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Hashing
From Forensics Wiki
Revision as of 00:47, 16 December 2007 by Simsong (Talk | contribs)
Jump to: navigation, search
Hashing is a method for reducing large inputs to a smaller fixed size output. When doing forensics, typically cryptographic hashing algorithms like MD5 and SHA-1 are used. These functions have a few properties useful to forensics. Other types of hashing, such as Context Triggered Piecewise Hashing can also be used.
Tools
There are literally hundreds of hashing programs out there, but a few related to forensics are:
Hash Databases
National Software Reference Library
The largest hash database
Hash Lookup Services
There are several online services that allow you to enter a hash code and find out what the preimage might have been. One way to find these services is to google for 'd41d8cd98f00b204e9800998ecf8427e' (the MD5 of the null string).
Here are some services that we have been able to find:
http://nz.md5.crysm.net/
MD5 reverse lookup, operated by Stephen D Cope. As of December 2007 this database had 28 million MD5 hashes. The author states that the database is divided into 256 MySQL tables to make the problem more tractable. The database claims to include every two, three, and four digit combination, all dictionary words, and a pile of user-submitted data." But the author also states that they are attempting to calculate and index all possible MD5 indexes. Of course, this is an impossibility.
http://us.md5.crysm.net/
Similar to the NZ server, but with only 16 million MD5 hashes.
http://md5.benramsey.com
A nice forward and reverse demonstration system, with an XML and AJAX interface.
http://www.hashcrack.com/
reverse hash lookup of MD5, SHA1, MySQL, NTLM, and Lanman hashes. Claims 75million hashes of 13.2 million unique words.
http://gdataonline.com/seekhash.php
MD5 reverse lookup with approximately 1 million entries.
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Navigation:
About forensicswiki.org:
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About this Journal Submit a Manuscript Table of Contents
Mediators of Inflammation
Volume 2012 (2012), Article ID 643609, 7 pages
doi:10.1155/2012/643609
Research Article
Differential Expression of Sphingosine-1-Phosphate Receptors in Abdominal Aortic Aneurysms
Division of Vascular Surgery, Department of Surgery, The University of Hong Kong, Hong Kong
Received 8 November 2011; Accepted 19 January 2012
Academic Editor: Aldo Pende
Copyright © 2012 Z. Qu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Objective. Inflammation plays a key role in the pathophysiology of abdominal aortic aneurysms (AAAs). Newly discovered Sphingosine-1-Phosphate Receptors (S1P receptors) are critical in modulating inflammatory response via prostaglandin production. The aim of the current study was to investigate the expression of different S1P receptors in AAAs and compared with normal aortas at the protein level. Materials and Methods. Aortic specimens were harvested during aortic reconstructive surgery for the AAA group or during organ transplant for the control group. The protein expression of S1P1, 2 and 3 in AAAs and normal aortas was assessed by Western blotting and immunohistochemical analysis. Results. There were 40 AAAs and 20 control aortas collected for the receptor analysis. For Western blot analysis, S1P1 expression was not detected in either group; S1P2 protein was constitutively detected in both types of aortas but its expression level was significantly decreased by 73% () in AAAs compared with the control group. In contrast, strong S1P3 expression was detected in AAAs aortas but not in normal aortas. Immumohistochemical staining showed similar results, except a weak S1P3 signal was detectable in normal aortas. Conclusions. Western blot and staining results consistently showed the down-regulation of the S1P2 protein with simultaneous up-regulation of the S1P3 protein in AAAs. Since those newly discovered receptors play an important role in the inflammatory cascade, the modulating of S1P signaling, particularly via S1P2 and S1P3, could represent novel therapeutic targets in future AAA treatments.
1. Introduction
Abdominal aortic aneurysm (AAA) is the localized dilation of the infrarenal aorta. If surgical treatment is not applicable, an AAA progresses to rupture with a high mortality rate and causes 1%–3% of elderly male deaths in developed countries each year [1]. Analysis of the aneurysmal wall has demonstrated that connective tissue degradation, increased atherosclerosis, and chronic inflammation are the common pathological features of AAAs [13].
Sphingosine-1-phosphate (S1P) is a newly discovered low-molecular-weight zwitterionic lysophospholipid molecule that is generated from the metabolism of sphingomyelin by a series of enzymes including sphingosine kinase, S1P phosphatase, and S1P lyase in mammals [4]. The main sources of S1P are platelet cells in plasma, while other cell types such as erythrocytes, neutrophils, and mononuclear cells can also produce and release S1P upon activation [4, 5]. S1P exerts a wide range of physiological activities, particularly inflammatory reactions through the interactions with five different receptor subtypes 1, 2, 3, 4, and 5. They are the members of the endothelial differentiation gene family of G protein-coupled receptors [4], and differential expressions of S1P receptors are thought to modulate the cellular inflammatory response [6]. A precise S1P/S1P receptor balance is found to be responsible for the signaling of cell growth and regulation of cell metabolism in mammal [7, 8]. An imbalance of this system also participates in pathologic conditions such as cancer and inflammatory diseases [9, 10]. S1P2 is the major expressed S1P receptor, while S1P1 or S1P3 is only weakly expressed in healthy vascular endothelial cells [11] and vascular smooth muscle cells (VSMCs) [12]. Consistently with this receptor multiplicity and pleiotropic signaling mechanisms, S1P receptors influence numerous cell functions. Particularly, differential expressions of S1P receptors have been demonstrated to either promote or inhibit the inflammatory infiltration in diverse cell types by inducing cyclooxygenase 2 (COX-2) expression [6] with subsequent prostaglandin E2 (PGE2) or prostacyclin (PGI2) production [1315]. Our previous study showed that inflammatory mediators such as Cox-2 and prostaglandin E2 are also widely expressed in AAA explants [16]. Those phenomena implicating S1P receptors may play some roles in the pathogenesis of AAA.
S1P1, S1P2, and S1P3 receptors are the major S1P receptor subtypes in the vascular system [11, 12]. However, the expressions of these three S1P receptors in AAA remain unknown. In the present study, we aimed to investigate the S1P1, 2 and 3 receptor protein expressions in AAAs and compare them with healthy aortas.
2. Materials and Methods
2.1. Human Abdominal Aorta Tissues Collection
Cross-sections of aneurysm wall, which were dissected of luminal thrombus, were removed from the AAA patients who underwent open surgical aneurysmal repair in a local hospital. Control aortic tissues were obtained from the corresponding location of healthy organ donors without known cardiovascular diseases and connective tissue disorders during the transplant operation. Aneurysmal patients with the Marfan syndrome and other connective tissue disorders were excluded from this study.
Each collected specimen was thoroughly washed with normal saline solution, and then the tunica intima elimination procedure was conducted using a scalpel and forceps. All specimens were divided into two parts for the western blotting which was kept in a −80°C freezer and immunohistochemical analysis, respectively.
All experiments were performed with the approval from the local institution’s ethics committee. Informed consent was obtained from AAA patients and organ donors’ relatives.
2.2. Western Blot Analysis
Frozen tissues were first thawed and then lysed with cell lysis buffer (Cell Signaling. Technology, Danvers, MA, USA) containing protease inhibitor (Roche, Basel, Switzerland). The protein concentration of each specimen was measured based on the Bradford method utilizing the Bio-Rad Protein Assay Kit (Bio-Rad Laboratories, Hercules, CA, USA) with bovine serum albumin (BSA) as the standard. After the protein denaturing procedure with loading buffer (pH 6.8 24 mM Tris-HCl, 684 mM glycerol, 14 mM SDS, 142 mM beta-mercaptoethanol, 0.3 mM bromophenol blue), each sample (50 μg) was resolved on 12% SDS-polyacrylamide gel electrophoresis (PAGE) gel (Bio-Rad Laboratories) at room temperature then transferred onto a polyvinylidene fluoride (PVDF) membrane (Bio-Rad Laboratories) at 4°C. After blocking in 10% TBS–0.01% Tween 20 (TBST) diluting nonfatty milk (Bio-Rad Laboratories) for two hours at room temperature, the membranes were then incubated overnight at 4°C with primary antibodies against S1P1 receptor (Catalogue no. sc-48356, dilution 1 : 100, Santa Cruz Biotechnology, Santa Cruz, CA, USA) or S1P2 receptor (Catalogue no. sc-25491, dilution 1 : 200, Santa Cruz Biotechnology) or S1P3 receptor (Catalogue no. sc-30024, dilution 1 : 100, Santa Cruz Biotechnology) with GAPDH (1 : 1000, Cell Signaling Technology) as the positive control. After membrane washing using TBST solution, HRP-conjugated goat anti-mouse (1 : 2000) or goat anti-rabbit (1 : 4000) secondary antibody (Dako, Glostrup, Denmark) was added and the membranes were then incubated for 1 hour at room temperature. After washing, signals were visualized by luminol reagents (Bio-Rad Laboratories) and the densitometry of each exposing blotting was analyzed by ImageJ 1.44 software (National Institutes of Health, Bethesda, MD, USA). The relative expression of the studied receptors’ protein was calculated by the detected signal divided by the internal positive control (GAPDH) expression signal in each sample.
2.3. Immunohistochemical Study
The staining procedure was performed on paraffin-embedded aortic tissue (5 μm) sections according to the manufacturer’s instructions (DakoCytomation EnVision + System-HRP (DAB) Kit (Dako)). Specificity of S1P receptor antibodies was firstly validated by positive and negative tests using healthy adult rat brain paraffin sections. Briefly, all sections were antigen retrieved with boiling sodium citrate buffer (pH 6) and incubated with either mouse anti-S1P1 receptor antibody (1 : 25), rabbit anti-S1P2 receptor antibody (1 : 100), or rabbit anti-S1P3 receptor antibody (1 : 100) (Santa Cruz Biotechnology) overnight at 4°C. After staining, all specimens were subjected to the dehydration procedure and sealed for microscopy observation.
To avoid staining underestimation due to considerable regional variations, 5 continuous × 200 microscopy views of each stained specimen, which had the largest amount of positive stained VSMCs, were captured and recorded (Nikon, Tokyo, Japan). Two researchers scored the positive immunostaining using the scoring system according to the Wang and colleagues study [17]. Briefly, a proportion subscore from 0 to 4 (i.e., 0—0% positive stained, 1—1%–25% positive stained, 2—26%–50% positive stained, 3—51%–75% positive stained, 4—76%–100% positive stained) and an intensity subscore from 0 to 3 (i.e., 0: no staining, 1: weak staining, 2: moderate staining, 3: intense staining) were first assigned by each observer for each slide. A weighted score was then determined by multiplying the proportion subscore and the intensity subscore. Finally, a mean value of the five weighted scores for each specimen was calculated.
2.4. Statistical Analysis
All data were expressed as means ± SD. Statistical analysis was performed by SPSS 18.0 software (SPSS, Chicago, IL, USA). Any statistical differences between the two groups’ experimental results were determined by independent sample -tests. Correction for ages and sex of patients on receptor expression levels were made using a linear model. A value < 0.05 was considered as statistically significant.
3. Results
3.1. Patient Characteristics
There were 40 AAA specimens and 20 control aortas obtained from the corresponding surgical patients and organ donors. Most of patients were male, and the control patients were younger than the AAA patients. Patient characteristics are listed in Table 1.
Table 1: Patient characteristics of AAA patients group and control group.
3.2. Western Blot Analysis
S1P1 receptor protein (38 kDa) was undetectable in both tissues (Figure 1(a)). For S1P2 receptor protein (45 kDa), positive signals were detected in both AAA and control aortic tissues, with AAA tissues had a significantly lower protein expression level compared with control aortas (Figure 1(b)). In contrast, S1P3 receptor protein (45 kDa) was highly expressed in AAA aortas but was undetectable in control aortas (Figure 1(c)).
Figure 1: Representative pictures of western blot analysis of S1P receptors in AAA and control aortic tissues. S1P1 expression was undetectable in both AAA and normal aortas, while it became detectable in rat brain tissues (a). Expression level of S1P2 protein was significantly decreased in AAAs compared with control aortas (b). S1P3 expression was detectable in AAAs only (c). GAPDH antibody was used as internal positive control in each WB experiment.
The relative intensities of S1P1 and 2 receptors expression by western blot analysis are shown in Figure 2 upper and lower panels, respectively. The protein level of S1P2 receptor was decreased by 73% () in the AAA tissues (mean relative intensity of 0.29) compared with the control aortic tissues (mean relative intensity of 1.08). S1PR3 protein levels were significantly upregulated in AAA tissues with average relative intensity of 0.65, whereas it was undetectable in normal aortas.
Figure 2: Quantitative analysis of S1P2 (upper panel) and 3 (lower panel) protein expression levels in western blot analysis. The relative S1P2 protein level was decreased by 73% () in AAAs (relative expression intensity of 0.29) compared with normal aortas (relative expression intensity of 1.08). S1PR3 protein levels were significantly upregulated in AAA tissues with average relative intensity of 0.65, whereas it was undetectable in normal aortas.
3.3. Immunohistochemical Staining Analysis
S1P1 receptor expression level was undetectable in both AAA (a) and normal aortas (b), as shown in Figure 3. A Positive control of S1P1 receptor was performed in healthy adult rat brain for validating its specificity (Figure 3(c)). S1P2 receptor protein was expressed in both types of aortas, with pronounced S1P2 receptor staining observed in control aortas (Figure 4). S1P3 receptor protein was found in the AAA tissues (Figure 5(a)), but it was almost undetectable in normal aortas (Figure 5(b)). The staining scores of both types of tissues sections are shown in Table 2.
Table 2: Staining scores of immunohistochemical analysis of S1P receptors in both types of tissues.
Figure 3: Representative staining pictures of S1P1 protein in AAA (a), control aortic (b) sections, and healthy adult rat brain paraffin sections (c) (×200). S1P1 protein was undetectable in both types of tissues.
Figure 4: Representative staining pictures of S1P2 in AAAs and control aortic sections (×200). S1P2 protein was more pronounced in the normal aortas (b) than that in the AAAs (a).
Figure 5: Representative staining pictures of S1P3 in AAA and control aortic sections (×200). More S1P3 protein was found in the AAA (a) than that in the normal aortas, in which it was almost undetectable.
Positive staining of S1P2 and S1P3 receptors in the aortic walls showed that they were localized in VSMC plasma membrane and cytoplasm but absent in the nucleus (Figures 4 and 5).
3.4. Correction for Ages and Sex
Giving the age and sex discrepancy existed in the patients, corrections for ages and sex of the receptor protein expressions was made. The association between S1P2 and S1P3 protein (both IHC and WB expression levels) in the patients were robust to correction in a linear model with age and sex ().
4. Discussion
Among the studied S1P receptors, only S1P2 and S1P3 receptor proteins were differentially expressed in AAA tissues compared with the control aortas, while S1P1 receptor protein was absent in both types of tissues. Differential S1P receptors expressions have been shown to participate in diverse physiological processes, such as cell survival and apoptosis [18], and pathological processes, such as angiogenesis, inflammation, cancerogenesis, and immune regulation [9]. Inflammation is one of the common pathological features of AAAs [3]. Thus, the present novel findings may implicate the importance of these receptors in the inflammation attribute to AAA pathogenesis. Nevertheless, atherosclerosis is indeed regarded as a chronic inflammatory disease with atherosclerotic plaques containing inflammatory infiltrates, which implicated in the formation of AAA [19]. Thus, the possibility of S1P receptor expression related to the atherosclerotic event cannot be excluded.
S1P1 receptor is undetectable in both types of aortic tissues. Other researchers found that only some specific cell types, such as endothelial cells, cardiomyocytes, neural stem cells, as well as B cells, and T cells, express marked S1P1 [4]. Healthy rat adults’ VSMCs express S1P1 receptor weakly [20], and the deletion of S1P1 receptor is embryonically lethal since it causes the failure of dorsal migration of VSMCs to form the tunica media layer of arteries [21], suggesting that S1P1 receptor should be critical in vascular development rather than in maintaining VSMCs metabolism [21]. A more recent study suggested that S1P1 is involved in the phenotype regulation of adult smooth muscle cells [22]. They utilized a rat carotid artery balloon injury model and demonstrated that there was a transient over expression and activation of S1P1 receptor after injury. This action can facilitate VSMCs transfer into the proliferative and migratory phenotype. However, such S1P1 receptor over expression will be restored to the basal value by 7 days after injury, suggesting that this irritable S1P1 receptor activation may be a short-term injury response. Thus, we postulated that the S1P1 receptor protein may be transiently increased during early AAA lesion, but its high expression will subsequently return to the basal level or become undetectable at the advanced stage of AAA development. In addition, S1P1 receptor is possibly responsible for the development of circulation system and expressed in the endothelial cells, rather than expressed in smooth muscle cells in mature aortas [21] which may explain for absent of S1P1 levels in the late stages of aneurysm.
S1P2 receptor protein was detected in both types of aortic tissues, particularly in control aortas. Indeed, S1P2 receptor has been previously shown to be the major S1P receptor expressing population in a wide variety of tissues in humans, like vascular endothelial [11] and smooth muscle cells [12], but not in inflammatory infiltrates [9]. This particular receptor can facilitate VSMCs’ contractile phenotype expressions and negatively regulate their proliferation and migration [22]. Moreover, S1P2 receptor is capable of inducing Cox-2 expression and producing prostacyclin (PGI2) in response to exogenous S1P stimulus [15, 23, 24]. PGI2 possesses anti-inflammatory functions and simultaneously relaxes VSMCs and suppresses their proliferation and migration [25]. Thus, the decreased expression of anti-inflammatory S1P2 receptor in VSMCs of AAAs, and probably not expressed in the inflammatory infiltrates, may impair the production of PGI2 and ultimately lead to the pronounced inflammation response in AAA patients [16]. Therefore, the S1P2 receptor downregulation of VSMCs is obviously an important etiological factor in AAA development.
Markedly S1P3 receptor protein was found in AAA tissues. S1P3 receptor possesses a promoting inflammatory response property as it can induce Cox-2 expression and concomitant PGE2 production in various cell types [13, 14, 26, 27]. As a pronounced inflammatory infiltrate, PGE2 was also found in AAA explants in our laboratory previously [28] though the extent of its involvement in vascular inflammation is still unclear. In addition, a very recent study suggested that S1P3 mediates the chemotactic effect of its ligand-S1P in macrophages in vitro and in vivo, which plays a crucial role in atherosclerosis by promoting inflammatory monocyte/macrophage recruitment and altering smooth muscle cell behavior [29]. We suggested that the S1P3 receptor protein may be critical in the strengthened inflammatory response and thus atheroslcerosis via the chemotactic property and the PGE2 pathway during AAA development. However, the causal relationship between the inflammatory cells recruitment and the prostaglandins needed to be further explored.
In the present study, a weak S1P3 staining signal was found in normal aortas, though it became undetectable using western blot analysis. This staining result was consistent with Ryu et al. study that S1P3 is found to be weakly expressed in human healthy VSMCs [12].
Though age and sex discrepancy existed in the studied patients, the present analysis found that the expression of the S1P2 and 3 receptor proteins are not age and sex dependent. Thus, the up- or downregulated receptor probably related to the inflammatory cascade underlying the AAA pathogenesis but is not simply a feature of aging or sex difference.
The limitation of the present study is only an observational analysis on surgical aneurysmal aortas. Thus, we cannot extrapolate the observations to the initiation or promotion of aneurysm formation. Nevertheless, the present work has provided evidence that aneurysmal aortic tissue exhibits a decreased activity of S1P2 and enhanced S1P3 receptor, which may contribute to the inflammation of aortic walls involved in AAA pathology.
Our findings of the differential expression of S1P receptors in AAA compared with normal aortas are novel and may be helpful to delineate the important inflammatory mechanisms in AAA development. This investigation has provided a new concept in the inflammatory response in the lesions, and the regulation of S1P receptor via S1P2 and S1P3 may open a new regime for AAA treatment in the future.
Acknowledgment
Thanks are due to Dr. Vincent Lui for his generously advice on the protein expression experiment.
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27. K. Masuko, M. Murata, H. Nakamura, K. Yudoh, K. Nishioka, and T. Kato, “Sphingosine-1-phosphate attenuates proteoglycan aggrecan expression via production of prostaglandin E2 from human articular chondrocytes,” BMC Musculoskeletal Disorders, vol. 8, article no. 29, 2007. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
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29. P. Keul, S. Lucke, K. von Wnuck Lipinski et al., “Sphingosine-1-phosphate receptor 3 promotes recruitment of monocyte/macrophages in inflammation and atherosclerosis,” Circulation Research, vol. 108, no. 3, pp. 314–323, 2011. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
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Bibliography: Introduction (Miss Atomos)
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Title: Introduction (Miss Atomos)
Author: Jean-Marc Lofficier
Year: 2011
Type: ESSAY
Language: English
ISFDB Record Number: 1378520
User Rating: This title has fewer than 5 votes. VOTE
Current Tags: None Add Tags
Variant Titles:
Publications:
Copyright (c) 1995-2011 Al von Ruff.
ISFDB Engine - Version 4.00 (04/24/06)
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× You must be logged in to change this data. If you don't have an account, Please join.
Settings : Code Locations
Analyzed 6 days ago based on code collected 6 days ago.
Showing page 1 of 1
Repository URL SCM Type Update Status Ignored Files
http://git.etc.gen.nz/app-bcvi-autoinstall.git master Git Ohloh update completed 6 days ago. All files included.
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Copyright © 2013 Black Duck Software, Inc. and its contributors, Some Rights Reserved. Unless otherwise marked, this work is licensed under a Creative Commons Attribution 3.0 Unported License . Ohloh ® and the Ohloh logo are trademarks of Black Duck Software, Inc. in the United States and/or other jurisdictions. All other trademarks are the property of their respective holders.
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Low Activity
Estimated Cost
Analyzed 1 day ago based on code collected 1 day ago.
Project Cost Calculator
$ .00
6,491 lines
1 person-years
$ 76,499 *
*Using the Basic COCOMO Model
Estimate seems way too high?
Ohloh scans all files at any given code location to calculate the cost estimate.
Ohloh lets you exclude files and direc-tories from this calculation on the Code Locations page. You can get a more realistic estimate by excluding:
• External dependencies or libraries
• Non-code files
About Cost Estimates
• Software cost estimation is tricky business even when all the variables are known -- knowlegdge which we certainly don't have.
• We calculate the estimated cost of the project using the Basic COCOMO model.
• For those familiar with the details, we are using coeffcients a=2.4 and b=1.05.
• Please note that COCOMO was created to model large institutional projects, which often don't compare well with distributed open-source projects.
• COCOMO is meant to include the design, specification drafting, reviewing and management overhead that goes along with producing quality software.
• This model seems to be most accurate with mature, large projects. Young projects with little activity are typically overvalued.
Copyright © 2013 Black Duck Software, Inc. and its contributors, Some Rights Reserved. Unless otherwise marked, this work is licensed under a Creative Commons Attribution 3.0 Unported License . Ohloh ® and the Ohloh logo are trademarks of Black Duck Software, Inc. in the United States and/or other jurisdictions. All other trademarks are the property of their respective holders.
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Very High Activity
Contributors : Ævar Arnfjörð Bjarmason
Analyzed about 3 hours ago based on code collected about 3 hours ago.
Recent Kudos...
... for MediaWiki given by:
Antoine Musso
Siebrand Mazeland
xantus
Project Commits
Ohloh did not measure any commits by this contributor.
Project Languages
Ohloh did not measure any lines of code written by this contributor.
Copyright © 2013 Black Duck Software, Inc. and its contributors, Some Rights Reserved. Unless otherwise marked, this work is licensed under a Creative Commons Attribution 3.0 Unported License . Ohloh ® and the Ohloh logo are trademarks of Black Duck Software, Inc. in the United States and/or other jurisdictions. All other trademarks are the property of their respective holders.
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"url": "www.ow2.org/view/Events/ICARSummerSchoolNiceFrance",
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ICAR Summer School, Nice, France
ICAR Summer School
(Intergiciels et Construction d'Applications Réparties)
25-29 August 2008
Nice, France
This training program offers to participants a consistent and up-to-date vision of the technologies in the field of distributed applications. The program includes lectures about up-to-date technologies (including JavaEE, CCM, Web Services,OSGi, .Net) See detailed program at http://rainbow.essi.fr/icar08/pages/programmepag.html
OW2 will be a partner of the event.
Read more at : http://rainbow.essi.fr/icar08/pages/accueilpag.html
Venue :
Maison des séminaires
29, boulevard Franck Pilatte
06300 Nice
Tél 04.93.89.39.57
Fax 04.93.26.79.99
Contact : Michel Riveill - riveill@unice.fr
Created by Catherine Nuel on 2008/07/04 14:15
Legal Notice
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}
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CMD sent two reporters to track ALEC in Oklahoma
Click here to help support our future investigations.
Shimon Peres
From SourceWatch
Jump to: navigation, search
Shimon Peres (Labour), "Minister of Foreign Affairs, was born in Poland in 1923 and immigrated with his family as a child. He studied at the Ben Shemen Agricultural School, and was one of the founders of Kibbutz Alumot in the Jordan Valley. In 1943, he was elected secretary of the Hano'ar Ha'oved youth.
"In Israel's War of Independence, Mr. Peres was responsible for arms purchases and recruitment, and in 1948 was appointed head of the naval services. In 1949, he headed the Defense Ministry's procurement delegation to the United States.
"Mr. Peres was appointed Deputy Director-General of the Ministry of Defense in 1952 and served as its Director-General between 1953-1959.
"Mr. Peres has been a Member of the Knesset since 1959 and served as Deputy Minister of Defense from 1959-1965. In 1965, he left the Mapai Labour Party with Ben-Gurion and became Secretary-General of Rafi. In 1968, he was instrumental in bringing Rafi back to Mapai to form the Israel Labour Party.
"Mr. Peres became Minister of Immigrant Absorption in 1969 and served as Minister of Transport and Communications from 1970-1974. In 1974 he was appointed Minister of Information and later, Minister of Defense (1974-1977). The highlight of his tenure as Defense Minister was the Entebbe rescue operation.
"In 1977, Mr. Peres was elected chairman of the Labour Alignment. In 1984, a National Unity Government was formed, and he served first as its Prime Minister (1984-1986), and then as Vice Premier and Minister of Foreign Affairs (1986-1988). During his term as Prime Minister, Israel withdrew from Lebanon and an economic stabilization plan was implemented.
"In 1978, Mr. Peres was elected Vice-President of the Socialist International.
"In the National Unity government (1988-1990), Shimon Peres served as Vice Premier and Minister of Finance. From 1990-1992, he led the opposition in the Knesset.
"Mr. Peres began his second tenure as Israel's Minister of Foreign Affairs on July 13, 1992 with the establishment of the new, Labour-led government.
"Shimon Peres has authoured the following books: The Next Step (1965); David's Sling (1970); And Now Tomorrow (1978); From These Men (1979):;Entebbe Diary (1991); The New Middle East (1993); Battling for Peace (1995). He has written hundreds of articles and essays." [1]
Resources and articles
Related Sourcewatch articles
References
1. Shimon Peres, Nobel Peace Prize, accessed December 23, 2008.
2. 2009 Annual Report, International Crisis Group, accessed April 20, 2009.
3. Committees, Forum 2000 Foundation, accessed January 2, 2009.
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}
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Person:Francis Willis (4)
Watchers
Browse
Francis Willis
Facts and Events
Name Francis Willis
Gender Male
Birth? c1660 Kent, England
This page is a stub, being used to capture information about a particular subject, in preparation for development of a formal article. Please note that some of the data, perhaps much of, or even all of the data, presented here is derived from secondary and tertiary sources. The intent is to eventually tie everything to an "original" or primary source, or at least to something that can be accepted as a surrogate for such a source. See Category:Stub Warnings For Southwest Virginia Project for a list of articles with stub warnings.
___________________________________________________________
Quick Summary
Francis Willis IV, son of Henry Willis, and nephew of Francis Willis III inherited the Gloucester County estate of his uncle Francis known as "White Hall". Francis is said to have married a Lewis, but documentation for this is limited. The couple had two sons,lish the town of Fredericksburg, Virginia.
Notes
FRANCIS WILLIS (ca.1666-1719)
Born ca. 1666, England; died 1719, Gloucester Co., VA; son of Henry Willis (1630 - bef 1689). Married: ca. 1686??, Sarah Lewis??
Children:
• 1. Francis Willis, born ca. 1689, Gloucester Co., VA; died 1769, Gloucester Co., VA.;Married: 1) Lady Anne Rich; 2) Elizabeth Smith Harrison
• 2. Henry (Harry) Willis, born 1691, Gloucester Co., VA; died 1740, Fredericksburg, Spotsylvania Co., VA Married: 1) Anne Alexander Smith; 2) Mildred Howell Lewis Brown; 3) Mildred Warner Washington Gregory
Gloucester County Willis Male lines
Image Gallery
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{
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Surname:Singh
Watchers
the text in this section is copied from an article in Wikipedia
Singh is a common title, middle name, or surname used in South Asia, mainly in India, Nepal, Sri Lanka and Bangladesh, used originally by the Hindu Kshatriyas (warriors and kings). It is derived from the Sanskrit word सिंह Sinha meaning Lion. Apart from Rajput clans, it is also used by Sikhs, Marathas, Sinhalese people of Sri Lanka and Newa people of Nepal.
By the sixteenth century, "Singh" had become a popular surname among the Rajput warriors. It was adopted into Sikhism in 1699 as per the instructions of Guru Gobind Singh; the use of Singh as a last name is mandatory for all baptized male Sikhs since 1699, regardless of their geographical or cultural binding. Some Brahmins like Bhumihar Brahmins (see Kingdom of Kashi and Royal House of Benares) and Maithil Brahmins (see History of Mithila) also use this surname. The general editor of the book "People of India (Bihar and Jharkhand)", published by Anthropological Survey of India (ASI), and noted academician-bureaucrat, the late Kumar Suresh Singh, said that the surname "Singh", which used to denote connection with power and authority, was used in Bihar by Brahmin zamindars, like the surname "Khan" in Muslims. "Singh" has gradually emerged as a hereditary title to be used as a middle name, highlighting connections to a warrior status or occupation. The surname has also been widely adopted by other groups of India like Yadavs and Jats. However, this is not an exclusive usage, and many Hindu groups including Scheduled Castes and Vaishya have adopted this title without any significant warrior status or ties.
Sources
Manual translation of Wikipedia sources into WeRelate sources
This page uses content from the English Wikipedia. The original content was at Singh. The list of authors can be seen in the page history. As with WeRelate, the content of Wikipedia is available under the Creative Commons Attribution/Share-Alike License.
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HRM Practices and Organizational Performance: An Empirical Analysis
Kodjo Ezane Joseph, Changjun Dai
Abstract
We theorize about the assessment of HRM practices on perceptions of firm performance through Monte Carlo Method
(MCM), and the Hausman’s Specification Test (HST) in the Ivorian framework. 320 enterprises were surveyed and
factor analysis of 13 bundles of HRM practices was undertaken. The confirmation of the findings through simulation
(MCM) permitted the examiner to authenticate the reliability of the results in using the HST. The results of this paper
highlight that in the Ivorian context there are significant connections between HRM practices and firm performance;
that the strategic alignment of HRM is also a driver for firm performance.
Full Text: Untitled () PDF
This work is licensed under a Creative Commons Attribution 3.0 License.
International Journal of Business and Management ISSN 1833-3850 (Print) ISSN 1833-8119 (Online)
Copyright © Canadian Center of Science and Education
To make sure that you can receive messages from us, please add the 'ccsenet.org' domain to your e-mail 'safe list'. If you do not receive e-mail in your 'inbox', check your 'bulk mail' or 'junk mail' folders.
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Mobile Phones
Info
Search:
Differences:
version 101 (2012-08-18 01:24:04 by liweifr)
←previous edit
version 102 (2012-08-18 09:36:16 by TomGarberson)
next edit→
Deletions are marked like this. Additions are marked like this.
Line 27: Line 27:
[http://www.repairpartstock.com/products-big-list.asp?id=577 cell phone parts]
Line 163: Line 163:
*["Pocket Unitrans"] [http://www.repairpartstock.com/products-small-list.asp?id=508 ps3 parts] - Local bus route info *["Pocket Unitrans"] - Local bus route info
1. Mobile Phone Recycling
2. Coverage
3. Service Providers
1. Pre-Paid Providers
2. Retailers
4. Repair
5. Smartphone Apps
1. iOS (iPhone and iPad)
Mobile phones are nearly ubiquitous, either carried on most people's person as they move about Davis, or stuck to the ear of an oblivious pedestrian walking into traffic. Coverage and local availability in Davis has shifted and changed over the years. See below for tips on what current coverage is like.
Many cell phones, such as Apple's iPhone, offer internet access via WiFi access points. On campus, this allows you to browse the web and check e-mail rapidly, without needing a laptop or going to a computer lab. You have two choices for access: Moobilenet, and Moobilenetx. Moobilenet requires authentication every time you connect to it. On a handheld wireless device, this means that you may need to reauthenticate quite frequently, since your device will probably go to sleep and give up its connection while you are not using it. Moobilenetx allows you to store a username and password, and is also much more secure. Because your device can send the correct authentication information, connecting to Moobilenetx is a much better choice, if your handheld supports it. The iPhone will connect automatically after you set up Moobilenetx for the first time.
On July 1, 2008, Senate Bill 33 became law prohibiting all drivers under 18 years of age from using a cell phone or portable electronic device in any way (i.e. calling using an MP3 player or a laptop) while driving. A separate law making it illegal for anyone to drive a motor vehicle while using a cell phone without a hands-free capabilities went into effect on the same day. CHP says that they expect to only enforce the law as part of a pull-over, and not a reason to pull someone over. As of January 1, 2009 it will be illegal to text while driving.
In 2010, 11th District state Senator Joe Simitian sponsored the first bill to make it illegal to talk or text on a cell phone while bicycling.
Telemarketing to cell phone numbers has always been illegal in most cases and will continue to be so (link).
Mobile Phone Recycling
Some e-waste information:
In 2005 SB 20 (Sher, 2003) Electronic Waste Recycling Act was signed into law, ensuring consumers cost-free recycling of cell phones at all retailers and making improper disposal illegal. Check out the California Aggie article and campus Multi-bin locations.
Charitable Recycling of Cell Phones, Environmentally Friendly and Socially Conscious:
http://www.charitablerecycling.com/CR/home.asp
http://www.collectivegood.com/donate_phone_redjellyfish.asp
Coverage
Cellular coverage within Davis varies considerably, especially indoors. If you're looking for a new phone or service, try and find someone who already has it or take advantage of the 14-30 day trial period to make sure it will work where you want. If you're curious where the towers are located, you can see them on the City of Davis' Telecomm Site guide.
Verizon: Signal is poor to non-existent in northwest Davis. Signal is poor around campus and A street.
AT&T: Signal is (usually) very good in northwest Davis. Signal is poor on campus, although there are a few spots (mainly towards the tops of buildings) where it is reasonable. Signal is moderate downtown.
The newest GSM frequency is 850 so if you are using an older T-mobile/Cingular phone they won't be able to pick up the new signal. This is why some phones work better than others in certain areas. When purchasing a new phone make sure to pick up a quad band, for continous coverage in America and abroad.
In Kemper Hall, you can pick up a very strong AT&T signal, but not be able to make a call at all! There is supposedly a microcell or picocell installed in the basement of Kemper, which is the source of the signal.
To post and read information about cellphone reception in Davis, search for "95616" on Deadcellzones.com. It might also be useful if someone wanted to summarize postings here.
see also Improve Campus Cell Coverage
Service Providers
Lots of people moving to Davis for the first time want to know the track records of various cellular providers, and how good their service is in Davis. Please comment on your experiences.
Cingular(Now AT&T) and T-Mobile share 1900MHz GSM towers in California. Cingular(Now AT&T) also has its own 850MHz GSM towers in the area.
Pre-Paid Providers
Retailers
When shopping for a new phone and/or service, the magic number is $39.99. If you get a plan at this monthly rate or higher, the dealer gets a much larger commission than for lower plans. Thus, they will offer lower prices and/or larger rebates. Keep in mind that in addition to the above mentioned retailers, many phones/plans can also be purchased at stores like Safeway, 7-Eleven and other non-phone specific locations.
Note that there may be an activation fee for new accounts. Also, the monthly rate does not include fees and taxes, which may be anywhere from $3/month to over $10/month.
Note also that, contrary to prior belief, most pay as you go plans are now much less costly than contracted plans at all dealers.
Repair
Smartphone Apps
Since the debut of the iOS and Android operating systems, there has been a growing number of applications to help in just about any task you can imagine. There are now several Davis-centric apps available. Perhaps we will someday see a DavisWiki app?
iOS (iPhone and iPad)
For more information on telephones in Davis generally, see Telephones.
Comments:
Note: You must be logged in to add comments
2005-01-03 20:41:07 My phone switches between cingular and AT&T. Even though the two carriers share towers, i tend to get different reception depending on which carrier my phone selects. However, I tend to get coverage everywhere in Davis. The weakest coverage is around campus, but is not terrible. —JaimeRaba
2005-01-03 21:02:22 In north-east Davis (north of Covell), indoor reception is pretty poor with T-Mobile and Cingular. I can get a strong signal outside but it drops to 0 once I step a few feet away from any windows. Maybe my walls are lined with lead or something. —AndrewChen
2005-01-04 00:43:02 I used to have horrible coverage (AT&T) in north davis, but since they combined with cingular, I get good to great coverage all over davis —PaulLanzi
2005-01-05 14:29:16 I use cingular, and don't get reception in some places in Kemper Hall, and inside other large buildings like the MUKenBloom
2005-03-05 11:26:10 If you have free roaming and a phone that is not locked to a particular network, GSM is the way to go. So that means AT&T or Cingular (basically the same now) or T-Mobile. —JaimeRaba
2005-10-05 22:38:17 I have cingular, but my reception is really crappy around campus (no bars at all in many places) and at my house (along 8th street). I DO have a really cheapy flip phone...does anyone know whether the quality of the phone makes a difference? —YumikoHenneberry
2005-10-08 13:53:15 I have a pretty good Verizon plan, but I get poor reception around campus. Outside reception is 2-3 bars give or take. Indoors you might get lucky and get 1 bar, but don't count on it. Other people in my building have Sprint and they get much better reception. —RyanCoates
2005-11-06 10:06:13 I hate this to sound like a plug, but I never have bad reception with my cheapie Siemens phone on T-Mobile and I always hear of people complaining with the other carriers. I recommend T-Mobile. —SteveDavison
2006-01-14 21:48:36 I live near the high school, have Verizon and lousy reception. We're changing to Cingular but having both services for a month just in case. I got Verizon to waive my early cancellation fees by asking to speak to your supervisor 3 times. But they won't port my numbers. They "own" them. Its a catch 22 with the early cancellation concession. Would like to know if there is Nextel coverage in Davis. —BarbaraClowers
2006-01-14 21:50:34 There is Nextel coverage in town. Fairly good on campus and around town. —JasonAller
2006-05-15 14:25:41 I'm in the Tercero dorms and I have T-mobile. I always have service outside (1-3 bars) but I might lose it inside (usually it's 1 bar max). Whenever I speak to my parents, they complain about a "wooshing" sound that I can't hear, but I'm not sure if that's my phone or my phone service. I have one of those free phones they give you when you sign up. Bleah, but it's my first cellphone and I didn't want to waste money in case I had to cancel. T-mobile is okay... I think I'll try Metro PCS next year, though. My dad has that... —NumiaCairaguas
2006-05-15 15:00:38 If you have a Motorola go to settings>>Network>>>network set up and set the band to 1900/850, search to manual and search speed to continuous that will help..... —JonathanNasca
2006-08-02 00:35:13 I lived in Alder Hall and I have t-mobile. Worked great! I had full reception in the dorm halls. No reception in lecture halls though. —WaylandLee
2006-09-01 18:19:19 I have sprint/nextel and the coverage is very good. My boyfriend just got a cingular razor phone and seems to have good reception too. So far I've had good reception with Sprint most places I need it (the Bay Area), so I would recommend them, except they just cut their minutes so now I'm looking around. I used to have at&t back when the network sucked. How is it now? —GreenThing
2006-10-29 21:35:28 I live at Fountain circle and I get horrible reception with T-Mobile. I'l have 1-2 bars, then itll drop to 0 or even die on me. :/ Cingular has pretty good reception up here though. —WaylandLee
2007-05-28 14:52:20 in my opinion, t-mobile has the worst service for on-campus usage other then that, t-mobile is really great around davis —DonaldJaye
2007-09-08 08:40:19 I totally agree with the above user, I barely get service in Tercero and Olson, and in no other campus buildings, but in the U Mall I get five bars. I've been all over Davis with excellent reception. A note about campus usage though, usually once you step well outside whatever building you were in, service will return. —KellyCorcoran
2008-03-12 20:07:30 I have AT&T and live near Pole Line & Covell...not sure what changed in the last couple of months, but cell reception at my place went from 1-3 bars, to 4-5 bars on my phone. —DukeMcAdow
2008-05-01 12:14:45 T-Mobile Update for on Campus reception: T-Mobile has a new tower in the center of UC Davis Campus scheduled to go on September 1st. This will help T-Mobile become one of the best options for reception throughout Davis. Please let us know if when you see a drastic improvement on campus. Go here for a picture: http://www.facebook.com/photo.php?pid=448840&id=5671963257Aaron.Vorbau
2008-06-18 21:40:50 T-Mobile on G Street was most accomodating to a particular problem I had. I want to give kudos to their employees and manager. —bar775 (This review is the only edit this user account has made on the wiki. While it does not invalidate this review, please keep this in mind)
2008-06-26 12:45:59 Around 8th & J (College Square Apartments), Sprint has some pretty spotty coverage. I am unable to place or receive cell phone calls unless I am roaming :( —BrandonMinow
2008-10-06 07:59:57 Where is That new tower in ucd? another scam?I just wait till end of october and then change it to AT&T —Frederick
2008-10-09 17:19:09 In the past several months Verizon service has gotten much worse in north Davis, to the point that I can't even make a call from inside my house. There is a huge area around Drake Dr/Sycamore/Alvarado which is pretty much dead. Is AT&T any better in north Davis? —twblalock
2008-12-08 18:15:49 I live in the Tercero buildings and all of a sudden about 3 days ago, many students that have t-mobile have been getting service everywhere from wellman underground floor to the social science humanities room 1100 where hardly anyone gets reception. so I'm pretty happy with t-mobile right now. —rmsanchez
2009-04-18 17:07:15 I use Virgin Mobile and I have never been disappointed. This service doesn't have any contracts and you can change your plan every month. It is a prepaid service and you can recharge with top up cards from [[Radio Shack]] or through their website. This helps me a lot since I can switch plans. When I will be working in the summer, I will have a desk phone in my office and I don't require a lot of minutes. Also, their website has a feature called SugarMama through which you can watch ads and earn airtime. I live in East Davis and the quality of their network (Sprint) network is excellent. Phones can be bought from as less as $30 from either Radio Shack or Wal-Mart. —Praveen
2009-06-09 22:43:36 metropcs sucks if you enter a building, or your own apartment for that matter. It is suppose to have good service in Davis, but I guess they omitted the part about zero service inside your own room! —blastoff
2009-11-03 15:37:20 T-Mobile seems to be at least partially broke today. My wife and I get "number not in service" if we call each other on our cell phones, but we can still call to landline numbers. Get some sort of "not available" message if I call 611. Very strange. —JimStewart
2010-02-12 22:37:37 I have Verizon Wireless and it costs a TON and I don't even have all the features (the only real feature I have is unlimited Text and Image transfer). A friend of mine got Sprint (he doesn't live in the area) with a decent phone and got everything for about what I pay. If I wanted to get everything he got for Verizon then I'd have to pay like $30 more than what I'm already paying. Does anyone know if Sprint works well in Davis and specifically in central Davis around Covell? Any current info? BTW, Verizon coverage seems to be pretty good everywhere I've been in Davis. —davisRez
2010-10-04 15:43:08 Mobile Connections has never closed and definitely still exists. We now only carry T-Mobile pre-paid and MetroPCS pre-paid service. We also carry chargers, cases, bluetooth headsets, and other cellphone accessories. —MobileConnections
2011-10-01 22:14:31 Cell phones are absolutely worthless if people don't use them for at least two damn seconds to send response texts once in a damn while. —Wes-P
This is a Wiki Spot wiki. Wiki Spot is a 501(c)3 non-profit organization that helps communities collaborate via wikis.
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Error!
Success!
Content Manager and Editor
0
kicks
Content Manager and Editor (Unpublished)
Tonight I am introducing a new application I have been working on for just a few days called "Content Manager by Focused Games" or FGCM for short. The main goal of the Content Manager is to bring realization to my goal for the website.
Kicked By:
Drop Kicked By:
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Cortex
From eLinux.org
Revision as of 18:51, 10 February 2008 by Glenn (Talk | contribs)
Jump to: navigation, search
The ARM Cortex family comprises three series, which all implement the Thumb-2 instruction set to address the increasing performance and cost demands of various markets:
• ARM Cortex-A Series, applications processors for complex OS and user applications.Supports the ARM, Thumb and Thumb-2 instruction sets
• ARM Cortex-R Series, embedded processors for real-time systems. Supports the ARM, Thumb, and Thumb-2 instruction sets
• ARM Cortex-M Series, deeply embedded processors optimized for cost sensitive applications. Supports the Thumb-2 instruction set only
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Fairview Pennsylvania Family History CenterEdit This Page
From FamilySearch Wiki
This article describes the services and resources available at a Family History Center, a branch facility of the Family History Library.
(Add a brief paragraph about your center here and the area it serves. Information in italics below is guidance for you and should be deleted as you fill out the page. Remove italics from other text by selecting the text and clicking the "I" box in the Toolbar above.)
Contents
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Holiday Schedule:
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Upcoming Events
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Center Resources
Collections
• Family History Library Catalog: This center has the ability to order any of the films and fiche available through the Family History Library Catalog.
• (List additional collections you have such as the types of books and microfilm you have on indefinite loan; though you will not want to list every single item you have. Just give visitors to this page a general idea of your resources.)
Databases and Software
• FHC Portal This center has access to the Family History Center Portal page which gives free access in the center to premium family history software and websites that generally charge for subscriptions. (Note to FHC: Not all FHCs have access to this portal. If you do not, you will want to remove this entire bullet. If you do have access to it, just remove this text in italics.)
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Lawyers in England and WalesEdit This Page
From FamilySearch Wiki
Justice, finial figure of the Old Bailey
Contents
History of Profession
From early times, the legal profession in England and Wales has been divided into two groups, barristers and solicitors, the latter usually being called attorneys until 1875. A solicitor cannot be a barrister and speak at the bar, and a barrister cannot be enrolled as a solicitor.
Professional pleaders, who were laymen and not ordained clerics, appear in the King's court in the 13th century and by the end of that century the judges were being appointed from amongst their number. Schools of English common lawyers (as opposed to clerics schooled in canon law) quickly arose in London and were the first in England where men could study for a profession without the necessity of being ordained. In the 14th century these schools developed into four Inns of Court that flourished from the 15th century.
In the reign of Elizabeth I these Inns, the Inner and Middle Temple, Lincoln's Inn and Gray's Inn, all on the Westminster side of London, attained their zenith. Anthony Wagner says they "became in effect the third university of England, to which the nobility and gentry sent their sons to acquire knowledge of the world and of a subject then as useful as any for the management of property and the pursuit of worldly and political ambitions". In fact, as time passed, the majority of students went to Oxford or Cambridge before entering an Inn.
The number of those who qualified at the Inns of Court and were "called to the bar" grew by about 40% between the 1590s and the 1630s. By 1689 there were perhaps 3,000 barristers in England with more than twice as many attorneys. Students for the bar had to keep a certain number of terms at their Inn before being called, a public examination being introduced only in 1853.
Throughout the 16th and 17th centuries and into the 18th century successful lawyers formed a large proportion of the "new" men who entered county society by purchasing land and building manor houses. Their fortunes came from fees and perquisites of the legal and other offices to which they were appointed and it was not until after 1660 that fortunes were made from legal expertise alone. Many, but by no means all, had gentry backgrounds.
Affiliated to the Inns of Court were seven Inns of Chancery that acted as preparatory colleges for younger students. Staple Inn and Barnard's Inn were affiliated to Gray's Inn, Clifford's and Clement's Inn to the Inner temple, New Inn to the Middle Temple, and Thavie's and Furnival's Inns to Lincoln' Inn. Many of the students of these Inns proceeded to the appropriate Inn of Court, but others, without further study, became either solicitors acting for litigants in the Court of Chancery, attorneys acting for litigants in the common law courts, or proctors acting in the church or admiralty courts where Roman law was practised.
Although the more reputable attorneys were beginning to be recognised as gentlemen in the late 15th century, they were in general of less social standing than the barristers who regarded them as inferior. From the 16th century the barristers began to exclude attorneys from the Inns of Court (a process completed in the 17th century), thereby further depressing their status. Thus it was that the remainder of the legal profession developed outside the self-governing guild-like organisation that the barristers attained through their Inns. The Inns of Chancery suffered a long decline and the last was closed in 1900.
Outside London, attorneys were found only in the main towns in each county, particularly those where the assizes and quarter sessions were held. Without traditional guilds, apprenticeship became the only means of entry into the occupation. Giving advice but not selling any product or possessing manual skills, they were perhaps the most genteel of all those who learned their occupation in this way. They paid the highest premiums, nearly always for only a five-year term. In the first half of the 18th century the average fee was £100 or 100 guineas (£105) and this was paid in about a third of cases. The highest premium paid in Wiltshire was £262 10s 0d to an attorney in Devizes but much higher fees could be obtained in London where three Sussex boys were apprenticed for 300 guineas each. They included Bysshe Shelley, the poet's grandfather, who, in 1748, paid an extra £30 for better food. In 1721 an attorney in the Exchange Office in the City of London obtained £450 with an apprentice from Putney. These apprentices were nearly always the younger sons of minor gentry, of clergy and of widows. They were often sent far from home, many to London where the largest fees might eventually be earned.
Attorneys in practice, as they grew more prosperous, might take, over a period of time, several apprentices. Parents looking for suitable masters were advised to consider only those of known integrity with sufficient business. In the provinces a strong family thread ran through many law firms, It was a widespread belief in the first half of the litigious 18th century, when the number of apprentice attorneys doubled, that attorneys were too numerous and easily became dishonest.
David Hey says that in no other professions in late 17th and early 18th century Britain did so many men make so much money, or make it so quickly, as in the law, drafting wills, drawing up deeds and settlements, arranging mortgages and loans, and acting as stewards, estate managers and rent collectors.
The 18th century saw an expansion in legal work in country towns as a result of Poor Law disputes, when parish officials had often to pay heavy fees to attorneys in settlement and bastardy cases. The historian Joan Lane says that attorneys, profiting from the misfortunes of others, "seem never to have been held in general regard". Frequently their expertise was distrusted and their fees greatly resented. Indeed, Samuel Johnson commented about an acquaintance that he, "did not care to speak ill of any man behind his back, but he believed the gentleman was an attorney".
An Act in 1728 attempted to suppress the less reputable attorneys and the term of apprenticeship (or "articles") was fixed at five years (it is now two years). A society of practitioners was established in London that year, and by the end of the century local law societies had been founded. From 1749 affidavits that their articles had been completed had to be filed in the court in which they practised within three months of their admission to that court, and from 1785 an annual certificate of admission was required. Although the Society in London failed in 1817 it was the forerunner of the Law Society, formed in 1823 and given a charter in 1831 to regulate the profession.
The status of the attorney rose with the reforms of the 19th century when the more successful made further money from property and transport speculations; they became valuable members of town corporations and other governing bodies, and many married into land-owning families. Prior to 1871, however, no "man of the law" was allowed to stand for Parliament. In 1872 there were 13,824 attorneys and solicitors and the following year the Judicature Act merged the two into a single body, from November 1875 all attorneys being styled solicitors. The articling system continued and solicitors, to the end of the 19th century, were seldom university graduates. That is not infrequently the case today.
Records
Law Lists
Following the Act in 1728, lists of those attorneys and solicitors admitted in the two years 1729 and 1730 were printed by Parliament [not in FHL].
Law was the first profession to have a regularly published list of its practitioners, and these should be the searcher's first port of call. Browne's General Law List appeared annually, 1775-97, and has been continued as The New Law List, 1798-1840, and, from 1841, as the Law List, by other publishers. Up to 1789 the names of some lawyers who had not been formally admitted are listed, but from 1790 the List was based on the record of their annual certificates of admission (and omits those without a certificate in a particular year). The Family History Library has 1799 [FHL 942 N24b; film 897090.2]; 1802 [FHL 924 N24L; not filmed]; 1808, 1818, 1827, 1840 [all FHL 942 N24L; film 1696676.4]; 1812 [FHL fiche 6202650]; and 1843 [FHL 942 N24L; film 1696626.8].
The Lists contain separate lists of barristers and of London and country solicitors but give no indication of age or parentage. For a solicitor the List shows his name and the name of the firm and place where he practised. The date of qualification appears from 1861. The disappearance of a name may suggest death and a will, but it is not uncommon for a solicitor not to make a will. There are good runs of theList at Guildhall Library, London, from 1799 at The National Archives, Kew, and from 1812 at the Society of Genealogists.
Attorneys and Solicitors
As mentioned above, those solicitors who practised in the courts had, from 1728, to take oaths and be formally admitted and, from 1749, to file an affidavit of due execution of articles. If the articles themselves were also filed they generally show the name of the father or guardian. Most of the surviving records (at The National Archives) are described in The National Archives' Research Guide 36,Lawyers: Records of Attorneys and Solicitors (available at http://www.nationalarchives.gov.uk) but for each court there are various series that may need to be checked. Most of the records prior to 1749 are for the Court of Common Pleas where the admission books start in 1724 (with supplementary entries back to 1656), but from 1749 a good series starts in the Court of King's Bench. The Palatinate Courts of Chester (from 1697) and Durham (from 1660) seem to have the earliest entries. Most courts have some indexes. The National Archives also has a microfilm of a 'roll' in four volumes with indexes of the solicitors admitted in the Court of Chancery, 1729-1858 (C216/21-25), the original of which is on loan to the Law Society.
Between 1710 and 1811 the apprenticeship of an attorney may also be traced through the volumes of Apprentices of Great Britain (indexed to 1774), also at The National Archives, though they do not give the fathers' names after 1752.
The Law Society maintains a Register of Attorneys and Solicitors listing all those admitted since 1845 (with admissions from about 1790 for most courts) and some Registers of Articles of Clerkship since 1860. This is held at the Law Society's Solicitors Regulation Authority, Ipsley Court, Berrington Close, Redditch, B98 OTD (http://www.sra.org.uk).
Barristers
There were formerly three degrees of barristers: ordinary barristers, King's or Queen's Counsel and Serjeants at Law.
Serjeants at Law were the highest in status, and before 1846 had a monopoly of pleading in the Court of Common Pleas, but the last appointed was in 1868 and they were abolished in 1873. See J.H. Baker, The Order of Serjeants at Law: a chronicle of creations (Selden Society Supplementary Series, vol. 5, 1984) [FHL 942 H2bj]. Lives of a select 58 were compiled by H.W. Woolrych, Lives of Eminent Serjeants at Law of the English Bar (2 vols. 1869) [not in FHL].
King's or Queen's Counsel, first appointed in 1604, are listed by Sir John Sainty in A List of English Law Officers, King's Counsel and Holders of Patents of Precedence (Selden Sociey, 1987) [not in FHL].
As most barristers are university graduates, some details of them may be found in university and college registers. Like these registers the admission registers of the Inns of Court are uneven in the detail they provide, though most show the name, status or occupation, and place of residence of the father. The age of the student appears in the 19th century, when the university attended and the date of being called to the bar may be added.
For Gray's Inn there are Joseph Foster, The Register of Admissions to Gray's Inn 1521-1889 (1889) [FHL film 844906.1] and R.J. Fletcher, The Pension Book of Gray's Inn 1569-1800 (2 vols. 1901-10) [FHL 942.1/L1 C4gr; film 1426151.1-2]. Admissions 1521-1889 are online[1]
For Lincoln's Inn there are The Records of the Honourable Society of Lincoln's Inn: Admissions 1420-1799 and 1800-1893 (2 vols. 1896) [not in FHL] and W.P. Baildon, The Records of the Honourable Society of Lincoln's Inn: the Black Books (4 vols. 1897-1902) [FHL film 845175-6]. Admissions 1420-1799 are online[2]
For the Middle Temple there are H.A.C. Sturgess, Register of Admissions to the Middle Temple ... to 1944 (3 vols. 1949) [FHL 942.1/L1 C4st; film 873850-1], C.H. Hopwood, Middle Temple Records (4 vols. 1904-5) [FHL 942.1/L1 C4m; film 873848.1-2] and J.B. Williamson, The Middle Temple Bench Book (2nd edn. 1937) [FHL 942.1/L1 U2t; not filmed]. Records 1501-1603 are online[3]
For the Inner Temple, W.H. Cooke's Students Admitted to the Inner Temple 1547-1660 (1877) [not in FHL] only covers the early period, though some admissions appear in F.A. Inderwick and R.A. Roberts, Calendar of the Inner Temple Records (5 vols. 1869-1937) [FHL 942.1/L1 C4in; film 845173-4]. For details of students since 1660 one has to write to the Librarian at the Inner Temple, London EC4. Admissions Database 1547-1920 is online[4]
The genealogist Joseph Foster circulated barristers and judges and compiled a most useful biographical dictionary of those alive in 1885 that he called Men at the Bar (1885) [FHL 942 U24fj; film 845204; fiche 6028223] and that may include parents, wives and children.
Few records of the Inns of Chancery have been published, but D.S. Bland's Bibliography of the Inns of Court and Chancery (Selden Society Supplementary Series, vol. 3, 1965) [FHL 942 A3bb] describes the surviving manuscripts as well as the printed sources. The admission registers of Clement's Inn, 1656-1883, are at The National Archives, and its Pension Books, 1658-1883, were published in volume 78 of the Selden Society series (1960) [FHL 942 P3ss]. A list of admissions to Staple Inn, 1716-1884, appears in E. Williams, Staple Inn (1906) [FHL 942.1/L1 H2ws; not filmed].
Judges
Judges, being normally chosen (until the middle of the 19th century) from amongst the serjeants at law, will be found in the above-mentioned sources. They are listed in Sir John Sainty, The judges of England 1272-1990; a list of judges of the superior courts (Selden Society Supplementary Series, volume 10, 1993) [FHL 942 N2sj]. Short accounts of those in the higher courts may be found in Edward Foss, Biographical Dictionary of the Judges of England 1066-1870 (1870) [FHL 942 D3fo; fiche 6036846] and in A.W. Simpson, Biographical Dictionary of the Common Law (1984) [not in FHL]. John Campbell compiled Lives of the Chief Justices of England (3 vols. 1849-58) FHL 942 U24cj; film 845191-2]. Many judges appear in the Oxford Dictionary of National Biography.
Justices of the Peace
Justices of the Peace (or magistrates) were unpaid laymen. Until very recent times they had no formal legal training, though a stipendiary magistrate in the busier courts was salaried and legally qualified. Magistrates were appointed by the Crown and in order to qualify, by an Act of 1439, they had to have an estate within the county in which they served worth at least £20 a year. This was increased to £100 in 1731, but occupation of a house rated at £100 per annum became an alternative in 1875. These requirements were abolished in 1906 and anyone residing within seven miles of the county then qualified.
From 1745 justices were required to register their qualifications under oath and the records were filed with the Clerk of the Peace. They are now in county record offices along with those of the other oaths that they took, but rarely show more than names and addresses. From 1665 the appointment of justices features irregularly in The London Gazette and there are some lists and entry books amongst the Crown Office records at The National Archives.
Canon Lawyers
In the church courts as well as the Court of Admiralty and the Court of Delegates, the solicitors were known as advocates and the barristers as proctors.
Advocates were generally doctors of law with university degrees. At the end of the 15th century they formed an association that developed into the College of Advocates, situated in an area that had become known as Doctors' Commons near St Paul's Cathedral. In spite of the requirements of canon law, very few advocates worked in the church courts, most of them for the Archbishops of York (at York) and Canterbury (at London) and for the Bishop of London. The records of the College of Advocates are at Lambeth Palace Library and were used extensively by George Squibb in his Doctors' Commons (1977) [FHL 942 C4sq]. This includes an annotated transcript of the Subscription Book, 1511-1855. A list of the graduates admitted before 1803 was published by Charles Coote in 1804 [not in FHL].
Outside London and the courts centred at Doctors' Commons the proctors (or procurators) worked almost universally in the local archdeaconry and bishops' courts. They had usually been apprenticed to other notaries for a seven-year term and were not normally graduates. At the start of their careers, like the attorneys, they were formally admitted to practise by the various courts (though the records usually give only their names).
Bibliography
Brian G.C. Brooks and Mark D. Herber, My ancestor was a lawyer (Society of Genealogists, 2006) [FHL 942 D27bbg].
Article by John Titford, 'Old occupations: proctors' in Family Tree Magazine (UK), vol. 7, no. 3 (January 1991) pages 4-5.
[Adapted from an article by Anthony Camp on 'Records of lawyers in England and Wales' in Family Tree Magazine (UK), vol. 17, no. 5 (March 2001), pages 22-24].
References
1. Joseph Foster, The Register of Admissions to Gray's Inn, 1521-1889, Together with the Register of Marriages in Gray's Inn Chapel, 1695-1754 (London: The Hansard Publishing Union, Limited, 1889). Digitized by Google Books.
2. The Records of the Honorable Society of Lincoln's Inn. Vol. I. Admissions from A.D. 1420 to A.D. 1799 (Lincoln's Inn, 1896). Digitized by Google Books.
3. Charles Henry Hopwood, Middle Temple Records (London: Butterworth and Co., 1904). Digitized by Google Books.
4. The Inner Temple Database.
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Talk:Chambly CanalEdit This Page
From FamilySearch Wiki
WikiProject New York
This article is within the scope of WikiProject New York, a collaborative effort to improve the coverage of the U.S. state of New York on FamilySearch Research Wiki. If you would like to participate, please visit the project page, where you can join the discussion and see a list of open tasks.
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NOTE: If you are a developer, please use a private wiki based on foswiki/trunk on a daily base ...or use trunk.foswiki.org to view this page for some minimal testing.
Use Item9693 for docu changes for 1.2 and 2.0.
Item310: Managing webs redesigned for better usability.
Priority: CurrentState: AppliesTo: Component: WaitingFor:
Enhancement Closed Engine
Let me call it a usability nightmare. Made it urgent because I can't stand this any longer.
-- MichaelDaum - 26 Nov 2008
In templating or the corresponding core routines?
-- OliverKrueger - 29 Nov 2008
This isn't ready to be a task; it hasn't been through the feature request process, has no committed developer, is insufficiently detailed for anyone to pick it up and just do it, and for sure should not be a release blocker.
Changed to Enhancement and set to waiting for a feature request I just opened.
Dunno why this isn't a task as this is just a plain todo like a normal programing improvement with the only difference that this is no coding but creating the appropriate input form.
• Simple; the lack of detail in the report. Reports that are only useful to the reporter are useless to anyone else. If you were run over by a bus, no-one would be able to pick up the work. You were basically saying "this is a release blocker because I don't like it, but I'm not going to tell you why". Thank you for improving the report.
• Well, for most people it is obvious why the current ManagingWebs is bad simply because they feel pain. I could give you a detailed analysis of the causes but let me save this for later. Instead have a look at the proposed changes. I hope you will understand.
Anyway, I will bring it up in the UserExperienceTaskTeam and discuss it with Carlo. Improving it should be straight forward, i.e. separating blabla into a dedicated help section thus not being in the way when actually wanting create a new web.
There are a couple of similarly bad input forms e.g. for creating a new group. I consider these things a release blocker and thus upgrade this to urgent again.
See also RedesignManagingWebs.
-- MichaelDaum - 30 Nov 2008
Improved report by proposing the redesign at RedesignManagingWebs
-- MichaelDaum - 01 Dec 2008
I agree that such proposal needs a feature proposal.
I just raised concern. But because I am against the proposal, but I am against the part where half the form is hidden behind an non-obvious twisty. Without the hiding I am OK with the change.
This is in no way a release blocker. It is not even normal. It is an enhancement. Nothing in the current UI will prevent 1.0.0 from being released. We are on a feature freeze. Remember? Since this is a docu change and not code change I will allow it for 1.0.0 but I will not allow it to block a release.
-- KennethLavrsen - 01 Dec 2008
A fucked up usability is a similar sever issue for software like fucked up code: people can't use the product. So we should start treating userinterfaces with the same care.
-- MichaelDaum - 01 Dec 2008
To me the topic is a misnomer, because you cannot manage webs, only create new webs. I would expect an overview of all webs with the option to rename or delete directly. And add a web of course.
-- ArthurClemens - 05 Dec 2008
Re-added the feature proposal to the "Waiting for" field. You should not have a task in "Waiting for" state without saying what it is waiting for. If the link to that topic is meant to be broken, please change the state to a non"waiting" state.
-- CrawfordCurrie - 06 Dec 2008
Done.
-- ArthurClemens - 01 Sep 2009
A couple of spacing tweaks.
-- ArthurClemens - 19 Sep 2009
ItemTemplate edit
Summary Managing webs redesigned for better usability.
ReportedBy MichaelDaum
Codebase
SVN Range TWiki-4.2.3, Wed, 06 Aug 2008, build 17396
AppliesTo Engine
Component
Priority Enhancement
CurrentState Closed
WaitingFor
Checkins Foswikirev:4741 Foswikirev:4742 Foswikirev:4743 Foswikirev:4744 Foswikirev:5003 Foswikirev:5004
TargetRelease patch
ReleasedIn 1.0.7
Topic revision: r22 - 20 Sep 2009, KennethLavrsen
The copyright of the content on this website is held by the contributing authors, except where stated elsewhere. see CopyrightStatement.
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Research
Application of the comprehensive set of heterozygous yeast deletion mutants to elucidate the molecular basis of cellular chromium toxicity
Sara Holland1, Emma Lodwig1, Theodora Sideri1, Tom Reader1, Ian Clarke2, Konstantinos Gkargkas3, David C Hoyle2, Daniela Delneri4, Stephen G Oliver3 and Simon V Avery1*
Author Affiliations
1 School of Biology, Institute of Genetics, The University of Nottingham, University Park, Nottingham NG7 2RD, UK
2 North West Institute for Bio-Health Informatics, The University of Manchester, ISBE, School of Medicine, Oxford Road, Manchester M13 9PT, UK
3 Department of Biochemistry, University of Cambridge, Sanger Building, Tennis Court Road, Cambridge CB2 1GA, UK
4 Faculty of Life Sciences, The University of Manchester, Oxford Road, Manchester M13 9PT, UK
For all author emails, please log on.
Genome Biology 2007, 8:R268 doi:10.1186/gb-2007-8-12-r268
The electronic version of this article is the complete one and can be found online at: http://genomebiology.com/2007/8/12/R268
Received:15 November 2007
Revisions received:18 December 2007
Accepted:18 December 2007
Published:18 December 2007
© 2008 Holland et al.; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background
The serious biological consequences of metal toxicity are well documented, but the key modes of action of most metals are unknown. To help unravel molecular mechanisms underlying the action of chromium, a metal of major toxicological importance, we grew over 6,000 heterozygous yeast mutants in competition in the presence of chromium. Microarray-based screens of these heterozygotes are truly genome-wide as they include both essential and non-essential genes.
Results
The screening data indicated that proteasomal (protein degradation) activity is crucial for cellular chromium (Cr) resistance. Further investigations showed that Cr causes the accumulation of insoluble and toxic protein aggregates, which predominantly arise from proteins synthesised during Cr exposure. A protein-synthesis defect provoked by Cr was identified as mRNA mistranslation, which was oxygen-dependent. Moreover, Cr exhibited synergistic toxicity with a ribosome-targeting drug (paromomycin) that is known to act via mistranslation, while manipulation of translational accuracy modulated Cr toxicity.
Conclusion
The datasets from the heterozygote screen represent an important public resource that may be exploited to discover the toxic mechanisms of chromium. That potential was validated here with the demonstration that mRNA mistranslation is a primary cause of cellular Cr toxicity.
Background
Toxic metals are major environmental pollutants that are linked to a broad range of degenerative conditions in humans [1-3]. Metal toxicity is also widely studied in microorganisms, both as models to further our understanding of cellular metal toxicology, and because of the importance of metal toxicity in microbial biotechnologies [4-7]. Chromium toxicity is an issue of especially broad interest, Cr compounds having been among the earliest chemicals to be classified as carcinogens. Although the consequences of chromium toxicity are well documented [8], the underlying cause(s) of toxicity remains unknown. This is a key issue, as an understanding of mechanism should help develop appropriate therapies.
The yeast Saccharomyces cerevisiae is at the forefront of functional genomics and systems biology research [9] and provides an excellent model with which to tackle intractable biological questions. The yeast deletion strain collections have proven particularly valuable resources, the homozygous versions having been used widely for genome-wide assignment of function [10-13]. The heterozygous deletion strain collection [14] has been less commonly exploited. This reflects (in part) the more subtle phenotypes that the reduction in the copy number of a given gene (from two copies to one), as opposed to its complete removal, is expected to produce. This subtlety means that small differences in growth rate of individual heterozygous mutants must be detected, and this is most easily achieved by competition experiments. These experiments are generally carried out by pooling the entire collection of mutants and growing them in competition under the condition of interest [11,15]. Analysis of the competitions is facilitated by the fact that the gene replacement cassette for each mutant has a unique 20-mer strain-identifying sequence [10,14]. These molecular 'barcodes' are amplifiable with common primers, enabling a parallel analysis of all strains in the mixed culture and avoiding the need to culture each strain separately to assess growth effects. Total genomic DNA extracted from the mixed competitions is subjected to PCR with the universal primers, yielding a pool of amplified tag sequences in which the abundance of each unique tag corresponds to the abundance of a strain in the culture [14,16]. These abundances can be determined quantitatively by hybridization to oligonucleotide arrays, the data revealing the relative growth of each yeast mutant under the growth condition(s) of interest.
A major advantage of the heterozygous deletion strain collection is that it encompasses essential gene functions that, by definition, are not represented in the homozygous collections. Therefore, exploitation of the heterozygous mutant collection through competition analyses should provide a considerably richer pool of information. Essential gene products are likely cellular targets of drugs and other xenobiotics. Consequently, existing data from screens of the homozygous mutant collections against agents such as mutagens and toxic metals [17-19], although very useful, exclude potentially key information. Furthermore, mutation to heterozygosity is common in nature, and such heterozygosities can underlie human genetic diseases [20].
The proof-of-principle of competition analyses employing the heterozygous yeast deletion mutants involved confirmation or identification of essential proteins as targets of drug action [14,15,21]. For those purposes, large collections of pooled mutants were co-incubated with the drug and the relative growth effect of the drug on each strain assayed as outlined above. Genes were identified that yielded haploinsufficiency phenotypes. Haploinsufficiency describes the situation where halving the copy number of a gene (to create a heterozygous mutant) provides insufficient gene product for optimal growth under a particular condition. Therefore, the above studies identified (essential) genes that are required for optimal growth in the presence of the drugs, revealing putative drug targets. Another phenomenon, not yet exploited in the above context, is haploproficiency (that is, a fitness benefit arising from heterozygosity). Recent work has highlighted the value of considering haploproficiency. For instance, genes with functions related to protein turnover showed haploproficiency under conditions of nitrogen limitation, where protein conservation might be expected to yield a selective advantage [22].
Armed with these convincing proofs of principle, the present study extends the use of competition analyses, beyond the identification of drug targets, to a natural stressor that is not necessarily expected to have a primary protein target - the toxic metal chromium. Prior to our study intense efforts to characterize the toxic action of chromium have been made, but the primary molecular mechanisms causing toxicity have, nevertheless, remained elusive. Here we show that mRNA mistranslation is a primary cause of cellular Cr toxicity.
Results
Identification of heterozygotes with altered chromium resistances
The experimental system involved co-culture of >6,000 heterozygous (hemizygous) deletion strains in carbon-limited continuous culture. A number of similar studies have co-cultured the heterozygotes in batch culture [15,21], whereas a more recent study with the heterozygotes has used the same continuous culture system as that employed here [22]. The use of continuous culture for competitions enables detection of the more subtle phenotypes, expressed as small growth rate differences and revealed over a large number of generations. In addition, use of the chemostat for continuous culture offers high reproducibility, owing to a defined and constant growth rate and physicochemical environment at steady state. CrO3 was supplied at a sub-lethal dose (0.1 mM), pre-determined to cause an approximately 30% increase in the mean doubling time of the mixed cultures. The relative growth of each strain in the cultures (that is, change in relative abundance between the start and end of a chemostat experiment) was derived from signals assigned to the strains' unique identifying (barcode) sequences (see Background, and Materials and methods). The effect of Cr was determined by comparing the relative growth of each strain in the Cr-treated cultures versus that in control cultures. This yielded a value for each strain for the size of the growth effect of Cr (see the Data analysis section in Materials and methods). The data for each strain are given in Additional data file 1.
The range of growth effects of Cr across the strains indicated a normal distribution centered around zero (Figure 1). The relative growth of some strains was decreased by Cr (negative growth effect; tendency towards haploinsufficiency with Cr), whereas others showed improved relative growth (tendency towards haploproficiency). A similar normal distribution was evident for growth effects on strains that were heterozygous specifically for essential gene functions. The growth data were analyzed further to identify strains that showed significant (false discovery rate, q < 0.05) haploinsufficiency or haploproficiency (see the Data analysis section in Materials and methods). There were fewer significantly haploinsufficient strains than haploproficient ones, that is, 115 strains exhibited a Cr-specific growth defect (indicating gene functions that normally protect against Cr), whereas the relative competitiveness of 203 strains was enhanced by Cr (indicating functions through which metal toxicity could be mediated). This suggests that S. cerevisiae has not been routinely exposed to Cr stress during its evolutionary history, as Fisher [23] demonstrated that when selection occurs in the environment to which an organism is adapted, then most mutations will be deleterious; whereas, when selection occurs in increasingly suboptimal conditions, then an increasing proportion of mutations will be beneficial. Knowledge of genes that exhibit haploproficient phenotypes in the presence of Cr could be exploited to increase the rate of biotechnological processes that may be limited by metal toxicity [4,7].
Figure 1. Analysis of the global effects of Cr treatment on the heterozygous mutants. The plot shows the distribution of the sizes of the growth effects caused by Cr for all genes (black line) and essential genes (grey line). Mutants were grouped into bins according to the size of growth effect. Each bin encompasses a 0.0025 range of growth-effect sizes, and the frequency denotes the number of strains in each bin. The calculation for determining size of growth effect is described in the Data analysis section in Materials and methods.
In contrast to the therapeutic compounds that were the subjects of previous haploinsufficiency analyses [14,15,21,24], there is no a priori expectation that the primary target of Cr will be a specific essential protein [5]. Nonetheless, closer analysis of our data showed that, under the condition of Cr stress, five of the eight most significant haploinsufficient phenotypes (that is, those with the lowest q-values) were found in strains heterozygous for an essential gene (Additional data file 1). These included NHP2 (involved in 18S rRNA processing), and ARP3 and ARC19 (involved in actin nucleation and actin patch function). As with the drugs, these observations could, in principle, be explained by direct interference of the metal with the essential function of its target protein, reducing its activity to a level below that required to sustain the growth of a diploid cell at wild-type rates. Alternatively (and this also applies to the haploinsufficient phenotypes observed for non-essential genes), there may be a synthetic lethal interaction with the principal target of chromium, or the haploinsufficient protein may contribute to the intrinsic resistance of the cell to the toxic action of the metal.
Over-representation of specific Gene Ontology terms in the annotations of genes found in the haploinsufficiency and haploproficiency datasets
GoMiner [25] was used to associate Gene Ontology (GO) terms with all genes whose heterozygous mutants exhibited significant haploinsufficiency or haploproficiency under Cr stress (Additional data file 2). Not unexpectedly, GO terms related to transport and metal homeostasis were significantly over-represented in the annotation of those genes that displayed either haploinsufficient or haploproficient phenotypes. Gene functions involved with chromatin structure were also significantly over-represented in the haploinsufficient and haploproficient data, indicating an involvement of chromatin organization and its possible effects on gene expression in Cr resistance. Schnekenburger et al. [26] have described how Cr cross-links complexes of histone deacetylase 1 and DNA methyltransferase 1 to gene promoters, inhibiting histone modifications and decreasing recruitment of RNA polymerase. Cr may also provoke aberrant DNA methylation, with the potential to silence tumor suppressor genes in higher cells [27]. Genes involved in nucleotide excision repair also were evidently important for Cr resistance, consistent with previous work [28]. Cr is well known to promote DNA damage, but it is unresolved whether this is a primary cause (versus a secondary effect) of Cr toxicity.
The Cr treatment revealed haploproficient phenotypes for several genes involved in sulfur metabolism. The flux of sulfur in these heterozygotes could be re-directed towards molecules that may promote metal resistance, such as glutathione (GSH). Such re-programming of sulfur metabolism occurs normally in wild-type yeast responding to other metals [29,30]. In addition, Cr uptake may occur through sulfate transporters, which are regulated in response to Cr stress [31]. Actin was a highly over-represented haploinsufficient category for Cr, which might relate to targeting of actin function by Cr, as suggested above.
Proteins synthesized during chromium exposure tend to form aggregated toxic-products
Genes involved in proteasome function and regulation of protein stability were among those most significantly over-represented in the set showing haploinsufficient phenotypes in the presence of Cr (Additional data file 2). We decided to subject this evidence of the mechanism of chromium's toxicity to further investigation. Initially, we validated the output from the library screen by confirming in independent batch-culture assays the haploinsufficient phenotypes of several Cr-treated proteasome mutants (Additional data file 3). These data point to a requirement for protein degradation in Cr resistance and, therefore, to an involvement of cellular proteins in Cr toxicity. This hypothesis was supported by experiments involving cycloheximide, an inhibitor of translational elongation. Exposure of cells to Cr for 3 h resulted in a marked loss of viability (Figure 2a). However, this toxicity was suppressed in cells that were blocked for protein synthesis using cycloheximide.
Figure 2. Chromium causes accumulation of toxic protein aggregates. (a) Exponential phase cells of S. cerevisiae in YEPD medium were exposed to 9 or 12 mM CrO3 for 3 h, in either the absence or presence of 10 μg ml-1 cycloheximide (CHX) (the latter cells were also pre-incubated for 1 h with CHX before metal exposure). Viability (%) was subsequently determined according to colony-forming-unit counts, with reference to control cultures not exposed to Cr. (b) Protein was extracted from cells treated for 30 minutes with 0.5 mM CrO3 and an aggregated protein fraction (separated from soluble and membrane proteins) [49] was prepared from each sample. The data show protein determined in the aggregate fraction as a proportion of the total cellular protein. (c) Cells were cultured in YEPD medium that was either unsupplemented with protein (open circles), or supplemented with 24 μg ml-1 of the soluble (filled circles) or aggregated (squares) protein fractions isolated from cells that had been exposed to 0.2 mM CrO3 for 1 h. All values are means ± standard error of the mean from at least three independent determinations.
Previous evidence showed that Cr toxicity involves protein oxidation [32]. Oxidized proteins are prone to forming potentially toxic aggregates [33], but this can be countered by proteasomal degradation of the abberant proteins. Combining those observations with our new haploinsufficiency data, we hypothesized that Cr toxicity could involve the formation of protein aggregates. Protein aggregation is also linked to cancer [33], and the carcinogenicity of Cr is well-documented [8]. To test the effect of Cr on protein aggregation, insoluble aggregate fractions of proteins were isolated from cells (see Materials and methods) that had been incubated with or without Cr, and the levels of protein in these fractions were determined. The proportion of cellular protein occurring as insoluble aggregates was found to increase approximately two-fold during Cr exposure (Figure 2b), indicating that Cr promotes protein aggregation. Protein aggregates can be toxic, and the potential toxicities of aggregate preparations from cells can be tested by exposing fresh cells to these and measuring their inhibitory effect [34] on the growth of S. cerevisiae. Growth was not affected by supplementing the medium with soluble protein that was previously isolated from Cr-treated cells (Figure 2c). In contrast, growth was slowed in medium supplemented with an equivalent amount of aggregated protein from the Cr-treated cells. Therefore, aggregated protein formed in the presence of Cr can exert a toxic effect.
The observation that Cr resistance was enhanced by the simultaneous inhibition of protein synthesis (Figure 2a) suggested that proteins synthesized during Cr exposure were involved in toxicity. To explore this further, the source of Cr-induced protein aggregates was determined with pulse-chase experiments involving protein labeling with [35S]methionine. These experiments showed that Cr-dependent aggregation was attributable primarily to proteins synthesized during Cr exposure, rather than to aggregation of pre-existing proteins: the aggregate fraction isolated from cells that were [35S]methionine-labeled during the period of Cr exposure was enriched with labeled protein (Figure 3a), whereas the opposite was true for cells labeled prior to Cr exposure (Figure 3b). (In the latter case, there was a decrease in the proportion of labeled protein in the aggregate fraction following incubation with Cr. This could be due to dilution of pre-existing labeled aggregates with unlabelled aggregates formed during the incubation with Cr.) In other experiments, co-treatment with cycloheximide suppressed the Cr-dependent accumulation of protein aggregates (Figure 3c), supporting the conclusion that proteins that form insoluble aggregates in response to Cr are predominantly synthesized during Cr exposure.
Figure 3. Chromium causes aggregation predominantly of proteins synthesized during chromium exposure. Cells were exposed to 0.1 mM CrO3 for 60 minutes, either (a) at the same time as or (b) after labeling with [35S]methionine for 60 minutes. The data show the relative enrichment of isotope in the aggregate fraction [cpm per μg aggregated protein, corrected for labeling efficiency (cpm per μg total protein)]. (b) Due to the natural turnover of labeled proteins during the post-labeling 60 minute incubation ± Cr, the data from this experiment were normalized with respect to the minus-Cr control from (a). (c) Aggregated protein as a proportion of total protein was determined after incubation of cells for 1 h in the absence or presence of 0.4 mM CrO3 and 10 μg ml-1 cycloheximide (CHX). All values are means ± standard error of the mean from three independent determinations.
Mistranslation of mRNA is a primary cause of chromium toxicity
The finding that Cr causes aggregation primarily among proteins being synthesized during exposure suggested that the metal might be targeting the protein synthesis or folding machineries. Mistranslation of mRNA transcripts provides a major potential source of aberrant proteins that form aggregates [33]. To test whether Cr provokes mRNA mistranslation, the rate of translational read-through of a UAA nonsense (stop) codon was monitored in a short-term dual-luciferase assay (see Materials and methods). The rate of read-through was increased more than two-fold by the addition of CrO3, at a concentration that increased the population doubling time by about 15% (Figure 4a). A similarly inhibitory dose of another metal, Cu(NO3)2, did not significantly affect read-through across the stop codon. The ribosome-targeting drug paromomycin caused a stimulation of mistranslation comparable to that observed with Cr. These data were supported by results from a longer-term qualitative assay, based on read-through of the ade1-14 UGA codon and suppression of the red pigmentation associated with this allele. Treatments with agents such as H2O2 or Cu(NO3)2 gave no change in colony color compared with untreated controls, whereas red pigmentation was suppressed with paromomycin or CrO3 (Figure 4b), indicative of mistranslation [35]. Red pigmentation was restored when pale colonies from Cr-supplemented medium were sub-cultured onto non-supplemented medium (not shown), indicating that Cr-dependent nonsense suppression did not stem from a prion switch or other heritable change. Translational read-through due to Cr, but not paromomycin, was abolished under anaerobic conditions; this indicates an oxidative basis for Cr-induced mistranslation (Figure 4c).
Figure 4. Chromium causes errors in mRNA translation. (a) Cells transformed with the dual-luciferase plasmid [50] were exposed or not to 200 μg ml-1 paromomycin ('Paro'), 0.6 mM Cu(NO3)2 or 0.1 mM CrO3, in YNB medium for 90 minutes. The activities of the firefly and renilla luciferases in derived protein extracts were determined luminometrically. The ratio of luminescence from the firefly versus renilla luciferase indicates the short-term level of translational read-through of the UAA stop codon that separates the two open reading frames. All values are means ± standard error of the mean from at least three independent determinations. RLU, relative light units. (b, c) Exponential-phase S. cerevisiae L1494 (ade1-14) cells (OD600 ~1.0, plus a 10-fold dilution) were spotted in 6 μl aliquots on to YEPD agar supplemented or not with 150 μg ml-1 paromomycin, 8 mM Cu(NO3)2, 0.15 mM CrO3 or 3.6 mM H2O2. Plates were incubated for 3 days at 30°C either aerobically (b) or anaerobically (c). In the latter case, plates were incubated aerobically at 4°C after the 3 days incubation to allow development of the red pigment before images were captured. The stressors were supplied at doses that produced similar degrees of mild inhibition of aerobic growth (versus controls) within each experiment on the different media.
The hypothesis that induction of mRNA mistranslation causes Cr toxicity was tested first by assaying for synergistic toxicity between Cr and paromomycin. These agents together caused a far stronger growth-inhibitory effect than their combined individual effects (Figure 5a), indicating that paromomycin (which provokes mistranslation via ribosome binding) and Cr target a common process. No synergy was found between H2O2 and paromomycin (data not shown). Second, we examined Cr resistance in 18S ribosomal RNA mutants that carry out mRNA translation with differing degrees of accuracy [36]. The L1583 mutant, which is characterized by highly error-prone translation, was markedly sensitized to Cr in comparison to the wild type (L1494); in contrast, increased translational accuracy (strain L1597) caused increased Cr resistance (Figure 5b). These results substantiated the proposal that induction of mRNA mistranslation is the main cause of chromium's toxic effect on yeast cells.
Figure 5. mRNA mistranslation causes chromium toxicity. Exponential phase cells were sub-cultured in 300 μl volumes of YEPD in 48-well plates, and growth (OD600) was subsequently monitored at 30°C with continuous shaking in a plate reader. (a) Growth of S. cerevisiae BY4743 in unsupplemented medium (control; open circles), or in medium supplemented with 0.1 mM Cr (filled circles), or 100 μg ml-1 of the ribosome-targeting drug paromomycin (open squares), or 0.1 mM Cr + 100 μg ml-1 paromomycin (filled squares). (b) Growth of S. cerevisiae L1494 (wild type; circles), L1583 (error-prone translation; squares) and L1597 (high translational fidelity; triangles) strains in the absence (open symbols) or presence (filled symbols) of 0.1 mM CrO3. Typical results from one of three independent experiments are shown.
Discussion
The lack of understanding of the cellular and molecular mechanisms that cause metal toxicity has contrasted starkly with our appreciation of the detrimental consequences of metal toxicology for human and animal health. Chromium exposure, for example, is linked with carcinogenicity, liver and kidney necrosis, and allergenicity [8]. In this study, the complete collection of heterozygous deletion mutants of protein-encoding genes in the yeast S. cerevisiae was used to determine the contribution of every gene, essential and non-essential, to cellular resistance to chromium. This provides the most comprehensive dataset yet available for elucidating this metal's mode of action. Moreover, we have validated this potential through the novel finding that the induction of mistranslation is a major cause of Cr toxicity. This finding stemmed from an observation that proteasomal functions were over-represented in the annotations of genes that displayed haploinsufficiency in the presence of Cr. Given that most of the proteasomal genes are essential, this result would have been missed in a conventional homozygous-mutant screen, underscoring the importance of including essential gene functions in this type of investigation.
Although metals are not necessarily expected to have essential proteins as their targets [5], we did identify candidate toxicity targets of that type, that is, haploinsufficient essential genes. However, the concept of loss-of-function of an essential protein target (the focus of the drug-induced haploinsufficiency studies [14,15,21,24]) could be less relevant to mode-of-action than toxic gain-of-function, for example, resulting from Cr-induced formation of toxic protein aggregates. In this scenario, candidate protein targets of Cr-mediated toxicity would be among the haploproficient genes. The association between protein aggregation and Cr toxicity remains to be resolved in full. However, we demonstrated that mRNA mistranslation is a primary cause of Cr toxicity, and propose that this toxicity is mediated by aggregation of the mistranslated polypeptides.
It is known that protein (but not DNA) oxidation is required for the process of Cr toxicity [32]. Chromium promotes the generation of superoxide radicals in cells and there are overlaps in the phenotypic effects of Cr and superoxide [32,37,38]. The superoxide-generating provitamin menadione is the only classical pro-oxidant for which haploinsufficiency data are already available [21]. The two genes giving the strongest haploinsufficiency in that report, GIM1 and RPN10, have functions related to the same principal GO categories identified here for Cr-induced haploinsufficiency: actin and proteasome. Therefore, the present data support the superoxide-related mode of toxicity suggested elsewhere for Cr [32]. These conclusions may be particularly relevant to toxicity in humans as 80% of non-essential gene functions that influence yeast resistance to the superoxide-generating toxicant, paraquat, have highly conserved human homologues [39].
Oxidative stress in yeast is associated with a Gcn2p-dependent repression of translational initiation [40] and similar responses occur in mammalian cells [41]. Combined with translational inhibition additionally at a post-initiation step, this results in a slowdown of protein synthesis that is thought to preclude the potentially deleterious effects of continued mRNA translation under the error-prone conditions of oxidative stress [40]. This strategy of decreased mRNA translation during oxidative stress appears to work in the case of H2O2, as our data provided no evidence for H2O2-induced mistranslation. In contrast, the key role for oxygen-dependent mRNA mistranslation in Cr toxicity, revealed here, indicated that translational shutdown is ineffective for Cr. This is despite the fact that assays of translation initiation (C Mascarenhas and CM Grant, personal communication) and [35S]methionine incorporation (S Holland and SV Avery, unpublished data) have indicated that Cr provokes a decrease in protein synthesis that is at least as marked as that provoked by H2O2. Therefore, the ability to respond by decreasing the rate of protein synthesis is not the only factor determining resistance of cells to stressor-induced mistranslation. The specific targeting of the translation process by Cr, indicated by our work, provides a useful new tool for elucidating the molecular mechanisms by which translational fidelity in cells can fail.
Conclusion
This study has validated the use of the heterozygous yeast mutant collection for mode-of-action discovery beyond therapeutic compounds, with a natural agent not necessarily expected to have essential proteins as its targets. This was also the first study of this nature to exploit the stringency of continuous culture in performing the necessary competitions in a manner that is both highly reproducible and highly sensitive. It is also unique in revealing haploproficient, as well as haploinsufficient, phenotypes with a toxic agent. The screening data presented here provide the research community with an authoritative resource for elucidating the molecular basis of Cr toxicity. Moreover, the data led us to the discovery that Cr induces the mistranslation of mRNA (and increased protein aggregation) and that this is a primary cause of Cr toxicity. Development of new therapies for metal toxicity relies, at least in part, on such advances and these aims should now be closer at hand.
Materials and methods
Strains, oligonucleotides and plasmids
The heterozygous deletion strains, in the diploid BY4743 background (MATa/MATαhis3Δ 1/his3Δ 1 leu2Δ 0/leu2Δ 0 met15Δ 0/MET15 LYS2/lys2Δ 0 ura3Δ 0/ura3Δ 0) were obtained from the Saccharomyces deletion consortium [42]. The strains were pooled as described elsewhere [22]. BY4743 was used for aggregate extraction, protein labeling and the luciferase assay. The ribosomal mutant strains (L1494, L1597 and L1583) were kindly provided by Dr Susan Liebman (University of Illinois at Chicago).
Growth conditions
Competition experiments in chemostat culture were carried out according to Colson et al. [43] using a small-scale multiple fermenter system (Fedbatch-pro, Das Gip Technology, Julic, Germany). Inoculation with the heterozygote pool and culture in carbon-limited medium were as described by Delneri et al. [22], but with the inclusion of CrO3 (0.1 mM) or no stressor. In brief, an aliquot (1 × 107 cells) of the pool of heterozygous strains was inoculated into 120 ml of carbon-limiting medium [44]. These were grown in batch for 24 h at 30°C with shaking at 170 rev min-1, before continuous culture was initiated at a dilution rate of 0.1 h-1 and a constant pH of 4.5. Each competition experiment was conducted in two biological replicates for at least 24 generations. Other experiments were with strains cultured individually in YEPD or YNB media [45,46]. Where specified, organisms were cultured in 300 μl volumes in 48-well plates (Greiner Bio-One, Stonehouse, Gloucestershire, UK) with shaking at 30°C in a BioTek Powerwave microplate reader (BioTek, Vinooski, VT, USA). Where specified, an anaerobic atmosphere (H2 + CO2) was generated with an Oxoid Gas Generating Kit (Oxoid, Basingstoke, Hampshire, UK).
Genomic DNA extraction, tag amplification, and hybridization to tag-3 DNA microarrays
Samples (15 ml) of the organisms from competition experiments were collected from the culture outflow as soon as the continuous cultures reached steady state (time zero sample; approximately 72 h after original inoculation) and also after at least 24 generations of steady-state growth. Genomic DNA was extracted from these using the DNA tissue kit (Qiagen, Crawley, West Sussex, UK). The concentration of DNA in the extract was determined using a Nanodrop device (Agilent Technologies, South Queensferry, West Lothian, UK). The universal primers used for amplification of the unique barcodes in the genomic DNA of the heterozygotes and the hybridization protocol are those used by Winzeler et al. [10]. Amplifications and hybridizations for each genomic DNA sample were carried out in duplicate, and each sample was from one of two biological replicates of the relevant competition.
Data analysis
Data from hybridizations were globally normalized by median centering the intensity values from tags corresponding to each heterozygous deletant (two tags per mutant). Log.-ratios for each strain were then calculated between the initial and final chemostat time points [22]. This served to eliminate tag-specific biases and further normalized the data. The log.-ratios were expressed as change (in relative strain abundance) per number of cell generations; the latter correction accounted for differences in the generations elapsed between control and Cr-treated cultures (31 and 24 generations respectively). For each strain, the differences in the mean log.-ratios between the control incubations and incubations with Cr indicated the size of the growth effect of Cr. These growth effects were assessed for significance using the p value obtained from an independent-samples t-test. To account for multiple testing, false discovery rates (q-values) were estimated [47], using the Qvalue v1.0 library implemented in the statistical package R, version 2.4.1. Differences yielding a q-value < 0.05 were considered as statistically significant and the corresponding open reading frames selected for further analysis with GoMiner.
Intensity values from tags that do not correspond to deletion mutants were taken as being representative of the background intensity. This was used as a baseline, enabling determination of the presence or absence of individual deletion strains in the experiments. Several strains giving a median signal that was not significantly different to this background were strains that characteristically yield poor hybridization signals [48] (termed 'PH'; Additional data file 1). Data for these were removed from subsequent analyses. Some other strains were lost (out-competed) during competitive culture. Such strains that were not detected in the Cr condition but were in the control condition (termed 'absent'; Additional data file 1) were considered haploinsufficient. Strains that were not detected in the control condition but were in the Cr condition (termed 'present') were considered haploproficient. These strains were included with the relevant haploinsufficient or haploproficient datasets, although the absence of a hybridization signal under either the stressed or the control condition precluded assignment of a q-value.
Protein extraction and metabolic labeling
Protein extraction (total, and the aggregated fraction) was as described in Rand and Grant [49], with the modification of an additional final wash in lysis buffer (minus Igepal), prior to protein quantification with the Bradford assay (Bio-Rad Laboratories, Hemel Hempstead, Hertfordshire, UK). The technique for isolation of aggregates involves solubilization and separation of membrane proteins, so reducing the background of insoluble proteins in aggregate fractions. The term 'aggregated protein', as used in this paper, refers to those fractions that include residual insoluble protein, separated from total protein [49]. For radio-labeling, exponential-phase cells (OD600 ~0.5) in 25 ml YNB medium were incubated with 1 μl (10 μCi) [35S]methionine (MP Biomedicals, Cambridge, Cambridgeshire, UK) ± CrO3 for 1 h at 30°C with shaking. Cells were washed twice in chase medium (YNB plus 1 mg ml-1 unlabeled methionine) and protein was extracted and quantified, as above, either immediately or after 1 h incubation in chase medium + CrO3. Incorporated isotope was quantified in 5 ml scintillation fluid (Emulsifier Safe, Perkin Elmer, Beaconsfield, Buckinghamshire, UK) using a Packard Tri-Carb 2100TR liquid scintillation analyzer. Incorporation of [35S]methionine was expressed as counts-per-minute (cpm) per μg protein.
Dual luciferase assay
Cultures (5 ml) of cells transformed with the dual-luciferase plasmid [50] (a kind gift from Dr David Bedwell, University of Alabama), were grown to OD600 ~0.5 and treated with Cu(NO3)2, CrO3 or paromomycin as specified. At intervals, 5 ml of cells were pelleted by centrifugation and resuspended in 60 μl of Passive Lysis Buffer (Promega, Southampton, Hampshire, UK) before vortexing with 40 μl glass beads (0.5 mm diameter, Biospec Products, Bartlesville, OK, USA)) for 10 × 30 s, with a 30 s incubation on ice between each disruption. The subsequent assay was with the Dual Luciferase Assay system (Promega). Extracts were centrifuged at 15,000 g, 30 s and 5 μl of supernatant added to 20 μl Luciferase Assay Reagent II. Samples were read in a Berthold Lumat LB9507 luminometer for 10 s, 20 μl of Stop and Glo reagent was added and the luminescence was again read for 10 s. Background measurements obtained for cells that lacked the plasmid were subtracted from test measurements. The derived ratio of luminescence attributable to the firefly versus Renilla luciferases indicated the level of UAA mis-translation.
Abbreviations
GO, Gene Ontology.
Authors' contributions
SVA and SGO conceived the study. DD and EL performed the genome-wide screen. SH and TS performed all other experiments. IC, KG, SH, DCH, and TR analyzed the data from the screens. SVA, SH and SGO wrote the paper. All authors approved the final manuscript.
Additional data files
The following additional data are available with the online version of this paper. Additional data file 1 is an Excel workbook that gives the growth data for each heterozygote strain under Cr stress. Additional data file 2 is an Excel workbook that lists the over-represented GO terms among genes that gave significant haploinsufficiency or haploproficiency. Additional data file 3 is a figure showing confirmation of chromium sensitivity in individual heterozygous proteasome mutants. Additional data files 4 and 5 are Excel workbooks that give the raw Affymetrix data and log.-ratios, respectively, for each strain under the control and Cr conditions.
Additional data file 1. Growth data for each heterozygote strain under Cr stress.
Format: XLS Size: 792KB Download file
This file can be viewed with: Microsoft Excel Viewer
Additional data file 2. Over-represented GO terms among genes that gave significant haploinsufficiency or haploproficiency.
Format: XLS Size: 38KB Download file
This file can be viewed with: Microsoft Excel Viewer
Additional data file 3. Exponential-phase cells were sub-cultured, in 300 μl volumes of YNB in 48-well plates, and growth (OD600) was subsequently monitored at 30°C with continuous shaking in a plate reader. Doubling times were determined during the period of exponential growth in the absence or presence of 0.1 mM CrO3, and the percent increase in doubling time attributable to Cr (a measure of Cr sensitivity) was calculated for each strain. The values are the means of three independent experiments ± standard error of the mean.
Format: EPS Size: 398KB Download file
Additional data file 4. Affymetrix data for each heterozygote strain under the control and Cr conditions
Format: XLS Size: 5.6MB Download file
This file can be viewed with: Microsoft Excel Viewer
Additional data file 5. Log.-ratio data for each heterozygote strain under the control and Cr conditions
Format: XLS Size: 2.1MB Download file
This file can be viewed with: Microsoft Excel Viewer
Acknowledgements
This research was supported by grants from the NIH (R01 GM57945) and the NERC (NER/T/S/2001/00343) to SVA and SGO, respectively.
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Research
Genomic linkage map of the human blood fluke Schistosoma mansoni
Charles D Criscione1*, Claudia LL Valentim2,3, Hirohisa Hirai4, Philip T LoVerde2 and Timothy JC Anderson3
Author affiliations
1 Department of Biology, Texas A&M University, College Station, TX 77843, USA
2 Departments of Biochemistry and Pathology, University of Texas Health Science Center, San Antonio, Texas 78229, USA
3 Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Texas, 78245, USA
4 Primate Research Institute, Kyoto University, Inuyama, Aichi 484-8506, Japan
For all author emails, please log on.
Citation and License
Genome Biology 2009, 10:R71 doi:10.1186/gb-2009-10-6-r71
Published: 30 June 2009
Abstract
Background
Schistosoma mansoni is a blood fluke that infects approximately 90 million people. The complete life cycle of this parasite can be maintained in the laboratory, making this one of the few experimentally tractable human helminth infections, and a rich literature reveals heritable variation in important biomedical traits such as virulence, host-specificity, transmission and drug resistance. However, there is a current lack of tools needed to study S. mansoni's molecular, quantitative, and population genetics. Our goal was to construct a genetic linkage map for S. mansoni, and thus provide a new resource that will help stimulate research on this neglected pathogen.
Results
We genotyped grandparents, parents and 88 progeny to construct a 5.6 cM linkage map containing 243 microsatellites positioned on 203 of the largest scaffolds in the genome sequence. The map allows 70% of the estimated 300 Mb genome to be ordered on chromosomes, and highlights where scaffolds have been incorrectly assembled. The markers fall into eight main linkage groups, consistent with seven pairs of autosomes and one pair of sex chromosomes, and we were able to anchor linkage groups to chromosomes using fluorescent in situ hybridization. The genome measures 1,228.6 cM. Marker segregation reveals higher female recombination, confirms ZW inheritance patterns, and identifies recombination hotspots and regions of segregation distortion.
Conclusions
The genetic linkage map presented here is the first for S. mansoni and the first for a species in the phylum Platyhelminthes. The map provides the critical tool necessary for quantitative genetic analysis, aids genome assembly, and furnishes a framework for comparative flatworm genomics and field-based molecular epidemiological studies.
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BME103:T130 Group 13
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On the smartphone folder click on '''import pictures and videos''' and a new icon will appear downloading all the pictures on your smartphone onto your laptop.
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Revision as of 01:32, 2 November 2012
BME 103 Fall 2012 Home
People
Lab Write-Up 1
Lab Write-Up 2
Lab Write-Up 3
Course Logistics For Instructors
Photos
Wiki Editing Help
Contents
OUR TEAM
Name: Sudarshan Iyer
Research and Development Specialist
Name: Ujwala Vaka
Experimental Protocol Planner
Name: Emily Herring
Experimental Protocol Planner
Name: Garrett Repp
Open PCR Machine Engineer
Name: Joseph Del Rosario
Open PCR Machine Engineer
LAB 1 WRITE-UP
The Original Design
Experimenting With the Connections
When we unplugged the PCB Board of the LCD from the Open PCR Circuit Board, the machine's LCD screen turned off.
When we unplugged the white wire that connects the Open PCR Circuit Board to the 16 Tube PCR Block, the machine could not register or measure the temperature.
Test Run
On October 18, 2012, our group first tested the Open PCR Machine. At first the machine seemed overwhelming in its design. However, after following the instructions and advice from peers and professors, we were able to determine how to properly setup, program, and run a simple test.
Protocols
Polymerase Chain Reaction
Polymerase Chain Reaction is a technology that amplifies a single piece of DNA. This technology works very similarly to the natural DNA replication cycle. One PCR cycle consists of three basic steps, denaturation, annealing and extension. In the denaturation step, heat (usually about 95 degrees Celsius) is used to separate the DNA into two strands. Then in the annealing step, the temperature is decreased to 50 degrees Celsius and the DNA primer, specific to the target sequence for that organism, anneal to the separated strand of DNA. The primers mark the beginning and the end of the targeted DNA sequence. Finally, the extension step required the temperature to be raised to 72 degrees Celsius so that the DNA polymerase is activated. The DNA polymerase begins synthesis at the DNA primer. This results in two double stranded target DNA sequences. The PCR cycle is repeated many times to amplify the targeted strand.
There are typically many cycles that need to take place in the PCR in order to amplify a patient's DNA.
Cycle 1: The PCR master mix contains Taq DNA polymerase, dNTP's, MgCl2, forward primer, and reverse primer. The thermal cycler heats up to 95 degrees Celsius, or 203 degrees Fahrenheit, which is almost at boiling point. At this temperature, DNA double helix separates, creating two single-stranded DNA molecules. Gradually the temperature begins to cool to 50 degrees Celsius so the primers will attach. Then the temperature is raised to 72 degrees DNA polymerase is activated and locates primers attached to the single-strand DNA, which will then begin to add complementary nucleotides onto the strand. This process continues until it gets to the end of the strand and falls off.
Cycle 2: The same three steps occurring in cycle happen in cycle 2. The temperature is raised again to separate the DNA strands, the temperature is lowered so that the primers may attach, and the temperature is raised again slightly to stimulate DNA polymerase to copy the strand.
Cycle 3:the two desired fragments begin to appear—two strands that begin with primer one and end with primer two—and these are the DNA copies of the segment of DNA you’ve targeted. These products will increase (become the majority) as the cycle continues.
Cycle 4: At the end of this cycle, you‘ll have 8 fragments that contain only your target sequence.
Cycle 5: At the end of this cycle, you‘ll have 22 fragments that your target sequence and only ten longer length copies.
After 30 cycles there are over a billion fragments that contain only your target sequence and only 60 copies of the longer length molecules. You now have a solution of nearly pure target sequence.
Reagent Volume
Template DNA (20ng) 0.2 μL
10 μM forward primer 1.0 μL
10 μL reverse primer 1.0 μL
GoTaq master mix 50.0 μL
dH2O 47.8 μL
Total Volume 100.0 μL
We ran a total of 8 samples. We made 3 samples from Patient 1 (ID#65685) was female and aged 58. We made 3 samples from Patient 2 (ID#58278) who was also female and aged 53. The remaining 2 samples were the positive and negative controls. The positive control for this experiment was the cancer DNA template and the negative control was the no DNA template.
Flourimeter Measurements
Fluorimeter Assembly Procedure
1) Turn on the excitation light using the switch for the blue LED.
2) Place a smart phone on the cradle at a right angle from the slide.
3) Adjust your camera settings as follows:turn off the flash, set the ISO to 800 or higher, increase the exposure to the maximum, and turn off autofocus (optional).
4) Move the smartphone in the cradle as close possible to the first two rows of the slide so that you will get a clear image.
5) The pipette should be filled with liquid only to the bottom of the black line. Then use the pipette to place two drops of water (each drop should be between 130-160 microliters) in the middles of the first two rows of the slide.
6) Move the slide so that the blue LED light is focused on the the drops of water to the middle of the black fiber optic fitting on the other side of the drop.
7) Cover the fluorimeter with the light box so that much of the stray light will removed, but make sure you can still access your smartphone to take pictures.
8) While being careful not to move the smartphone, take three picture of the water droplet.
9) When removing the light box, be careful not to move the smartphone because that could make the analysis more complicated.
10) Use a clean plastic pipette to remove the water droplets from the slide.
11) Push the slide in so that you are npo in the next set of two holes.
12) Repeat steps 5-10 four more times in 5 different positions.
13) Record the following: type of smartphone used, the distance from the base of the smartphone cradle to the measurement device (in cm), and attach one image for each position of the drop (5 images total).
Transferring the images from your smartphone to the laptop that has ImageJ
1) Connect your smartphone to your laptop using a USB sync cable.
2) Click Start and then click My Computer or Computer where under Portable Devices, you should find your smartphone icon and double-click on this icon.
3) Once you have opened it, double click folder DCIM, and next double-click the folder Camera.
4) From the Camera folder, press down on CTRL and click on the images you want to transfer and right-click and copy these images. NOTE: Do not take your finger off the CTRL key until after you right-click.
5) Under the Libraries folder, click on the Pictures tab and right-click and go to New and select Folder. Name this new folder ImageJ Pictures and double click on this folder. You can now right-click and paste the images taken by your smartphone into this folder.
6) Go to your desktop and double-click on the ImageJ icon and when ImageJ opens, go to the top left of the bar and click on File, next click Open.
7) A folder will appear on your screen, and on the left click the Libraries icon, next double-click the Pictures icon. In the Pictures folder, find the ImageJ Pictures folder you previously created and double-click on that folder.
8) In the ImageJ Picture folder, select an image (you can only select one image at a time) and click Open. In a few seconds, the image will be appear on your screen.
Research and Development
Specific Cancer Marker Detection - The Underlying Technology
The reason that the cancer-associated sequence of r17879961 will produce a DNA signal while the non-cancer DNA sequence of the same SNP (single nucleotide polymorphism) will not produce a DNA signal lies in the arrangement of nucleotides at the molecular level. The lack of a DNA signal is due to the inability of the reverse primer to bind to the forward strand during the annealing phase of PCR. To detect the cancer-associated sequence of r17879961, the reverse primer AAC TCT TAC ACT CGA TAC AT is used. This is because the cancer-associated mutation is represented by a single nucleotide in a particular triplet: instead of the normal ATT, the middle T mutates into a C, thus rendering a triplet of ACT (which you can see in the reverse primer shown above). At the protein level, this mutation of 1 nucleotide changes the coded protein from isoleucine to threonine. As a result, the primer will not attach to the normal r17879961 DNA sequence as it will not have the corresponding base pairs (TGA) in the particular section of DNA that the mutated sequence would have.
(BONUS points: Use a program like Powerpoint, Word, Illustrator, Microsoft Paint, etc. to illustrate how primers bind to the cancer DNA template, and how Taq polymerases amplify the DNA. Screen-captures from the OpenPCR tutorial might be useful. Be sure to credit the source if you borrow images.)
Results
(Your group will add the results of your Fluorimeter measurements from Week 4 here)
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Biomod/2011/MIT/Origami
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''Effective Drug Delivery Vehicles Exhibiting Specific Deformation Programmability''
''Effective Drug Delivery Vehicles Exhibiting Specific Deformation Programmability''
Revision as of 19:37, 2 November 2011
Image:INSERT BANNER HERE.jpg
Home Motivation Process Potential Scrapped Ideas Team Members Literature Software
==Abstract== Effective Drug Delivery Vehicles Exhibiting Specific Deformation Programmability
The synthetic technique of DNA origami, involving a single scaffold strand being folded into arbitrary shapes through the attachment of smaller staple strands to various locations along its sequence, has provided a powerfully programmable framework for the spatial design of nanostructures. Our research has involved adding an additional layer of programmability to these constructs, the ability to respond to external stimuli viz. electromagnetic radiation and pH by means of conformational changes. In particular we are exploring how these stimuli stabilize/destabilize linkers in the DNA origami so as to cause the structure to collapse and expand; thereby dramatically enhancing the utility of DNA nanostructures in controlled particle release. An immediately apparent application for such a technology is the precise delivery of drugs at certain targets as a result of stimulated release.
Contents
Team
Undergrads
• Aliya Dincer
• Maria Elena Martinez
• Michael Hernandez
Graduate Student Mentors
• Matthew Adendorff
• Ishan Gupta
Faculty Mentor
• Professor Mark Bathe
Useful Websites
• News story on the MIT webpage about work currently being done in the LCBB on DNA Origami - [1]
• Laboratory for Cell Biology and Biophysics, MIT- [2]
• Laboratory for Biomolecular Nanotechnology, TUM - [3]
• International Bio-Molecular Design Competition - [4]
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Cfrench:KodPCR
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Cloning parts by PCR using Kod polymerase
18 July 2008.
Kod Hot Start is a proof-reading polymerase distributed by Novagen. It is claimed to be as accurate as Pfu and 4 to 5 times faster. It comes with three solutions: 10 x reaction buffer, 2 mM dNTP mixture, and 25 mM MgSO4. These are stored in the 'PCR reagents' box in the freezer. before you start, take these out, thaw them, making sure they are completely thawed and well mixed before use, and store them on ice. Then, to a 0.5 ml PCR tube add:
• about 32 microlitres of water (adjust the amount to get 50 microlitres total volume at the end)
• 5 microlitres of 10 x reaction buffer
• 5 microlitres of 2 mM dNTP mix
• 3 microlitres of 25 mM MgSO4
• 1.5 microlitres of primer mixture (at 10 pmol/microlitre each)
• 1 to 2 microlitres of template (DNA or cell suspension)
• 1 microlitre of Kod polymerase (in the blue freezer box with the other enzymes).
To mix the reaction, set your P200 to 50 microlitres and pipette it gently up and down a few times, making sure that you don't introduce bubbles.
The cycling protocol is as follows: Program 1: initial denaturation at 95 C for 2 minutes. Links to program 3. Program 3: 30 cycles. Segment 1, 95 C for 20 seconds. Segment 2, annealing temperature for 10 seconds. Segment 3, extend at 70 C. Links to program 4. Program 4: chase at 70 C for 10 minutes, then cool to 4 C and hold.
The recommended extension time is 10 seconds/kb for fragments below 0.5 kb; 15 seconds/kb for fragments of 0.5 to 1 kb; 20 seconds/kb for fragments of 1 to 3 kb; and 25 seconds per kb for fragments of greater than 3 kb. (By comparison, Taq uses 1 minute/kb and Pfu 2 minutes/kb).
We have had good success with Kod Hot Start. The short extension time makes it ideal for fusion PCR, site-directed mutagenesis and other protocols where relatively long fragments (vector plus insert) are to be amplified.
Modification for high-GC templates
For high-GC templates or other difficult templates, we have found it advantageous to
• Add 10 microlitres of 50% v/v glycerol to the reaction mixture, decreasing the amount of water to maintain the same final volume. (We also tried DMSO, but glycerol seemed to work better.)
• Increase the length of the 95 C denaturation step in each cycle from 20 seconds to 1 minute.
In those cases where we have tried it, doing both of these things together works much better than just doing either one of them without the other. Theoretically, glycerol should decrease the strength of GC bonds (I think), so it might be necessary to use a slightly lower annealing temperature - we have not investigated this in any systematic way.
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Quotation added by staff
Why not add this quote to your bookmarks?
Our Constitution was made only for a moral and religious people. It is wholly inadequate to the government of any other. Adams, John
This quote is about freedom · Search on Google Books to find all references and sources for this quotation.
A bit about Adams, John ...
John Adams (October 30, 1735 July 4, 1826) was the first (1789 1797) Vice President of the United States, and the second (1797 1801) President of the United States.
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Quotation added by staff
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But I believe this: by and large, the United States ought to be able to choose for its President anybody that it wants, regardless of the number of terms he has served. That is what I believe. Now, some people have said You let him get enough power and this will lead toward a one-party government. That, I dont believe. I have got the utmost faith in the long-term common sense of the American people. Therefore, I dont think there should be any inhibitions other than those that were in the 35-year age limit and so on. I think that was enough, myself. Eisenhower, Dwight D.
Source: President DWIGHT D. EISENHOWER, answer to question seeking his views on limiting U.S. presidents to two terms, news conference, Washington, D.C., October 5, 1956.Public Papers of the Presidents of the United States: Dwight D. Eisenhower, 1956, p. 862. · This quote is about uncategorised · Search on Google Books to find all references and sources for this quotation.
A bit about Eisenhower, Dwight D. ...
Dwight David "Ike" Eisenhower (October 14, 1890 March 28, 1969) was an American soldier and politician. He served as the 34th President of the United States (19531961) as well as Supreme Commander of the Allied forces in Europe during World War II, with the rank of General of the Army.
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SR04
built by David P. Anderson
Click on an image to enlarge it
Target Environment Locomotion Method
Indoors 3 Wheels
Sensors / Input Devices Actuators / Output Devices
bumper switches
IR proximity detectors
stereo sonar
photo detectors
passive IR motion detectors
shaft encoders
2 DC motors
Can gripper
LCD readout
LED state indicators
Speaker for audio indications
Control Method Power Source
Autonomous Battery
CPU Type Operating System
Motorola HC11 None
Programming Lanuage Weight
C N/A
Time to build Cost to build
N/A N/A
URL for more information
http://www.geology.smu.edu/~dpa-www/robots/sr04/sr04.html
Comments
SR04 is a small mobile robot suitable for exploring human habitats unattended. It is controlled by a Motorola HC6811 microprocessor running in an M.I.T. 6.270 CPU card, similar to the commercially available "Handy Board." Two 12-volt DC gear-head motors maneuver the robot in a dual-differential drive configuration, balanced by a non-driven tail wheel caster and powered by a 12 volt 2.2 amp-hour sealed lead acid battery. Sensory input is provided by (in order of priority): front bumper switches, IR collision avoidance, stereo sonar ranging, photo detectors, passive IR motion detection, and shaft-encoder odometry.
This is my fourth robot project, the prior three were constructed with Lego Techniques ® and variously controlled by analog hardware, a New Micros HC6811 Forth CPU, and the "Rug Warrior" CPU card sold in conjunction with Flynn’s excellent "Mobile Robots" book. This design has evolved from those robots and from many long conversations with friend and veteran robot builder Duane Gustavus.
Sorted by Robot
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Sorted by Builder
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SCP-387
rating: +149+x
SCP-387 spread out
Item #: SCP-387
Object Class: Safe
Special Containment Procedures: Due to the nature of this object and the almost nonexistent harm it poses, it is stationed in a storage container in Site-19, with a standard lock on it as the SCP does not present any danger. The red tub in which SCP-387 is contained does not possess any unusual properties itself, as has been determined through testing but SCP-387 will not duplicate itself unless at least a layer of it covers the bottom of the aforementioned container. A sheet is available for those wishing to utilise SCP-387, and access will be revoked if it is not properly restored.
Description: SCP-387 is a tub of commercially available Lego, normal in design. Irregular shapes not featured in normal sets, such as circular “wheels,” and prisms, are also available. It has no brand name, and every company interviewed by undercover Agents thus far has denied ever making irregular Lego. When the tub is not full (i.e. when it is partially or almost-fully emptied) the Lego will slowly duplicate themselves, stopping when the container is full.
The interesting property of SCP-387 is that, when constructed by a human hand (see Addendum 387-d) the constructions will animate themselves, performing activities based on their surroundings. For example, if a Legoman – which is a “man” constructed using the provided humanoid parts - is placed within a car, it will begin to drive it. Further experimentation has revealed that the car (and indeed, any complex machine) needs no internal engine or power source. The legopeople have some form of sentience, as they interact with each other quite readily.
If left over time, the constructed people and buildings will evolve. They will take on occupations based on the buildings around them, (e.g. some people will become firemen and use firetrucks if the corresponding objects are there). They will also use SCP-387 to construct more things to expand their society. Humans can interact with them quite peacefully, but if a human becomes hostile to them, they will immediately cease all activity and become inanimate.
SCP-387 was found in February of 20██ by Agent H████. During a long train ride back to the city he lived in, Agent H████ idly constructed a man from SCP-387 (which was in the seat beside him at the time). Several seconds later it became animated. Agent H████ quickly disassembled the man and delivered the item to Site 19 for analysis, where it now remains. The security tapes from the train were confiscated and destroyed before they could be reviewed.
Optional information: SCP-387 should not be given to children under the age of 10, especially if said child(s) is influenced by cartoons and television shows. See Addendum 387-b.
Experiment 387-a: A small community of SCP-387 is formed in a testing chamber. A plane constructed from normal Lego was placed to the side of the community. Over the next three (3) hours, the following changes were observed:
- Several Legomen procured some equipment from SCP-387, heading over towards the plane.
- With incredible efficiency, the Legomen constructed what was, for all intents and purposes, a working airport, the specific pieces having been supplied by SCP-387, without visible signal.
- A petrol tank zoomed over to said plane, apparently filled it with fuel (despite earlier observations that vehicles constructed from SCP-387 do not require fuel) and the plane proceeded to literally take off, flying around the room at low speeds and altitude, seemingly to avoid crashing.
- More planes, of different make and design, were formed soon after.
Addendum 387-1: Judging by this, I’d say that constructions of SCP-387 have some form of understanding of the surrounding environment and they are able to convert existing Lego to 387. – Dr. Arch
Experiment 387-b: Several young children were given SCP-387 and were given instructions to use their imagination. The children, who had their memories of this experiment removed, began constructing various objects. After having noticed that they were animate, they excitedly conferred, and began building several objects that they intended to use in battling each other. These included a Transformer, an M1 Abrams Tank and several [EXPUNGED] The children were instantly removed, at which point the creations began to fire and the creations destroyed, though not after considerable effort.
Addendum 387-1: How the fuck did these children gain knowledge of the workings of a M1 Abrams Tank, no less [EXPUNGED]!? I’m not responsible for cleaning out the mess those things make, if anyone is stupid enough to let children go at SCP-387. I am not recommending an upgrade to Euclid, as the constructions did not fire whilst in the presence of humans. This has been tested with adults and proved just as correct. - Dr. Arch
Experiment 387-c: The red tub that contains SCP-387 is emptied of Lego. Commercially available Lego is then placed in the tub for a minute. Constructed objects are inanimate, and remain so. SCP-387 replaced. It is noted that the Lego placed within the tub also did not duplicate itself.
Experiment 387-c-2: A single block of SCP-387 is placed within the red tub. It does not replicate. More of SCP-387 is added until the bottom layer is covered, at which point it began to replicate itself quite rapidly until it had been filled. The amount of SCP-387 removed from the tub continued to work. Similarly, when an amount of SCP-387 higher than the tub’s capacity was placed upon the tub, it shrank until the red tub was fully filled.
Addendum 387-3: It appears that the red tub itself has no abilities by itself, but SCP-387 will not duplicate itself unless in that particular tub. Perhaps this is a copyright mechanism that stops copies of 387 being made. Further experimentation needed. – Dr. Arch
Experiment 387-d: A robotic arm was used to construct a car out of 387. It did not animate. This test was repeated with a human hand, at which point the car animated as usual. A dead hand from a recently-dismembered Agent was used, to no response. The hand was then heated, which still provoked no response.
Addendum 387-4: It appears that 387 responds to a pulse, or some other detection of human life. – Dr. Arch
Addendum 387-5: This SCP has been in high demand for extended use, as further testing has revealed no more anomalies or features. In the personnel tested, SCP-387 has improved morale and attitude by 87%. People are really kids at heart here. As such, I am recommending that all personnel be given free access for recreational use. – Dr. Arch
Request approved.
Experiment 387-e: Once a normal community of 387 was constructed, a small mound of Megablocks (a common copy of Lego) was placed near the community. When this happened, everything constructed of 387 stopped moving, turned slowly towards the Megablocks and [EXPUNGED].
Addendum 387-6: Jesus fucking Christ. - Dr. Arch
Unless otherwise stated, the content of this page is licensed under Creative Commons Attribution-ShareAlike 3.0 License
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Help Wikitravel grow by contributing to an article! Learn how.
Rajshahi
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Rajshahi is the capital of Rajshahi Division in Bangladesh.
[edit] Understand
Rajshahi is the capital of Rajshahi District and Division in northwestern Bangladesh. The Rajshahi municipality was established in 1876, one of the first in Bangladesh. There is a total population of 700,000 people. One of the major rivers of the Indian subcontinent, the Padma, runs along the southern end of the city.
The city is home to many educational institutions, leading to a large student population and the nickname of "education city". The city is in proximity to many ancient capitals of Bengal, notably 'Lakhnoiti' or 'Lokhnaboti' and 'Pundra'. Rajshahi is famous for trade in many exotic items, including pure silk, mangoes and lychees. Attractive silk products are cheaper in Rajshahi than anywhere else in the country, with the city often referred to as the 'silk city'. There are also a number ancient mosques, shrines and temples in and around Rajshahi. The city of Rajshahi was declared as the happiest city in the world by the World Happiness Survey in 2006.
[edit] Get in
[edit] By plane
Shah Makhdum Airport is the primary airport of the city. At the time of writing, United Airlines had flights to Dhaka on Thursdays and Sundays, as well as flights to Saidpur. But the schedule changes frequently, and sometimes the airport has no services at all.
[edit] By bus
It takes approximately 5 hours by road to reach Rajshahi from the capital, Dhaka. A number of bus services are available from Dhaka via Natore, some with air-conditioning. Bus services to other major districts are also available from the bus terminal.
Some bus services for Dhaka to Rajshahi are
• Greenline Volvo -
• Hanif Enterprise - Tk 1000
• NP Elegance
• Modern Enterprise
• National Travels - Tk 400
• Shamoli Paribahan
[edit] By train
There are a number of luxurious intercity services between Dhaka and Rajshahi each day. The main ones are the Padma Express, the Silksity Express and the Dhumketue Express.
• Silk City Express - Dhaka to Rajshahi at 2:40 PM and from Rajshahi to Dhaka at 07:35 AM.
• Padma Express - Dhaka to Rajshahi at 22:45 and from Rajshahi to Dhaka at 04:00 PM.
• Dhumketue Express - departs Dhaka at 6:00AM, reaching Rajshahi at 12:00 PM, and departs Rajshahi at 11:20PM, reaching Dhaka at 4:50AM
The Silk City Express does not operate Sundays, the Padma Express has no service on Tuesdays, and the Dhumketue Express does not run Mondays.
[edit] By car
The journey from Dhaka is 261km, taking approximately 6 hours, depending on traffic. One must cross the famous Jamuna Bridge to reach the city.
[edit] Get around
The usual forms of Bangladeshi transport are available in the city; taxis, rickshaws and auto-rickshaw CNGs. Negotiated and metered fares will usually be cheaper than in Dhaka. Like anywhere in the country, there are a lot of people and vehicles on the road, but the traffic is significantly quieter than in the capital.
[edit][add listing] See
• Banks of the Padma. A lovely sight of one of the largest rivers in South Asia. During the Monsoon season, the water level rises, along with its beauty. edit
• Varendra Research Museum, [1]. Established in 1910, the museum is dedicated to ancient history and culture. It is recognised as the oldest museum in the country. It has a rich collection of artefacts, relating to Hindu, Buddhist and Muslim heritage. Some of these date back to the 16th century. It is maintained by the University, located in the heart of town. Free. edit
• Shrine of Hazrat Shah Makhdum(Rh.). A Majar (shrine) was established to mark the resting place of Hazrat Shah Makhdum in 1635 AD. He was the first preacher of Islam in the region. Legend has it that he arrived by riding down the Padma on 2 crocodiles. To preserve this myth, some crocodiles are kept in the pond next to the shrine. edit
• Central Park and Zoo. The park is a wide area with lush green trees and grass. The zoo houses a variety of different animal species. It is located by the bank of river Padma. edit
• Puthia Palace. Situated a little far away from the city. Its an ancient palace which attracts all to visit. edit
• Shahid Zia Park. An amusement park for pleasure. It has mono rail, bumping cars and many other exciting things for amusement. It is under the Rajshahi City Corporation. edit
• Bagha Mosque. A historical mosque situated in Bagha of Rajshahi. There is a picture of this mosque in one side of 50 taka note. edit
• Rajshahi University (University of Rajshahi). You must see this well-planned beautiful green campus before leaving Rajshahi. It is within a few kilometers from the city centre and easily accessible. edit
• Ghoramara. The oldest part of Rajshahi City, consisting most of oldest (70-100 year old) buildings. edit
• Kashia-Danga. From this area massive mango tree garden area of Rajshahi starts. Anyone can have a glimpse of famous mangoe's tree of Rajshahi from this area. The area is at the west part of the city, near to Rajshahi court railway station. edit
• Santal Para. Located inside the Mahish-Bathan Area. Some santal tribes people lives here. Anyone can have a look to their tribal life. edit
[edit][add listing] Do
• Rajshahi University. You must see this well-planned beautiful green campus before leaving Rajshahi. It is within a few kilometers from the city centre and easily accessible. edit
[edit][add listing] Buy
• Shopping Mall & Fashion Stores: These fashion clothing stores and mall are located in the center of the city. Both traditional and western style clothes are available here.
• Shaheb Bazaar
• RDA Market
• Rani Bazaar
• New Market
• Madrasha Market
• Style Zone
• Look Me
• Nanking Bazar
• Index plaza
• Cats Eye
• Iota Style Zone
• Uposhahor New Market,Uposhahor
• RDA Market, Shaheb Bazaar, Zero Point, Sahebbazar, Rajshahi. (The oldest market of the city) edit
[edit][add listing] Eat
Some nice restaurants and fast food places are available in the city.
• Nanking Chinese Restaurant, Monibazar, 774120. The best Chinese restaurant in the town. Also provides Indian fast foo edit
• Party Point, Shalbagan, 01711346484. edit
• Razia Chinese Restaurant, Shalbagan. edit
• Aristocrat Chinese Restaurant and Catering, Shaheb Bazar. 100 tk. edit
• Chili's Chinese Restaurant, Shaheb Bazar. edit
• Safa Wang Chinese Restaurant, Greater Road. edit
[edit][add listing] Sleep
Hotels rates are cheap in the city($13.50 per night). Most accommodations are available in these hotels.
• Red Castle Inn. One of the better places in town. However, backup generator cannot run air conditioning. Tk3,000. edit
• Rajshahi Parjatan Motel. edit
• Hotel Nice International, Shaheb Bazar. edit
• Way Home. edit
• Hotel Galaxy, Laxmipur. edit
• Hotel Haq's International. edit
• Hotel Mukta International, Batar Mor. Renovation is going on at the moment (March 2012) A/C room cost 1200. 1200. edit
• Hotel Century, Luxmipur, 0721-775063. This is one of the nice hotels in Rajshahi. Price is cheap here with Air-Conditioned Rooms and Parking. edit
[edit] Internet Service
• ISP
1. Librabd - [2] -
2. SKYLINK -Rajshahi Malopara, Ghorama, Rajshahi 610
• CyberCafe
1. Zeropoint Computing - Location: Top of the Ground Floor, Jamal Super Market, Saheb Bazar, Rajshahi.
2. Syenthiya Computer
3. Chartered Computer
• Web Development Company
1. Zeropoint Computing, Jamal Super Market, Saheb Bazar - [3]
1. GIIT(Global institute of Information Technology)-(http://www.giitbd.com)
belder para more,Rajshahi.
[edit] Get out
This article is an outline and needs more content. It has a template, but there is not enough information present. Please plunge forward and help it grow!
[edit] Recreation Place
: Sopnobilas Horticulture Park, Kazir Para,
Near Bharuapara, aHarian, P.S Puthia,
Rajshahi Bypass Road
there are 2storied Guest House, 2 Swimming Pool, 2 Picnic Spot,Mini Zoo, THOUSANDS OF TREE, 10 TOWER, 1 POND, & mORE...........
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
8731.0 - Building Approvals, Australia, May 2010 Quality Declaration
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 01/07/2010
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Provides the number and value of dwelling units approved by sector (public/private) and by state, number and value of new other residential dwelling units approved by type of building, and the number and value of non-residential building jobs approved by type of building (i.e. by function such as 'retail and wholesale trade', 'offices') and value ranges. State data includes the number of private sector houses approved; number and value of new other residential dwellings by type of building such as flats, units or apartments in a building of one or two storeys; number and value of non-residential building jobs by type of building and sector; and for Capital City Statistical Divisions, the total number of dwelling units approved broken down by Houses, Other Dwellings and Total Dwelling Units. Seasonally adjusted and trend estimates by state are included for the number of dwelling units and value of building approved. The quarterly value of building approved is shown in chain volume measure terms.
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Catalogue Number
4500.0 - Crime and Justice News, July 2011 to June 2012
Latest ISSUE Released at 11:30 AM (CANBERRA TIME) 26/07/2012
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Welcome from the Director
New series released! In Focus: Crime and Justice
Expanded range of information now available about federal offences
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Upcoming publications
Cybercrime: Framework development consultations
Review of the Corrective Services Collection
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Category:BahamasEdit This Page
From FamilySearch Wiki
Revision as of 06:08, 27 March 2008 by DiltsGD (Talk | contribs)
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Welcome to the Bahamas category page.
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Contributor
31May2010,15:53 #31
we can hide any folder/file by the folder option properties in control panel(Do not show hidden files and folders).
we can also hide folder by using any folder lock software which provides password facility .
Light Poster
17Jun2010,16:32 #32
Awesome article. Eager to try this to protect my Important files and folders.
Thanx a lot for sharing your knowledge with us...
Newbie Member
30Jul2010,00:27 #33
Great tool to use
**** ytour all
Contributor
30Jul2010,20:26 #34
What happens if you encrypt your windows?
Go4Expert Founder
31Jul2010,09:12 #35
Quote:
Originally Posted by johnny.dacu
What happens if you encrypt your windows?
It gets encrypted.
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View Poll Results: Would i will be able to learn complete hacking
100% 1 50.00%
Dont know 0 0%
50-50 1 50.00%
dont care 0 0%
Voters: 2. You may not vote on this poll
Adi The First Intro
Go4Expert Member
2Jul2007,17:36 #1
Hi its me adi I wnat to learn ethical hacking tht's why i have joined this huge site
i am happyfdg
Go4Expert Founder
2Jul2007,18:25 #2
Welcome to the forum and there is nothing called complete hacking.
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About this Journal Submit a Manuscript Table of Contents
ISRN Meteorology
Volume 2012 (2012), Article ID 625318, 7 pages
doi:10.5402/2012/625318
Research Article
Influence of Stratospheric Intrusion on the Surface Ozone Levels in India
Department of Physics, St. Xavier's College, Ahmedabad 380009, India
Received 5 April 2012; Accepted 21 June 2012
Academic Editors: S. Iizuka, N. A. Mazzeo, and D. Moreira
Copyright © 2012 Nandita D. Ganguly. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Linked References
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17. E. L. Avol, W. C. Navidi, E. B. Rappaport, and J. M. Peters, “Acute effects of ambient ozone on asthmatic, wheezy, and healthy children,” Research Report, no. 82, pp. 1–30, 1998. View at Scopus
18. R. J. Delfino, A. M. Murphy-Moulton, and M. R. Becklake, “Emergency room visits for respiratory illnesses among the elderly in Montreal: association with low level ozone exposure,” Environmental Research, vol. 76, no. 2, pp. 67–77, 1998. View at Publisher · View at Google Scholar · View at Scopus
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20. World Meteorological Organization, “Atmospheric ozone 1985: global ozone research and monitoring report,” WMO Report 16, Geneva, Switzerland, 1986.
21. P. Cristofanelli, A. Bracci, M. Sprenger et al., “Tropospheric ozone variations at the nepal climate Observatory-Pyramid (Himalayas, 5079 m a.s.l.) and influence of deep stratospheric intrusion events,” Atmospheric Chemistry and Physics, vol. 10, no. 14, pp. 6537–6549, 2010. View at Publisher · View at Google Scholar · View at Scopus
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24. J. P. Peixoto and A. H. Oort, Physics of Climate, American Institute of Physics, New York, NY, USA, 1992.
25. V. H. Annes, K. Mohankumar, and P. V. Joseph, “Winter and summer hadley circulations over Peninsular India as monitored by mst radar at Gadanki (13.47°N, 79.18°E),” International Journal of Climatology, vol. 21, no. 5, pp. 593–601, 2001. View at Publisher · View at Google Scholar · View at Scopus
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A primer on water law and policy in India
The objective of this primer is to introduce the water law and policy framework in India, including the ongoing water sector/ law reforms, to members of the public, civil society organisations, and government representatives. The primer encapsulates water laws, the current water law reforms; their impacts and issues for further advocacy. It is hoped that the contents of this primer will raise more questions about the ongoing reform process, which will facilitate dialogue and a better understanding of the problems plaguing the sector, and eventually result in more effective and equitable solutions.
Attachment(s):
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}
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The free office suite
Download LibreOffice
LibreOffice Windows, version 3.6.2, Sinhala. Not the version you wanted? Change System, Version or Language
You need to download and install these files in order:
• Source code
LibreOffice is an open source project and you can therefore download the source code to build your own installer.
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Pharmaceuticals 2010, 3(10), 3212-3239; doi:10.3390/ph3103212
Review
Malaria Prophylaxis: A Comprehensive Review
1 Institute for Infectious and Tropical Diseases, University of Brescia, Piazza Spedali Civili, 1 - 25123–Brescia, Italy 2 Institute for Infectious Diseases, University of Catania, Via Palermo 635 – 95100 Catania, Italy
* Author to whom correspondence should be addressed.
Received: 1 September 2010; in revised form: 7 October 2010 / Accepted: 11 October 2010 / Published: 13 October 2010
(This article belongs to the Special Issue Tropical Medicine)
Download PDF Full-Text [202 KB, uploaded 13 October 2010 12:41 CEST]
Abstract: The flow of international travellers to and from malaria-endemic areas, especially Africa, has increased in recent years. Apart from the very high morbidity and mortality burden imposed on malaria-endemic areas, imported malaria is the main cause of fever possibly causing severe disease and death in travellers coming from tropical and subtropical areas, particularly Sub-Saharan Africa. The importance of behavioural preventive measures (bed nets, repellents, etc.), adequate chemoprophylaxis and, in selected circumstances, stand-by emergency treatment may not be overemphasized. However, no prophylactic regimen may offer complete protection. Expert advice is needed to tailor prophylactic advice according to traveller (age, baseline clinical conditions, etc.) and travel (destination, season, etc.) characteristics in order to reduce malaria risk.
Keywords: malaria; prophylaxis; traveller
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Cite This Article
MDPI and ACS Style
Castelli, F.; Odolini, S.; Autino, B.; Foca, E.; Russo, R. Malaria Prophylaxis: A Comprehensive Review. Pharmaceuticals 2010, 3, 3212-3239.
AMA Style
Castelli F, Odolini S, Autino B, Foca E, Russo R. Malaria Prophylaxis: A Comprehensive Review. Pharmaceuticals. 2010; 3(10):3212-3239.
Chicago/Turabian Style
Castelli, Francesco; Odolini, Silvia; Autino, Beatrice; Foca, Emanuele; Russo, Rosario. 2010. "Malaria Prophylaxis: A Comprehensive Review." Pharmaceuticals 3, no. 10: 3212-3239.
Pharmaceuticals EISSN 1424-8247 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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Contributors : parafin
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Tell me more ×
Answers OnStartups is a question and answer site for entrepreneurs looking to start or run a new business. It's 100% free, no registration required.
I have created an affiliate program for my web site selling single property websites. I have set everything up on my website to handle it and I don't want to use an affiliate network like Commission Junction to promote it. My marketing place basically consists of
• Promotion via the websites existing Twitter account
• Ramp up the Facebook friends page
• Regular blog posts
• Article submissions
• Being involved in affiliate forums
Is there anything else I should be doing and how would you prioritize these activities.
share|improve this question
2 Answers
Figure out where your customers hang out, which blogs they visit, which forums they visit, which LinkedIn groups they use, who they follow on twitter, everywhere they hang out.
Then choose the top place and try and speak to them directly - ask for an introduction if possible, email them, call them on the phone and explain to them why they should promote your product.
Simples.
share|improve this answer
Google always has free $100 coupons for Adwords. Get a coupon, and experiment with PPC (I would stick with just the Search network, don't try the content network yet). Spend your free $100, and measure your ROI.
Also, do some keyword research (both for your articles and your PPC), and target highly search keywords.
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101 reputation
1
bio website None
location Nashville, TN
age 22
visits member for 7 months
seen Sep 25 '12 at 19:30
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I'm a senior Computer Science/Audio Engineering Technology major at Belmont University. My general hobbies include programming, electronics, and music. Long term electronics project would be a fully analog synth, since I just so happen to be a keys a player and a synth enthusiast. Mostly here to learn but would love to soon know enough to be able to help.
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Research article
Quantification of the whole-body burden of radiographic osteoarthritis using factor analysis
Amanda E Nelson1*, Robert F DeVellis1,2, Jordan B Renner1,3, Todd A Schwartz1,4, Philip G Conaghan5, Virginia B Kraus6 and Joanne M Jordan1
Author affiliations
1 Thurston Arthritis Research Center, University of North Carolina, 3300 Thurston Building CB 7280, Chapel Hill, NC, 27599, USA
2 Department of Health Behavior and Health Education, Gillings School of Global Public Health, University of North Carolina, 302 Rosenau Hall, Chapel Hill, NC, 27599, USA
3 Department of Radiology, University of North Carolina, 101 Manning Drive, Chapel Hill, NC, 27514, USA
4 Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina, 3106E McGavran-Greenberg Hall, Chapel Hill, NC, 27599, USA
5 Section of Musculoskeletal Disease, University of Leeds & NIHR Leeds Musculoskeletal Biomedical Research Unit, Chapel Allerton Hospital, Chapeltown Road, Leeds, LS7 4SA, UK
6 Department of Medicine, Duke University Medical Center, 595 La Salle St, Durham, NC, 27710, USA
For all author emails, please log on.
Citation and License
Arthritis Research & Therapy 2011, 13:R176 doi:10.1186/ar3501
The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/content/13/5/R176
Received:26 April 2011
Revisions received:5 July 2011
Accepted:25 October 2011
Published:25 October 2011
© 2011 Nelson et al.; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Introduction
Although osteoarthritis (OA) commonly involves multiple joints, no widely accepted method for quantifying whole-body OA burden exists. Therefore, our aim was to apply factor analytic methods to radiographic OA (rOA) grades across multiple joint sites, representing both presence and severity, to quantify the burden of rOA.
Methods
We used cross-sectional data from the Johnston County Osteoarthritis Project. The sample (n = 2092) had a mean age of 65 ± 11 years, body mass index (BMI) 31 ± 7 kg/m2, with 33% men and 34% African Americans. A single expert reader (intra-rater κ = 0.89) provided radiographic grades based on standard atlases for the hands (30 joints, including bilateral distal and proximal interphalangeal [IP], thumb IP, metacarpophalangeal [MCP] and carpometacarpal [CMC] joints), knees (patellofemoral and tibiofemoral, 4 joints), hips (2 joints), and spine (5 levels [L1/2 to L5/S1]). All grades were entered into an exploratory common factor analysis as continuous variables. Stratified factor analyses were used to look for differences by gender, race, age, and cohort subgroups.
Results
Four factors were identified as follows: IP/CMC factor (20 joints), MCP factor (8 joints), Knee factor (4 joints), Spine factor (5 levels). These factors had high internal consistency reliability (Cronbach's α range 0.80 to 0.95), were not collapsible into a single factor, and had moderate between-factor correlations (Pearson correlation coefficient r = 0.24 to 0.44). There were no major differences in factor structure when stratified by subgroup.
Conclusions
The 4 factors obtained in this analysis indicate that the variables contained within each factor share an underlying cause, but the 4 factors are distinct, suggesting that combining these joint sites into one overall measure is not appropriate. Using such factors to reflect multi-joint rOA in statistical models can reduce the number of variables needed and increase precision.
Keywords:
Radiography; osteoarthritis; factor analysis
Introduction
Generalized osteoarthritis (OA) as a disease entity has been described for well over 100 years [1]. In 1952, Kellgren described multiple joint OA involvement (feet, facet joints, knees, hips, and other limb joints) among individuals with Heberden's nodes and/or carpometacarpal (CMC) OA [2]. He states in this paper that although many individuals had "polyarticular OA" without nodes or CMC OA, "we are not yet prepared to make this diagnosis [primary generalized OA] in the absence of Heberden's nodes or arthritis of the first CMC joints [2]." Since that time, published reports have defined generalized OA in a variety of ways, including nodal with large joint OA, more than three or five joints or joint sites involved [3], summed numbers or grades of affected joints [4-7], multiple hand joints [8], or nodal hand OA with other joints involved [9]. However, there remains no widely accepted and universally used definition of generalized OA in the literature despite widespread use of the term itself.
This lack of an accepted definition makes it difficult to quantify the effect of multiple joint involvement on OA outcomes, leading to the common practice of focusing on a single joint site without considering the contribution of other involved sites. This is particularly problematic in the setting of systemic factors, such as functional disability, performance-based outcomes requiring the use of multiple joint sites, serum/urine biomarkers, and genetics, which are necessarily a reflection of the whole-body burden of OA and the impact of that burden on the individual. In this setting, it would be advantageous to have a parsimonious composite measure(s) that could be included in a statistical model to account for the whole-body burden of OA.
Factor analysis, a method used for 80 years in the social sciences [10-12], provides a way to determine whether a set of variables has one or more relatively global underlying variables that can account for the observed correlations among the analyzed items [10]. Thus, this analytic approach can clarify the extent to which one or more explanatory concepts or dimensions account for most of the shared variation among the variables. Composite scores combining such variables can then be used in further statistical modeling of an outcome of interest, reducing dimensionality of models and increasing estimate precision. Factor analysis was developed for intelligence testing [11], then expanded to other psychological variables, and now frequently used in validation of multi-item questionnaires in a variety of disciplines [13-16]. Factor analysis and related psychometric methods have been used to evaluate multiple clinical instruments used in arthritis, including the Arthritis Impact Measurement Scales Health Status Questionnaire (AIMS2) [17], Western Ontario and McMaster Universities Arthritis Index (WOMAC) [18], and Australian/Canadian Osteoarthritis Hand Index (AUSCAN) [19].
To our knowledge, these methods have only twice been applied to radiographic data, and then only for the hand [20,21]. However, the potential strength of factor analysis in understanding the whole body burden of radiographic OA (rOA) lies in its ability to account for presence and severity of rOA in multiple joint sites by including the full range of all of the individual radiographic scores. We were therefore interested in applying factor analytic methods to Kellgren-Lawrence global (KL, 0 to 4) and Burnett atlas joint features (0 to 3) radiographic grades [22,23] across multiple joint sites as a way to formulate composite scores of multi-joint rOA, encompassing both presence and severity, using data from participants in the Johnston County Osteoarthritis Project (JoCo OA).
Materials and methods
The analysis used data from the JoCo OA, a population-based prospective cohort study of non-institutionalized African American and white men and women, living in rural North Carolina, aged 45 years and older, both with and without OA, which has been described previously [24]. All participants signed informed consents, and completed two home interviews and one clinic visit with physical examination, including functional measures and radiographs, administered by trained study personnel. Multi-joint radiographs were added at the cohort enrichment (2003 to 2004) and second follow up (2006 to 2010), so data from these time points were used for the current analysis (total n = 2121). Data from a given individual was included from only one time point.
Self-reported age, gender, and race were obtained from interviewer-administered questionnaires, while body mass index (BMI) was calculated in kg/m2 from height (cm) and weight (kg) measured during clinic examination by trained study examiners. This cross-sectional analysis included demographic, clinical, and radiographic data collected at the same time for each participant (either during the 2003 to 2004 or 2006 to 2010 time period). The JoCo OA has been continuously approved by the Institutional Review Boards of the University of North Carolina and of the Centers for Disease Control and Prevention in Atlanta, GA.
Radiographs
Posteroanterior radiographs of the bilateral hands were read for KL grade [22] at each of 30 joints (distal interphalangeal (DIP), proximal interphalangeal (PIP), metacarpophalangeal (MCP), CMC, thumb IP and MCP). Fixed flexion, weight-bearing posteroanterior views of the tibiofemoral joint (TFJ) using the Synaflexer™device (CCBR-Synarc, San Francisco, CA, USA) were read for KL grade. Sunrise views of the patellofemoral joints (PFJ) were read for osteophytes (OST) [25] using the Burnett atlas [23]. PFJ films were added later in the study and had not all been read at the time of this analysis (see also Figure 1). Anteroposterior supine pelvis films were used to assess KL grade at the hips; these films were not performed in women under age 50 years. Lateral lumbosacral spine (LS) films (taken with the participant lying on his/her left side) were read for OST and disc narrowing (DN) at five levels (L1/2 through L5/S1). Joints that had undergone replacement were not included, because no KL or OARSI score could be assigned. Individuals with radiographs suggestive of an underlying inflammatory condition were excluded. All films were read by a single experienced musculoskeletal radiologist (JBR) previously shown to have high intra- and inter-rater reliability (κ = 0.89 and 0.86, respectively) [26].
Figure 1. Participant inclusion and exclusion. Flow diagram showing sample size and exclusions for the analyses. Individuals with evidence of inflammatory changes were excluded, as were those missing radiographic data for each factor; the reasons for missing data are detailed.
Prior to factor analysis, a priori definitions for rOA were determined, such that 1) joints that were not included in any factor could still be included in a model to allow estimates to reflect the whole body burden of rOA and 2) sample characteristics for OA could be summarized. For the hand joints, TFJ, and hip, a KL grade of 2 or more was considered to be diagnostic of rOA in any given joint. For the PFJ, any OST of 2 or more was considered to indicate PFJ OA. LS OA was defined if both OST and DN graded 1 or more were present at a single level [9].
Factor analysis
In this paper, the term factor analysis refers to an exploratory common factor analysis, in which the factors represent hypothetical (latent) variables that are being estimated. Determination of the number of factors to retain can be performed utilizing eigenvalues, scree plots, factor interpretability, and/or parallel analysis, although there remains a level of subjectivity to this decision [10]. We used a scree plot, which allows visual comparison of relative eigenvalues [27]. Variables that did not load well (≤ 0.4) or had cross-loadings, indicating weak relations to the latent variable, were dropped. An oblique rotation, which allows the factors to correlate with each other, was then applied. Higher order factor analysis was used to determine whether the identified factors represented a single latent variable (and could therefore be combined) or contained independent information that would be lost through combination. Cronbach's alpha statistic was calculated as a measure of internal consistency reliability for all factors. Separate factor analyses were performed for each gender (men and women), race (African American and white), age (< 65 compared with 65+ years) and cohort (cohort enrichment versus second follow-up cohorts) subgroup; qualitative comparisons of factor structure and Cronbach's alpha were performed. All analyses were performed in Stata 11.0 (StataCorp, College Station, TX, USA).
Results
Sample characteristics
The inclusion of subjects in the current analysis is presented, along with reasons for exclusion, in Figure 1. Sixteen individuals were excluded due to evidence of inflammatory disease on radiographs; the remainder of excluded individuals were missing radiographic data as shown. Detailed sample characteristics for the total sample (n = 2,092) and the subset with interpreted radiographs for all joint sites (n = 1,373) are shown in Table 1. The subset with all radiographs was slightly older (67.3 versus 65.1 years), with a similar mean BMI and proportion of men and African Americans. About 45% of the participants had OA of the DIP joints, 30% had PIP OA, and 9% had MCP OA. Slightly under one third had CMC OA, while slightly over one third had hip OA. Forty percent had TFJ OA, about 10% had any PFJ OST grade 2 or more, and 60% had LS OA by our definition, with the subset overall similar to the total population (Table 1).
Table 1. Sample characteristics
Factor analysis
All radiographic variables (KL or Burnett atlas joint features scores) were entered into a factor analysis simultaneously as continuous scores, such that each joint site had a score of 0 to 4 or 0 to 3. We explored three-, four-, and five-factor solutions, as all of these were reasonable based on eigenvalues above 1 and scree plot findings (Figure 2). Balancing interpretability and simple structure, we selected a four-factor solution. Then, variables with weak or cross-loadings were dropped from the analysis. The hips had loadings of less than 0.2 in all solutions and were dropped. The first MCPs also had poor loadings (< 0.4), as well as cross-loadings, and were dropped. In a three-factor solution, the separate LS variables (first the DN grades, then the OST grades) had low loadings and so these were dropped, as were the CMC variables (loadings < 0.4). However, when all LS variables were simultaneously included and a four-factor solution was used, these variables had acceptable loadings, as did the CMC joint, and all were retained in the present four-factor solution. In contrast, a five-factor solution caused the LS variables to cross-load onto factors 4 and 5 with lower loadings overall. An oblique rotation was then applied, as we deemed it unlikely that radiographic variables at different joint sites would be entirely independent. In this final solution, we identified four factors that can be thought of as latent variables underlying the individual radiographic variables contained in each (Table 2). The four factors were moderately correlated, with Pearson correlation coefficients ranging from 0.24 to 0.40 (Table 3).
Figure 2. Scree plot. Scree plot using Johnston County Osteoarthritis Project radiographic data. Based on the eigenvalue (the dashed line indicates an eigenvalue of 1.0) and scree plot criteria, a three-, four-, or five-factor solution would be acceptable. Subjective examination based on interpretability and simple structure led the authors to use a four-factor solution.
Table 2. Factor loadings* for each radiographic variable in the four-factor solution after oblique rotation
Table 3. Pearson correlation coefficients between factors in the rotated four-factor solution
The first can be defined as an IP/CMC Factor, and contains the thumb IP and CMC, DIPs 2 to 5 and PIPs 2 to 5 of both hands (factor loadings 0.43 to 0.84). The lowest loadings on this factor were observed for the CMC (0.43 to 0.44), compared with 0.51 to 0.84 for the other included joints. The second factor is an MCP Factor, and includes the MCP joints of the second to fifth fingers of both hands (loadings 0.55 to 0.67). The third is the Knee factor, including the TFJ and PFJ of both knees (loadings 0.70 to 0.86). The fourth factor is the spine factor including DN and OST variables from the five LS levels L1/2 to L5/S1 (loadings 0.38 to 0.70). The lowest loadings were observed for DN and OST at the L4/5 and L5/S1 levels (0.38 to 0.47) compared with the other levels (0.55 to 0.70), but for interpretability, all LS levels were retained. Cronbach's alpha statistic was calculated for each of the final factors to give a measure of reliability, and ranged from 0.80 for the spine factor to 0.95 for the IP/CMC factor (Table 4). The results were essentially unchanged when stratified by gender (α = 0.77 to 0.96), race (α = 0.78 to 0.96), age (α = 0.74 to 0.95), or cohort (α = 0.77 to 0.95) subgroups.
Table 4. Cronbach's alpha (internal consistency reliability) and average inter-variable correlation for the 4 factors
We were interested in the possibility of a single, higher order factor that could be defined as a "generalized rOA" score. However, in our analysis, higher order factor analysis of the four factors showed that they should not be combined into a single factor. For comparison, the individual factors had eigenvalues ranging from 11.7 (IP/CMC factor) to 1.7 (spine factor), compared with values not exceeding 1.1 for the higher order analysis. The loadings of the four factors on the higher order factor ranged from 0.47 to 0.56. In addition, the reliability for this single higher order factor was lower than any of the individual factors at 0.65.
Discussion
We have employed factor analysis as a way of understanding the latent factors underlying radiographic variables in OA. We report a four-factor solution as follows: 1) IP/CMC factor (20 joints), 2) MCP factor (eight joints), 3) knee factor (four joints), and 4) spine factor including DN and OST (5 levels, 10 variables). Use of a composite (e.g., an average or a standardized score) for each of these four factors in a multiple regression model would result in representation of all 20 + 8 + 4 + 10 = 42 underlying variables (or 37 distinct joint sites) through only four explanatory variables. Taking the MCP factor as an example, the individual scores from the eight MCP joints could be added and divided by eight, resulting in a single, average value for the MCP factor rather than eight individual scores. This allows consideration of the whole body burden of rOA in a parsimonious model, resulting in reduced dimensionality and increased precision of the resultant estimates. This is particularly important when considering a systemic outcome, such as a molecular or genetic biomarker, or a performance or disability score, which is likely influenced by the overall rOA burden and not only by the specific joint of interest in a study. The results were similar by age, between men and women, between African Americans and whites, and between members of the two cohorts.
Factor analysis involves some subjective decision-making, particularly when selecting the number of factors to retain and dropping variables that do not load well. The benefits of the four-factor solution are inclusion of the LS and CMC variables, which were not part of the three-factor solution. However, the spine factor has the lowest reliability and contains one variable (osteophytes at L5/S1) with loading less than 0.4, and the reliability of the knee factor is slightly reduced in the four-factor (α = 0.85) compared with the three-factor (α = 0.87) solution. The elimination of the hip variables was robust and similar across all solutions, however, supporting the idea that the hip is not part of the generalized OA construct. Also dropping out in all solutions were the first MCP variables, for reasons that are not immediately obvious, as these joints were involved at a similar frequency to the other MCP joints.
Our results do not support a single underlying latent variable for all joint sites, and are therefore not consistent with the concept of "generalized OA." This is in agreement with a study by MacGregor, et al, who used structural equation modeling to assess relations between knee, hip, PIP, DIP, and CMC rOA (also using the KL grading system) in a population of female twins accounting for shared genetics [28]. The authors found that, while each individual joint site demonstrated genetic influence (heritability estimates 28 to 68%), there was a moderate genetic correlation only between DIP and PIP joints, and little or no correlation between other joint sites [28]. MacGregor et al, conclude from their study that there was "little evidence of the phenotype 'generalized OA,'" consistent with what we found using a different methodology in the present report.
The DIPs and PIPs have long been thought to group together, and bony enlargement of these sites is the basis for a clinical diagnosis of hand OA [29]. MCP involvement is generally thought to be less common than other hand joints and to represent a secondary OA process such as calcium pyrophosphate deposition disease (CPPD) or hemochromatosis. However, as shown by several studies reporting the patterns of hand OA, MCP involvement is not infrequent in radiographic or ultrasonographic OA [6,30], with prevalence estimates ranging from 8% to 36% in Caucasian populations [9,31-33]. MCP rOA has been shown to be more common among African American compared with white women in one study [34]. Our preliminary work on the frequency of hand rOA in the JoCo OA showed that although African Americans were much less likely to have DIP or PIP rOA compared with whites, the frequency of MCP rOA was not different by race [35].
Principal components analysis (rather than exploratory factor analysis as described in the current paper) has been used in other studies of radiographic hand OA [20,21]. Marshall et al, reported on a principal components analysis of radiographic variables in the hand [20]. They identified a four-component model where the DIPs (second to fifth digits, right and left), PIPs (second to fifth digits, right and left), and MCP (only included the second and third bilaterally) joints each grouped onto one component and the thumb joints (IP, MCP, CMC, and trapezioscaphoid) onto the fourth. In contrast to the current study, Marshall et al used binary variables in the factor analysis (rOA defined as KL ≥ 2 at each joint), which is not consistent with the assumptions of factor analysis and does not include information about KL severity. In addition, the authors of that study simplified their results to subgroup patients into finger only, thumb only, and thumb and finger together. Although such phenotyping is useful, it does not fully utilize the power of factor analysis to create meaningful composites. Hunter et al, using osteophyte and joint space narrowing scores in addition to KL scores in a principal components analysis of hand OA, chose a 10-factor solution [21]. The DIP joints loaded on a single factor, as did the PIP joints, with other joints (CMC, individual MCPs, thumb IP) loading on separate factors, and these factors were then used in a genetic association study [21]. We found, in common with Marshall et al and Hunter et al, that the MCPs did not load onto the same factor as the IP joints. However, the DIP and PIP joints grouped together in our study along with the CMC, and we did not identify a separate thumb factor, which may be due to our larger sample size or the above-noted differences in methodology.
Although we included data on the hips in our analysis, we found that the hip joints did not load onto any factor. There has long been controversy whether hip OA is part of the "generalized OA" construct, or a separate entity [36-41]. Our attempt to develop a composite measure of multi-joint OA has shown, in agreement with other researchers [6], that the hip is a separate entity, but it remains unclear whether this is a measurement issue or a true difference in the nature of OA at the hip compared with other sites. Arden, et al, in a study assessing different radiographic definitions of hip OA, found that composite measures such as the KL grade had superior construct and predictive validity compared with single radiographic features (such as osteophytes or joint space narrowing alone), and recommended such measures for defining incident hip rOA [42], supporting our use of this grading system. Hip OA is less influenced by obesity in comparison with knee OA [43-45], and may therefore have other unique risk factors that vary by gender and race. For example, among African Americans compared with Caucasians [46], we have reported a higher prevalence of specific radiographic features, such as superior joint space narrowing, previously found to be predictive of progression to hip replacement [47]. Other recently recognized aspects of hip anatomy, such as femoroacetabular impingement and hip shape as described through active shape modeling, may contribute to hip-specific OA risk [48-51] while not reflecting "generalized OA."
Limitations to the current study include the lack of PFJ joint space narrowing data (although PFJ osteophytes were included due to better reproducibility and associations with knee pain [25]), and of radiographs of other joint sites, such as the feet or cervical spine, although we did have radiographic data for many of the joint sites most commonly affected by rOA. Although we used primarily KL grades for the present analysis, use of individual radiographic features (osteophytes and joint space narrowing), could lead to different conclusions and will be the focus of future analyses. Differences in scaling can cause variables to group on a factor due to differences in scale alone, but while we had some radiographic grades that were based on a 0 to 3 scale while others were on a 0 to 4 scale, we did not observe groupings based solely on this difference in scaling. The factor structure presented here has not yet been replicated in an independent population, and should be considered specific to the JoCo OA study until replication has been confirmed. The factors we have identified should therefore not be used in other populations without confirmation of a similar structure. We have used only radiographic data in this analysis, although other projects are underway to consider symptoms and other variables of importance to an individual's experience of OA.
Conclusions
Combination of multiple radiographic variables using composite scores as described allows consideration of the whole body burden of rOA in parsimonious regression models, resulting in reduced dimensionality and increased estimate precision. This methodology provides a way to define more complete phenotypes in individuals with rOA in statistical models, thus improving study of systemic outcomes in this common and debilitating disease.
Abbreviations
BMI: body mass index; CMC: carpometacarpal joint; DIP: distal interphalangeal joint; DN: disc narrowing; IP: interphalangeal joint; KL: Kellgren-Lawrence; L1/2, etc: lumbosacral spine level; LS: lumbosacral spine; MCP: metacarpophalangeal joint; OA: osteoarthritis; OST: osteophytes; PFJ: patellofemoral joint; PIP: proximal interphalangeal joint; rOA: radiographic osteoarthritis; TFJ: tibiofemoral joint.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
AEN, RFDeV and JMJ were responsible for study conception and design, data acquisition, analysis and interpretation, drafting and critical revision for important content. PGC and VBK were responsible for study conception and design, drafting and critical revision for important content. JBR and TAS were responsible for data acquisition, analysis and interpretation, drafting and critical revision for important content. All authors have read and approved the final manuscript for publication.
Acknowledgements
We would like to thank the staff and participants of the Johnston County Osteoarthritis Project without whom this work would not have been possible. Funding for this work was provided in part by: Nelson: American College of Rheumatology Clinical Investigator Fellowship Award 2009; NIH/NIAMS Loan Repayment Award L30-AR056604
Jordan/Renner: CDC/Association of Schools of Public Health S043 and S3486
Jordan/Renner/Schwartz: NIAMS P60-AR30701
The funding sources were not involved in study design, data collection or interpretation, writing or approval of the manuscript for publication.
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1
Cannot uninstall 3.4 due to "Please exit LibreOffice"
asked 2012-04-02 22:32:09 +0200
jetpeach
46 1 1 5
I've searched for a while, and the methods say to open task manager and ensure any LO related programs are killed. None are running. I don't even have the quickstarter component installed. There are so many bug duplicates and reports, but none have fixes that worked for me.
I have never had Openoffice or any previous LO version installed.
However, when attempting to uninstall 3.4, the program errors. This also happens when attempting to install 3.5.
Some people have mentioned running the uninstall program as admin, and others say the problem is that the uninstall attempts to rename a directory that doesn't exist and then quits.
The primary question I have is: what is the workaround for me to uninstall LO?
Related to this: 1) Where is the uninstall executable for LO so that I can navigate to it and attempt to run it as admin? And 2) Can I create this directory so the uninstaller has something to rename and then won't just quit?
Thanks, Joe
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answered 2012-04-04 02:02:16 +0200
jetpeach
46 1 1 5
Well, I've somehow got upgraded to 3.5.1 now, I'm not exactly how I got around the bugs, but here's what I did.
From control panel, modified the install of 3.4.2 that I was on and removed all programs but then added the quickstarter (which I hadn't installed previously, I added thinking that maybe because it wasn't installed it was glitching and thinking it was running even though it wasn't)
Still couldn't upgrade to 3.5.1, so upgraded to the latest 3.4.x (6 i think).
Then was able to remove LO.
Couldn't install 3.5.1 because of a possibly unrelated problem with a corrupt CAB, but not sure if related or not, but 3.5.0 worked and installed.
Removed 3.5 because upgrade to 3.5.1 still didn't work after redownloading.
Redownloaded from a different server, tried 3.5.1 install again and it worked.
I'm really not sure what "fixed" it, but I hope it's easier next time! Wow, I know why I run Linux whenever possible (I can't on this machine though). Package managers are so much easier than all this garbage and glitchiness of Winblows 7...
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answered 2012-04-03 10:48:36 +0200
Florian Reisinger
209 4 16
http://flosmind.wordpress...
Are you able to update to the latest 3.4??
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On the Disintegration of the Soviet Union - From the Perspective of Soft Power in Culture
Yuzhi Zhang, Fengwei Xue
Abstract
The disintegration of the Soviet Union is widely discussed in academic circles. From the perspective of soft power in culture, stating the gradual loss of soft power in the publican and political culture, at last led to the disintegration of the Soviet Union.
Full Text: PDF
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Asian Social Science ISSN 1911-2017 (Print) ISSN 1911-2025 (Online)
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"uncompressed_offset": 40933825,
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Purposes of Performance Appraisal System: A Perceptual Study of Civil Servants in District Dera Ismail Khan Pakistan
Malik Ikramullah, Bahadar Shah, Shadiullah Khan, Faqir Sajjad Ul Hassan, Tariq Zaman
Abstract
Performance Appraisal System (PAS) in the civil service of Pakistan has been established to fulfill various
purposes. Previously, this aspect of PAS in the civil service has not been investigated. In this study we examine
perceptions of the civil servants regarding various purposes of the PAS. Data was collected from the civil
servants working in the two departments of far flung district Dera Ismail Khan, Khyber Pakhtunkhwa. The
results show that appraisees have mixed responses regarding purposes of PAS. It implies that appraisees are not
fully aware to all the purposes of PAS, with exception of a sole purpose i.e. support to promotion decisions. In
the article we discuss the factors affecting appraisees’ perceptions about purposes of the appraisal system.
Subsequently, we proffer few recommendations for making the appraisal system purposeful in minds of
appraisees. Finally, we give directions for future research in the PAS of civil service.
Full Text: PDF DOI: 10.5539/ijbm.v7n3p142
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International Journal of Business and Management ISSN 1833-3850 (Print) ISSN 1833-8119 (Online)
Copyright © Canadian Center of Science and Education
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Chicago Manual of Style (Reference, in Author-Date style):
Abboud, P. 2011. Adaptation Rubric - Sony Pictures Group. Connexions, April 25, 2011. http://cnx.org/content/m38097/1.1/.
Modern Languages Association (MLA) Style Manual:
Abboud, Peter. Adaptation Rubric - Sony Pictures Group. Connexions. 25 Apr. 2011 <http://cnx.org/content/m38097/1.1/>.
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92648
Skilled Nursing Homes and Getting a Power of Attorney Explained Via the Happy Hospitalist–Good Advice To Read Up On For Any Patient
I have just a couple clips of his entire blog post but you really should read his entire post on this topic. I did and as always I learn from everyone and the question he answers relates to the question of whether or not a hospital can force a patient to go to a nursing home and Medicare covering the visit. I think this is especially good information for seniors to be aware of and what a palliative care consult is. He advises all to get a power of attorney as there are some avenues to go through to get one if a doctor or hospital needs one but a power of attorney will trump it, but almost any doctor can make a decision to send you to one if it is determined you lack the capacity to make that decision. Read the last comment regarding the time of death at the bottom of his clip, interesting and provokes a few thoughts for sure. With the abbreviated jargon of SNF as he stated is pronounced sniff, this kind of gives a new meaning to sniffing one out if there’s a bit of slang chatter involved:)
He also clarifies that nursing homes are not prisons either and that you can leave if you want if you have the capacity to make that decision and the power of attorney or court appointed guardian can also release you without penalty of Medicare paying. Good stuff and well written. I would say even if one is not a senior, the power of attorney is a good idea as you never know what could happen, especially when having any surgical procedure. BD
Many elderly patients get admitted to the hospital with profound weakness due to their acute and chronic medical conditions. Many of them will leave the hospital with profound weakness from their acute and chronic medical conditions (and unfortunately without a palliative care consult). In many situations, these patients will be too weak to take care of themselves. They will need extra help with their activities of daily living either from family or from trained home health care representatives. Patients who cannot safely return to the community often need to transition through a nursing home (with skilled nurses) before returning home. These are called skilled nursing facilities, or SNF for short (pronounced sniff).
Can a hospital force a patient to go to a long term nursing facility or short term skilled nursing facility (SNF)? The answer is no. No doctor, no nurse, no physical, occupational or speech therapist anywhere in America can force you or your loved one to go anywhere they don't want to go. If a patient wants to go home, they have every right to go home, with one caveat. They have to have the capacity to make their own medical decisions.
I implore everyone to get a POA. If you're in the hospital, you can get these from from the hospital. You can also find free POA forms off the internet. Discuss your wishes with your POA so they will always make decisions for you that are consistent with your wishes should the time come someday that you can not. Otherwise some family member may force your doctors to resuscitate your decomposing body over and over again just to document your time of death past the midnight hour so they could collect one last VA disability check from your cold dead body. Yes, that really happened to me.
http://thehappyhospitalist.blogspot.com/2012/07/Can-Hospitals-Force-Patients-To-Go-To-SNF-Nursing-Homes.html
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Franklin North Carolina Family History CenterEdit This Page
From FamilySearch Wiki
This article describes the services and resources available at a Family History Center, a branch facility of the Family History Library.
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Research
Evolutionary rates and centrality in the yeast gene regulatory network
Richard Jovelin* and Patrick C Phillips
Author affiliations
Center for Ecology and Evolutionary Biology, 5289 University of Oregon, Eugene, OR 97403, USA
For all author emails, please log on.
Citation and License
Genome Biology 2009, 10:R35 doi:10.1186/gb-2009-10-4-r35
The electronic version of this article is the complete one and can be found online at: http://genomebiology.com/2009/10/4/R35
Received:9 October 2008
Accepted:9 April 2009
Published:9 April 2009
© 2009 Jovelin and Phillips; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background
Transcription factors play a fundamental role in regulating physiological responses and developmental processes. Here we examine the evolution of the yeast transcription factors in the context of the structure of the gene regulatory network.
Results
In contrast to previous results for the protein-protein interaction and metabolic networks, we find that the position of a gene within the transcription network affects the rate of protein evolution such that more central transcription factors tend to evolve faster. Centrality is also positively correlated with expression variability, suggesting that the higher rate of divergence among central transcription factors may be due to their role in controlling information flow and may be the result of adaptation to changing environmental conditions. Alternatively, more central transcription factors could be more buffered against environmental perturbations and, therefore, less subject to strong purifying selection. Importantly, the relationship between centrality and evolutionary rates is independent of expression level, expression variability and gene essentiality.
Conclusions
Our analysis of the transcription network highlights the role of network structure on protein evolutionary rate. Further, the effect of network centrality on nucleotide divergence is different among the metabolic, protein-protein and transcriptional networks, suggesting that the effect of gene position is dependant on the function of the specific network under study. A better understanding of how these three cellular networks interact with one another may be needed to fully examine the impact of network structure on the function and evolution of biological systems.
Background
Understanding of the function and evolution of any specific gene or protein requires knowledge of the context in which that gene operates, because change in any single component of a complex system can have ramifications for all other components. This system-orientated view, largely enabled by the omics revolution, has sparked increasing interest in the investigation of biological networks and has yielded promising results in the understanding of cellular [1], developmental [2] and ecological [3] processes. A major challenge within this area is to determine how the various parts of a system interact in order for the system as a whole to function. With a more global understanding of system function in hand, a larger question then emerges: in what ways does the structure of the network influence the evolution of the components of that network? For example, in the yeast protein-protein interaction (PPI) and metabolic networks, central and highly connected proteins tend to evolve more slowly than peripheral genes [4-7]. Is this a global feature of all such networks, or does the specific function of a given network have a strong influence on its evolutionary properties? Here, we address these questions by analyzing the evolution of the yeast transcription factors in the context of the structure of the transcriptional regulatory network.
The premise that biological systems are more than the sum of their parts implies that such systems possess emergent properties that cannot be captured by a purely reductionist approach. For a network, one such emergent property is its topology. Comparisons of entirely different types of networks, including social, technological and biological networks, have revealed intriguing shared topological properties, such as an overall hierarchical organization, similar node-degree distributions, and a tendency toward a small-world structure in which most nodes are connected by only a few other intervening nodes [1]. The observation that both metabolic and PPI networks display approximately scale-free topologies, with a few highly connected nodes and a majority of nodes with only a few connections, leads to the proposal that network structure may be the result of selection, perhaps as a means of providing mutational robustness [8]. This hypothesis remains uncertain, however, because networks with node connectivity following a power-law distribution can be assembled without natural selection [9] and because natural selection is very weak on second order network properties such as robustness [10]. Further, networks with similar power-law distributions can have different fine-scale architectures, which may be functionally important [11].
In this study we examine the evolution of the yeast transcription factors and ask whether fine differences in network structure and function lead to different evolutionary impacts on the elements of those networks. Gene regulatory networks are of particular interest because they allow the cell to modify its physiology, cycle and shape in response to environmental or developmental demands [12]. Metabolic and gene regulatory networks have a different level of complexity than PPI networks because they are directed and explicitly model the flow of information passing through the nodes. Moreover, even though all three cellular networks are characterized by having a small number of highly connected nodes, these networks differ in their node-degree distribution [1]. The yeast transcription regulatory network consists of a mixed scale-free and exponential topology: only the number of target genes follows a power-law distribution whereas the number of regulators is exponential [13]. These structural and functional differences may result in different effects on the evolution of network components. For instance, underlying the power-law distribution of target genes is a distributed architecture that may cause the apparent independence between connectivity and the retention of regulatory proteins across genomes [14].
Overall, we show that network structure does indeed lead to different evolutionary dynamics that depends more specifically on the overall function of the network. Therefore, understanding the relationship between network structure and the evolution of network components will depend on a deeper knowledge of gene function.
Results
Central transcription factors tend to evolve faster
We obtained node statistics, specifically the number of regulatory inputs (in-degree, kin), the number of target genes (out-degree, kout), and betweenness, measuring the centrality of a gene in the network, from two separately derived representations of the yeast transcriptional network. The first dataset (YTN1) [15] includes 286 transcription factors, 3,369 target genes and 8,372 regulatory interactions. The second dataset (YTN2) [14] includes 157 transcription factors, 4,410 target genes and 12,873 regulatory interactions. Only transcription factors clearly identified as orthologs in the yeast genome database (Saccharomyces Genome Database (SGD)) were retained for analysis of evolutionary rates, leading to the retention of a set of 256 genes for YTN1 and a set of 138 genes for YTN2. Because the first network contains 85% more transcription factors than the second, we have much more power to detect significant effects using the first network and therefore focus most of our discussion on that dataset. Nevertheless, both datasets yield qualitatively similar results for each of our major conclusions.
Large-scale analyses have shown that multiple genomic variables have an effect on the rate of protein evolution [16,17]. Among them, expression level has been shown to correlate strongly with a gene's evolutionary rate [18-22], leading to a wide debate about the importance of other genomic variables such as essentiality [21-25] and connectivity [7,21,24,26-28]. Therefore, we first examine the separate effects of expression, function and network related variables on rates of transcription factor sequence evolution in turn, and then tease apart their independent effects using a multivariate approach.
As noted in previous studies, expression level has a strong effect on transcription factor sequence evolution (Figure 1), with more highly expressed genes being under stronger purifying selection against both amino acid replacements and synonymous changes, as predicted by the translational robustness hypothesis [20]. Further, essential transcription factors (those having a lethal phenotype in deletion-mutants [29]) also tend to evolve slower than non-essential transcription factors, at least in the network that includes more transcription factors (YTN1: dN/dS: t249 = 3.62, P < 0.001; Wilcoxon two-sample P < 0.0001). Similarly, we find a correlation between protein evolutionary rates and genes' essentiality estimated by the growth rate of deletion strains [19] (Figure 1).
Figure 1. Correlation between expression (blue), function (green), and network topology (red) related variables with evolutionary rates. Darker colors represent results from analyses of YTN1, and lighter colors represent results from analyses of YTN2. Correlations are Spearman's nonparametric ρ. *P < 0.05, **P < 0.01, ***P < 0.001.
To further investigate the impact of functional constraints on sequence evolution, we used the number of Gene Ontology (GO) terms [30,31] as a proxy for a gene's pleiotropic effects. GO describe a gene's properties and functions by assigning attributes under the categories 'cellular component', 'biological process' and 'molecular function'. There is a correlation between the number of GO terms and essentiality (YTN1: Spearman's ρ = 0.171, P = 0.007), indicating that pleiotropy has direct fitness consequences. Accordingly, transcription factors with more GO terms tend to evolve more slowly (Figure 1), presumably because mutations arising in genes with larger pleiotropic effects are more likely to be deleterious and are thus selected against.
Finally, the position of a gene within the network, or its centrality, has a significant influence on its evolutionary rate (Figure 1). Previous studies have determined that central metabolic enzymes and central proteins in the PPI network are under stronger selective constraints and evolve slower [4,6]. In contrast, we find that for the transcriptional network, protein evolution is positively correlated with betweenness, indicating that transcription factors that occupy a more central position in the network tend to evolve faster (Figure 1). Similarly, contrary to metabolic and PPI networks, protein sequence divergence correlates positively with connectivity. However, the relationship between out-degree and evolutionary rate differs between the two network datasets (Figure 1).
The effect of centrality on protein sequence evolution is independent of other genomic variables
Interpretation of these simple correlation patterns is complicated by the fact that different genetic properties are correlated with one another and so any single correlation between two characteristics might actually be generated by a shared correlation with a third causal element. To correct for this, we examined the relative contribution of function, network and expression-associated constraints on transcription factor evolution using multivariate analysis.
We first used multiple regression analysis with network connectivity and network centrality separately with function and expression-related predictor variables in order to estimate the contribution of each of these elements to variation in evolutionary rates among transcription factors. Consistent with the univariate patterns, our analysis reveals that transcription factors having larger effects on organismal fitness when deleted tend to evolve more slowly than those with lesser fitness effects (Table 1). In the same vein, transcription factors with a larger number of GO terms are subject to stronger functional constraints and tend to evolve more slowly (Table 1). These results indicate that sequence divergence for the yeast transcription factors depends at least in part on the cost of mutations altering protein function and affecting organismal fitness. Among the genomic variables analyzed, only expression level has a strong effect on the rate of synonymous changes (Table 2)
Table 1. Multiple regression of genomic variables and protein evolutionary rates
Table 2. Multiple regression of genomic variables and rates of synonymous changes
We find no significant correlation between in-degree and essentiality (kin: YTN1: Spearman's ρ = -0.082, P = 0.2; YTN2: ρ = 0.033, P = 0.7), although the relationship between out-degree and essentiality differs between the two datasets (kout: YTN1: Spearman's ρ = -0.071, P = 0.26; YTN2: ρ = 0.27, P = 0.002). However, when growth rate is measured under different conditions, transcription factors with numerous target genes in YTN2 are not enriched in essential genes [14]. Nevertheless, the correlation between the number of target genes and protein sequence divergence is fairly weak, as multiple regression analysis failed to disentangle the effect of out-degree from the causal effect of other predictor variables (Table 1). Therefore, contrary to the PPI [4,8] and metabolic [5,6] networks, there is no significant correlation between connectivity and essentiality, while in-degree is in fact positively correlated with protein sequence divergence.
Importantly, this analysis also shows that the contribution of network centrality to protein divergence is independent of expression and function-related variables (Table 1). Thus, a striking difference among cellular networks lies in the influence of the position of a gene within the network on its rate of evolution. However, transcription factors that are more central in the network do tend to show higher variability in their expression level under changing conditions (YTN1: Spearman's ρ = 0.178, P = 0.004), but centrality is not correlated with expression level (YTN1: Spearman's ρ = 0.006, P = 0.924) and essentiality (YTN1: Spearman's ρ = -0.022, P = 0.735).
The high degree of correlation among predictor variables has led some to question the use of multiple regression for these types of analyses [21]. We therefore also analyzed these data using principal component regression analysis [21]. For YTN1, the first principal component, composed mostly of contributions from network-related variables, is positively correlated with protein divergence but the second principal component, mostly composed of expression and function-related variables, correlates negatively with substitution rates (Tables 3 and 4). Both principal components explain a similar amount of the total variance in the data, indicating that no single variable dominates the rate of protein evolution for the yeast transcription factor genes. The pattern is more complex for YTN2 because the principle components tend to confound expression and network properties. For instance, the first principle component for YTN2 does not show a significant effect on evolutionary rate, presumably because the positive and negative effects of the network, function, and expression variables are counterbalancing one another (Tables 3 and 4).
Table 3. Principal component regression analysis: principal components PC1 to PC4
Table 4. Principal component regression analysis: principal components PC5 to PC8
To get around these issues, we defined a new set of variables composed of principal components derived separately from the expression, network and function-related variables. Multiple regression analysis on these composite variables shows that each of these causal components has independent effects on the rate of nonsynonymous changes (Table 5). Results from the two network datasets are qualitatively and quantitatively very similar to one another, although particular coefficients from YTN2 tend to be less significant because of reduced power.
Table 5. Results of multiple regression analysis on composite variables
In summary, our results on the yeast transcription network and previous work on the yeast metabolic and PPI networks [4-6] show that the structure of cellular networks influences the evolution of proteins within these networks. However, the system-level pattern of selective constraints at individual nodes differ despite the three networks having grossly similar topologies, perhaps in relation with the function and the nature of the network.
Discussion
Genomic information generated in recent years has not only offered new insights into biological processes at various levels of organization [1-3,32], but has also enabled a shift from studying the evolution of single or few genes to a system-level view of molecular evolution that integrates interactions among genes within their cellular context. A first consequence of this new perspective is the recognition that several factors in addition to protein function control rate divergence in coding sequences [16,17], with expression level having a strong effect [20,21].
A second consequence of this systems molecular evolution perspective is that it yields novel insights into how cellular networks and their components evolve. Previous studies have noted that metabolic enzymes with high degree are no more essential than those with low degree, perhaps because rerouting of metabolic fluxes in highly connected regions circumvents loss of function mutations at a given node [5]. The absence of correlation between connectivity and essentiality observed here may be the consequence of a similar mechanism of genetic robustness achieved through rerouting of information flow through the transcriptional network. This hypothesis is further suggested by a recent study showing that the mean sequence divergence among intermediate regulators between a top regulator and its target gene increases with the number of alternative pathways between the regulator-target gene pair [33].
We obtain qualitatively similar results from our analysis of both representations of the transcriptional network [14,15]. This is especially true if we account for the overall correlation structure among the variables within the network, function, and expression classes (Table 5). Many more transcription factors are represented in the first network, however, which makes it much easier to detect significant evolutionary associations. It is clear, therefore, that completeness of the network will influence conclusions from global analyses such as that conducted here. Nevertheless, the fact that similar results are obtained from different network datasets, which undoubtedly capture different levels of network complexity, suggests that the results presented here are somewhat robust to overall sampling issues.
Our results on the yeast transcription network and previous work on the yeast metabolic and PPI networks [4-6] show that the structure of cellular networks influences selective constraints at individual nodes, but that these system-level constraints differ despite the three cellular networks having similar, although not identical, topological properties [1,13]. These differences may ultimately be due to the nature of the networks and how they function. Highly connected proteins in the PPI and metabolic networks are subject to stronger purifying selection, presumably because of a larger fraction of sites involved in interactions and because of kinetic constraints due to highly used metabolites, respectively [5,7].
In contrast, transcription networks play fundamental roles in regulating cell state during developmental processes and during physiological adjustment to changing environmental conditions [12]. For instance, changes in growth conditions lead Escherichia coli to regulate transcript and protein levels to maximize growth rate and maintain stable metabolite levels, whereas when enzymes of the carbon metabolism network are disrupted, system stability is achieved through redundancy and flux rerouting [34]. In eukaryotes other than yeast, transcriptional variability (which might serve as an indicator of environmental sensitivity), rather than expression level per se, seems to correlate better with protein divergence [35]. Here, transcription factors that are more central in the network tend to show higher variability in their expression level in changing conditions. At a local scale, expression variability within a regulatory motif also depends on network structure [36]. However, we do not find a significant effect of expression variation on transcription factor evolution (Table 1). The influence of centrality on the rate of protein evolution in the yeast transcription factor network is therefore not a secondary effect of selection acting directly on transcriptional variability. Because central transcription factors have rapid access to many regions of the network and may act to control the flow of information across the network, they may be important components of sensory systems that transduce environmental changes and coordinate the response of the regulatory network. It is possible that the higher level of amino acid change seen in central transcription factors is therefore the result of historical adaptation to changing environmental conditions. An alternative hypothesis is that more central transcription factors are instead more buffered from outside influences and therefore less subject to strong purifying selection.
Although the relationship between centrality and evolutionary rate is somewhat unexpected, examination of the fine scale structure of other networks indicates that this may be a general property of control systems. For example, although highly connected proteins (hubs) in the yeast PPI network evolve slowly [4,7], intermodule hubs (those that display temporal variation in their connections) are more divergent than intramodule hubs (those displaying static patterns of interactions) [37]. Similarly, directional selection has recently been inferred at controlling, branch-point enzymes in four out of five metabolic pathways converging to glucose-6-phosphate in Drosophila [38]. Thus, proteins that exert some control in flux distribution, information processing or in connecting various protein complexes may, in general, be the target of adaptation because mutations arising in these proteins have the potential to affect the entire system and may, therefore, be more exposed to natural selection.
Conclusions
The system-level pattern of evolutionary rates is different from that observed in the protein-protein interaction and metabolic networks: central transcription factors tend to evolve faster. This suggests that the higher nucleotide rate divergence in central transcription factors may result from the role that these proteins play in controlling the flow of information and may be the result of adaptation to changing environmental conditions. The conclusions derived from network level analyses of molecular evolution can clearly vary depending on the functional role played by the components of that network. In the same way that we have shown that the particular function of a network can influence how one interprets the impact of its structure on protein evolution, it is clear that we must begin to link all of these networks (regulatory, protein-protein, and metabolic) together so that the complete nature and consequences of network structure on the function and evolution of biological systems can be examined.
Materials and methods
We used two distinct datasets of the yeast transcriptional network. The first dataset [15], YTN1, includes 286 transcription factors, 3,369 target genes and 8,372 regulatory interactions. The second dataset [14], YTN2, includes 157 transcription factors, 4,410 target genes and 12,873 regulatory interactions. The two networks were derived from largely independent genetic, biochemical and ChIP-chip experiments. Node statistics, including in-degree (kin), out-degree (kout) and betweenness, were obtained for each dataset using the tYNA platform [39].
Protein sequences of orthologous genes from Saccharomyces cerevisiae [40] and S. paradoxus, the most closely related species [41] having its genome sequenced [42], were retrieved from the SGD [43], aligned [44], and subsequently used to generate codon-based DNA sequence alignments. Maximum likelihood estimates of the rates of amino acid replacements (dN) and synonymous changes (dS) were computed in CODEML [45]. In addition, we computed the rate of synonymous changes corrected for selection at silent sites (dS') [46]. We also attempted to correct for the correlation between dN and dS by using the residuals of the regression between dN with dS in our analyses.
Essentiality was defined by a lethal phenotype in deletion strains [29]. For a quantitative measure of a gene's essentiality we used growth rates measured in deletion mutants [19]. The number of GO terms [30,31] used as a proxy for a gene's pleiotropic effect was obtained from the SGD. Protein and mRNA abundance have been used as estimates of gene expression in studies of evolutionary rates in yeast [18-22,24,25,37]. We obtained protein [47] and mRNA [48] abundance from the literature. However, in our sample faster evolving genes are more likely to be missing from the mRNA abundance (YTN1: N = 206; YTN2: N = 108) and protein abundance (YTN1: N = 195; YTN2: N = 96) datasets, leading to an obvious bias (YTN1: protein abundance: dN/dS: Wilcoxon two-sample P = 0.004; mRNA abundance: dN/dS: Wilcoxon two-sample P = 0.04; YTN2: protein abundance: dN: Wilcoxon two-sample P = 0.03; mRNA abundance: dN/dS: Wilcoxon two-sample P = 0.06). Nevertheless, the translational robustness hypothesis suggests that the frequency of translation events is a better indicator of evolutionary rate than the number of proteins per cell [20]. Therefore, we used the codon adaptation index (CAI) [49], which measures synonymous codon usage bias and correlates with mRNA abundance [50], as well as direct measures of expression level, as substitutes for other abundance measures. CAI was computed [51] using the reference gene set defined by Carbone et al. [52]. Expression level is the average level of expression across 198 microarrays from a wide range of conditions [35]. Expression variation is measured by the coefficient of variation defined as the mean over the standard deviation [35].
Statistical analyses were performed using JMP 4.0.4 (SAS Institute Inc., Cary, NC, USA). The number of GO terms and kout were natural-logarithmic transformed to approximate a normal distribution. One unit was added to betweenness and kin, as well as kout in YTN2, prior to the natural logarithmic transformation because of null values for these variables. All variables, including predictor and response variables, were standardized to a mean of 0 and 1 standard deviation unit. In addition to Spearman's rank correlations and multiple regression analysis, we also performed principal component regression analysis, first using single predictor variables together and then by defining a new set of principal components separately from the expression, network and function-related variables. These composite variables were obtained from the first principal component of expression (CAI, expression level, expression variability), network (betweenness, kin, kout) and function (GO, essentiality) related variables. Principal component analyses were performed on correlations.
Abbreviations
CAI: codon adaptation index; dN: rate of nonsynonymous changes; dS: rate of synonymous changes; dS': rate of synonymous changes corrected for selection at silent sites; GO: Gene Ontology; kin: in-degree; kout: out-degree; PPI: protein-protein interaction; SGD: Saccharomyces Genome Database.
Authors' contributions
RJ designed the study and collected the data. RJ and PCP analyzed the data and wrote the paper.
Acknowledgements
Support was provided by a Doctoral Dissertation Improvement Grant (NSF DEB-0710378), the UO IGERT program in Evolution, Development and Genomics (NSF DGE-9972830) and by grants from the National Science Foundation (DEB-0441066) and the National Institutes of Health (AG029377).
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Sana Saleem
Contributor profile · 35 posts · joined 12 May 2009
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The author is a blogger at The Guardian and Dawn. Her archive of published and unpublished work can be found on her personal blog.
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11 January 2013
Pakistani Activist Khudi Ali Killed in Bombings Targeting Hazaras
On 10 January, 2013 in Pakistan's southwestern city of Quetta, 82 people lost their lives in back-to-back bombings that hit an area populated primarily by ethnic Hazara Shia Muslims. Irfan Khudi Ali, a prominent human rights activist who tirelessly highlighted the persecution of the Hazara in Pakistan, passed away in the second attack. His killing has sparked a tribute to his struggle and reignited protests on Shia killings in Pakistan.
11 December 2012
Global Voices: Where Every Voice Counts
The idea that every voice counts is one that is very close to the notion of Global Voices as a platform and as a community. As netizens unite to have their voices heard when the world's authorities argue on who should run the internet, we decided to ask our diverse community speak out on issues that matter to them and look back at issues we have covered over the year bearing in mind that every voice counts.
31 August 2012
Pakistan: Conflicting Reports in #SaveRimsha Blasphemy Case
The blasphemy law in Pakistan has been the focus of a heated debate yet again, after a minor christian girl named Rimsha was accused of blasphemy and was sent to jail. There have been a few conflicting reports about the case, and the most significant one being a picture of a girl being used, that has now become the face of the #SaveRimsha campaign.
21 June 2012
Pakistan: Video Leak Sends Shock Waves Across The Country
A leaked video showing popular anchorpersons Mehar Bokhari and Mubashar Lucman involved in a set-up interview has sent shock waves across the Pakistani media industry and the citizens, triggering a debate on the credibility of the journalists.
28 February 2012
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The recent blow to the internet freedom in Pakistan has been the announcement of a request for proposal (RFP) for national “URL filtering and blocking system” by the ICT R&D Fund under the Ministry of Information Technology (MoIT). The $10 million system is required to be able to ”handle a block list of up to 50 million URLs".
25 November 2011
Pakistan: The Death of Nusrat Bhutto
The recent demise of Nusrat Bhutto, former first lady and wife of Zulfiqar Ali Bhutto, was mourned across Pakistan. A public holiday was declared as a part of the mourning, which triggered a wave of reactions from Twitter users questioning the logic behind such a move.
23 November 2011
Pakistan: Twitter Reactions to the SMS Filtering Announcement
The Pakistan Telecom Authorities' possible attempt at SMS filtering for abusive contents, had twitter timelines flooded with reactions; mostly humorous. Sana Saleem compiles Twitter reactions and provides update on the issue.
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Pakistan: Political Satire Becomes Internet Sensation
A recent song released on YouTube, by a group of young men from Lahore, has become an Internet sensation. The songs lyrics are heavily loaded with political satire, something that is rarely witnessed in Pakistan in recent years.
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Pakistan: Bloggers Dismayed at Google Adsense Ban
A recent ban on Google Adsense accounts has left many Pakistani bloggers dismayed. Scores of genuine publishers have fallen prey in a move aimed for crackdown on fraudulent websites and blogs. Sana Saleem reports.
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Pakistan: Demanding Justice For Saleem Shahzad
Many suspect that Pakistan's intelligence agency was behind the May 2011 abduction and murder of Pakistani journalist Syed Saleem Shahzad, bureau chief of Asia Online. The judicial commission set up to investigate the murder is struggling from lack of help, and many fear that justice will be denied.
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User:Pranav Rathi/Notebook/OT/2010/05/12
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Contents
AOM Characterization
Introduction:
The motive of doing this is to attend enough information, to use AOM as power modulator for the tweezer. AOM (Gooch & Housego R23080-2-1.06-LTD; 138252) operates in CW and normal mode. We use 1st order diffracted beam. First CW mode operation is characterized, to know the usable power (of the diffracted beam) Vs ascending input laser power. Second normal mode operation is characterized: Computer controlled ascending input voltage for RF signal power Vs usable power of the diffracted beam, at several input laser powers. The laser temperature is kept constant at 62F.
Setup:
Relatively simple setup ThorLabs power meter is place infront of the diffracted beam from AOM. An aperture is used infront of the power meter to keep off all the stray beams.
CW mode operation characterization:
The AOM is operating in CW mode. Data is recorded; laser power (.25W to 4W in .25W increments) Vs 1st order beam power. This 1st order beam power is the usable power for tweezer. The data is presented below:
View/Edit Spreadsheet
Result:
The relationship is linear. So the AOM gives output power in 1st order diffracted beam, of average around 70% of the input power (in CW mode). This help us calculating the usable power of any input power without measuring; for example if I set the laser on .10W, then the usable power at the tweezer is 70% of it, which is .07W or 70mW.The maximum usable power for the tweezer is 2.66W. If we want to stay in the single mode operation regime, it is 1.4W (at room temperature). When the laser is cooled down to 60F, it is stretched to 1.9W (2.75W input).
Normal mode operation characterization
In normal mode, AOM is controlled by our LabView program. Voltage input for RF signal is from –ve1 Volt to –ve5 Volts in –ve.1 Volt increment. 1st order diffracted beam power is recorded for every ascending voltage increment for .5W, 1.5W, 2W and 2.5W input laser powers. Different laser powers are used to check if any how the characteristic of the AOM is input power dependent, which it should not be. RF signal Vs diffracted beam power will help us in obtaining the best workable range of voltages over which power increases linearly. I will also help us in characterizing the relationship between the voltage and diffracted power. The data is presented below:
View/Edit Spreadsheet
Result:
• Data Sheet 1 and Chart 1: By looking the chart it’s clear; diffracted beam power is not linearly related with voltage. It has strange characteristic, which is same for all laser powers: So there is no laser power dependence and any laser power can be chosen to define the AOM characteristic. Characteristic: It runs somewhat exponentially in the beginning from 1 to 1.4 volts, somewhat linear between 1.5 to 3.1 volts and second degree polynomial in the end from 3.2 to 5 volts. So the most appropriate workable range for linear power modulation (in relatively same size of steps) is from 1.5 to 3.1 Volts at any input laser power.
• Data Chart3: Shows how power increases in % over 1 to 5 Volts at 2W of laser power. By joining the head of each histogram the characteristic curve can be traced out. Between 1.5 and 3.1 Volt the power increases almost in same step size of avg 3.45% (.069W) /step in comparison to .8% (not linear; over range of 1 to 1.4 Volts) and .42% (not linear; over range of 3.1 to 5 Volt). 3.45% step size is more convenient for power modulation and power is also linear over the step size.
• Data Chart 2: Shows power step in %; the difference between the two consecutive power-increments over the difference in the two consecutive voltage increments (.1 Volt; steps). It gives us the better idea of over what range of voltage, the steps are over all large with somewhat of same histogram height difference. The region between 1.5 to 3.21 Volts contains that.
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Quotation added by staff
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There must be more to life than having everything. Sendak, Maurice
This quote is about materialism · Search on Google Books to find all references and sources for this quotation.
A bit about Sendak, Maurice ...
Maurice Sendak (born June 10, 1928) is an artist and creator of children's literature who is best known for his book Where the Wild Things Are, published in 1963.
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It's easy! Just pick the product you like and click-through to buy it from trusted partners of Quotations Book. We hope you like these personalized gifts as much as we do.
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Finance, like time, devours its own children. Balzac, Honore De
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212 - The Extra Degree
The one extra degree makes the difference. This simple analogy reflects the ultimate definition of excellence. Because it's the one extra degree of effort, in business and life, that can separate the good from the great. This powerful book by S.L. Parker and Mac Anderson gives great examples, great quotes and great stories to illustrate the 212° concept. A warning - once you read it, it will be hard to forget. Your company will have a target for everything you do ... 212°
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Quotes by Bell, Alexander Graham
Alexander Graham Bell (March 3, 1847 August 2, 1922) was a British-American-Canadian scientist and inventor. He was, until recently, widely considered to be the inventor of the telephone, although this matter has become controversial, with a number of people claiming that Antonio Meucci was the 'real' inventor and others holding out for Elisha Gray, the founder of the Western Electric Manufacturing Company. In addition to his work in telecommunications technology, he was responsible for important advances in aviation and hydrofoil technology..
"What this power is I cannot say; all I know is that it exists and it becomes available only when a man is in that state of mind in which he knows exactly what he wants and is fully determined not to quit until he finds it."
Bell, Alexander Graham on determination
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"Great discoveries and improvements invariably involve the cooperation of many minds. I may be given credit for having blazed the trail, but when I look at the subsequent developments I feel the credit is due to others rather than to myself."
Bell, Alexander Graham on invention and inventor
"A man, as a general rule, owes very little to what he is born with -- a man is what he makes of himself."
Bell, Alexander Graham on responsibility
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Chip's Challenge/Level Pack 2/Levels 121-140
From StrategyWiki, the video game walkthrough and strategy guide wiki
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Levels 121 (Flame Boy) through 140 (Keep Trying) will be discussed on this page.
Contents
[edit] Level 121: Flame Boy
Level 121, time limit 300, no chips. Put a little spring in your step this time...you'll need it.
In Flame Boy, Chip can move the fireball through the level to access the further stages, which is instructive, but instead Flame Boy teaches about the value of the spring step.
Follow the fireball out, then move DLU and take the block all the way out to the top of the force floors. When you push the block onto the first force floor, perform a spring step LU. As Chip cannot push blocks in the direction they are already sliding, he runs into it as if it were a normal wall. Normally, this would not be enough, as Chip would have to wait an entire move before he is allowed to move U. Because of the spring step, though, Chip is only on [0, 1] for half a move, and therefore has enough time to step U into the exit!
FLAME OFF - 283 seconds.
[edit] Level 122: Warehouse II
Level 122, time limit 999, no chips. Oh, please don't make a Warehouse III...no! NO! NO!!
This level contains four major rooms: the north room with eight blocks and eight buttons in it, the west room with a bunch of blocks, the central room with a series of circular pathways, and the south room with a lot of buttons. Your goal is to complete the puzzle in the north room with the eight blocks, then move the seven blocks in the west room through the central room and into the south room to stay. However, the tricky part is that you can't complete the north room without blocking off a vital pathway through the central room. An already long puzzle with many turns is made much more difficult, causing Warehouse II to be one of the hardest levels in CCLP2. Blocks are counted by north room and then west room, only using reading order within each room. When the southeast room is reached, blocks are counted by the order they enter it.
Start by entering the north room and throwing block 5 4U, block 2 U 5R, and block 1 4D U 2R, and then block 2 2U, block 6 3U 5R, and block 2 out to button 3. In stage three, move block 7 L, block 6 2U, block 4 2R, and block 3 U 3R, then move the loose block 6 R off button 8 and run 2U, and out to block 8, wedged between the areas. This belongs U, and then move to the west room.
As Chip walks around to block 14, move block 11 2U, and on the way back over, move block 13 2L and block 15 R. When you can turn north from moving block 14, shove it L 3D 6U L; Chip will use this maneuver for all the remaining blocks in the west room. Start as such by circling around the top of the west room, moving block 13 D and using block 15. When you can turn north, move the block back L, then go back to the north room, pass the buttons, and shove block 8 3L, then do some more work here: Take block 3 2U, block 7 4U 3R under it, and drop block 3 onto button 6, then move to the center, throwing the block 4R. At this point, block 15 in the 4-way intersection will use a similar method to the L 3D 6U L: simply 3D 6U L, as the L has already been performed. After this, go back to the west room and take block 13 out, moving it L when you can. Next, carry block 14 4R D 5R 5D, then return to the north and move the loose block from button 6 to button 1, and perform more work: Shove block 4 L, drop block 7 onto button 6, and then return to the center, shove the block 4R, and again use 3D 6U L before returning to the west room.
Now, move through the straight passageway, carry block 11 out, move the northeast block 4R again, and only then knock block 11 back L. Enter the area where block 14 is jammed and sidle it 7L for use below, then carry the northeast block D 5R 5D to replace it. Walk straight through the north room, moving the block from button 6 to 5, and use 4R and 3D 6U L in the same way. Take the straight path to the top of the block room, drop block 10 L, block 9 U, and use block 10, ready to intercept block 9 on the next run. Again, use 4R and then L, then carry block 14 10D 6R for use in the second button room. Replace this block with the next one 7L, then that block with the northeast one, and walk straight through the north room and use 4R and 3D 6U L again.
Take the top fork to the west room, intercepting block 9 L 2D 2L, and use block 10, again performing 4R and then L. Now, move another block 10D, southeast block 1 2D 9L, and replace it with block 2, then replace the upper blocks, and run back through the north room to use 4R and 3D 6U L. Return to the west room for the final time, take the side path, and move block 9 down to use 4R and L. Again, move another block 10D, then southeast block 2 D and block 3 7R, and walk DRURUL and replace the blocks with 7L and D 5R 5D. However, after this, leave out the L from the next 4R and 3D 6U movement, as Chip has emptied out the west room and does not need to open the north intersection from the 4-way. Instead, move the northeast block 4R and go straight to the 10D move. When you enter from the east, move the block from button 3 to 1, the new block 6R, and then replace the upper two blocks and enter the north room to finish it.
Start with block 8 2L, then block 4 2U 3R, block 8 R 4U, and with no further need for the passage, move block 4 to button 6, and block 8 to button 2. Exit the room, move the block in the way 3R U 4R, then move a block 10D and enter to the east. Nick the loose block U, the new block 6R, then move URD2RUL, replace with 7L, and before replacing with D 5R 5D, enter the east of the north room and finish the puzzle. Return to the center, jam the one remaining block 10D, and then move a block from button 3 to button 2. Move the new block 7R, take the last block from above and jam it 7L and 10D, and then walk in to finish.
Of the movable blocks, run block 1 R, block 2 L, and block 6 5L, then block 2 RUL onto button 3, and with block 1 out of the way, Chip can circle around to the other three; move block 1 6R and around, then U onto button 4, and then blocks 6 and 5 onto buttons 7 and 6. This ends it - go to the center and exit to collect the 451 hours...oops, seconds. It took that long! :)
[edit] Level 123: BlockSlide
Level 123, time limit 800, 18 chips. When has skating become so diff - *CRASH!! &$@^(&@*
It's possible that this is not just in the tough area of CCLP2, but actually the toughest non-random bold in the entire set. You will not need superhuman boosting skills as in Follow the Glacier Brick Road, but instead you will need superhuman timing skills, as well as a computer, a CC copy, a week alone, and...well, maybe another week. Sorry!
BlockSlide's structure is very unconventional, as it requires Chip to actually catch blocks as they are sliding on ice, sort of like a soccer game. The trouble is when more than one block is used; slide delay will make the level painful in more ways than one! Even one block at a time can be extremely annoying, as Chip must get the timing exactly right on every turn to survive. Four blocks are necessary; this route will use five clones, as the unused block 1 will alter the slide delay in Chip's favor. For easier routes, simply take one block at a time, as this removes slide delay from the equation.
At the beginning, the cloning is as follows: D [1/2] DUDUDU [1 1/2] DU [1/2] 2D. From here, skate over 8R, and spring step [1/2] DU as blocks 4 and 5 suddenly return, keeping Chip out of danger from block 3. Continue R [1] DUR to knock out block 5, then move 2D as a spring step as block 3 comes through; block 2 can be caught directly with LU. Continue R 3U L, then L, and then move R to shove block 2 R, then drop back LD and move block 5 R as well, and then R again to catch block 3.
One space away from the wall, step 2D to catch block 5, then skate 2U R, catch block 2, and then move [1/2] DL (as a spring step) L 4D R (catches block 5) 2D and wait for block 2 to hit itself on the wall. To avoid being hit by block 3, Chip must use a spring step RL; he can then continue to follow 8R D, then [1/2] UR as another spring step, sending block 2 north and south. Slide delay is noticeably taking its toll on block 5; to catch it, move at 783.8. To free the chips, skate R 4U 2L [1/2] RU (spring step). When coming back out, block 3 can be seen sliding; catch it directly from column 3, then sprint over column 2, barely catching block 2 to the west. When it returns back to you, move it into the central bomb (this is as a spring step) for the best effect.
Run to the left side; at 769.0, block 4 is visible. Run it L, then skate U 4R and directly catch it D. To finish the chips, skate: L5D, then RU spring step, 3L [1/2] DL spring step, 5D, and then R as a normal move. Wend your way back through the level all the way to the strip on the extreme right of the level, and when the clock comes to the end of 752, block 3 can be seen coming down. This will be used to reach the exit: move it L off column 3, as moving it R will not allow Chip to throw it south in time, forcing him to wait longer, and then drop it U onto column 1 and skate 6D R [1/2] LU spring step, and L 2D [1/2] UL spring step, and 4D 4R naturally. This last move will drop Chip to the exit with 746 seconds.
[edit] Level 124: Paramecia
Level 124, time limit 340, no chips. Why do they have to make it so difficult to link to the paramecium page?
Each stage of Paramecia is a tussle with, well, paramecia. Some stages are ingenious puzzles, and some are just dodging.
Follow the path to the ice skates, which includes a Russian Roulette sliding bullet, then jump behind the paramecium with the red keys and move 3U LD 2R 4D and up through the teleport, which is a convenient shortcut. Open the rest of the locks to the east, dodge to the west at the end of the path, and then switch to the right side when the paramecium moves up. When it moves away, take the fire boots and follow the ice path to the suction boots. You can also collect the ice skates at the very start by simply jumping back U, but without fire boots, you can't get back through.
Skate back to the center, hiding on the gravel as the paramecium slides by, then skate through the center area, waiting again, and then run to the very top to take the fire boots. Hide as paramecia close in: 3L D and on the gravel, then sneak out to the west and return to the teleporting paramecium near the start. Climb two rows to the next rung on the right, then L 2U L, and Chip can now exit with a time of 228.
Because there is no boosting in Lynx, the ice slide at the beginning makes Paramecia unsolvable in this mode.
[edit] Level 125: Blocks 'n Bombs
Level 125, time limit 300, 3 chips. System of a Down suggests you Bring Your Own Bombs to this level.
It turns out that an entire section of this level is not required, so you can finish it in only 68 seconds. As such, move to the top section and take the blue key, then hit the blue button, which allows Chip to take the other goodies to the right. Now, go to the very bottom end, move DR to override the force floors, and touch the green button to release the pink ball that clones the blocks. As the clock goes to 282, the first block will clone; move it 2R and north, then use another two blocks, wait [1] before stepping on the button for block four, and then finish the bridge north. With both keys, open the two locks in the center of the level.
Go directly over to the red button in the bug circle, then move the block DRL to trap the bug in a 2x1, and now clone another block to stuff him in a 1x1, allowing Chip to collect the goodies under the block including the last chip. Move the free block against the sockets, then remove the sockets on the right, move the block to the teleport and follow it, and move it U to stop the fireballs cloning. After the last two sputter out, you can reach the exit with 232 seconds remaining.
[edit] Level 126: Dodge!
Level 126, time limit 200, no chips. If great big balls of fire are coming at you, what else are you going to do?
This level is a very easy little jumble when you figure out the patterns, and with only a few seconds spent in the namesake maneuver, it won't be long.
Zigzag DRUR to the ice skates, then move 2D 2L and repeat ULDLULDLD. Halfway done...continue [3] D 3R [1] D [1] U 3R [1] D [1] UR 3D. For the last area, step 3L DLU 3L 2D LR 2D, which will send you on a long ice slide to the exit located just under you, and no more dodging! It's 156.
[edit] Level 127: Escape from Chipkatraz
Level 127, time limit 200, no chips. "Don't let the guards see you"? Well, the monsters do see you, even if they don't catch you.
In this small prison, Chip has to move several blocks past a teeth and across a pair of paramecia circling in a smaller area. Even step is preferable, as although odd step will initially save a move, it is lost later, and it throws off the timing for further endeavors.
Escape from the prison, pass the paramecia, and step on the gravel. To outrun the teeth, feint L [1], then 2R 2D, and walk out to the green and yellow keys. Emerge from the gliders, move block 4 3L and up through the paramecia, and then take a detour into the upper yellow lock to pick up a red key under the dirt. Move block 4 2U to save four moves at the cost of just two, open both locks, and then drop it in the water, followed with block 1.
Now, run across the east, move block 5 3L, block 3 UL, and then block 2 out. As you go to use block 5, move block 3 2L, then push blocks 5 and 3 to the bridge to exit the level...INMATE 112 MISSING. 112 SECONDS.
[edit] Level 128: Fantasy Island
Level 128, time limit 400, 264 chips. A real fantasy island would be without that glider clone machine!!
This island contains many, many chips, and also a glider clone machine which slowly adds more and more gliders. There is a block available to stop it, but you won't need it if you watch how you collect the chips. There are many, many possible routes through without stopping; a sample route is shown below.
Collect row 23, U 4L, across row 21, and zigzag DRUR to collect rows 21 and 22, then pick up the edge of rows 20 and 19 and zigzag ULDL, collecting all of these rows. Continue to run east and west for rows 18 and 17, then with gliders messing around near you, walk as such: U 2L ULURUR 2D 2R D. Pick up the remainder of rows 16, 15, 14 and 13, and then 12 and 10 around the block on row 11, removing the chips here as well - except for the extreme right column on rows 12 all the way up to 6, which will be the finishing run.
As most of the gliders are deflecting off the chip in front of the socket, never passing row 13, with very few exceptions which can be dodged in almost all routes, Chip is generally free to take the remaining nine rows in any pattern. When you finish, coming across the far eastern column, take the flippers and swim around to the exit. 336 seconds have become a reality.
[edit] Level 129: Miscellaneous
Level 129, time limit 600, 4 chips. What about this level is miscellaneous? It's all been seen before, right?
This level looks like it's going to be a multisectioned, extensive affair, going along with the name of Miscellaneous - but the blue wall section under the exit, while possibly added as a joke, is actually passable, causing the level to be busted. To enter this, move 2R 3D R 6D 2R D 5R DUR 2D RDL [3] 2L R [1] 2L U. 593 seconds are left.
[edit] Level 130: Frozen Birdbath
Level 130, time limit 400, 51 chips. Do you really want to touch those chips now that you know you're in a birdbath?
In this small ice diamond, Chip moves through hidden recessed walls, hidden ice spaces, blue walls, and some force floors, to collect 51 chips. As there is no convenient way to describe such a route otherwise, only the directional notation is shown:
R 2D L 3R U 2R UR 3L DUL 2U 3R LU 2L 3U LUDR 4D 2L DL 2D L 2U 2L U 3R 3U RU 4D RDLRDR 3D LDULUL 2U 2L ULURL 2U L, which leaves 385 on the clock.
[edit] Level 131: Time Bomb
Level 131, time limit 300, 3 chips. So explain this to me again...if you hit the bomb, time explodes?
Specifically, Time Bomb looks like it will require eight blocks to complete due to the nature of the glider's left turns and the fire through which it must move, and Chip only has four blocks available. The trick is to reuse some of the blocks, meanwhile keeping the glider occupied.
Drop underneath block 1, pick up the chips, and leave it where it is, where it can temporarily trap a glider in the chip room. Open the second socket, leaving the first as another obstacle, then play (2R) to collect a few items, and open the remaining sockets, meanwhile revealing blocks 3 and 4. Off the final socket, run ULD (2R) LD 4R 3U, which will set up some of the apparatus. Pick up the other tools, jog north to free block 2 from the five locks, and push this block 2U 5R 19D 4R 2U in total. Block 3 belongs D, which will redirect the glider north and then west, north with the single socket, into the chip room and back out, and then to a spot where Chip can intercept him towards the exit.
Now, clone a glider in the southeast, and then push blocks 4 and 3 3D and 3D, 5L and 7L, and U (to intercept the glider north) and 21U. Now, this block is ready to turn the glider west towards the exit, but Chip must first move block 1 3U to redirect the glider UR into the "time bomb"; otherwise, he will die by moving D. Run back out, as the glider will be directly behind you, and move block 3 into place, which allows the bomb to detonate. Chip can now exit with 241 remaining.
[edit] Level 132: Captured
Level 132, time limit 300, no chips. Sure, I'll go to a prison camp island where the only thing you can eat is mice.
If you want the bold, the Mouse Panel Glitch is required. Captured requires Chip to move three blocks around, using two of them to drop the third into a thin wall maze, where it is flicked westward one column at a time. In the meantime, Chip has to avoid gliders cloned from both directions!
Mouse route for 250: Run over the sinking floor, move block 2 R, block 3 3U for later use, and block 2 U to reach block 1. Flick this out a total of 3D, and now use block 3 to bridge to the main section, while intercepting block 1. Stick this in the main section 3R D 2R 2D 5L 2D 2L, then circle back through the water maze, move the block U, then run RU and *D. When you make such a mouse maneuver, make sure to hit the keys hard in order to override the mouse, otherwise Chip will continue going in the direction he was directed to.
Follow this route through the rest of the level from where the mouse click moves Chip down: LDLUL 2U RDRD *D LDL 2U RU *U LULD [1] DRD *U LUL 2D RD *U LUL 2D RD *D 5:[LDL 2U RU *D]. Chip approaches the exit, and in this case, move slightly different towards the exit: LDL 4U RU *D, then move the block into the water below the exit and exit the level.
Key-only route for 246: Move the same in the beginning until you get ready to start moving block 1 west. Drop the block D instead, and then follow the route as posted: RD -L U [2] LULDL 2D RURU -L DLDL 2U RU -L UL 3D [1] L 2U RU -L DLDL 2U RU -L ULUL 2D RD -L 2:[DLDL 2U RU -L] ULUL 2D RD -L DLDL 2U RU -L DLDL 2U [5] RU [1] -L 2:[DLDL 2U RU -L] ULDLDL 3U.
[edit] Level 133: Block Maze
Level 133, time limit 999, 14 chips. We're sorry, this caption has been blocked. Please enter a password.
Block Maze is, of course, a block maze; it is more unconventional, as it moves blocks through different sections containing monsters, locks, water, and bombs, and walking through dirt corridors.
Free yourself with the given two blocks, then and move the block into the second water, then continue with D 2R 2U, around to the gravel, and step DR onto the gravel rather than RD. Follow with RU [1], then step into the bugs and collect the 12 keys, which will be used throughout the level's area. One dirt, U off gravel 1, is left behind to block the bugs from running through the corridor and interfering with other parts of the level. From the keys, collect the three chips on the left of the ball room, then 2R and collect up, 2L and open the yellow lock to the paramecium room.
Start with 2L 4D 3R-D, use blocks 9 and then 7 and 2, and move block 6 D on the way to using block 8, which will redirect the paramecia around it. Immediately erase block 1, then drop block 3 D and use block 5, and use blocks 2, 6 and 3 individually. The subtle rearrangement will allow Chip to avoid any clashes with paramecia.
With the blue key in your possession, turn west 4L from the first lock, then 4U 6L to open some key dirt, and enter the small room below with two yellow locks, moving L 2D L off the second one to pick up the red key. Walk directly north to the next row of gravel, to avoid releasing bugs into this area, and then open the red lock and move block 3 here L 3U 4L and 5U 7D through the start. Drop block 1 2U off this, then move block 3 through the open dirt, and then divert below, passing all the bombs, to reach the green button before moving this block north. Continue to exchange the other two blocks 5U 7D to complete the bridge to the other locks and chips, and afterwards run across the west side to pick up the other chips.
The first one is easy; off the blue lock, run 2U and both directions for another two; the final chip is also easy to collect, with a simple clone machine. Now, move further east, through the final yellow lock, and U and 2:2R2U2L2U (2R 2U) to the green key, then LULULDLU 2L to exit. You get 832 seconds.
[edit] Level 134: Microcosm
Level 134, time limit 400, 39 chips. Sorry, but there's already a map here!
This type of level, with a grid of squares and random assortment of items in Chip's square, is actually a mini-map: room 13 contains a tile that best represents what is in each square of Microcosm: hidden fire, a clone machine room, force floors, tanks, etcetera.
Pick up the green key, chip 1, down to chip 2, the key and chip 3, then power south through room 18 and some yellow locks for another chip. Remove the 9 chips in room 24, then move through 25 and in 20, avoid all blue walls. Pass 19, then move directly north, with this timing ignoring the paramecia, for a chip, then U 2R DR into room 15, where Chip must stay on the blue walls.
Continue ULUL to room 3, hold south into the southeast corner of this, and then run through rooms 8 and 7, then enter room 2 and walk 2L U and U to room 1 and all the way south into room 16. Finish the level through rooms 17 and 12, then exit to the west; you score a microscopic 361 (!) seconds.
[edit] Level 135: Zartacla
Level 135, time limit 500, 9 chips. This is the last level in the alphabet; does this mean anything? ...No.
Run the name backwards, and Zartacla is the famous Alcatraz! Despite the bombs everywhere under the block prison, Zartacla is not quite as difficult as it seems, as the exits are obvious.
Escape! Open lock 5, then lock 4, press the green button twice to send the bug out, and then remove locks 2 and 1, leaving lock 3 for another passage through here. On the left is one safe area; block 2 will lead to the exit when Chip finds fire boots. Move block 1 to a dirt bloc, and walk 3U R 2U to allow a teeth onto the brown button. Before using this, Chip needs the blue keys on the south edge; move both blocks, then collect both sets of keys, and then push block 3, open the blue locks, and touch the red button before standing on the trap. It will take 11 moves on the trap before the teeth release you; run out of this and turn north to bridge the water into another area.
Take the left fork and open the red lock, then step 2U RU 3L DRDLD specifically to get the block out the quickest. Free the tank from the dirt, swap it, and follow the dirt to the ice skates, then switch the tank again to escape. With the ice skates, Chip can enter the east section; open the trap to explode the bomb, then remove the red locks and follow the recessed walls, which stays away from the teeth to pick up more chips. Now, finally return to lock 3 at the start, with the bug opening the toggle wall, to pick up the final chip, and then use this to enter the socket.
To pick up the fire boots safely, run L 4D L 2D 2R U, and then escape 2U L and run out when it is safe. Now, Chip can move block 2 on the west side to access the exit, worth 402 seconds.
This is the only CCLP2 level busted in Lynx; because Chip can push blocks without moving them, he can solve Zartacla in five seconds.
[edit] Level 136: Switch Hit
Level 136, time limit 600, 1 chip. Which switch do you hit, you snitch?
Switch Hit contains many obstacles in the form of simple toggle walls, creating a rather difficult maze. What you learn from it will help you in Key Color, so be mindful!
Clone block 1 and push it onto the green button, which frees all use everywhere else, then block 2 and move it 5U 4L to water 1, and a third 5U 7L 3U to water 2. Touch the button twice, then take block 4 to water 2, swap walls, and drop the block west onto the next water and leave the dirt. Now, switch the walls back and take block 5 to water 2, switch the walls twice and put block 6 3L off water 1, and now move block 5 RD off the dirt, pass the dirt and switch the walls, which allows Chip to keep moving the block. Drop this 3D LD, switch again, and now move the block southeast. In this type of situation, Chip wishes to switch the walls in order to ram the block off; do this twice, but Chip can click *L on the second push, which will save one second in the end.
When this is done, walk to the south and switch the walls, and remove the water under the block and switch the walls. Use the passageway above this to collect block 6, move it through in the same way (the mouse is not required for the bold now), and this time, after it goes on the most recent water space, swap the walls again and you can use the block to reach the green key. Go back to the old location of the dirt from block 4, take the chip above, and now go back to the clone machine to exit.
Before cloning, Chip must switch the walls away from their starting position; build east with block 7, slightly south with block 8, then move block 9 east and the tenth a total of U 7R D. Now, switch the walls and drop the block through the second shaft on the right. You can flick the block to the bottom row; now, switch the walls back to normal and build to the south of the shaft with blocks 11 and 12, which will link up with block 10 so as to reach the exit at 423.
[edit] Level 137: Iron Mysticus
Level 137, time limit 500, 23 chips. Welcome to Let's Make a Deal...do you want door number 1, 2 or 3....or 4, 5, 6, 7, 8?
Here's a fun level: it's a bunch of tanks blocking out alternate locks, each containing goodies, in different sections, growing in difficulty with the addition of the fireballs and toggle walls.
Start with [1] 2U 3L UR, then teleport west to the green key and out. Shove east, open locks 4, 7 and 6, and now continue through the level as follows, with teleports in brackets and lock numbers in parentheses: [LD] (swap tanks) [UR] (2, 5) [LD] (swap tanks) [UR] (1) [LD] (swap tanks) [UR] (8, 3) [UU] (5) [D] (swap tanks) [UU] (3) [D] (swap tanks) [UU] (6, 4) [D] (swap tanks) [UL] (3) [RLD] (swap tanks) [UL] (2, 5) [RLD] (swap tanks).
At this point, there are 8 chips remaining and about 440 on the clock. Continue by collecting the yellow and red keys below, touch the green button with no further need for the fire boots, swap tanks again and collect the blue key. At this point, the two fireballs blocking some of the chips are released, and accurate movement is required.
Swap the tanks again, and finish the level as such: [UU] 4U L (wait) R 3U (2, 1, wait) R 3D L (wait) [D] (swap tanks) [UL] 4L D (wait) U 2L (1, wait) D 3L U (wait) [RLD] (swap tanks) [UL] 4L D (wait) U 3L (4) U 3R D (wait, 6) [RL]. Now, jump after the fireball and sneak past it using the ice to reach the exit. I'm mystified...you got 400?
[edit] Level 138: Patrolled
Level 138, time limit 600, 21 chips. Behind that door is...a bunch of toy tanks!
Patrolled contains many tanks circling around the level with the assistance of some ice, but changing every now and then. Switching the tanks will alter their self-switching point, which makes it a little harder.
Wait as a tank runs east, then take the two yellow keys, use ice 8 and take the chip by the exit. You require six yellow keys to exit the level, and you can only get four without the socket, two of which you took earlier. You'll use one key somewhere, so the three keys behind the socket will be enough. Return to the start, hit the blue button above twice, then run 2U R 5U and hold west to the yellow lock. Slide back over ice 3 and south to a red key, circle above the tank on your head, and take the blue key to the east, while you can sneak past the moving tank to take the red. Return to the northwest corner, take the blue key, and hold to the south to collect a red key. At this point, make the transition to the south: 3U 3R 7D R and squeeze west when you can.
Start with the first lock to the east, then move 3L 6D 2L behind the tank for the next key, further east for the next one, and more east to another key, plus a chip. Touch ice 11 and the blue button, then continue L 5U 5L U, take the key and chip, and just slide across ice 8 to safety and another key below. Now, slide across the blue button twice, move through the green and red locks on the far southeast corner, and retreat back out. Directly above the start is the next key, and as you come out, the tanks will swap and you can slide up.
Continue all the way over ices 4 and 2, take the chip and blue key, and wait for the approaching tank, at which point you dart through the western shaft to a blue lock, and then slide back over 2 and 4 to the final red lock. You can visibly see the chip, so go towards the chip; a tank is about to hit you, so dodge above, and then dive in to take only the chip before you enter the socket to collect the keys. Now, touch the blue button above the start twice, again slide over ice 8, and open all the yellow locks to finish the level. The tanks are fired and you score 481.
[edit] Level 139: Frostbite
Level 139, time limit 400, 148 chips. In this weather, I betcha can eat just one!
This common type of level (see Bounce) contains chips with ice under them, forcing Chip to plan routes through by avoiding specific chips and using boosting to maximize efficiency. In addition, there is a teeth, but he won't bother you in this route.
This level was the last level that I (the person writing this guide) finished in this set, as this type of puzzle is quite hard! Most of the level is composed of steps rather than routes; thus, move as directed:
Northwest: 2U LDLDL (this takes Chip into the room) URLDLRURDULRULRD 2U RU (2D) 2D LDLD. Now you are exiting this section and the clock should be at 394.8. Ride the ice to the next chip.
Southwest: DLDRDRD (inside the area) LUDRDULURLDULDUR 2L UL (2R) 2R DRDR. Notice the pattern is identical in this and the next section! You are now leaving this area and the clock should be at 387.8. Ride the ice again.
Southeast: RDRURUR (inside now) DLRURLDLUDRLDRLU 2D LD (2U) 2U RURU. Here, you are leaving at 380.8.
Northeast and exit: URULULDU (inside) RDULUDR, and here the pattern changes slightly, as Chip has to exit here: UDLRUDLRUDL 2R DR (2L) DR 2L (U) and exit. The UDLR section here is very likely the hardest move in the level, as it moves quicker than other boosting in the level because of continuous bent boosting. Think the key presses as you're doing them.
If you don't have "bite", don't expect to get 373; this is the bold score on this level and it is nearly impossible unless you remember the patterns.
[edit] Level 140: Keep Trying
Level 140, time limit 600, 30 chips. The caption cannot be displayed. Try again.
And that you shall have to do. This could just be the hardest bold in existence just because of the sheer amounts of randomness required, maybe even harder than straight random routes such as Mads' Rush II. In MS CC, it's going to be all but impossible. When I angled towards beating the previous record of 476, I made sure to use Tile World v. 1.2 to make the job a million times easier. However, even with my new route, it took about 2 hours straight to pull it off. Over time, my routes of 477, 479, and 480 received noticeable attention and work, which eventually got broken at 481. This is why Keep Trying is level 140!
Hold all the way west, teleport west, then step DRU and hold left to four red keys, and finally teleport RL to reach the locks they belong with. Pick up the three yellow keys, then open lock 2, lock 1 above, and move the block RD 4R U into the teleport, then [2] and follow it. Splash through the dirt and continue L 2U and through a zigzag six horizontal and two vertical, waiting for the tanks when necessary, and then finally up to the chip, green key, and then [4] and follow the tank as it bounces east for two more yellow keys.
Retrace back out to the entrance, and turn to the left and under the first yellow key. Keep moving [3] 4U 2D 4L 2D 2L (5D 5R) for a blue key, and then run onto the two locks and 3U 10R into the blue walls, then follow the tank out and U. Above are several teeth guarding several chips at once; they must be separated to take the chips. Move 2R U 4R URUR 3L DU 2L [1] 3L D to pick these up, then move through the water and open the five yellow locks from the bottom. With this timing, the tanks should avoid you; take the chips on the far right, zigzag south to take the rest of the chips, and then D 2L and into the socket. Wow! You made it this far?! But you're just starting...this is where it's going to get tough.
Slide through west, then down, up, and into a central room. Step into the toggle wall at the south, which should leave 518 on the clock, and power west to the fire boots at about 515. Return back out, being at the very top turn at a 511 minimum, and power through the up and down turns. This ends most of the random areas; touching the gravel at 508 will lead to 481, and at 507 will lead to 480.
At this time, move the block D into the water, and listen to the bouncing tank on the left. It will take six moves to reach the brown button and come back out. The tank is going 4R 4L repeatedly without pause, so watch its movement. If you see that taking the six moves will cause you to wait less, hit the button, and if not, go through now and do this later. At the 481 time diary, you should be able to touch the button; at 480, leave it.
Open the wall under the left fire and pass the fire to a force intersection; under the block at the end of the southern path are suction boots. The other one has nothing, so watch out!! Step back out, wait for the tank, continue out with D 2R UR, and very important: move D onto another green button! Now, smash the brown button if you haven't yet, then go back to the random section and walk through the toggle walls. The wait time will be noticeably decreased at any time, more than the 2 moves spent on the button. Step into the consecutive toggle walls, then hold left to get to the exit. Your time depends on your luck, but you can take a check on your status by following the "goal" times for completing each section.
The theoretical maximum was calculated to be 488 seconds, but this was before I fixed the teeth room and other spots, and in any case, it's only in theory - in practice, it would likely never happen unless God was playing it.
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
9314.0 - Sales of New Motor Vehicles, Australia, May 2003
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 19/06/2003
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Passenger vehicles
Includes vehicles designed primarily for the carriage of people, such as cars, station wagons and people movers. Please note that this description is not directly comparable to the definition of passenger vehicles in ABS collections (such as the Motor Vehicle Census) which includes four-wheel drive passenger vehicles.
Other vehicles
Describes light trucks which includes: trucks, buses, vans, all terrain wagons, pick-up/cab chassis (whether four-wheel drive or not) with a gross vehicle mass of 2.5 to 3.5 tonnes. Also included are heavy trucks and buses, with a gross vehicle mass exceeding 3.5 tonnes. Includes four-wheel drive passenger vehicles.
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
4902.0 - Australian Culture and Leisure Classifications, 2001
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 28/08/2001
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1701
Motor vehicles (other than motor cycles) built or modified specifically for motor sports
1702Motor vehicles, for the transport of persons, specially designed for travelling on snow; and golf cars and similar vehicles
1703Trailers and semi-trailers of the caravan type, for housing or camping
1704Trailers for the transport of boats and other water craft
1705Horse floats
1706Motor cycles (with or without sidecars) built or modified specifically for motor sports
1707Bicycles and other cycles, not motorised
1708Other land vehicles for leisure or sports, not mechanically propelled
Includes:
- land yachts, harness racing sulkies and soap box derby vehicles.
Excludes:
- golf buggies (included in Class 1620).
1709Boats, yachts, and other vessels for pleasure or sport of 5 tonnes or more but less than 50 tonnes displacement (excluding inflatables)
1710Canoes, rowing boats and pedal-operated boats (excluding inflatables)
1711Other small boats and yachts under 5 tonnes displacement (excluding inflatables)
1712Inflatable vessels
1713Sails
1714Marine outboard motors
1715Marine radios
1716Boat fittings and accessories
Includes:
- oars.
1717Gliders and hang gliders
1718Balloons, dirigibles and other non-powered aircraft
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
1105.0 - Release Advice, 23 Nov 1999
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 23/11/1999
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• About this Release
ABOUT THIS RELEASE
Previously: Publications Advice (ISSN: 0156-4722)
Lists products released by all ABS offices on the day of issue of the Release Advice and those expected to be released on the following four working days.
Copies are available free of charge on Tuesdays and Fridays over the counter from ABS bookshops, or by subscription. A daily Release Advice is also available from the ABS Statsite on the Internet (www.abs.gov.au).
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
4517.0 - Prisoners in Australia, 2005
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 15/12/2005
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MEDIA RELEASE
December 15, 2005
Embargoed: 11:30 AM (AEST)
135/2005
Over 25,000 prisoners in Australia
There were 25,400 people in adult prisons in Australia at 30 June 2005, an increase of 5% from the previous year, according to figures released today by the Australian Bureau of Statistics (ABS).
This represented an imprisonment rate of 163 prisoners per 100,000 adult population.
The most common offences for sentenced prisoners were: acts intended to cause injury (15%); unlawful entry with intent (13%); sexual assault and related offences (12%); robbery, extortion and related offences (11%); homicide and related offences (10%); and illicit drug offences (10%).
The majority (60% or 15,300) of prisoners in custody had served a sentence in an adult prison prior to the current episode.
Over half (51% or 10,400) of sentenced prisoners were sentenced in the 12 months preceding 30 June 2005. Of these prisoners two-thirds (67%) had served a sentence in an adult prison prior to the current episode being served. Sentenced prisoners had an average sentence length of 3 years, while the average expected time to serve was 23 months.
Indigenous prisoners comprised 22% (5,700) of the total population, an increase of 12% from 30 June 2004. This was the largest annual increase since 1999.
Other characteristics at 30 June 2005 were:
• Men were almost 14 times more likely to be in prison than women (23,600 men and 1,700 women)
• The number of male prisoners increased by 5% (or 1,100 prisoners) from 30 June 2004 while the number of female prisoners increased by 4% (62 prisoners)
• The median age of all prisoners was 32 years
• The majority (71%) of prisoners were aged between 20 and 39 years
• There were 5,100 unsentenced prisoners on remand, an increase of 4% from 30 June 2004
• Unsentenced prisoners in custody were on remand for an average of 2.8 months.
Further details are available in Prisoners in Australia (cat. no. 4517.0).
Media note: The average sentence length excludes prisoners with indeterminate, life and periodic detention sentences.
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
6405.0 - Export Price Index, Australia, Apr 1995
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 16/06/1995
Past Releases
First Release
• First Issue: Jan 1937
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
1105.0 - Release Advice, 04 Jun 1999
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 04/06/1999
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• About this Release
ABOUT THIS RELEASE
Previously: Publications Advice (ISSN: 0156-4722)
Lists products released by all ABS offices on the day of issue of the Release Advice and those expected to be released on the following four working days.
Copies are available free of charge on Tuesdays and Fridays over the counter from ABS bookshops, or by subscription. A daily Release Advice is also available from the ABS Statsite on the Internet (www.abs.gov.au).
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< Previous
Attack Poker >
I Was Tech Support For James Gosling: He came to the retreat to talk. He had an incidental question about private projects in Sourcecast. I answered it. I was proud of this, which is probably pretty sad.
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< Anacrusish #2
Speaking of Granola >
(5) Granola: The thing I've missed most while having braces turns out to be granola, so I've been making a lot of it and it's great. I'm using Alton Brown's recipe but with different nuts and fruits. Macadamias are great, peanuts are less great. Dried berries are better than raisins. Alyson, would you post or send me the recipe for the granola you made when I came to visit last year?
Filed under:
Comments:
Posted by Rachel at Mon Jan 31 2005 01:48
mmmm macadamia....
Posted by frances at Mon Jan 31 2005 18:55
A far cry from when I was the only person in the family who ate granola. Now, I can't have it. I miss it.
Posted by Alyson at Tue Feb 01 2005 10:44
Here it is:
Granola
Modified from Deborah Madison’s recipe in Vegetarian Cooking for Everyone
6 cups flaked or rolled grains
2 cups chopped nuts (I always add a combination of sunflower seeds, pumpkin seeds, sesame seeds, halved pecans, and slivered almonds)
1 cup wheat germ
1 tsp. nutmeg
1 Tbsp. cinnamon
Salt (about1 tsp.)
2 cups raisins
½ cup safflower or canola oil
¾ cup honey or maple syrup
Preheat oven to 300 degrees F. Toss the dry ingredients together (all except for the raisins), then add the oil and sweetener and toss again to coat them thoroughly. Spread the mixture on two baking sheets and bake until golden, turning every 10 minutes so that it browns evenly. When done, after about 30 minutes, add the raisins and let cool. As the granola cools, it will lose its stickiness and become crunchy.
I've always wondered what the copyright laws are concerning recipes. Sometimes I am tempted to post things I've made, but then I don't because I don't want mad cooks to come after me. This one is modified enough that I'm not worried about it, though. I've played around with it a lot, and this is what I've settled on. Last year, when you came for your visit, I was using only one cup of nuts, but I say one can never have too many nuts in granola!
Posted by Kristen at Tue Feb 01 2005 16:55
I love Alyson's granola!
Posted by Leonard at Tue Feb 01 2005 17:02
Alyson, I say don't worry about sharing recipes. For hundreds of years people have shared them and that's a big part of how people improve their cooking skills. As long as you don't reprint big chunks of a book I think you'll be fine.
The next time I make granola it will be yours.
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Public Health Statement for Asbestos
Public Health Statement for Asbestos
Asbestos, anthophyllite. Source: USGS.
This article has been reviewed by the following Topic Editor: Sidney Draggan Ph.D.
This article is a verbatim version of the original and is not available for edits or additions by EoE editors or authors. Companion articles on the same topic that are editable may exist within the EoE.
September 2001
En Español
Public Health Statement for Asbestos
CAS#: 1332-21-4
Asbestos Fibers
This Public Health Statement is the summary chapter from the Toxicological Profile for Asbestos. It is one in a series of Public Health Statements about hazardous substances and their health effects. A shorter version, the ToxFAQs™, is also available. This information is important because this substance may harm you. The effects of exposure to any hazardous substance depend on the dose, the duration, how you are exposed, personal traits and habits, and whether other chemicals are present. For more information, call the ATSDR Information Center at 1-888-422-8737.
This public health statement tells you about asbestos and the effects of exposure. The Environmental Protection Agency (EPA) identifies the most serious hazardous waste sites in the nation. These sites make up the National Priorities List (NPL) and are the sites targeted for long-term federal cleanup activities. Asbestos has been found in at least 83 of the 1,585 current or former NPL sites. However, the total number of NPL sites evaluated for this substance is not known. As more sites are evaluated, the sites at which asbestos is found may increase. This information is important because exposure to this substance may harm you and because these sites may be sources of exposure.
When a substance is released from a large area, such as an industrial plant, or from a container, such as a drum or bottle, it enters the environment. This release does not always lead to exposure. You are exposed to a substance only when you come in contact with it. You may be exposed by breathing, eating, or drinking the substance, or by skin contact.
If you are exposed to asbestos, many factors determine whether you’ll be harmed. These factors include the dose (how much), the duration (how long), the fiber type (mineral form and size distribution), and how you come in contact with it. You must also consider the other chemicals you’re exposed to and your age, sex, diet, family traits, lifestyle (including whether you smoke tobacco), and state of health.
What is asbestos?
Asbestos is the name given to a group of six different fibrous minerals (amosite, chrysotile, crocidolite, and the fibrous varieties of tremolite, actinolite, and anthophyllite) that occur naturally in the environment. One of these, namely chrysotile, belongs to the serpentine family of minerals, while all of the others belong to the amphibole family. All forms of asbestos are hazardous, and all can cause cancer, but amphibole forms of asbestos are considered to be somewhat more hazardous to health than chrysotile. Asbestos minerals consist of thin, separable fibers that have a parallel arrangement. Nonfibrous forms of tremolite, actinolite, and anthophyllite also are found naturally. However, because they are not fibrous, they are not classified as asbestos minerals. Amphibole asbestos fibers are generally brittle and often have a rod- or needle-like shape, whereas chrysotile asbestos fibers are flexible and curved. Chrysotile, also known as white asbestos, is the predominant commercial form of asbestos; amphiboles are of minor commercial importance. Asbestos fibers do not have any detectable odor or taste. They do not dissolve in water or evaporate and are resistant to heat, fire, chemical and biological degradation. Because of these properties, asbestos has been mined for use in a wide range of manufactured products, mostly in building materials, friction products, and heat-resistant fabrics. Since asbestos fibers may cause harmful health effects in people who are exposed, all new uses of asbestos have been banned in the United States by the EPA. Please see the toxicological profile for more information on the properties and uses of asbestos.
What happens to asbestos when it enters the environment?
Asbestos fibers do not evaporate into air or dissolve in water. However, pieces of fibers can enter the air and water from the weathering of natural deposits and the wearing down of manufactured asbestos products. Small diameter fibers and fiber-containing particles may remain suspended in the air for a long time and be carried long distances by wind or water currents before settling. Larger diameter fibers and particles tend to settle more quickly. Asbestos fibers are not able to move through soil. They are generally not broken down to other compounds in the environment and will remain virtually unchanged over long periods. However, the most common form of asbestos, chrysotile, may have some minor mineral loss in acidic environments. Asbestos fibers may break into shorter pieces or separate into a larger number of individual fibers as a result of physical processes. When asbestos fibers are breathed in, they may get trapped in the lungs. Levels of fibers in lung tissue build up over time, but some fibers, particularly chrysotile fibers, can be removed from or degraded in the lung with time. Please see the toxicological profile for more information on the behavior of asbestos in the environment.
How might I be exposed to asbestos?
Asbestos minerals are widespread in the environment. They may occur in large natural deposits, or as contaminants in other minerals. For example, tremolite asbestos may occur in deposits of chrysotile, vermiculite, and talc. Asbestos may be found in soil that is formed from the erosion of asbestos-bearing rock. You are most likely to be exposed to asbestos by breathing in asbestos fibers that are suspended in air. These fibers can come from naturally occurring sources of asbestos or from the wearing down or disturbance of manufactured products including insulation, automotive brakes and clutches, ceiling and floor tiles, dry wall, roof shingles, and cement. However, these products do not always contain asbestos. Low levels of asbestos that present little, if any, risk to your health can be detected in almost any air sample. For example, 10 fibers are typically present in a cubic meter (fibers/m3) of outdoor air in rural areas. (A cubic meter is about the amount of air that you breathe in 1 hour.) Health professionals often report the number of fibers in a milliliter (mL) (equivalent to a cubic centimeter [cm3]) of air rather than in a cubic meter of air. Since there are one million cm3 (or one million mL) in a cubic meter, there typically would be 0.00001 fibers/mL of asbestos in air in rural areas. Typical levels found in cities are about 10-fold higher.
Close to an asbestos mine or factory, levels may reach 10,000 fibers/m3 (0.01 fibers/mL) or higher. Levels could also be above average near a building that contains asbestos products and that is being torn down or renovated or near a waste site where asbestos is not properly covered up or stored to protect it from wind erosion.
In indoor air, the concentration of asbestos depends on whether asbestos was used for insulation, ceiling or floor tiles, or other purposes, and whether these asbestos-containing materials are in good condition or are deteriorated and easily crumbled. Concentrations measured in homes, schools, and other buildings that contain asbestos range from about 30 to 6,000 fibers/m3 (0.00003–0.006 fibers/mL). People who work with asbestos or asbestos-containing products (for example, miners, insulation workers, asbestos abatement workers, and automobile brake mechanics) without proper protection are likely to be exposed to much higher levels of asbestos fibers in air. In addition, custodial and maintenance workers who are making repairs or installations in buildings with asbestos-containing materials may be exposed to higher levels of asbestos. Since vermiculite and talc may contain asbestos, occupational workers and the general population may be exposed to asbestos when using these products.
You can also be exposed to asbestos by drinking asbestos fibers that are present in water. Even though asbestos does not dissolve in water, fibers can enter water by being eroded from natural deposits or piles of waste asbestos, from asbestos-containing cement pipes used to carry drinking water, or from filtering through asbestos-containing filters. Most drinking water supplies in the United States have concentrations of less than 1 million fibers per liter (MFL), even in areas with asbestos deposits or with asbestos-cement water supply pipes. However, in some locations, water samples may contain 10–300 million fibers per liter or even higher. The average person drinks about 2 liters of water per day. Please see the toxicological profile for more information on how you could be exposed to asbestos.
How can asbestos enter and leave my body?
If you breathe asbestos fibers into your lungs, some of the fibers will be deposited in the air passages and on the cells that make up your lungs. Most fibers are removed from your lungs by being carried away or coughed up in a layer of mucus to the throat, where they are swallowed into the stomach. This usually takes place within a few hours. Fibers that are deposited in the deepest parts of the lung are removed more slowly. In fact, some fibers may move through your lungs and can remain in place for many years and may never be removed from your body. Amphibole asbestos fibers are retained in the lung longer than chrysotile asbestos fibers.
If you swallow asbestos fibers (either those present in water or those that are moved to your throat from your lungs), nearly all of the fibers pass along your intestines within a few days and are excreted in the feces. A small number of fibers may penetrate into cells that line your stomach or intestines, and a few penetrate all the way through and get into your blood. Some of these become trapped in other tissues, and some are removed in your urine.
If you get asbestos fibers on your skin, very few of these fibers, if any, pass through the skin into your body. Please see the toxicological profile for more information on how asbestos enters and leaves your body.
How can asbestos affect my health?
To protect the public from the harmful effects of toxic chemicals and to find ways to treat people who have been harmed, scientists use many tests.
One way to see if a chemical will hurt people is to learn how the chemical is absorbed, used, and released by the body; for some chemicals, animal testing may be necessary. Animal testing may also be used to identify health effects such as cancer or birth defects. Without laboratory animals, scientists would lose a basic method to get information needed to make wise decisions to protect public health. Scientists have the responsibility to treat research animals with care and compassion. Laws today protect the welfare of research animals, and scientists must comply with strict animal care guidelines.
Information on the health effects of asbestos in people comes mostly from studies of people who were exposed in the past to levels of asbestos fibers (greater than or equal to 5 µm in length) in workplace air that were as high as 5 million fibers/m3 (5 fibers/mL). Workers who repeatedly breathe in asbestos fibers with lengths greater than or equal to 5 µm may develop a slow buildup of scar-like tissue in the lungs and in the membrane that surrounds the lungs. This scar-like tissue does not expand and contract like normal lung tissue and so breathing becomes difficult. Blood flow to the lung may also be decreased, and this causes the heart to enlarge. This disease is called asbestosis. People with asbestosis have shortness of breath, often accompanied by a cough. This is a serious disease and can eventually lead to disability or death in people exposed to high amounts of asbestos over a long period. However, asbestosis is not usually of concern to people exposed to low levels of asbestos. Changes in the membrane surrounding the lung, called pleural plaques, are quite common in people occupationally exposed to asbestos and are sometimes found in people living in areas with high environmental levels of asbestos.
Effects on breathing from pleural plaques alone are usually not serious. There is conflicting evidence as to whether their presence in a person accurately predicts more serious disease development in the future.
Asbestos workers have increased chances of getting two principal types of cancer: cancer of the lung tissue itself and mesothelioma, a cancer of the thin membrane that surrounds the lung and other internal organs. These diseases do not develop immediately following exposure to asbestos, but appear only after a number of years. There is also some evidence from studies of workers that breathing asbestos can increase the chances of getting cancer in other locations (for example, the stomach, intestines, esophagus, pancreas, and kidneys), but this is less certain. Members of the public who are exposed to lower levels of asbestos may also have increased chances of getting cancer, but the risks are usually small and are difficult to measure directly. Lung cancer is usually fatal, while mesothelioma is almost always fatal, often within a few months of diagnosis. Some scientists believe that early identification and intervention of mesothelioma may increase survival.
The levels of asbestos in air that lead to lung disease depend on several factors. The most important of these are (1) how long you were exposed, (2) how long it has been since your exposure started, and (3) whether you smoked cigarettes. Cigarette smoking and asbestos exposure increase your chances of getting lung cancer. Also, there is a scientific debate concerning the differences in the extent of disease caused by different fiber types and sizes. Some of these differences may be due to the physical and chemical properties of the different fiber types. For example, several studies suggest that amphibole asbestos types (tremolite, amosite, and especially crocidolite) may be more harmful than chrysotile, particularly for mesothelioma. Other data indicate that fiber size dimensions (length and diameter) are important factors for cancer-causing potential. Some data indicate that fibers with lengths greater than 5.0 µm are more likely to cause injury than fibers with lengths less than 2.5 µm. (1 µm is about 1/25,000 of an inch.) Additional data indicate that short fibers can contribute to injury. This appears to be true for mesothelioma, lung cancer, and asbestosis. However, fibers thicker than 3.0 µm are of lesser concern, because they have little chance of penetrating to the lower regions of the lung.
The health effects from swallowing asbestos are unclear. Some groups of people who have been exposed to asbestos fibers in their drinking water have higher-than-average death rates from cancer of the esophagus, stomach, and intestines. However, it is very difficult to tell whether this is caused by asbestos or by something else. Animals that were given very high doses of asbestos in food did not get more fatal cancers than usual, although some extra nonfatal tumors did occur in the intestines of rats in one study.
Several government offices and regulatory agencies have considered all of the evidence regarding the carcinogenicity of asbestos. The Department of Health and Human Services (DHHS) has determined that asbestos is known to be a human carcinogen. The EPA has determined that asbestos is a human carcinogen. The International Agency for Research on Cancer (IARC) has determined that asbestos is carcinogenic to humans. Please see the toxicological profile for more information on how asbestos can affect your health.
How can asbestos affect children?
This section discusses potential health effects from exposures during the period from conception to maturity at 18 years of age in humans.
Asbestos exposure in both children and adults may occur while breathing air in or near buildings (public or private) containing asbestos building materials or near asbestos-related industrial operations. Children breathe differently and have different lung structures than adults. It is not known if these differences may cause a greater amount of asbestos fibers to stay in the lungs of a child when they are breathed in than in the lungs of an adult. Children drink more fluids per kilogram of body weight than adults and can also be exposed through asbestos-contaminated drinking water. Eating asbestos-contaminated soil and dust is another source of exposure for children. Certain children intentionally eat soil, and all young children eat more soil than adults through hand-to-mouth activities. Historically, family members have also been exposed to asbestos that was carried home on the clothing of other family members who worked in asbestos mines or mills. Breathing of asbestos fibers may result in difficulty in breathing, lung cancer, or mesothelioma (another form of cancer associated with asbestos exposure). These diseases usually appear many years following the first exposure to asbestos and are therefore not likely to be seen in children. But since it may take up to 40 or more years for the effects of exposure to be seen, people who have been exposed to asbestos at a young age may be more likely to contract these diseases than those who are first exposed later in life. In the small number of studies that have specifically looked at asbestos exposure in children, there is no indication that younger people might develop asbestos-related diseases more quickly than older people. Developing fetuses and infants are not likely to be exposed to asbestos through the placenta or breast milk of the mother. Results of animal studies do not indicate that exposure to asbestos is likely to result in birth defects.
How can families reduce the risk of exposure to asbestos?
If your doctor finds that you have been exposed to significant amounts of asbestos, ask whether your children might also be exposed. Your doctor might need to ask your state health department to investigate.
The most important way that families can lower their exposures to asbestos is to be aware of the sources of asbestos in their homes and avoid exposure to these sources. The most important source of asbestos in a home is from damaged or deteriorating asbestos-containing insulation, ceiling, or floor tiles. Should you suspect that your house may contain asbestos, contact your state or local health department or the regional offices of EPA to find out how to test your home for asbestos and how to locate a company that is trained to remove or contain the fibers. Federal law requires schools to identify asbestos-containing material in school buildings and take appropriate action to control release of asbestos fibers.
If you live close to where asbestos and certain other ores are mined or processed, where a building that contains asbestos products is being torn down or renovated, or a waste site where asbestos is not properly covered, then the levels of asbestos in dust and wind-blown soil may be higher. Pets can also bring asbestos into the home by carrying dust or dirt on their fur or feet if they spend time in places that have high levels of asbestos in the soil. Swallowing of asbestos in house dust or soil is a potential exposure pathway for children. This problem can be reduced in many ways. Regular hand and face washing to remove asbestos-containing dusts and soil, especially before meals, can lower the possibility of asbestos fibers on the skin being accidentally swallowed while eating. Families can lower exposures to asbestos by regularly cleaning the home of dust and tracked in soil. Door mats can help lower the amount of soil that is tracked into the home; removing your shoes before entering will also help. Planting grass and shrubs over bare soil areas in the yard can lower the contact that children and pets may have with soil and reduce the tracking of soil into the home.
You can bring asbestos home in the dust on your hands or clothes if you work in the mining or processing of minerals that contain asbestos, in asbestos removal, or in buildings with damaged or deteriorating asbestos. Federal law regulates work practices to limit the possibility of asbestos being brought home in this way. Your occupational health and safety officer at work can and should tell you whether chemicals you work with are dangerous and likely to be carried home on your clothes, body, or tools, and whether you should be showering and changing clothes before you leave work, storing your street clothes in a separate area of the workplace, or laundering your work clothes at home separately from other clothes. Your employer should have Material Safety Data Sheets (MSDSs) for many of the chemicals used at your place of work, as required by the Occupational Safety and Health Administration (OSHA). Information on these sheets should include chemical names and hazardous ingredients, important properties (such as fire and explosion data), potential health effects, how you get the chemical(s) in your body, how to handle the materials properly, and what to do in an emergency. Your employer is legally responsible for providing a safe workplace and should freely answer your questions about hazardous chemicals. Either OSHA or your OSHA-approved state occupational safety and health program can answer any further questions and help your employer identify and correct problems with hazardous substances. OSHA and/or your OSHA-approved state occupational safety and health program will listen to your formal complaints about workplace health hazards and inspect your workplace when necessary. Employees have a right to seek safety and health on the job without fear of punishment.
Is there a medical test to determine whether I have been exposed to asbestos?
The most common test used to determine if you have received sustained exposure to asbestos is a chest x-ray. A chest x-ray is recommended for detecting exposure to asbestos only in persons who have sustained relatively heavy exposure. A chest x-ray is of no value for detecting evidence of asbestos exposure in a person whose exposure to asbestos has been only brief or transient. The x-ray cannot detect the asbestos fibers themselves, but it can detect early signs of lung disease caused by asbestos. While other substances besides asbestos can sometimes produce similar changes in the lungs, this test is usually reliable for detecting asbestos-related effects produced by long-term exposures at relatively high concentrations of asbestos fibers. Other tests, such as gallium-67 lung scanning and high-resolution computed tomography, are also useful in detecting changes in the lungs. However, there are currently no means of detecting exposure-related effects from commonly encountered environmental exposures.
The most reliable test to determine if you have been exposed to asbestos is the detection of microscopic asbestos fibers in pieces of lung tissue removed by surgery, but this is a very invasive test. A test can also be run to determine the presence of asbestos fibers in material rinsed out of the lung. However, this test can cause some discomfort. Asbestos fibers can also be detected in mucus (sputum), urine, or feces, but these tests are not reliable for determining how much asbestos may be in your lungs. Low levels of asbestos fibers are found in these materials for nearly all people. Higher-than-average levels can show that you have been exposed to asbestos, but it is not yet possible to use the results of this test to estimate how much asbestos you have been exposed to, or to predict whether you are likely to suffer any health effects. Please see the toxicological profile for more information about how asbestos can be measured in people and in the environment.
What recommendations has the federal government made to protect human health?
The federal government develops regulations and recommendations to protect public health. Regulations can be enforced by law. Federal agencies that develop regulations for toxic substances include the Environmental Protection Agency (EPA), the Occupational Safety and Health Administration (OSHA), and the Food and Drug Administration (FDA). Recommendations provide valuable guidelines to protect public health but cannot be enforced by law. Federal organizations that develop recommendations for toxic substances include the Agency for Toxic Substances and Disease Registry (ATSDR) and the National Institute for Occupational Safety and Health (NIOSH).
Regulations and recommendations can be expressed in not-to-exceed levels in air, water, soil, or food that are usually based on levels that affect animals; then they are adjusted to help protect people. Sometimes these not-to-exceed levels differ among federal organizations because of different exposure times (an 8-hour workday or a 24-hour day), the use of different animal studies, or other factors.
Recommendations and regulations are also periodically updated as more information becomes available. For the most current information, check with the federal agency or organization that provides it. Some regulations and recommendations for asbestos include the following:
The federal government has taken a number of steps to protect citizens from exposure to asbestos. First, on July 12, 1989, EPA established a ban on new uses of asbestos. Uses established before this date are still allowable. Second, EPA has established regulations that require school systems to inspect for asbestos and, if damaged asbestos is found, to eliminate or reduce the exposure, either by removing the asbestos or by covering it up so it cannot get into the air. In addition, EPA provides guidance and support for reducing asbestos exposure in other public buildings. Third, EPA regulates the release of asbestos from factories and during building demolition or renovation to prevent asbestos from getting into the environment. EPA also regulates the disposal of waste asbestos materials or products, requiring these to be placed only in approved locations. Fourth, EPA has proposed a limit of 7 million fibers per liter on the concentration of long fibers (length greater than or equal to 5 µm) that may be present in drinking water. Fifth, FDA regulates the use of asbestos in the preparation of drugs and restricts the use of asbestos in food-packaging materials. NIOSH has recommended that inhalation exposures not exceed 100,000 fibers with lengths greater than or equal to 5 µm per m3 of air (0.1 fibers/mL). OSHA has established an enforceable limit on the average 8-hour daily concentration of asbestos allowed in air in the workplace to be 100,000 fibers with lengths greater than or equal to 5 µm per m3 of air (0.1 fibers/mL). Additional sources of information about asbestos are the 10 regional offices of the EPA. Most EPA regional offices have an asbestos coordinator.
Please see the toxicological profile for more information about regulations and guidelines to protect people from exposure to asbestos.
Where can I get more information?
If you have any more questions or concerns, please contact your community or state health or environmental quality department or:
Agency for Toxic Substances and Disease Registry
Division of Toxicology and Environmental Medicine
1600 Clifton Road NE, Mailstop F-32
Atlanta, GA 30333
Phone: 1-800-CDC-INFO • 888-232-6348 (TTY)
Email: cdcinfo@cdc.gov
Information line and technical assistance:
Phone: 888-422-8737
FAX: (770)-488-4178
ATSDR can also tell you the location of occupational and environmental health clinics. These clinics specialize in recognizing, evaluating, and treating illnesses resulting from exposure to hazardous substances.
To order toxicological profiles, contact:
National Technical Information Service
5285 Port Royal Road
Springfield, VA 22161
Phone: 800-553-6847 or 703-605-6000
References
Agency for Toxic Substances and Disease Registry (ATSDR). 2001. Toxicological Profile for Asbestos. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service.
Editor's Notes
• The Encyclopedia of Earth article "Animal testing alternatives" supplements this entry.
• Hyperlinks were created by the Encyclopedia of Earth, not by the Content Source.
Citation
Agency for Toxic Substances and Disease Registry, National Center for Environmental Health (Lead Author);Sidney Draggan Ph.D. (Topic Editor) "Public Health Statement for Asbestos". In: Encyclopedia of Earth. Eds. Cutler J. Cleveland (Washington, D.C.: Environmental Information Coalition, National Council for Science and the Environment). [First published in the Encyclopedia of Earth September 11, 2008; Last revised Date June 26, 2012; Retrieved May 18, 2013 <http://www.eoearth.org/article/Public_Health_Statement_for_Asbestos>
The Authors
The mission of the Agency for Toxic Substances and Disease Registry (ATSDR), as an agency of the U.S. Department of Health and Human Services, is to serve the public by using the best science, taking responsive public health actions, and providing trusted health information to prevent harmful exposures and disease related to toxic substances. ATSDR is the principal federal public health agency involved with hazardous waste issues. The agency helps prevent or reduce the harmful effects of exposu ... (Full Bio)
NCEH Mission The National Center for Environmental Health plans, directs, and coordinates a national program to maintain and improve the health of the American people by promoting a healthy environment and by preventing premature death and avoidable illness and disability caused by non-infectious, non-occupational environmental and related factors. NCEH Main Activities National leadership in prevention programs, global health, and the use of human genetic knowledge, tests, and services Publ ... (Full Bio)
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FamilySearch Wiki:Contributors MeetingEdit This Page
From FamilySearch Wiki
Revision as of 19:34, 6 March 2012 by AdkinsWH (Talk | contribs)
Welcome to the Wiki Contributors Meeting
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The Wiki currently has 73,271 articles in English
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Come forge solutions with other community contributors. We discuss content, best practices, community, and strategy. This is a conference call meeting every Tuesday from 1:00-2:00 PM (mountain time). Community members are welcome to suggest topics for the agenda by posting in the Contributor's Corner Forum thread or by adding to the weekly agenda discussion pages.
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|Meeting agenda]]
Purpose of the meeting
<div>
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The Technical Meeting previously handled many of these issues. It has recently evolved into technical issues that may not interest all contributors.
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SIMCon
From Forensics Wiki
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SIMCon
SIMCon is a program that securely images all files on a GSM SIM Card with a standard smart card reader. After imaging, the forensic investigator can then analyze the contents of the card. Specific information regarding stored numbers, call history, and text messages are available.
SIMCon's features:
• Acquire all available files on a SIM Card and store in an archive file
• Analyze and interpret content of files
• Recover deleted text messages stored on the card
• Manage PIN and PUK codes
• Compatible with SIM Cards and USIM Cards
• Print reports of evidence
• Secure file archive using hashing
• Export items to popular spreadsheet programs
• Supports international charsets
All GSM cell phones today have a subscriber identity module (SIM) to identify the phone onto the network. SIMCon is an application to acquire all of the information from the SIM Card.
The SIM Card provides secure storing of the key identifying a mobile phone service subscriber, subscription information, preferences and text messages. Network state information, such as the current location area identity (LAI), is also stored on the card. When a handset is turned off and then back on, it will search for the LAI that it was in, rather than having to search all frequencies that the phone operates in. This saves time when trying to log on to the network. (Subscriber, 2006, para. 1)
By using SIMCon and a smart card reader, all of the above information and more can be pulled off of the card without knowing the PIN or the PUK of the card. The PIN and the PUK are ways to keep the information on the card secure. They also can be used as a security feature on the phone, not allowing anyone to use a phone to access the SIM Card without knowing the codes.
SIMCon is an application developed by Inside Out Forensics in Norway. It is designed for use by the law enforcement community, and it can be obtained free of charge by emailing SIMCon and identifying the officers and unit. However, for anyone outside the law enforcement community, it is not free.
Review
SimCon makes the acquisition of data very easy, simply inserting the Sim card to the appropriate Sim card reader, and clicking acquire is all that is needed to start analyzing evidence. After the acquisition of the data is complete SimCon will show the user a screen with two halves.
On the left panel is the different data sectors of the SIM Card that can either be checked on or off depending on what is needed. After choosing what data sectors are needed, the right panel will be populated with the selected data. Some of the most useful pieces of information that are shown are: the International Mobile Subscriber Identity number, every contacts name and number, and all SMS messages sent and received both stored and deleted.
SIMCon also comes with two more handy features that are key to an investigation and in a court of law. The first is SIMCons' feature that allows the printing of a report. SIMCon will format and populate a report with the contents of the users’ choosing. This can list all the key pieces to an investigation and is an excellent piece of evidence to be used in a court of law. The second feature is the exportation of the acquired data. SIMCon allows the exportation of all SMS messages and also of all contacts. When these exported files are opened in a program such as Microsoft Excel the data can be read, sorted, and analyzed in a format of the users design.
When SMS messages are exported SIMCon automatically adds the following information about every message: file, item, status, service center, message type, number, time stamp, and text. When the contacts are exported SIMCon automatically adds the following information about every contact: file, item, identifier, and number. For reference a report of an acquired SIM card is enclosed as well as a document that tells what information is added into an exported file at the end of this document.
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Publication Listing
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• Title: Cat's Cradle
• Authors: Kurt Vonnegut, Jr.
• Year: 1970-07-00
• Catalog ID: #1149
• Publisher: Dell
• Price: $0.95
• Pages: 191
• Binding: pb
• Type: NOVEL
• Title Reference: Cat's Cradle
• ISFDB Record Number: 295488
• Notes: 5th New Dell edition printing, (6th printing over all). Date from the 10th New Dell edition printing.
• Bibliographic Comments: Add new Publication comment (CTSCRDLPFB1970)
Verification Status
Reference Status
Primary Not Verified
Clute/Nicholls Not Verified
Clute/Grant Not Verified
Contento1 (anth/coll) Not Verified
Locus1 Not Verified
Reginald1 Not Verified
Reginald3 Not Verified
Tuck Not Verified
Miller/Contento Not Verified
Bleiler1 (Gernsback) Not Verified
Currey Not Verified
Primary (Transient) Not Verified
Bleiler78 Not Verified
OCLC/Worldcat Not Verified
Primary2 Not Verified
Primary3 Not Verified
Primary4 Not Verified
Primary5 Not Verified
Copyright (c) 1995-2011 Al von Ruff.
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Bibliography: Noise is Beautiful!
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Title: Noise is Beautiful!
Author: Fox B. Holden
Year: 1943
Type: SHORTFICTION
Storylen: shortstory
Series: Probability Zero
ISFDB Record Number: 114536
User Rating: This title has fewer than 5 votes. VOTE
Current Tags: None Add Tags
Publications:
Copyright (c) 1995-2011 Al von Ruff.
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Bing Powered Yahoo Images Brings Back Old Yahoo Search Features
Jan 14, 2013 • 8:22 am | (4) by | Filed Under Yahoo Search Engine & Yahoo SEO
Yahoo announced that Yahoo Image search now has the ability to search Flickr images, as well as filter images based on re-use or re-posting under Creative Commons terms.
When I first saw this news, I thought, didn't Yahoo already offer this years and years ago. And yes they did. As Matt McGee reports, they had Flickr results in 2007 and creative commons filters in 2009 - both stories I covered, which is why I remembered it.
So why is Yahoo reporting that this is new? Well, it is the new old.
When Yahoo switched to search results powered by Bing, they quietly removed images on Flickr and the creative commons filter. Now they added it back. So, in a sense, Yahoo is catching up to itself.
Forum discussion at WebmasterWorld.
Previous story: Daily Search Forum Recap: January 11, 2013
blog comments powered by Disqus
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CMD sent two reporters to track ALEC in Oklahoma
Click here to help support our future investigations.
Egypt APPG
From SourceWatch
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The Egypt Group exists 'to promote friendship and understanding between our countries and parliaments'
Officers
Gulf Centre for Strategic Studies provides administrative assistance by organising meetings.
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Friday, August 24, 2012
The America That Once Championed Human Rights, Freedom And Democracy Is No More
by Michael Payne
America has, over many years, done an excellent job of portraying itself as the bastion of human rights, freedom and democracy. However, there is only one problem with that wondrous self-assessment; it is simply not the case as it has become very evident that, based on this nation's hubristic actions around the world and it continued repressive actions domestically, it has forfeited the right to that distinction. We might say that a nation that no longer practices what it preaches, should just stop preaching.
At the end of the Second World War, when America had established itself as the premier military power, it had to choose whether it would exercise this power as the facilitator of peace or if it would use this power as a dominating force. We now are well aware of what role America chose to take as illustrated by its succession of wars and the building of a massive military empire. War is in and peace is out.
After America had come to that critical crossroads and had chosen the entirely wrong direction here is what has transpired. While it once vigorously promoted itself as the leading proponent of world peace, freedom, democracy and the champion of human rights it no longer adheres to those principles that it once considered to be sacred. In the following, let's see how this government's actions around the world are actually the opposite of what it wants the world to believe.
Starting with the issue of human rights: The general definition of human rights is: "The basic rights and freedoms to which all humans are entitled, to include the right to life and liberty, freedom of thought and expression, and equality before the law." Now let's add a few associated excerpts from the Universal Declaration of Humans Rights of the United Nations:
"Everyone has the right to life, liberty and security of person."
"No one shall be subjected to torture or to cruel, inhuman or degrading treatment or punishment."
"No one shall be subjected to arbitrary arrest, detention or exile. No one shall be subjected to arbitrary arrest, detention or exile."
Now let's discuss human rights to a greater degree, not just those of Americans, but of people in nations around the world; and then let's see what the self-proclaimed champion of human rights record has been in recent times, especially since the year 2000.
Here is how America has clearly and severely violated the human rights of people in other nations. Does a nation that champions human rights invade and occupy sovereign nations at will, regardless of the international laws that prevail? Borders of other nations mean nothing to this government; airspace can be violated at any time it deems appropriate. International laws are to be strictly adhered to by all other nations but, in the case of the U.S., it all depends on whether this government agrees with them or not.
What about the human rights of all those families in Iraq who had the doors of their homes knocked down by U.S. troops; people who had the "right to security of person" and should not have been subjected to "cruel, inhuman or degrading treatment" at the hands of U.S. troops? Or when their country's national infrastructure and most of its important institutions were demolished? Or when the people of Fallujah watched in horror as their city was virtually destroyed? What about the rights of the several million people of that nation who were forced out of their homes or were involuntarily sent into exile in surrounding countries? How can this nation's leaders continue to criticize other nations for their alleged violation of human rights when they bring such misery and destruction upon other innocent human beings? That is the epitome of hypocrisy.
The human rights of hundreds of innocent civilians have been grossly violated by U.S. "pilots" in Afghanistan or at bases in the U.S. who sit before computer screens and systematically launch deadly Reaper and Predator drones and missiles that, no matter how much the military tries to deny it, do not have the absolute ability to distinguish between suspected terrorists and innocents, and rain death upon one and all. That is not mere conjecture, those are the proven facts.
Is that what human rights are all about? Or does it even matter since those on the receiving end of those missiles and bombs are just those "other kinds" of people? This rapidly escalating use of drones is the perfect example of how American now believes it can operate in this world; this government makes its own rules and bends and breaks international laws as it sees fit.
Is there any way that this government can even begin to defend or justify these violations of human rights? Is this what America has now become? Once the most admired and respected nation it has now become the most feared military power in the world. America has now made the following statement a part of its national credo; "Don't do as I do, just do as I say."
Now let's turn to another important issue, the one dealing with the American people's rights and freedoms under the Constitution. It seems like the people of America don't comprehend the great extent to which their rights and freedoms have been restricted or entirely eliminated by legislation that has been enacted and put into practice by this government, its presidents and the Congress. There was the Patriot Act of 2001 that gives the government extensive powers to wiretap, have easy access to citizens' records, and the use of search warrants; this was followed by the NDAA, the National Defense Authorization Act of 2012 that, in effect, eliminates habeas corpus and allows for indefinite military detention of anyone, including any American citizen, without charge or trial.
And then we have the final issue, the current deteriorating state of our democracy, the cornerstone of America; this government; of, by and for the people used to work in this nation and this society but, since our entry into the 21st century it has come under a massive attack by the masters of Corporatism who use vast sums of money to control the outcomes of our nation's elections. The richest corporations and CEO's are using their power and pervasive influence in these elections to assure that those that "they own" are reelected. These actions pose an extremely dangerous threat to our very frail democracy.
This deceitful, anti-democratic agenda seems to be working beautifully as several GOP controlled governorships and legislatures have enacted voter suppression legislation that, if allowed to be fully put into effect, will disenfranchise millions of voters in several key swing states because they do not have photo ID's, typically drivers' licenses. The nations of the world are witnessing the emergence of the real America as they watch the rapid dissolution of its famed democracy.
This assembled evidence represents concrete proof of how this country has now gained a solid reputation as one whose actions and behavior are exactly the opposite of those that it tries to project to the world. "It's not what you say, it's what you do." Or as some might put it, "America talks the talk but doesn't walk the walk." The world sees America for what it is, for what it has now become; a nation that still attempts to portray itself as the symbol of human rights, freedom and democracy, but one that has now forfeited all rights to that distinction.
#Michael Payne
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User talk:RandyHanna
Topics
Welcome
Welcome to WeRelate, your virtual genealogical community. We're glad you have joined us. At WeRelate you can easily create ancestor web pages, connect with cousins and other genealogists, and find new information.
Video Tour
We strongly recommend that you spend a few minutes taking our video tour. It provides a brief overview of how to use the features of WeRelate. A little time spent here may save you time later. There are also in-depth text tutorials available from the Help button.
Create Webpages
The next thing to do is launch Family Tree Explorer, then select File in the Family Tree Explorer menu and give your family tree a name. You can either upload your GEDCOM or create person and family pages one at a time. To upload your GEDCOM, select File in the Family Tree Explorer menu and then click on Import and choose the GEDCOM file to import. The system will create an editable web page for each person and family in your GEDCOM. To create a page manually, select Add in the Family Tree Explorer menu and click on Add new person; enter the given (first name) and surname (last name), select Add, then fill in the blanks and save.
The Family Tree Explorer is a Flash application and will need to use some space in your computer to cache the files. That's computer talk for "If you store some ancestor page information on your computer, you will be able to view more pages faster. Otherwise, the system has to fetch each page every time you edit or look at it. This would make navigating your tree very slow.
Connect with other genealogists
You should always sign in when you are editing or adding pages. Use the signature button (second button from the right in the menu bar above the edit box) to sign your comments on discussion pages. That way others with similar interests can find you. If you click on the blue user name on any page, you will go to that person's home page. You can leave a message on his/her Discussion page. The Discussion page button is in the light green second level menu bar above.
Shared research pages
Shared research pages act like specialized message boards. Be careful to use only one name spelling and one location in each field; do not use abbreviations. Including postal codes and multiple spellings, names, or locations in these fields will cause your pages to be improperly indexed. It will make it harder for your cousins to find your pages and work with you. For more information see Shared research pages.
Great things you can do at WeRelate
Please see the Great things you can do at WeRelate article.
Thanks for participating in your virtual community. --Ronni 08:23, 23 April 2007 (MDT)
Help in getting started
Hi RandyHanna! My name is Ronni and I'm one of the volunteers here and I just wanted to give you a few pointers when creating your User Page, should you need it, especially in regards to listing names and place you are researching.
On your User Page when listing the surnames and places you are interested in, put only one surname per field and only one place name per field. The reason for this is because as you enter the names and places you are interested in, a corresponding category is also being created. A category such as SMITH in Ohio, Virginia and Kentucky is very specific. For a cousin to easily find your information, he or she would have to create the very same category. The more simple the category, the easier it is for someone to find your research.
You can also list a county or town along with the state or country you are interested in, but again, keep in mind that you are narrowing the field of possibilities. Cast your net wide. :)
After you've listed a few names and places you are researching, save your work and then look at the bottom of your User Page and see the various categories that were created from the names and places you listed. Now click on the categories and see if there are any other pages already there. If so, then you are already on your way to making a possible connection with a cousin!
As you explore WeRelate, you'll also notice that abbreviations is another area we want to avoid when listing places. Ohio should be used instead of OH, for instance. Columbus, Franklin, Ohio, United States is the correct version of Columbus, Franklin Co., OH. To help you with typing in all that information each time though, just type in the name of the city or town followed by a comma and wait a few secs. A little window will come up with all the possible links. Just click on the one you want. The more you type, the narrower the choice.
By the way, all of this is covered in the Shared Research Pages mentioned above in the Welcome letter and it's one of the pages you should really try to read first when you get the chance.
I'm a fairly new user here myself and every day I'm learning new things about how powerful wiki can be in allowing us to network with others. If you are experienced in the area of wiki, then great, you can jump right in and get started. If on the other hand, wiki is something new to you and the site seems a little overwhelming, don't be discouraged. There are plenty of people that are willing to help you get started. In addition to the various HELP pages throughout the site, you can also stop by the Watercooler to see if a problem you are having has already been addressed. You can also visit by my User Page and leave me a message.
Good luck in your research! --Ronni 09:00, 23 April 2007 (MDT)
HannaHaney.ged Imported Successfully
The pages from your GEDCOM, "HannaHaney.ged" have been generated successfully. You may view them by launching the Family Tree Explorer and opening the family tree into which this GEDCOM was imported.
-WeRelate agent 09:21, 23 April 2007 (MDT)
We need to ask you to clean up or remove your tree [19 June 2009]
Hi,
I'm one of the administrators here at WeRelate. We're in the midst of an effort to merge all of the duplicate pages at WeRelate so that there is just one page for each person, so that multiple contributors can work together on the same page. We noticed in doing this that the GEDCOM you uploaded in 2007 contained a lot of internal duplicates and generated multiple pages for the same people. For example: Family:Alexander Danley and Sarah Hanna (1) and Family:Alexander Danley and Sarah Hanna (2). Would you please visit Special:ShowDuplicates/RandyHanna and combine these duplicates, or visit Special:Trees and remove your tree? If you don't respond to this message we'll remove your tree on Monday. Thank you.--Dallan 21:10, 19 June 2009 (EDT)
Hannah Ball - spouse of Rawleigh Travers [29 June 2009]
Hello, I noticed that you removed Hannah Ball (4) as a spouse for this family. Can you give the reasoning for this removal? Thank you:)
http://www.werelate.org/wiki/Family:Rawleigh_Travers_and_Hannah_Ball_%281%29 Family:Rawleigh Travers and Hannah Ball (1)--Delijim 18:16, 23 June 2009 (EDT)
It's because I removed the tree (see the message above). I'll restore Person:Hannah Ball (4).--Dallan 13:13, 29 June 2009 (EDT)
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Western CIO Summit: Enterprise Architectures
One of the panels is on Enterprise Architectures. The panel consists of:
• Curtis Wolf, CIO, North Dakota
• Val Oveson, CIO, Utah
• Robb Stoddard, CIO, Alberta
• Moira Gerety, CIO, new Mexico
• Bob Haycock, Manager, FEAPMO
Curtis is talking about North Dakota's Enterprise architecture program. They have made a lot of progress, although Curtis says its been sidetracked a little by agency angst over a legislatively mandated centralization of many IT functions, including email, database, and server administration. Curtis believes that the EA process would have eventually led to the same conclusions and done so in a way that wasn't so upsetting to the business. I think he's right. I've always believed that more centralized administration of IT functions is a fact of life that will happen and its much better for an IT organization to decide on their own how that should happen than it is to wait for someone else to decide for you.
Val is describing Utah's governance structure, put in place by the Governor last August, that uses the Cabinet as the IT project portfolio managers and a dotted line organization between the CIO's office and the CIOs in each agency that . Still, he says uncertain related to governance is the hardest question in putting an EA into place (every other CIO on the panel shakes their heads). Vision in Utah is clear. Application development is moving forward (witness eRep, for example). Infrastructure consolidation has not happened because the required political capital isn't available. Val also mentioned the new strategic plan and the hard work that went into it by agencies. This strategic plan does an excellent job of outlining seven great goals for eGovenrment in Utah and listing objectives for each one. As always, the proof will be in the implementation, but getting the governance done is a greate start.
Moira is one of the new CIOs who came into office from last year's election cycle. Her background is private sector. Its clear as you hear her speak that she's got an aggressive new Governor who's ready to make some changes. This translates into a desire to move money from IT into programs, in this case. This leads to less emphasis on technical architectures. She makes a case for open source and open systems. Architecture is impacted by procurement. Being new, she's concentrated on the governance issue and working toward a sub-cabinet group of agency CIO's. They are focused in three main areas of state functions: client services, resource management, and government operations.
Robb started off talking about the creation of Alberta SuperNet, a network that connects every school, library, health facility, and government office. This gave Robb a wide area network that allowed him to ask the agencies: how would you do business if bandwidth and storage were not an issue. The natural outcome in many cases was more consolidation. Robb views his role as defining the rules and creating the rulebook (the EA) and playing the part of referee as the agencies "play the game." Interestingly, after getting a governance model in place, Alberta started with a data architecture. This is unusual, but also a good way to promote data sharing. Its hard to do because executives want to fund "programs" not data.
Bob, as director of the Federal EA Program Management Office and, given OMB's mandate that new money won't go to programs without an EA, is in much demand. He's responsible for directing the development and implementation o the Federal EA. There are four primary objectives:
• identity opportunities to leverage technology and alleviate redundancy. or to highlight were agency overlap limits the value of IT investments.
• establish "line of sight" contribution of IT to mission and program performance.
• facilitate horizontal (cross-Federal) and vertical (Federal, State, and Local) integration of IT resources.
• support a more citizen-centered, customer-focused government that maximizes IT investments to better achieve mission outcomes.
I've written about the FEA's reference models before. Bob specifically calls attention to the Performance reference model and deals with business inputs, business outputs, and desired outcomes. This is unique in enterprise architectures, but tells Federal agencies how their architectures ought to address the subject of metrics for business process improvement.
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Document Engineering
At the InfoWorld SOA Executive Forum last week I met Bob Glushko who's on the faculty at Berkeley's School of Information, what they're calling the "i-school" (with no royalties to Apple, apparently). Bob's the director of the Center for Document Engineering. The mission of the CDE is to "invent, evaluate, and promote model-based technologies and methods that enable the automation of document-centric business processes and the implementation of business relationships as a network of document exchanges." As XML technologies have made documents machine-readable and automatically processed, the notion of engineering these documents has become more important.
Bob's also the author, along with Tim McGrath of Document Engineering : Analyzing and Designing Documents for Business Informatics and Web Services, a book I've had recommended to me by more than one person. I've ordered it and I'm anxious to read it.
When I spoke to Bob he mentioned that he'd just started blogging at Doc or Die. His latest entry references the SOA Forum and makes this statement about course-grained, doc-style vs. fine-grained, RPC-style Web services:
[T]he best argument for coarse document exchanges is that if you go that way you’ll be making a conscious design choice and almost certainly have invested some effort into designing the document models or evaluating standard document ones. The documents you exchange will more likely be ones that are easy to process because they’ll have unambiguous semantics and use robust code sets and identifiers. They’ll be easier to reuse across a range of related partners and services.
From Doc Or Die
Referenced Mon Mar 20 2006 15:15:45 GMT-0700 (MST)
RPC-style interfaces are almost invariably angle brackets around an interface designed for some other purpose.
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Catalogue Number
8921.2 - Towns in Time: Analysis and Data, Census Statistics for Victoria's Towns and Rural Areas, 1981 to 1996
Latest ISSUE Released at 11:30 AM (CANBERRA TIME) 31/03/1999
Page tools: Print Page Print All RSS Search this Product
• About this Release
ABOUT THIS RELEASE
Provides 1981, 1986, 1991 and 1996 Census data for Victoria's 308 towns, 52 'rural balances' of local government areas and the 8 Murray Valley local government areas of New South Wales.
It is an easy-to-use snapshot of key variables from the 1981, 1986, 1991 and 1996 Censuses. Variables include total population, age structure, income, household size, dwellings and vacancy rates, religion, labour force and industry. There are quick comparisons between different towns of similar size in the same region or local government area. It also provides useful information for planning infrastructure and services at the local level, as well as critical input to informed investment decisions.
This publication complements other Department of Infrastructure products such as Victoria in Time (8910.2) and Victoria in Future (8913.2).
© Commonwealth of Australia 2013
Unless otherwise noted, content on this website is licensed under a Creative Commons Attribution 2.5 Australia Licence together with any terms, conditions and exclusions as set out in the website Copyright notice. For permission to do anything beyond the scope of this licence and copyright terms contact us.
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TeraStationPro
From NAS-Central Buffalo - The Linkstation Wiki
Revision as of 04:01, 18 December 2006 by Omita (Talk)
Jump to: navigation, search
Contents
Background
In March 2006 Buffalo relased a new version of the TeraStation.
It is supposed to feature more current hardware like S-ATA disk.
For now please refer to the official site.
Hardware
See hardwarePro for the new mainboard.
Where to upload Software?
If you have anything (Firmwares, Custom Firmwares, useful software packages) that might be useful for other Tera/Tera HS/TeraPro-users then send mindbender a private message in the forums. He will provide you with the needed information to upload files to
http://downloads.linkstationwiki.net/terastation/uploads/
All linkstationwiki-admins & itimpi have full access and administrate the terastation-section:
http://downloads.linkstationwiki.net/terastation/
Firmware
Official
v1.01
The TeraStation Pro can be a member of Active Directory Enviroment of a Windows200x network.
To enable this Buffalo has released a beta firmware for this feature.
This firmware can be downloaded from http://de.buffalotech.com/downloads/TSPro-1.01-0.51-withAD.zip
And it uses an known password
v1.03
Some newly purchased units are coming out with a version 1.03 firmware. This firmware seems to have some issues, including the inability to set Active Directory settings(stays greyed out even after checking the AD checkbox, apparently not all 1.03 users are having this issue). Flashing with the 1.01 linked above seems to fix this issue.
In late June I had trouble with my TS Pro. Buffalo tech support suggested reinstalling the firmware. My box was at 1.03 but only 1.01 was available on the Buffalo website. I inquired and was told by Buffalo tech support 1.03 created more issues than it solved and was pulled for rework. My TS Pro subsequently died and I did a warranty exchange with the distributor (Dell). The replacement box contained 1.01, not 1.03.
Buffalo tech support does not recommend using 1.03.
v1.04
Buffalo has a Beta 1.04 firmware available on their (originally temporary) FTP site. According to Buffalo this should fix the issues that some users have been having when joining to their AD domains. It still does not appear to fix the name resolution issue(can connect to the device using AD users by connecting to "\\IPaddress" but not "\\Name").
-It seems that download link does not working, If someone have this firmware please let me know and I will provide hosting for it.
-It's working right now, but it seems go down intermittently. If someone has more reliable storage that would be great. Also, they have a new one out today: TSPro-1.04-0.01-CharFix. It is 1.04-0.01 instead of 1.04-0.00. Probably some sort of minor revision. --Wastedlife 05:09, 4 October 2006 (CEST)
Non-Official Firmware
The following firmware files have been provided by Entropy. There is always an inherent risk associated with updating your system. If your system breaks, you own both pieces. If you have feedback on the firmware, please leave a message on the Talk Page.
Terastation Pro Firmware by Entropy
Version Base Image Status Released Includes
1.01-1 Buffalo US 1.01-0.51-withAD Stable 2006-May-20 dropbear v??
user_nfs v??
1.01-2 (test1) Buffalo US 1.01-0.51-withAD TEST 2006-Dec-06 dropbear v?? (*)
less-358
md5*sum/sha*sum from busybox-0.60.5
openssh-3.5p1
rsync-2.6.9
strace-4.4.93
unfs3-0.9.16
user_nfs v??
• Backup ssh on port 1022, to be removed in released firmware.
Release Notes 1-01-2
Please test this version and let me know if there are any problems. The highlights of this version is that it replaces dropbear with openssh for compatibility reasons and includes a NFS v3 daemon so that files larger than 2G can be written to the Terastation via NFS. Most of the additional tools for this package are built using the Denx ELDK
Known Issues 1.01-2 (test1)
1. sftp does not work.
Workaround: chmod 755 /usr/libexec </dd>
Entropy's firmware worked great for me. I am having couple of issues it might be my inexpertise.
• 1. Couldnt get the Pulic key authentication working. Tried using the tips on QandA.
• 2. NFS - i was able to mount both on mac and linux and i tried to copy a file little over than 2GB and got error. I would really appreciate any help.
Thanks a Million
- Nav
The UNFS that's included is V2 which has a 2G file limit. I'm going to try to get a V3 UNFS into a firmware but I've got too much going on at the moment
--Entropy
I have a working UNFS v3 server and will be creating the test firmware shortly. If anyone is interested in testing, let me know (normal caveats regarding bricking your system apply).
--Entropy 10:15, 30 November 2006 (CET)
Entropy could you tell me briefly how i can get V3 UNFS into the firmware. I will give it a shot. Appreciate your help.
- Nav
I think there are a couple of ways you could approach getting UNFS V3 in the firmware.
• Use Dan Kegel's crosstool to generate your own cross-compiler toolchain and compile the source yourself. On my 1GHz machine, just building the toolchain takes a couple hours and gigabytes of disk space. (Build for a PowerPC 603e) Whatever libraries that UNFS V3 needs will also have to be compiled. This will probably take a lot of effort and time as you will find bugs in packages that aren't tested to be cross-compiled.
• Start with #1, cross-compile gcc and family to your TS. Then build UNFS3 for your TS. This will take a lot of time too I would guess, as the TS does not have a hefty CPU.
• Try to find a cross compiler or gcc/toolchain already compiled for PPC 603e and work from there.
• Try to find UNFS V3 compiled for a PPC host. This will require a good deal of luck, because if it's not statically compiled, you will need to make sure that your version matches the system library versions on your TS.
Once you have working binaries (you can ftp, or copy them using samba to your TS to test them), you want to update the firmware with your changes.
--Entropy
Thanks a lot for the info. It seems little bit out of my skills.
-- Naveen
Entropy, could you either help me or document some details about your firmware? I am trying to log onto the Root account and can't find what the password is? Can you use "su" or "sudo -s" to do so, or is there a "myroot" user?
• "su" - doesn't seem to work.
• "myroot" account - doesn't seem to work
• "sudo -s" - does seem to work with the "admin" users account password.
Please verify.
- Hays
Could I request someone update a NFS3 howto for Mac support. This one is out of date with the "Test" Firmware. Hacking The Buffalo TeraStation to Work with Mac OS X. I have the "Test" firmware running, I have edited my "/etc/exports". But I am not sure how to test the connection... so far my Mac can't log onto the port.
- Hays
Talk: Hacking the TeraStation Pro
Follow this link: Talk:TeraStationPro what is the root password for TeraStation Pro for the non-official firmware
Using the serial console
Serial console TsP
Miscellaneous
Joining Windows Domains
One problem is that the TeraStation will not allow you to join a domain that begins with a number. I had to rename my Windows domain because it began with a number. What was the programmer at Buffalo thinking? -Mike 2006 May 25
If you have a PDC with leading number(s) running send an Email to the helpdesk@buffalo-technology.ie. They can help you. - Joergl 2006 July 6
Have Terastation Pro 1TB. I can join it to my Small Business Server 2003 Active Directory, just fine. The network sees the TS-Pro just fine, but the user accounts are not updated on the TS. I have tried working with buffalo tech support, but the just keep telling me it is a Active Directory problem, that my AD is setup wrong.
I explained to them that AD in a SBS network has to be created in a exact patteren or it will not work right. This is created during setup. Explained to them that if I join the TS as a workgroup and not part of the domain then it works correctly. This points to an issues with TS and not my PDC. The TS is not retreiving the AD information correctly. I did flash to 1.03 no good.
Have found other posts elsewhere with the same problem in a SBS network. Has anybody been able to join to the SBS 2003 AD? Bryan July 2006
Is it realy not possible to join a domain which isn't in mixed mode? Thaek Sept 2006
Samba Performance?
Seems that I am the only one having problems with the bad samba performance from Windows clients (when having a few 1000 files in a directory). I assume that it has to do with the case insensitivity needed for Windows clients.
Is there a simple hack resolving this?
--Mbob 10:24, 3 October 2006 (CEST)
Localization of This Page
Notice! :This page of Original is English version.
TeraStation Pro(日本語) - Japanese
Help/Howto/Walk-thoughs
TeraStation Pro and NFS Walkthough for OSX and OSX Server
Personal tools
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Get Involved
From NAS-Central Buffalo - The Linkstation Wiki
Jump to: navigation, search
How to get involved!
Every community has its own set of rules. Here are ours:
1. those who ask questions, update the wiki when they get the answers
2. those who complain about the documentation, update the wiki to make it better
Start here:
Be sure to check out the sales and marketing site.
Happy hacking! - The Kurobox developer community
About the Wiki
The user - waite - is the Wiki evangalist and admin but as with any wiki, the more the help the better the results.
There are still a few growing pains that are going to occur here as we really work out all the configurations. Please, Please, Please PM or email waite with any bug reports. Eventually there will be a wiki page for wiki bugs but till then please let waite know. His email is linwoes@gmail.com
A great way to start helping out on this wiki, (besides making your own little blog style wikis on the Blogs page) would be to gather some of the great work and knowledge from the mailing list, forum and generally in the community conscience, into the FAQs, HowTo and Info areas.
If you want to play around with Wiki text formatting, use the Wiki Sandbox.
You should have no problem creating your own account on the new wiki and getting started with some content.
You can send waite a private message (PM) from the Forum if you encounter any problems here.
Personal tools
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Child Labor and Child Education in Bangladesh: Issues, Consequences and Involvements
Md. Aoulad Hosen, Mohammad Sogir Hossain Khandoker, S. M. Mujahidul Islam
Abstract
The concepts of child labor and child education both are inversely linked with each other in terms of execution. Child labor does not allow child education and vice versa. Between the two types of economic ideologies normative approach promote child education but other ideology i.e. positive approach have preferred child labor. It is factual that, child labor, however, become a burden for every economy. It is a serious problem in any nation. Economy never accepts child labor and the high volume of child labor creates liability on economy. Any job of children always treated as the problem of underemployment through the labor market framework and all child work are strongly prohibited by ILO. The main aims of this paper find out the basic causes of children are recognized as child labor and try to know the causes behind existence a negative relationship between child education and child labor. In Bangladesh, the volume of child labor is so high, near about 4.7 million children, age limit of 5-14 years of age were economically active and percentage of labor force participation rate was 13.4 in the year 2002-03 [National Child Labor Survey (NCLS)]. On the other hand, the figure of informal activities of children is higher than above figure. If we compare with South–Asia, our labor force participation rate is higher than rest of the nations. So policy maker should concentrate to ameliorate education of children and reduce child participation (reduce in number) in economic activity as well as unpaid work.
Full Text: PDF
This work is licensed under a Creative Commons Attribution 3.0 License.
International Business Research ISSN 1913-9004 (Print), ISSN 1913-9012 (Online)
Copyright © Canadian Center of Science and Education
To make sure that you can receive messages from us, please add the 'ccsenet.org' domain to your e-mail 'safe list'. If you do not receive e-mail in your 'inbox', check your 'bulk mail' or 'junk mail' folders.
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An unofficial blog that watches Google's attempts to move your operating system online.
Send your tips to gostips@gmail.com.
December 11, 2007
Google's Navigational Bar Goes International
Google's navigational bar is now available for all international versions of Google, even though the services included in the bar are different from one country to another.
There are also changes for the US version of Google (or the global version, if you like). Google removed from the list of services: Blogger, Labs, orkut, Patent Search, but added YouTube, the most popular property after Google Search, and a link to the More Google Products page.
Even though this makes Google's interface more consistent, you'll still find services that have an old navigation. Some international Google versions have different services: for example, Google Brazil and Google India include orkut in the main list of links because orkut is very popular there. In many countries, the antiquated Google Directory is still on the homepage.
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{
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For the half-year to 30 June 2013, the IPKat's regular team is supplemented by contributions from guest bloggers Stefano Barazza, Matthias Lamping and Jeff John Roberts.
Two of our regular Kats are currently on blogging sabbaticals. They are Birgit Clark and Catherine Lee.
Tuesday, 20 January 2009
"For the loser now/Will be later to win"
Scholars and cognoscenti of twentieth century culture will instantly identify the source of the title of this post: Bob Dylan's "The Times They Are A‑Changin'", in which copyright in the classic Dylan recording is now, it seems, safely in Sony's hands following the ruling of the Court of Justice of the European Communities this morning in Case C-240/07, Sony Music Entertainment (Germany) GmbH v Falcon Neue Medien Vertrieb GmbH. The Advocate General's Opinion in this reference remains frustratingly beyond the linguistic grasp of this blogger, but today's ruling has been lovingly translated into his mother tongue from the original German (though Birgit, the most recent recruit to the IPKat team, would have been perfectly equipped to deal with it).
So what is this ruling, on a request for a preliminary ruling from the Bundesgerichtshof, all about? Falcon distributed two CDs containing recordings of performances by the artist Bob Dylan: "Bob Dylan – Blowin in the Wind" and "Bob Dylan – Gates of Eden". These CDs featured tracks that were originally featured in the long-playing vinyl albums "Bob Dylan – Bringing It All Back Home", "The Times They Are A‑Changin'" and "Highway 61 Revisited", all three of thse albums having been released in the USA before 1 January 1966.
Sony, the German subsidiary of the Japanese multi‑national of the same name, sought an injunction to stop Falcon copying and distributing its CDs, or from having others copy and distribute them on its behalf. Sony also sought orders of discovery against Falcon and to determine Falcon’s liability for damages. Falcon responded that no phonogram producer had any rights in Germany to any Bob Dylan albums recorded beore 1 January 1966.
The Landgericht dismissed Sony’s application. When Sony appealed, the appellate court said there was no doubt that the rights in the disputed tracks had been effectively transferred to Sony but still dismissed Sony’s appeal. This was because, under the 1971 Geneva Convention for the Protection of Producers of Phonograms against Unauthorised Duplication of their Phonograms, in force both in Germany and the United States, phonogram producers were entitled to copyright protection only in relation to activities that took place after 1 January 1966. If music recordings produced before that date were not entitled to copyright protection in Germany, the transitional provisions of German law that were intended to bring national law in line with Directive 93/98 (harmonising copyright term) did not apply to works that had never even been protected in Germany. Sony then sought revision of this ruling by the Bundesgerichtshof which, noting that the tracks in question were protected in another EU member state (the United Kingdom) even though they were not protected in Germany, decided to stay proceedings and to refer the following questions to the Court for a preliminary ruling:
"(1) Does the term of protection granted by Directive 2006/116 [the codified tidying-up of Directive 93/98 on copyright term] … under the conditions set out in Article 10(2) thereof apply also in the case of subject-matter that has not at any time been protected in the Member State in which protection is sought?
(2) If Question 1 is to be answered in the affirmative:
(a) Do national provisions governing the protection of rightholders who are not Community nationals constitute national provisions within the meaning of Article 10(2) of Directive 2006/116?
(b) Does the term of protection granted pursuant to Article 10(2) of Directive 2006/116 also apply to subject-matter that, on 1 July 1995, fulfilled the criteria set out in Council Directive 92/100 [on rental and lending rights etc] …, but whose rightholder is not a Community national?"
This morning the ECJ ruled as follows:
"The term of protection provided for by Directive 2006/116 ... is also applicable, pursuant to Article 10(2) thereof, where the subject‑matter at issue has not at any time been protected in the Member State in which the protection is sought.
Article 10(2) of Directive 2006/116 is to be interpreted as meaning that the terms of protection provided for by that directive apply in a situation where the work or subject‑matter at issue was, on 1 July 1995, protected as such in at least one Member State under that Member State’s national legislation on copyright and related rights and where the holder of such rights in respect of that work or subject‑matter, who is a national of a non‑Member State, benefited, at that date, from the protection provided for by those national provisions".
The IPKatbets that Sony feels pretty pleased with this ruling, which will now give it the means to ruffle Falcon's feathers. Merpel notes that this is a fairly short ruling, of just 39 paragraphs inclusive of recitations of the relevant law, facts, analysis and ruling. a relative novelty in IP cases these days is that the Court cites no case law in reaching its decision.
IPKat comment on the Advocate General's Opinion here
Report here from Bloomberg
How to train a Falcon here
Subscribe to the IPKat's posts by email here
Just pop your email address into the box and click 'Subscribe':
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Modify
Opened 16 months ago
Closed 16 months ago
Last modified 16 months ago
#7294 closed defect (fixed)
move "show object id" back to normal preference option
Reported by: skyper Owned by: team
Priority: normal Component: Core
Version: latest Keywords: show id preferenc
Cc:
Description
Please, move the option "show object id" back to normal preference option.
Even for us, it is not good if a normal user has to enter expert-mode to get a clue about the objects-id. I know there are other ways to determine the ID but these are more hidden and a user needs more knowledge about JOSM.
Thanks
Attachments (0)
Change History (5)
comment:1 Changed 16 months ago by akks
• Resolution set to fixed
• Status changed from new to closed
comment:2 Changed 16 months ago by akks
Last edited 16 months ago by akks (previous) (diff)
comment:3 Changed 16 months ago by bastiK
comment:4 Changed 16 months ago by akks
Last edited 16 months ago by akks (previous) (diff)
comment:4 Changed 16 months ago by akks
Modify Ticket
Change Properties
<Author field>
Action
as closed .
as The resolution will be set. Next status will be 'closed'.
The resolution will be deleted. Next status will be 'reopened'.
Author
E-mail address and user name can be saved in the Preferences.
Note: See TracTickets for help on using tickets.
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EDDY VISCOSITY PROFILES FOR WAVE BOUNDARY LAYERS: VALIDATION AND CALIBRATION BY A k-ω MODEL
Rafik Absi, Hitoshi Tanaka, Loreline Kerlidou, Alicia André
Abstract
Eddy viscosity in wave boundary layers is a key parameter in coastal engineering. Two analytical eddy viscosity profiles present a particular interest for practical applications: the parabolic-uniform profile (Myrhaug 1982, van Rijn 1993, Liu and Sato 2006) and the exponential-linear profile (Gelfenbaum and Smith 1986, Beach and Sternberg 1988, Hsu and Jan 1998, Absi 2010). The aim of our study is to assess and validate these two profiles by: (1) investigation of eddy viscosity in steady fully developed plane channel flow; (2) comparisons with numerical results of the two equation baseline (BSL) k-ω model (Menter 1994, Suntoyo and Tanaka 2009). Our study shows that these two profiles are able to describe the eddy viscosity distribution in the wave bottom boundary layer but for different wave conditions given by the parameter am/ks, where am is the wave orbital amplitude and ks the equivalent roughness. The exponential-linear profile is adequate for am/ks <500, while the parabolic-uniform profile is more appropriate for am/ks ≥500. We suggest empirical formulations for the different coefficients which appear in these two profiles based on numerical results of the BSL k-ω model.
Keywords
wave boundary layers; eddy viscosity profiles; two-equation k-ω model, validation, calibration
References
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Arai M., Cheng L., Kunamo A., Miyamoto T. 2002. A technique for stable numerical computation of hydrodynamic impact pressure in sloshing simulation. Journal of the society of naval architects of Japan, 191, pp 299–307.
Brosset, L, Lafeber, W., Bogaert, H., Marhem, M., Carden, P., Maguire, J. 2011. A Mark III panel subjected to a flip-through wave impact: results from the Sloshel project. Proc. 21st International Offshore and Polar Engineering Conference. 84-96.
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Richardson L.F. 1911. The approximate arithmetical solution by finite differences of physical problems including differential equations with an application to the stresses in a masonry dam. Philo Trans of Royal Soc of London, Series A, 210, pp 307-357.http://dx.doi.org/10.1098/rsta.1911.0009
Vinje, T. and Brevig P., 1981. Numerical Calculation of Breaking Waves", J. Adv. Water Res., 4, 77-82.http://dx.doi.org/10.1016/0309-1708(81)90027-0
Witte H.H. 1988. Wave induced impact loading in deterministic and stochastic reflection. Mitt Leichtweiss Inst. Wasserbau, vol. 102, Tech. Univ. Braunschweig, Braunschweig, Germany.
Wu G. 2007. Fluid impact on a solid boundary. Journal of fluids and structures, Vol. 23, pp 755–765.http://dx.doi.org/10.1016/j.jfluidstructs.2006.11.002
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Yettou El-M., Desrochers A., Champoux Y. 2007. A new analytical model for pressure estimation of symmetrical water impact of a rigid wedge at variable velocities. Journal of fluids and structures, 23, pp 501-522.http://dx.doi.org/10.1016/j.jfluidstructs.2006.10.001
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Thursday, July 31, 2008
same ol same ol
Been away... actually still away, but apologies for the bland posts which are mostly things I left in the system to be posted while I was away. But catching up on news what do we learn?
Football: What is up with the Steelers ownership melodrama? This has even reached into the musings of the NYT Freakonomics column which has a copy of Art Rooney's letter to his children portending the situation his sons now face. Professor Dubner does not mention it, but is this a classic example of rational expectations?
Baseball: You know its another lame Pirates season when again the opening of training camp displaces all the baseball news. I say it's a well thought out plan to put out news on trading deadline moves during the Steelers camp news crescendo. It hides the capitulation that is now an annual ritual. What other place in the country with a major league professional baseball team has its media coverage seconded to what happens to the football teams punter even. Which is a good excuse to repost this video of Daniel Sepulveda in college. But as for Pirate baseball: ugly.
Casino: Where to begin? Where to end might be a better question. I actually think that the North Shore site where this is all supposed to be built must be vexed or something. That same site is where Riverboat gambling was supposed to go at one point. Thus far the only 'winner' in the current casino imbroglio is John Connelly who was able to finally unload the parcel which he had been stuck with since buying it in anticipation of the Riverboat gambling license. Be careful what you anticipate may be a lesson for the here and now. Summary: uglier.
Casino/SEA/Arena: Some things really are odd in the fundamental fact that the media can't get a clear answer over who and how the arena bonds will be paid. I think we will have to get back to this, but for the moment: What Fester said.
Foreclosures: What O said.
more to follow.
Wednesday, July 30, 2008
Energy R Us
Speaking of energy, and more why Pittsburgh may already be Energy Burgh... take a look at the news on the beginning of construction of new nuclear power plants in China, but also this recent article from the Department of Energy on the status of new nuclear plant applications in the US. Not to forget about coal. Looks like the PG had a story on the impacts of high coal prices on consumers. That is very true, but that story overlooked the big local story on the impact of skyrocketing coal prices on local communities, especially metallurgical coal which has really jumped in recent months. There are significant economic impacts in the greater Appalachian economy resulting from coal price swings. If there are no other similarities, both the coal and nuclear industries are extreme cases of industries that saw very little growth in recent decades. The result was minimal hiring and a cohort of workers that aged in place which result in an imbalance in the timing of retirements. The nuclear workforce may be smaller more specialized, but the coal workforce in particular is resorting to new methods to find new recruits.
Monday, July 28, 2008
fuel-cell(less?)-burgh
This was going to be a post a couple weeks ago, but it got caught in the undertow with the casino implosion and other things.. so a little after the fact but.....
News is that Siemens is looking to sell off its fuel cell division here in Pittsburgh. It is actually part of a very large reorganization at the multinational firm involving over 17,000 job cuts. It may not be the end of the fuel cell work here, but it’s a quiet turning point for a story that was once pretty big here.
Westinghouse’s power division was bought by Siemens and would remain here in Pittsburgbe part of a division at Siemens actually named Siemens-Westinghouse until recently. One of their major projects was an attempt to commercialize fuel cell production. Their focus product was not a fuel cell for cars, but a larger product that could be used for small co-generation applications and other stationary applications.
They put a lot of money into the project and the site selection for where to put the manufacturing facility was highly sought after both nationally and within the region. So highly valued it was that no less than Ross Perot worked hard to put incentives on the table that would have enticed Siemens to build the plant in Texas. In the end they decided to keep the plant here in the region. Why? Talking to some of the folks involved, the reason was mostly a workforce issue. This was a highly specialized technology to get off the ground and the Siemens (formerly Westinghouse) workforce was likely one that was not going to relocate en mass down to Texas. So even with much greater financial incentives on the table, they chose to build there plant here. Where here? That was a regionalism debate unto itself. The final sites they considered included locations in Armstrong and Allegheny counties. When they chose a site at the Waterfront Complex in Munhall, there was a lot of consternation between county commissioners that the site had been stolen from Armstrong County.
In the end, plant would not be completed to production stage. Fuel cells work for sure, but I believe they could never get the engineering to work to make a product that was commercially viable cost-wise. The building destined to be the manufacturing plant would be empty for years and has since been bought to become a research operation for US Steel.
So this one project entailed some of the core issues of regional competitiveness, site selection, regionalism and technology commercialization. Maybe the story isn’t over.
Thursday, July 24, 2008
Yinzerwear everywhere
I am not sure how I came across this picture in flickr, but the best Pittsburgh-themed t-shirt I have ever seen may shown in this picture. I can't figure out where it came from though. Anyone?
But not to dis the other great products out there.. The Inner Yinzer in me really thinks the parking-chair motif t-shirt says it all. Nonetheless, I think there are a few other Pittsburgh themed fashion outlets out there, for years you could own some bridge-wear. Of course there are the I Heart Pgh tee's out there.
Wednesday, July 23, 2008
Pittsburgh, 1941
no reason, but just a neat picture of Pittsburgh in 1941
Tuesday, July 22, 2008
daily reading assignment
Reading assignment for the day.. a history disseration from 2006.
MINES, MILLS AND MALLS: REGIONAL DEVELOPMENT IN THE STEEL VALLEY by Allen J Dieterich-Ward
Monday, July 21, 2008
All Billboard All the Time
update: If you are reading this, I have updated some of the data and charts below in a subsequent post: Pension Update and Clarifications
No, this isn't about billboards at all. I thought I would try some bait and switch; otherwise who would want to read about boring Pittsburgh pension math.
I really am confused. Lots of news of late about the city's financial status and its now-denied request to leave Act 47 oversight. From news reports to the state's own press release, they all refer to the city's unfunded pension liability as being $462 million dollars. I am pretty sure that figure comes from reports reflecting the state of the pension system as of January 1, 2005 which is more than a little dated now. At the time the total pension liability for the city of Pittsburgh 3 main pension system was reported as $843 million. Since there was reported to be $373 in the bank at the time, the unfunded liability worked out to be $469 million, or alternatively that the pension system was roughly 44% funded.
What I don't understand is why there is no reporting of the more recent data which the city reported to the state in March. The more recent reports, reflecting the state of the pension systems as of January 1, 2007 showed that the total pension liability for the City of Pittsburgh exceeds a billion dollars for the first time ever, $1.04 billion to be more precise. Total value of assets to cover that was $375 million at the time, so the city's pension systems collectively were underfunded by over $660 million (not $460 or so) and have a funding ratio more like 36% (and not 44). Funny how the city does not go out of its way to mention how big the pension liability has increased in just the last few years. Well, not that funny, I can understand the motivation. But I don't quite get why the state does not read the actuarial reports the city sent to them in March.
If you want to dig into the painful details, or are overspending on Ambien and need an organic alternative, the most current actuarial reports for the 3 pension plans are here:
Looking back, here is the time series of the total pension liability for the three main pension systems. Anyone discern a trend??
The trend has a couple causes. Some of it comes from what may need to be conservative assumptions on future mortality. I'll get back to that, but there is a big jump between 2005 and 2007 that is a story unto itself. I believe that increase (biggest ever increase? maybe) results from a lot of early retirements that the Act 47 process induced. So instead of getting continued work from a lot of folks that anticipated decreased benefits down the road if they remained on the job, they did the logical thing and retired early. It might have saved some dollars up front which I am sure the Act 47 folks will take credit for, but realize there is a big chunk of those costs were really just displaced into future pension liabilities. Those early retirees are going to be collecting benefits for a lot longer time than they would have otherwise. That big pension liability jump from 2005-2007 amounts to $190 million dollars unto itself and obviates a lot of what is being counted as 'savings' that resulted from Act 47. Not all of it for sure, but enough to make note of.
In the long run it's about the funding ratio. The funding ratio which is the ratio of assets to that total liability looks like this over the last decade.
Something you won't notice in that top line funding ratio for the entire pension system: Not all of the pension systems are in the same state these days. If you look at each pension system individually, there are the funding ratios for each:
Which shows that relative to the other two, the police pension system is significantly less funded. This could become a pretty serious issue really soon. It is also interesting that the fire pension system used to be the highest funded system of the three, but because it has seen the largest percentage of its workers take early retirements, it has unsurprisingly seen the biggest jump in its pension liability, and as a corollary seen the biggest decrease in its funding ratio.
Again, these are all numbers for January 1, 2007 which is itself now over a year and a half ago. Both of the key numbers, the total liability and the value of assets invested to cover that future cost have surely changed since then. How have they changed? News reports say that as of April the total $ value in the pension system was down to $350 million. That in itself would put the funding ration down around 34%. But you may have noticed that the stock market has been pretty bearish over the last few months. If you think that $350 has gone down just 10% to say $315 million (the stock market is generally down by a bigger % from its recent highs, but let's hope the investment is well diversified into safer things), the funding ratio could easily be pushing 30% right now. The police pension system could easily be pushing down near 20%. All numbers that are not really qualitatively different from where the city was at before it floated a huge pension bond to fund the system in the 1990's. The point of that bond was to push the pension system to where it would be able to sustainably garner investment income and eventually sustain itself in the future. It hasn't worked out that way at all.
If that is not bad enough, go and look at the time series for the total liability numbers. For a lot of really boring reasons I could go into why I think that total liability number continues to go up. Some of it relates to the Act 47 issue earlier, but it also results from a lot of assumptions that you have to make when looking into these future actuarial projections. In a certain sense those assumptions have to be conservative, but I think there is no reason not to believe that the total liability number has continued to inch up. Basically retirees are living longer than is being presumed, and thus every time you recalculate this future liability you see that there are more folks still living and collecting pensions than were expected in the past. So it's UPMC's fault that the pension liability keeps going up. (joke ok, don't want the UPMC police coming after me). But if the average annual increase of roughly +5% has continued, for 2008 the total pension liability could be on the order of $1.08 billion, for 2009 it could be on the order of $1.14 billion. January 1, 2009 is just a few months away so that may be my best guess as to the current state of the pension system.
If there is $300 million or so in the bank for a 1.1 billion dollar liability puts you at a funding ratio of roughly 26% overall, which would probably put the police pension system at a funding ratio in the teens. That last sentence is my own educated guess, but the pension system could put a more definitive number on what the assets are in the police pension system alone if someone wanted to give them a call.
In the past, I have seen pension reports for the city that assume that at funding ratios below 25% or so, the system would switch into a Pay-as-You-Go type of system. That would have big implications for the city budget near term if that comes to pass. What it all means in the end is that the required payments the city has to make to pay the anticipated liability are shooting up at rates that I am pretty sure are not reflected in any budget plan I have seen. At funding ratio's that low, you have to consider that even if a bull market reappears, the assets will never have achance to appreciate enough to catch up to where the pension fund needs to be. If the trend continues, the unfunded liability will eventually come close to matching the total liability which is now that billion+ number. A billion that is falling mostly upon an ever smaller population base which generates most of the revenue capacity for the city. Without going off on another tangent, the big issue with the city's declining population overall is that there is probably a growing student and transient population in the city. Students, along with seniors, do not exactly have the revenue generating capacity that will ever help with the city's future liability. The city's household population that is it's real tax base has been declining faster than the overall population trend would imply. So per capita, the debt issues are huge and unlike most anywhere else in the country.
*****
For reference, current and some past pension documents and other ephemera I collect are on my Pittsburgh Policy Document Collection web page.
The data used for the above illustrations are in an excel file I have online here.
Shrinking Cities Detroit Movie
I wish I had time (and skill of course) to do something like this about Pittsburgh.. maybe someday. but h/t to Digital Urban for the pointer to the movie below from shrinkingcities.com on the development and undevelopment of Detroit:
Moving Datas from 1kilo on Vimeo.
The closest I ever came was my
Sunday, July 20, 2008
Transit mashup
PG talks about an epic journey in a converted veggie-oil Mercedes. I just thought it would be a good opportunity to plug the Pitt Veggiemobile which deserves a mention in that story.
on transit, I have already predicted that the Port Authority labor negotiations are going to be a painful path until there is a resolution. Here is something from last year I thought I would repeat since it really will be relevant pretty soon:
Philly Inquirer talked about a transit study done out east: http://www.phillyburbs.com/pb-dyn/news/147-05172007-1348077.html . The full report is here: http://www.economyleague.org/files/File/The%20Price%20of%20Inaction.pdf
Maybe while debating the drink tax, we should debate the value of doing a study like that here.
Saturday, July 19, 2008
Early Black Flyers of Western PA
Only for history buff's out there. Actually, for some unknown reason this blog keeps getting search engine hits on a post I had mentioning early Black Flyers. Almost as often as people searching for information on Mallow Cups. So for whomever is looking, here is a journal article some may be interested in:
Early Black Flyers of Western Pennsylvania, by George Edward Barbour. Western Pennsylvania Historical Review, April 1986
Friday, July 18, 2008
Desperately Seeking Sources
The County Controller (wait, don't look, can you name the County Controller?) is making news of late with his claim that if the Steelers are sold the public should get the money put into building Heinz Field back. One issue is that it was money put into the Stadium, not the team and a change in ownership of the team does not really affect who owns the stadium..... so whats the point? Then there is the question of whose money should be returned? RAD money? State money? Maybe those expensive seat licenses people paid for to help fund the stadium? It's all one of those ideas that sounds good in a press conference for sure, but how it would all work out is unclear.
At first glance I thought it was just an excuse for the County Controller to garner some name recognition, it being unlikely there was any realistic way that the public could recoup any money. Made sense to think of this as the County Controller (Mark Flaherty btw) gearing up the PR machine for a post-Onorato campaign for Allegheny County Chief Executive. What was Dan Onorato before being elected to the top job in the county? Controller of course. Remember the politics behind the election when Mark Flaherty was elected. At the time council rules forced Jim Simms to resign from his position on County Council, where he was no less than Chairman, in order to run County Controller. There was talk of various deals that was supposed to make that election a foregone conclusion. Like a lot of deals that might have worked in the past it didn't end up the way some intended and Mark Flaherty captured the Democratic Party nomination for controller and would win the post. If not for controller, I always thought Jim Simms would reemerge in local politics. He may be too smart to actually jump back in these days and the public record will detail the personal tragedies he has to deal with as well.
But back to the Steelers and their money. The news reports say there is some clause in the lease that says the county must approve a transfer of ownership. So even if it really has no claim to any actual ownership to the team, it might actually be possible to have a claim on the capital gains that will be realized when the team is sold.
The lawyers might be empowered to sort that out, or this will all be overcome by events eventually... but here is my thing. You can take a look at the Sports and Exhibition Authority website yourself. It has some minimal information there, but nothing terribly important. Is there any reason the lease between the Steelers and the SEA could not be put online for everyone to see. It would take all of a minute to scan I think. What about the agreement between the SEA and the state over how much funding it will get to support the yet to be built arena? An important document these days with the turmoil in the casino. Try and get your hands on that document and you might as well be trying to gain access to the secret archives of the Vatican.
Remember, this is a government body according to most laws. It should not be so hard to find this information. Just for fun, you can read the lease between the SEA and the Pittsburgh Pirates. Thanks to Tim (aka Carbolic) M. for sending me a copy of that contract. Why do these things need to be passed around like illicit blueprints for nuclear triggers? Another important document I have put online, the prospectus for the SEA bonds to fund the new arena which has a lot of details relevant to the public discourse these days? Again, not to be found on the SEA website. So all that neato web programming that makes it look like the SEA website is open and available to the public is mostly for show. One could argue it obfuscates more than it makes available.
To be fair, its not an issue limited to the SEA at all, although I would argue that what goes on at a lot of public authorities and special district governments is a lot more shrouded than other public entities. In the City of Pittsburgh uber-activist David Tessitor is trying to get an open government amendment on the ballot as a referendum this fall. So from the shores of the Monongahela all the way over the pond where the Guardian runs a Free Our Data series there is a long way to go with public data access. The best response I ever had to a request for a public document from a public official was "We don't have a public library for those types of things, but if you were able to fund a library for us we could make that available". I thought that was such a creative answer I didn't get mad at all, actually I laughed pretty hard.
Thursday, July 17, 2008
Walkable-Burgh
I first saw this last year and can't recall if I blogged about it.. but the WSJ's number guy reminds me of a neat site http://www.walkscore.com/ which you can use to figure out your own neighborhoods "Walk Score". Not a criticism, but what it misses is access to transit routes which I think is a part of the mix. But it's a neat site, check it out.
I found a nearly perfect score in the middle of Bloomfield. A score of 98 out of a hundred for 4700 Liberty Ave.
Let's have a contest. Can anyone find a higher score anywhere in the Pittsburgh region?
Where is the lowest score?
Rumornomics
County Council has been debating the recently imposed drink tax. Which reminded to take a look at the Port Authority's "Rumor of the Day" the other day and this is what I found:
Rumor: Allegheny County passed the drink and car rental taxes to provide an additional $27 million to Port Authority.
Truth: Prior to enacting the new taxes on January 1, Port authority’s county funding came from real estate taxes. That money can now be used to support other county initiatives and the Authority has a stable source of county funding through the taxes.
The thing is, I really can't quite figure what point they are even trying to make with that? It almost reads to me that they are arguing against the drink tax, or at least undermining its justification. Also, does it imply real estate taxes weren't stable? or less stable than drink tax revenue?
They really have a lot of work ahead of them trying to come up with a constant stream of 'rumors' out there like that. They seem to be a little light on material right at the beginning. I am also unclear if anything they have flagged as a 'rumor' as yet are really rumors to anyone other than themselves. They mostly seem to be generating foils to argue management's side in the ongoing labor negotiations. Yeah, I know that is kind of self-evident.
Wednesday, July 16, 2008
blog-what?
Pittsburgh blog-dom is agog over the developments in Lamargate, specifically the news today that local Blogger Bram was interviewed by staff of the US Attorney and asundry legal begals over his role in bringing certain things to light. I have commented on the whole situation before in Constant Bearing Decreasing Range. I have also said this before, but as a general rule: interview with US Attorney = need lawyer. I don't care if one thinks they are as guilt-free as Mother Theresa, it's a good idea to have counsel with you when being interviewed by Federal agents. Do I need to start up a collection for Bram? Someone ought to at least register freebram.com as a domain.
But some out of the way thoughts on the article in the PG. Just the semantics of refering to Bram as a "local blogger" without much explanation. Yes, I know anyone reading this is aware of what a blogger is, but I wonder what percentage of the PG readership is. My mother is a regular PG reader, and much like many I suspect she has no idea what a blogger is.
Further, Bram has been pretty up front in his role in all of this to date, or at least I think he has. What was there to interview him for an hour over. Probably a lot of background stuff they had to go over just for due diligence's sake. What is unclear to me from the PG story is whether Bram was brought in as part of something having to do with the Lamargate at all. A Housing Authority lawyer is reported to have been there. It is not inconceivable that his has little to do with Lamargate but more with issues involving the Housing Authority. Who knows at this point?
Tuesday, July 15, 2008
collateral damage
There is a lot of collateral damage to the ongoing crises in the financial industry. On February 19th when this story was written, the price of National City Bank stock had taken a beating and closed at $16.03/share. The big impact locally was on the McCune foundation whose history had left it with a large holding of National City Stock. Yesterday that stock closed at $3.40/share. If that story painted a scary story at $16.03 for National City stock, what does it say for the foundation and the bank at around $3/share. It's an issue not only for the foundation but what is still a big player in the local retail banking industry.
Other financial impacts - Newspapers
Is there a post-media world?
I can't quantify this in any meaningful way, it really is just a gut feeling. More and more of late it just seems that journalists in town are collectively kind of depressed. I know the media as an industry is not doing well, but it really is kind of bad, or at least more obvious than in the past. Then (via Editor and Publisher) from Reflections of a Newsosaur comes this quote on the state of media as an investment:
The shares of seven publicly held newspaper companies today plunged to the lowest point in modern history in perhaps the worst single trading day ever for the industry.
That blog link has a very scary picture of the trend in major media stocks in recent years. It makes even the Dow Jones of late look like a safe haven for your money.
More on the Post-Media World: Blogarama
Just on the changes impacting journalism in general, or the nexus of blog-dom and journalism at least. The buzz in some journalism circles of late is from a blog comment on some internal comments made following layoffs at the Tampa Tribune. Currently with over 200 comments see this blog post: '"It's Worth Fighting For"'. The author actually being an intern at the Tampa Tribune so you are getting the straight scoop. Not bad for an interns blog.
Monday, July 14, 2008
Barden-nomics
It's still beyond me to parse much more than what is in the headlines over the past/present and future of the Pittsburgh casino license. Still waiting for some of the shrapnel to fall to earth to try and figure out where we are.
But I was wondering what Don Barden has collateralized his now semi-defaulted bridge loan of $200 million with. I had presumed it was some of his other casino operations. It couldn't have been his Las Vegas operation. Barden had put his flagship Las Vegas operation: Fitzgeralds up as collateral for the ongoing project. He simultaneously announced the operation was for sale to make that commitment liquid.
But.. this just in. Looks like the deal is off and Fitzgeralds has been pulled off the market. So I take it's not at risk here any more, but I could be wrong about that.
There has to be something at risk here? If the license gets pulled, you have to imagine that most of the $200 million already spent somehow will be a complete write down. At one point there was talk of loans to be collateralized by Detroit municipal pension funds. Is any of that risk still in play? I dunno, just questions I have.
Daily Steelers Fix
That may be a bad way to phrase it.. but some Steelers notes beyond the local headlines:
Blog exclusive: Real insight on the state of the Steelers is over on MondesiHouse with this interview of Art Rooney Jr.
I didn't realize that Mark Madden had landed somewhere, sort of, but he has weighed in on the Steelers saga in the Beaver County Times: Monday Madden: Losing Rooneys not a bad thing.
Bloomberg also weighs in today: Pittsburgh Blood Feud Lets Goldman Sachs Inside: John Helyar
AP has: Steelers' founder had his own ownership struggles
An Analogy Too Far....
... I hope, but let's hope this is never fodder for any local story. Otherwise provided without formal comment:
The Onion: Entire City Council Session Devoted to Tree Stump
On local government. Some good stuff from NE Ohio via Brewed Fresh Daily. See recent work on the Cost of Local Government in Northeast Ohio. Coincidental to story in the Trib today: Big challenges confront small Allegheny County municipalities. Mentioned in the past if you want to see some similar numbers for Pittsburgh in my Primer On Local Government Fragmentation and Regionalism in the Pittsburgh Region
Saturday, July 12, 2008
Oil Capital Redux
When I graduated from college some years ago, a couple of my friends took jobs with Schlumberger, the international oil services firm. What they wanted young engineers for was to train them in operating their oil exploration equipment. They would typically set you up with one of their specialized trucks which had as much high tech equipment as you could pack onto it, then send you off to far flung places to find the next mbillion dollar hole in the ground. They would typically have the best stories when you ever caught up with them.
So I am driving on I79 this weekend and come up behind a truck that looks to me like a cross between a MAC truck, a street sweeping machine on steroids and something from Transformers. I couldn't figure what it was. Passing it I saw it actually said it was a Schlumberger truck as you might find tooling across some desert somewhere. I have put a fair number of miles driving across Pennsylvania over the decades and I have never noticed a Schlumberger truck in the state. I know the crazy price of oil, natgas and coal all are causing a re-evaluation of Appalachain energy reserves, but the thing that I couldn't quite figure is that given the long history of Pennsylvania oil, could there really be anything left to analyze. The truck itself must represent a pretty valuable and scare commodity in the oil crazy world these days.... but it was tooling through Pennsylvania.
Maybe it was passing through to go look for some Canadian Oil Shale? Maybe I just never noticed these trucks before? Maybe it was some other type of Shlumberger truck that did something entirely unrelated to the oil industry? It could have been designed to drill for water for all I really know about geo-engineering these days, but would be shocked if you need that much capital to find water in Western Pennsylvania and points north. Given a dowser I suspect I could find underground water if I had to.
I was willing to accept any of those possibilities or something else innocuous, but then came across this article from just the other day via Steve Sjuggerud's newsletter: Why Pennsylvania Land Prices are Skyrocketing. That real estate speculation that never got to us.... incoming?
Friday, July 11, 2008
More Variable Rate Bond Messes
From West Virginia is this news today: High Gas Prices Taking Toll on Turnpike.
Which has TWO big stories in it. One is the decline in use of the turnpike which is the headline. But read the story, almost hidden in there is another variable rate bond crisis for their Turnpike Authority and an:
“The emergency meeting was held to address the situation forced upon us with the downgrade of our bond insurance company,” Martin said. “The immediate effect of that refund was to drop the interest rates the parkway was paying on its outstanding debt.”
There just has to be more stories like this lurking all around.
missing stories
Where to begin?
It just isn't in me to start deconstructing what the Barden financial capitulation could mean for the city and region. At this point, the gaming board really has an obligation to provide at the very least some quick roadmap for what the resolution to all of this could be to make sense of it all. They can't fix the mistakes already made and we will have plenty of time to assign blame, but right now the sheer uncertainty of the way forward has the potential for ever more harm.
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The indictments handed down in Bonusgate as it were have all sorts of implications. The headlines go to the indictment of Mike Veon who was the minority whip in the Pennsylvania House, but from a political standpoint he was already booted from office. He can't lose again and it's unclear what successors running for his old seat will be impacted by this. As much as it is not being focused on by the media, what is much more important politically is the indictment of Sean Ramaley. He is currently the nominated D for the 47th State Senate District which has been held by a Democrat, the retiring Gerald LaValle. Can't be good for your election prospects to be indicted in such a high profile kind of way. If a reliable Democratic senate district goes Republican in a body as small as the state senate (50 senators total) it really bodes really ill for Democrats in the Harrisburg. Every single seat counts a lot, especially given how rare it is for a State Senate district in Pennsylvania to ever 'flip'. Basically the Senate is already decidedly Republican (29R-21D) and pushing that to 30R-20D has real repercussions. A supermajority margin like that means a lot things will have to have clear Republic support to be passed, not much chance for swing voters in the middle to be the deciding vote. Does Ramaley remain the nominee?
Turns out I am not the only person asking that question, check out the video opining from the Beaver County Times on that topic. Turns out that the Beaver County Times has it's own YouTube channel. Cutting edge stuff for the Pittsburgh region's media.
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OK. probably need to stick to the knitting a bit. Yes, lost in all the other news was the annual release of census data on the population estimates for municipalities in 2007. What is the headline? the City of Pittsburgh dropped in population from 313K to 311K.
The funny thing is that there is nothing really different about the estimate released today for the City of Pittsburgh and most of the other municipalities in Allegheny County. Within Allegheny County the percentage decline for the City of Pittsburgh was right in the middle when compared to other municipalities. 62 of Allegheny County's 130 municipalities had faster rates of decline over the last year while 67 declined a little less or grew a small amount. Other key points include a few things. These really are estimates. Nobody has gone out and counted anything really. These are small area estimates which are the hardest things to get right. County estimates are going to be much more accurate than municipal level estimates. Do I have any real reason to think the numbers are biased low or high? no, but at this point 7 years past the last decennial census we are in a period where there is a real likelihood these annual estimates will be proven to be off. How do they come up with these estimates? They take the county level population estimates which were released months ago and break up the population changes within the county based almost entirely on the number of building permits. Where there are new building permits being issued, more folks within the county are presumed to be moving in, where there is a lower than average number of building permits you figure there is lower growth or faster decline. Also, everyone keeps asking if we are seeing the impacts of say high gas prices on where people are living. These are estimates for 2007, so they are meant to mostly reflect the population in the middle of last year and can't reflect any changes since then. And given the methodology just explained, and given that building permits are applied for well before population movement happens, you really are seeing data reflecting economic decisions made earlier than mid 2007. So it may be some time before any data begins to reflect these things we are mostly conjecturing about such as a return to the city due to gas prices.
Thursday, July 10, 2008
As God is my witness I thought turkeys could fly
Oh the pain. Per the PG and the Trib.
Now what? How goes the Rumsfeld quote? there are known knowns, known unknowns and unknown unknowns. Closer to the 3rd option right now if you ask me.
How much are the Steelers worth anyway?
Quite a lot of emotional angst over the potential sale of the Steelers and the eventual role of the Rooneys. Who knew there were so many Rooneys in the greater Steelerverse? For more on the alter-ego horse racing empire of the Steeler clan take a read of: A steely eye for the ponies which was in the Albany Times Union last year.
So how much are the Steelers worth? I guess we will find out soon. Sort of a core maxim of economics is that something is worth what the market says it is. If there is some open bidding for the team, or parts of it, we may see what the market price really is.
But Forbes regularly values professional sports teams. When they last figured the value of the franchise it was $929 million in 2007. The Forbes valuation has gone up every year and was just $300 million in 1998 which works out to be a healthy 13.4% annual appreciation. If that trend were to continue it would put the Steelers value at just over a billion dollars right around now. As the Rooney family appears to be struggling with, thats a lot, but it is not necessarily the most liquid billion dollars out there.
Today the Wall Street Journal has a pessimistic look at the finances of the Steelers in: Behind the Steel Curtain, a Rusty Bucket: Pittsburgh Franchise Wanes As Rooneys Angle for Profit and Control; Outside Bidders Loom. That article imputes a value of $700 million for the team based on numbers being offered among the Rooney clan, but I don't think anyone really knows what outside bids could bring just yet. Sounds like the likely suitor, billionaire Stanley Druckenmiller is a rabid Steelers fan which could mean there is an emotional premia for the team as well. A the same time the WSJ article highlights a number of financial pressures on the team's bottom line that could hurt its valuation as well.
With the French buying Yellow Cab and the Spanish buying Kennywood, I wonder if there are some Dubai sheiks who might wind up on the short list of suitors for the Steelers?
Wednesday, July 09, 2008
This Week in Coal
I have said before that the best public dissemination of data comes out of the Department of Energy's Energy Information Agency. Every Wednesday they distribute their "This Week in Petroleum" report which has just about everything you can get in near real time data on oil usage in the US. It is also the only government report where the authors explaining the data have a bit of humor to help out the otherwise awfully dry content. In the past they have used for context to explain oil trends things like the college football, bad movies, marmots, professional football, major league baseball and all sorts of other things.
They do have lots of other data on their coal page. But one of the biggest stories for the region that is not being talked much is what is happening to the price of regional coal. Last week, the spot price of Pittsburgh Seam coal jumped by 10% over just the previous week. Here is a factoid: since Jan 2007 the price of oil had gone up around 230%. The price of Pittsburgh Seam coal is up around 300%. Almost all of that increase is over just the last 6 months!!
Here is one of those graphs that make you go 'hmmm':
Pittsburgh Seam Coal Price 2007-2008
Which all may explain why the coal industry is resorting to new recruiting tools to get more workers.
The Creative Class Meets Soylent Green
Not exactly what Richard F. was intending, but man is this funny. Via Adfreak is a tip about this YouTube 'documentary': Distilling creative juices, one vine at time.
Tuesday, July 08, 2008
Council Collapse Disorder
(Sir) Ed Heath is now officially part of the Pittsburgh Punditry given his comments in the Trib today on the ongoing saga in City Council. The Trib’s Jeremy Boren was probably given 3 inches to fit in a piece that would have taken 30 to explain in any meaningful way, yet one that I hope would have gotten no more than a paragraph for any minimally necessary closure.
At this point when it comes to internal politics of city council I am as confused as the beekeepers who are wondering what is happening to all the bees? For sure, City Council has always been a nexus of painful and personal politics. You don’t need to go far into the past to find stories of squabbling amongst themselves. For the local historians out there, some personal spats are legendary: Madoff/DePasquale, Ferlo/Masloff, Polack/Givens to name a few. Yet even when the machinations were pointedly painful, involving profanity or even a few physical altercations on the record you usually could tell what the point of the fighting was about and who was on what side.
The problem we have today over the continued squabbling is that the public is confused at this point over what the point really is. Even the most charitable interpretation would find fault with just about everyone involved. How this has dragged on this far is mind boggling.
What is at risk if this continues a day longer. it is worth noting what this has meant to city politics. Consider the brief history to date of the sitting government for the City of Pittsburgh. When first elected and early in their term city council had quotes like this:
All I can say is that never has a political body had its reputation fall so far, so fast, over so little?
Now what? Does anyone really talk much about what is going on with regards to Lamargate. Does anyone remember the mayor’s former press secretary. What issue does the public associate with the whole billboard imbroglio?
Yes, this very post has sort of a Heizenberg effect that contradicts itself.. but for anyone who is a public official I really plead: end all of this now. I am sure everyone has lots of things they want to say and get off their chest. We all want greater transparency and communication with our elected officials. Nonetheless, at this point there is absolutely nothing any of you can say on the record that is going to do anything to lessen the public’s confusion in this matter. Stop, end, cease and desist, invoke radio silence on just this issue. There is a point so sometimes just saying “No Comment”. When those pesky media folks ask for “just one comment” to respond to whatever… just say no. Sometimes discretion really is the better part of valor.
The good news is that nothing in politics is permanent and with luck this will all be forgotten.. if not by each of you then by the public. This will not be the first issue you all disagree, sometimes on very core value terms. You can’t blow everything up over every instance like this lest what will happen, has happened, is happening, is a complete disfunction where matters that have to be attended to are just completely forgotten. Vote your consciences and move on. Anyone looking at how the city’s pension fund has been faring of late? Add 5 zeros to the legal bill jamming the machine to understand the magnitude of that one issue.
Business Friendly PA?
Too much of a downer of late... Here is a fascinating story from New Jersey: Rendell poaching business from N.J. It's fascinating since Pennsylvania gets beaten up so much as a place uncompetitive in business attraction and formation for various reasons.. usually having to do with tax climate. The money quote in the article:
In 2006, Pennsylvania ranked first in the nation in cross-border investments, projects whose capital comes from outside a given state, according to an IBM analysis, the latest data available.
emphasis added.
first? I have to admit I don't have the current reference research by IBM so I can't comment too much. A summary of the previous years report is here and on page 25 you will see some interesting recent trends for Pennsylvania. If you had to pick the ultimate goal of economic development at the state level it would be to attract investment from other states.
Obligatory history reference. How long have Pennsylvania and New Jersey been fighting over new investment? years? decades? try centuries. It was Alexander Hamilton who located his Society For Useful Manufacturers in 18th century New Jersey aided by some ample tax breaks to the chagrin of Pennsylvania politicians who felt it was unfair. In many ways it is a battle we would still be fighting more than 2 centuries later.
but maybe the article is just a reflection of "always greener on the other side" mentality over in New Jersey?
Monday, July 07, 2008
about those SEA bonds.....
Just to state this up front, this may be a non-issue. But even if it is just a possibility it's important enough that someone ought to ask the question: are the SEA arena bonds in trouble? Also, this is clearly something that has Municipal Finance 102 as a prerequisite, but it's worth going through.....
A brief bit of background is needed first. The Sports and Exhibition Authority (SEA) is a public authority that is responsible for the building of the two sports arenas in town, namely PNC park and Heinz Field as well as the Convention Center. The SEA should not be confused with the Stadium Authority which has neither a stadium these days to call its own, nor much authority, but that is another story for another post. They also are the folks who will be building the new arena for the Penguins. Last year they issued roughly $315 million dollars in bonds to pay for constructing the new arena. Recent news from last week is the first major contracts that go with that construction are being let by the SEA. The bonds to pay for this were floated last year, so the SEA has the money in the bank and have been making required bond payments since November. While they have planned in a certain amount of reserves to make these payments currently, the plan is that $7.5 million/year of the required payments are to come from the yet to be opened Majestic Star Casino. The viability of Don Barden and the Majestic Star to make those payments is its own issue these days and not the point here. What I am wondering is whether the bond payments are going to cost a lot more than planned for given a lot of changes in debt markets of late. Diving into the muck, there are an awful lot of dots to connect to this......
Last week I pointed out that bonds issued by the Sports and Exhibition Authority to pay for the new Arena in town are variable rate bonds. I have the entire bond prospectus scanned here. Variable rate bonds are not that out of the ordinary these days, but its worth noting that a lot issuers of variable rate bonds have run into a lot of trouble of late. Many issuers of these variable rate bonds suffer from what has been described as bidders remorse at this point. Locally the biggest story was about UPMC which actually lost money last quarter for the first time in a long time in part because they had to unwind some variable rate bonds that were quickly becoming money pits.
The reason variable rate bonds (think adjustable rate mortgage... except with a few more zeros) are problematic of late has a simple and complex aspect. The simpler problem is that among all the other bad economic stories going on is that some interest rates are going up. Thus if you borrowed a chunk of change at a variable rate, you are finding out that the payments you owe on that loan is going up. The more complex story of some serious market failures in some of the markets setting these interest rates is a story unto itself.
Is the SEA bond in the same boat as the UPMC loan? Not necessarily. You can buy all sorts of financial instruments to 'hedge' your risk. The bond prospectus (linked above) and quotes I dug up from the SEA Executive Director all lead you to think the SEA was planning to buy some swaps to hedge their risk here. I don't have enough info to know if they did that thoroughly or not. Risk hedging is a lot more art than science and the question is whether they did it well is not a foregone question. Lots of the economic miasma in the country really comes from the top experts coming up with risk hedges that were worse than useless (remember Long Term Capital Management? or any of the billion dollar rogue traders of late?).
Even if they hedged their risk, what risk were they planning for? I was more than willing to give the SEA the benefit of the doubt that is all a non-issue, but got worried again when I saw this headline last week first in some trade publications and then in the Dallas Morning News on Thursday. See: "Dallas Cowboys stadium bonds rise in cost for Arlington". The circumstances sound awfully familiar at the very least.
Turns out the Dallas bonds were in trouble for a different reason than UPMC. Those bonds were being hit by the fact that they were variable rate bonds, but also that they were insured by MBIA, a company that sells bond insurance... or did until very recently. MBIA has really flatlined of late and recently has seen its bond rating pulled by some of the bond rating agencies. If you are in the bond insurance business, all you are really selling is your bond rating so to not have a rating is to essentially be out of business. As a company MBIA's equally near-death competitor AMBAC saw its stock fall below a dollar a share last week and was delisted from the NY Stock exchange as a result. If that is all gobbledygood to you, the bottom line is that its all bad news for both companies and anyone doing business with them.
Update1: MBIA has sent me an email to clarify that: "Fitch withdrew its ratings on MBIA in response to our request, we continue to be rated by S&P (AA, CreditWatchNegative) and Moody's (A2, Negative Outlook)". OK?
Thus in Dallas, bonds insured by a near-defunct bond insurer resulted in their variable interest rates going up. They were being forced to pay a lot more in their bond payments than they planned. Thus like UPMC they went to great effort and expense to call and refinance the debt in question to get out from under the rising bond payments.
But does that apply to the SEA here. Still no. Not yet at least. The SEA bonds are not insured by MBIA, as in Dallas, nor by the other bond insurer having similar problems: AMBAC. You might say, good job SEA for now.
Anyone still reading? Here is the punch line.
The company that the SEA used to insure the bonds is called FSA and until recently it has not been talked about as being in the same miasmic condition of its competitors. The 'until recently' part comes into play when you read about financial analyst Bill Ackman's critique of FSA. He say FSA is next in line to suffer the fates of MBIA and AMBAC. Just a lone voice in the woods? The problem is that Ackman was the single wolf sounding the alarm about MBIA and AMBAC's shaky financial situation for years. So much the lone wolf that the companys attacked and sued instigated an investigation against (see update2 below) him for his analysis which was published in a report he himself put out "Is MBIA Triple A". So of all people, for Ackman to now be saying FSA is racing toward a wall, it gives you pause.
update2: an email from MBIA tells me that MBIA did not actually sue Bill Ackman. From news accounts, what they did was ask then NY Attorney General to launch an investigation at, and I quote, "at MBIA's request". That same news article describes the industry's response to Ackman's report as "Swift and brutal". I'm not sure it's worth arguing the semantics there but.....
So... even if the SEA fully hedged their variable interest risk in the bonds... something I wonder about but give the SEA the benefit of the doubt over.. the bigger wonder is if they hedged the risk to account for the potential that the bond insurer would run into trouble in the future. A swap that provided a hedge against general interest rate volatility in the municipal bond market probably does not provide much help for higher rates that would result from another failed bond insurer. The big question then is whether the SEA hedged against the risk of their bond insurer losing its credit rating? It's not the type of thing you normally plan for. If you thought your bond insurer would lose its credit rating in the near future, you would choose another bond insurer I hope. Until recently, failed bond insurance was considered a zero probability event.
Down the road is the SEA going to be in the same situation as Dallas and be forced to refinance its bonds? They would be in a tough spot to refinance what are essentially revenue backed bonds given that the revenue source (i.e. Don Barden and the Majestic Star) has its own problems these days.
Don't forget the first sentence. This might not be an issue. For a positive conclusion: if indeed this is not an issue it is because the bonds in question were fully hedged to account for these potential risks. If that is true than the SEA did a better job than a whole lot of other financial superstars did in similar circumstances. If so then I will be the first to say somebody at the SEA and their financial advisers deserve a big raise for not only saving the SEA a big chunk of change, but saving the region from an almost unquantifiable amount of heartburn if the bonds were to go south. Either way, its a big story I would say. Either there is a big problem completely under everyone's radar, or we have some of the best financial managers in the country right here that saved us from some big landmines going off in lots of other places.
So just to be clear, questions I think should be asked and answered on the public record are:
1) Are the SEA bonds for the arena construction auction rate bonds similar to what has been problematic for UPMC and other issuers in recent months?
2) Have changes in market interest rates impacted the payments made on SEA bonds?
3) Does the SEA expect the rating of FSA to go down in the future and
4) Are there potential impacts on interest rates and bond payments if the bond insurer FSA has its bond ratings downgraded at some point in the future.
While we are at it, I'll throw this in for good measure. I have no reason to believe anything improper, but given that the SEA is holding the bond proceeds... how have they invested the cash they are holding.
update3: While we are clarifying things. It's amazing how these things all connect to each other. I realize some may not know, but MBIA, the bond insurer that has taken the most interest in this blog post is also the company that once bought out most of the tax liens in the city of Pittsburgh causing innumerable problems until they were guilted into selling them back to the city for cents on the dollar last year. A long story I will append to a little later.
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Postscript: while everything is connected one way or another, most of the above has little to do with the issues raised in the PG this morning about the fees and related costs to city related debt issuances in recent years. But if you want to look at a lot of the past , in addition to the SEA bond prospectus mentioned above, a lot of local debt documents are on my Pittsburgh Policy Document web page. It didn't occur t me until reading the PG story that some of the Water and Sewer Authority Debt is both variable rate and insured by FSA, which means the issues I mention above apply to them as well. See the PWSA's 2008 variable interest rate offering.
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Happy Monday..
Sunday, July 06, 2008
I think that's called Minimalist Architecture
Sent by a reader and just too funny. Check out this post on the Skyscraper Forum which shows the 'new rendering for Barden's casino. The casino building is on the left and the parking garage is on the right'
I really am surprised given the delays in getting casinos running here and in Philadelphia that the idea of temporary riverboat gambling has not resurfaced (some history). But with it's major proponent over the decades, State Senator Vince Fumo, essentially retiring this month I don't see it. But you never know.
Friday, July 04, 2008
transit roundup
Just for fun it's interesting to look at recent past prognostications on the impact of rising oil prices. From 2006 is this piece in Reuters: "NYC the place to be if oil hits $100/bbl ? study". $100 being as far a runup in price as could be conceived of at the time. Where do you go at $140 and rising?
News in AP and Trib on aging river infrastructure here in Pittsburgh. This is really a big story, bigger than the coverage it gets. They mention some numbers for the amount of rail or truck transport it would take to move just some of the coal or coke that currently goes via barge. The thing is, talk to folks who work in the rail industry and there just isn't capacity to dump that much new demand into the system. The US rail system in general, but especially through some of the chokepoints near here, is arguably past what is sustainable as it is. As for trucks which may be the most costly option of the three becasue of fuel prices? So see the first paragraph above.
Speaking of prognostications. News is that the Port Authority has a new web site to inform the public on the status of labor negotiations. It has a 'rumor of the day' section which could be fun. The first 'rumor' was that service would stop when the current contracts end on July 1st. Funny thing is I heard nobody talking about such a rumor so it's unclear the purpose of that. and read the story for the timing: the site went up Wednesday the 2nd and the first rumor it quashed was already in the past? Curious.
But no joking. I will put good money that there will be a strike at the Port Authority. All the talk I hear leads me to believe that the powers that be actually want there to be a strike. I will not be surprised if there is a plan in place early on to use substitute workers in the event of a strike in order to break the union which is really the goal.
How will it all turn out is beyond anything I can predict. If the strike is limited to just the port authority drivers then they may be in for tough going and the plan may work. If there is any sympathy labor actions in the region then I dunno how it will turn out. It may be the biggest test for organized labor in the region in decades. Think of it as a local version of the PATCO air traffic controllers strike in 1981, something that had a major impact on labor-management relations for decades.
In the end I hope all parties realize that the true cost benefit analysis of transit service is not all measured in the Port Authority's budget anywhere.
Thursday, July 03, 2008
The Prince and the or Pauper
The casino news of late is focused on the proposed changes Don Barden is making to save money on the construction of the Majestic Star. A lot of those changes have to do with the casino's river frontage and aesthetics. Unsurprisingly, the Riverlife Task Force has taken umbrage to these ideas.
What history is relevant? A lot. I am surprised this did not get more coverage a couple months ago. Last March was the 20 year anniversary of the visit to Pittsburgh of Prince Charles. It made a lot of news at the time and since. One of his big messages was that we needed to reopen access to the rivers by our communities. Read the New York Times coverage of his main speech when in town. More in depth coverage of the Prince's visit to the burgh was in Pgh Magazine way back when.
bipolar housing disorder
Just so you don't think it's just me out there making this stuff up.. from the PBT is this quote
Despite a nationwide housing slump, losing short-term value on a home in Pittsburgh is less likely than in nearly every other major market, according to a recent report. (emphasis added)
Who would've thunk that? Must be a crazy person.
The report it references is here. It says that Pittsburgh's housing market is safer than oil boomtown Houston these days?! What is just curious to keep observing is the coverage of housing issues locally. This is at least relatively positive story, we have the least likely chance of decline.. but that is still a far cry from pointing out that almost alone among major regions housing prices here continue to increase while rapidly rapidly deflating most everywhere else.
update: I don't take credit for this, but on the semantics of the news... the headline for this particular news blurb was actually changed. It started as "Housing prices in Pittsburgh less likely to decline in next two years, report says"... but then after I blogged about it it became: "Housing prices in Pittsburgh unlikely to decline in next two years, report says". I added the emphasis in both cases just to highlight the change. It may seen innocuous, but the former implies pretty strongly that there will be a decline in housing prices, we are just wondering by how much. The latter is closer to what the report in question says that there isn't anything observed thus far that says local housing prices are going down at all.
Wednesday, July 02, 2008
Teenie Harris and the circle of history
Maybe I am missing something?? It's strange I don't see this in the PG, but PG editor David Shribman has a piece in Bloomberg pointing out that today is the 100th anniversary of the birth of Teenie Harris and that his photos are now online at the Carnegie Museum.
It really is an amazing coincidence that Teenie Harris' birthday occurs right on the day there is news that the Sports and Exhibition Authority is letting the first contracts for the construction of a new arena. Harris' studio, along with the neighborhood it resided in were erased by the construction that would become Mellon (née Civic) Arena whose days are also now numbered.
A new beginning? or back to the future? It's up to us to determine.
diaspora illuminati redux
Should we talk more about the state of the casino? billboards? impending Port Authority strike? Arena funding? Pension liabilities? Ugh..... I depress myself. Maybe some trivia therapy will help.
I was joking when I first said this, but maybe the Pittsburgh diaspora does acts as the new Illuminati. In the political world there are more connections than most realize, at least beyond ex-Burgher Ron Paul's run for President. I watched the HBO movie Recount last week. Any political junkie know the big Pittsburgh(er) connection in the movie? That's too easy. For balance and something a little harder: Here is an interesting article on the race for President in the Washington Post from last weekend. There are several Virginia politicians mentioned in there, anyone know which one has Pittsburgh roots? it might not count as a diasporan technically... maybe better to call them Pittsburgh connections.
I should come up with a prize, but you would have to get both.
Tuesday, July 01, 2008
crap or do I mean craps
afternoon pontifications:
From JG is a heads up to a WSJ article on the travails of financing across the board these days in the gambling industry. See: Debt-Laden Casinos Squeezed by Slowdown. For fun... some interesting video history of Dan Barden when he first was awarded the casino license here. Update: The Riverlife Task force has a press release with some annotated illustrations of what is being cut from the casino plan in order to bring costs down. See the Press Release here..... for more, read the story here.
Speaking of gambling in general and stealing an idea from Florida, I expect to see Gus working the pumps pretty soon.
whiskey t...... %^*&(%........ can someone explain this to me.. No, please don't try. There is this little matter of a legal bill and city council. First it should be paid, then it shouldn't, then it will be paid and now... get this, the city solicitor says that HALF of it should be paid. Does this mean that half of Reverend Burgess should leave his council seat when they discuss the matter. Does the new opinion specify which half? Seriously, if I were in charge of a PSYOPS campaign to disrupt the politics of city council, I could not have thought of anything better than these opinions coming from the city. update: How much has this all cost? Burgher Jon does the back of the envelope analysis of the city's direct costs over just the legal bill pertaining to Lamargate. If you ask me he way underestimates all the people/time involved, but you get the point. And the cost of Lamargate itself? priceless.
and for the record... this is a crime. and an awfully lot more important than the matter of who pays $10K $5K.
Rust Belt divergence?
Jim Russell must not sleep. From Colorado he is organizing a Rust Belt Bloggers Summt in Erie, PA July 11-12. I will be making at least a part of it the evening of July 11 if anyone is nearby then. I think there are events over that weekend as well. See the link above for more info.
With that as a theme, and with new regional unemployment data released today, here is an update to the graph I put up on occasion that I track. This has the seasonally adjusted unemployment rates in those core 'Rust Belt' regions: Pittsburgh, Detroit and Cleveland.
It's a pretty striking time series and one which I suspect most Pittsburghers wouldn't quite believe. What is really important is not just that Pittsburgh is doing relatively well, it's that where once the three regions had nearly identical unemployment rates, you are seeing large and growing divergence. Detroit's seasonally adjusted unemployment rate just hit 9.3% in May (a huge jump from 7.4% the month before... the biggest one-month spike for them in decades) compared to 5.0% here. Cleveland is 7.3%. Looking at the graph, you can parse it even more, the big spikes up of late in Cleveland and Detroit are matched by only a minor 1/10th of a % increase here, and what is funny about that is even that is partially attributed to a strike at Latrobe Steel. Take that out and you will be close to no change at all here while (formerly?) similar regions are seeing historic jumps. I have to admit that this divergence story is one that I don't understand why it does not get any media attention at all.. or not much at least.
This divergence is not about to turn around anytime soon. Auto industry and housing turmoil is far from over for Cleveland and Detroit. While our traditional industries in metals and coal are if anything seeing spiking prices worldwide which means producers here are pushing to produce as much as they can. On local coal and energy, I was driving across Pennsylvania last week and for awhile was only getting reception from a local radio station that was covering live for some time a "oil and gas industry job-fair". I wonder how long it has been since that has happened.
A lot more going on of course. A more thorough look at all this is in some references I mentioned in Shiny Rust Belt a few months ago.
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Quotation added by staff
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A stockbroker urged me to buy a stock that would triple its value every year. I told him, At my age, I don't even buy green bananas. Pepper, Claude D.
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It's easy! Just pick the product you like and click-through to buy it from trusted partners of Quotations Book. We hope you like these personalized gifts as much as we do.
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23 Sep 2006 Botnerd » (Master)
I love Doctor Who! Marev, are they playing the new season there already? Just curious. I hate they got rid of the old doctor though, he was cool and fun. I can't wait for the new season to start anyway, but the new guy doesn't seem as good as the old one.
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Visualizing a medical Twitter hashtag: MDChat
I’ve recently got in touch with an amazing group, the Thesys Group. They invited me to their HQ to show me what kind of projects they are working on and we started a bit of brainstorming about what we could come up with together.
In our first project, the Thesys Group analyzed the network of discussions focusing on one of the most popular medical Twitter hashtags, MD_chat. In the figure below, a dot represents a Twitter user, lines connecting the dots represent their relationship. The bigger the dot is, the more tweets the Twitter user had. The thicker the line is, the more tweets the two users had with each other. Based on this, here is the network graph (click on the image below to access the interactive graph):
Dots in the middle account for active users, while dots in the periphery did not participate that often in these discussions. Graph includes only tweets including user names, therefore representing discussions. Here is a zoomed version of this graph just to show you how the dots are connected to each other on a smaller scale with @doctor_v and @jodyms in the focus.
A few numbers and facts:
• Tweets are dated between October, 2010 and October, 2011 (4815 messages).
• Data tables were obtained from a public Scridb database containing all the MD_chat discussions and can be downloaded in doc or PDF formats.
• 282 users are represented in the graph with 1972 connecting them to each other.
• Graph was visualized with the Gephi open-source platform.
The top 10 most active Twitter user using the MD_chat hashtag in discussions (largest dots in the graph):
Rank MD chat user name Number of addressed tweets
1 richmonddoc 559
2 ellenrichter 204
3 gailzahtz 190
4 peds_id_doc 181
5 mdstudent31 178
6 apjonas 159
7 ability4life 155
8 westr 145
9 chukwumaonyeije 140
10 md_chat 139
The aim of this short study was to point out the importance of medicine related hashtags and the growing popularity of these. The dynamic growth of MD_chat is a good example for the changes that we can see now in the everyday communication among peers. Therapeutic experience, news and opinions spread without geographical or linguistic limitations.
Please let us know what you think of this analysis and feel free to contact me or the Thesys Group for more details.
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Aiuta Wikitravel a crescere grazie al tuo contributo: scrivi un articolo! Ecco come.
Wikitravel:Politica relativa alle pagine protette
Da Wikitravel.
Versione delle 17:20, 6 ott 2006, autore: Archeologo (Discussione | contributi)
(diff) ← Versione meno recente | Versione attuale (diff) | Versione più recente → (diff)
Questa pagina non è ancora stata tradotta completamente dalla lingua inglese. Se puoi, terminala o riscrivila tu, eliminando il testo in lingua straniera quando hai finito. Non usare traduttori automatici! Per l'elenco completo delle altre pagine da tradurre dalla stessa lingua vedi la relativa categoria.
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The revolutionary nature of Wiki is the ability for any reader of any article to edit that page right now. Wiki is the enabling technology that is making Wikitravel into a really great travel guide. Wikitravellers know that we need to keep Wikitravel open and available to make it succeed. We depend on the distributed effort of the millions of people on the Internet to get high-quality, up-to-date and reliable articles.
However, in some circumstances, it may be necessary to protect a page on Wikitravel. When a page is protected, it can only be edited by administrators. This is an extreme measure and shouldn't be taken lightly. Whenever possible, we prefer to counteract abusive actions by some users with the ability of other users to edit a page.
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Administrators may protect a page whenever they feel that this step is warranted. They are expected to use their judgement, and to err on the side of openness. Some example reasons why a page should be protected would be:
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
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Australian Bureau of Statistics
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Contents >> Chapter 4. The Occupation Classification >> Detailed Occupation Classification >> 7 Intermediate Production and Transport Workers
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Alternative title
Printing bindery assistant
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International Journal of Business and Management
International Journal of Business and Management (IJBM) is an international, double-blind peer-reviewed, open-access journal published by the Canadian Center of Science and Education. The journal focuses on the following topics: corporate governance, human resource management, strategic management, entrepreneurship, marketing, e-business, services, information technology management, production & operations management, financial management, decision analysis, management research methods and managerial economics, etc.
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Macoupin County, IllinoisEdit This Page
From FamilySearch Wiki
Revision as of 20:01, 6 September 2011 by McBrideLW (Talk | contribs)
Macoupin County, Illinois
Map
Location of Illinois in the U.S.
Facts
Founded: January 4, 1817
County Seat Greenville
Courthouse
Photo courtesy Illinois Regional Archives Depository, Illinois State Archives
Address Macoupin County Courthouse
210 E. Main Street
Carlinville, Illinois 62626
217-854-3214
Macoupin County Website
United States Illinois Macoupin County
Contents
County Organization
Macoupin County's civil records start the following years:
Beginning Dates for Macoupin County Records
Birth Marriage Death Census Land Probate
1877
1829
1877
1830
1829
1829
County records are most often kept at the County Courthouse or another local repository. For further information about where the records for Macoupin County are kept, see the Macoupin County Courthouse page.
Historical Facts
Macoupin County is named for Macoupin Creek which is a tributary of the Illinois River, which it joins near the village of Hardin, Illinois.[1]
Parent County
• 1829--Macoupin County was created 17 January 1829 from Madison and Greene Counties. County seat: Carlinville [2]
Boundary Changes
See an interactive map of Macoupin County boundary changes.
Record Loss
Places / Localities
Populated Places
Barr (township)
Benld (city)
Bird (township)
Brighton (township & village)
Brushy Mound (township)
Bunker Hill (city & township)
Cahokia (township)
Carlinville (city & township)
Chesterfield (village & township)
Dorchester (village & township)
Eagarville (village)
East Gillespie (village)
Gillespie (city & township)
Girard (city & township)
Hettick (village)
Hillyard (township)
Honey Point (township)
Lake Ka-Ho (village)
Medora (village)
Miles Station
Modesto (village)
Mount Clare (village)
Mount Olive (city & township)
Nilwood (town & township)
North Otter (township)
North Palmyra (township)
Palmyra (village)
Plainview
Polk (township)
Sawyerville (village)
Scottville (village & township)
Shaws Point (township)
Shipman (town & township)
South Otter (township)
South Palmyra (township)
Standard City (village)
Staunton (city & township)
Virden (city & township)
Western Mound (township)
White City (village)
Wilsonville (village)
Womac
Neighboring Counties
Records and Resources
Biography
Cemeteries
Illinois cemetery records often identify birth, death, relationship, and military information, as well as religious affiliation.
• Find A Grave can be searched by the name of a person or family to find where a person is buried. Usually gives birth and death dates often with a picture of the tombstone. May give obituaries, names of family members and links to their information in Find A Grave.
Census
Historical populations
Census Pop.
18301,990
18407,826293.3%
185012,35557.9%
186024,60299.1%
187032,72633.0%
188037,69215.2%
189040,3527.1%
190042,2564.7%
191050,68519.9%
192057,27413.0%
193048,703−15.0%
194046,304−4.9%
195044,210−4.5%
196043,524−1.6%
197044,5572.4%
198049,38410.8%
199047,679−3.5%
200049,0192.8%
1840 Pensioners
• A Census of Pensioners for Revolutionary or Military Services: With their Names, Ages, and Places of Residence, as Returned by the Marshalls of the Several Judicial Districts, Under the Act for Taking the Sixth Census. Washington, D.C., 1841. FHL 973 X2pc 1840; FHL 2321; digital version at Google Books. [See Illinois, Macoupin County on page 187.]
Church Records
Court Records
Ethnic Research
African American
The following have information concerning African American research.
Genealogy
History
Land and Property
BLM GLO Records. Search original land patents for Macoupin County from the Govenment Land Office (GLO) or Eastern States Office. Some searches include images of the original warrants. All search results include the patant details needed for requesting copies of the land entry files at the National Archives. The GLO is the custodian of millions of land title documents. The General Land Office Automated Records Project is responsible for making these important documents available to the public.
Illinois Public Domain Land Tract Sales. The Illinois State Archives has an online index to the records of Public land sales held by the State Archives. The indexes are by purchasers name and by legal description. This is a statewide collection with nearly 550,000 land sales fro 54740 square miles.
IRAD holdings for Macoupin County include Land patents 1819 to 1917
Land records that include Macoupin County at Ancestry.com $:
• "Illinois Public Land Purchase Records" This record extract includes over 538,000 land sales from the 19th Century. Each entry includes the purchaser's name, purchase date, number of acres, price per acre, and in some cases the purchaser's sex and residence.
• "U.S. General Land Office Records, 1796 to 1907:" Records of Illinois are among the 13 states included in this set. It includes images of the land patents which contain the information necessary for ordering the complete case files from the National Archives. This appears to be the same information that is online at the Federal Land Office site http://www.glorecords.blm.gov/.
• Sheldon, Theodore. Land registration in Illinois. Chicago: Callaghan Co., 1901. Digital book. Expains the laws regarding land and the land systems used in Illinois. Includes court cases involving land issues. In addition to being on Ancestry, this book is available online at no cost at Internet Archives and Google Books.
Maps
Military
• Civil War
Civil War service men from Macoupin County served in various regiments. Men often joined a company (within a regiment) that originated in their county. Listed below are companies or regiments that were formed from men of Macoupin County.
- 3rd Regiment, Illinois Cavalry, Company L.
- 27th Regiment, Illinois Infantry, Company F
- 32nd Regiment, Illinois Infantry, Companies A, C and I
- 59th Regiment, Illinois Infantry, Company I
- 97th Regiment, Illinois Infantry, Company A
Naturalization
Newspapers and Obituaries
Probate Records
Original probate records are held by the circuit court clerk. Probate records include wills, inventories, settlements, and guardianship records. A few copies of probate records are held at IRAD. Explore how to search IRAD–UIS. The following copies are available at IRAD–UIS and in the Family History Library Catalog:
Other abstracted probate records for Macoupin County can be explored through a subject search of theFHLC.
Repositories
County Courthouse
County records are most often kept at the County Courthouse or another local repository. For further information about where the records for Macoupin County are kept, see the Macoupin County Courthouse page.
Macoupin County Historical Museum Library
920 W. Breckenridge St
Carlinville, IL 62626
Phone: 217-854-2850
Phone: 217-854-2561
Hours: Wednesday May - Nov 10 AM - 2 PM Sunday Jun - Aug 1 PM - 5 PM
Family History Center
Family History Centers (FHCs) are branches of the Family History Library in Salt Lake City, Utah (United States) and are located all over the world. Their goal is to provide resources to assist you in the research and study of your genealogy. Currently there are no Family History Centers located directly in Cass County.
You may search your address for a center near you on the FamilySearch site.
The following centers are located in surrounding counties. Their wiki pages may supply hours and other information.
Litchfield Illinois Family History Center
12367 Roberson Rd.
Litchfield, Illinois 62056
217-324-2396
Springfield Illinois Family History Center
3601 Buckeye Dr.
Springfield, Illinois 62707
217-529-7930
Alton Illinois Family History Center
6500 Humbert Rd.
Godfrey, Illinois
618-466-4352
Jacksonville Illinois Family History Center
1053 E. Vandalia Rd,
Jacksonville, Illinois 62650
217-245-8113
Illinois Regional Archives Depository (IRAD)
IRAD is a system of Illinois Regional Archives Depositories managed by the Illinois State Archives, housing the archival records of local Illinois counties, townships, municipalities and school districts. The seven Regional Depositories are housed on state university campuses scattered throughout Illinois.
The University of Illinois at Springfield (UIS) houses the records for Macoupin County. The link will help you find and use the records. There address is:
Illinois Regional Archives Depository
LIB144
University of Illinois at Springfield Region
One University Plaza, MS BRK 140
Springfield, Illinois 62703-5407
217-206-6520
Public Libraries
Social Groups Online
Societies
Taxation
Vital Records
Information and forms for ordering birth, marriage, and death records can be found at the Macoupin County clerk web page.
Marriage Records
Available through Ancestry.com $:
• Macoupin County marriages in "Illinois Marriages 1851 to 1900." The source of this collection is films in the Family History Library's collection
Death Records
Macoupin County Coroner's Inquest Files Index, 1835-1928 (courtesy: Illinois State Archives)
A list of Macoupin County Patient Deaths at the Illinois State Hospital (1910s-1930s) is available online, courtesy: Researching Your Roots in Central Illinois. The site also provides a list of WWII Deaths.
Web Sites
References
1. Macoupin Creek www.wikipedia.org
2. The Handybook for Genealogists: United States of America, 10th ed. (Draper, UT: Everton Publishers, 2002), 196. (FHL Collection Ref Book 973 D27e 2002). WorldCat entry.
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Hello every1
Newbie Member
25Aug2007,11:18 #1
Hello every1
Most of the members knows me by the name of starguy...i m 25 years old.....MBA by qualification....had a 2 yrs experience in manufacturing company....
my motto in life is
TOGETHER WE CAN AND WE WILL MAKE THE DIFFERENCE
starguy
Go4Expert Founder
25Aug2007,18:09 #2
Definitely and welcome to the forum.
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Bibliography: The Stranger That is Within Thy Gates
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Title: The Stranger That is Within Thy Gates
Author: Poul Anderson
Year: 1990
Type: SHORTFICTION
Storylen: shortstory
Language: English
ISFDB Record Number: 688469
User Rating: This title has fewer than 5 votes. VOTE
Current Tags: None Add Tags
Variant Titles:
Publications:
Copyright (c) 1995-2011 Al von Ruff.
ISFDB Engine - Version 4.00 (04/24/06)
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Sensors 2011, 11(1), 905-916; doi:10.3390/s110100905
Article
Detection of Single Molecules Illuminated by a Light-Emitting Diode
1 CQT, Centre for Quantum Technologies, 3 Science Drive 2, 117543, Singapore 2 Low Temperature Group, Chemistry Department, University of British Columbia, 2036 Main Mall, Vancouver, B.C., V6T 1Z1, Canada
* Author to whom correspondence should be addressed.
Received: 8 December 2010; in revised form: 11 January 2011 / Accepted: 12 January 2011 / Published: 14 January 2011
(This article belongs to the Special Issue 10 Years Sensors - A Decade of Publishing)
Download PDF Full-Text [341 KB, Updated Version, uploaded 17 January 2011 09:43 CET]
The original version is still available [377 KB, uploaded 14 January 2011 16:59 CET]
Abstract: Optical detection and spectroscopy of single molecules has become an indispensable tool in biological imaging and sensing. Its success is based on fluorescence of organic dye molecules under carefully engineered laser illumination. In this paper we demonstrate optical detection of single molecules on a wide-field microscope with an illumination based on a commercially available, green light-emitting diode. The results are directly compared with laser illumination in the same experimental configuration. The setup and the limiting factors, such as light transfer to the sample, spectral filtering and the resulting signal-to-noise ratio are discussed. A theoretical and an experimental approach to estimate these parameters are presented. The results can be adapted to other single emitter and illumination schemes.
Keywords: single molecules; fluorescence microscopy; light-emitting diode; LED; signal to noise ratio; single photon detection
Article Statistics
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Cite This Article
MDPI and ACS Style
Gerhardt, I.; Mai, L.; Lamas-Linares, A.; Kurtsiefer, C. Detection of Single Molecules Illuminated by a Light-Emitting Diode. Sensors 2011, 11, 905-916.
AMA Style
Gerhardt I, Mai L, Lamas-Linares A, Kurtsiefer C. Detection of Single Molecules Illuminated by a Light-Emitting Diode. Sensors. 2011; 11(1):905-916.
Chicago/Turabian Style
Gerhardt, Ilja; Mai, Lijian; Lamas-Linares, Antìa; Kurtsiefer, Christian. 2011. "Detection of Single Molecules Illuminated by a Light-Emitting Diode." Sensors 11, no. 1: 905-916.
Sensors EISSN 1424-8220 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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Saturday, October 29, 2011
Some creative signs from Occupy Wall Street protest in Bellingham
* Compiled from some of my earlier blog posts
Good message about rebooting our country's operating system, held at Magnolia and Cornwall October 14.
So many issues interrelate. People often ask what Occupy Wall Street is about. I'm not even sure I'm a hundred percent "sold out" fan of Occupy Wall Street, but there is a whole "raft" of interrelated issues being discussed.
I see it as just another part of our cultural "paradigm shift."
Seeking an economy that's better than what we have now. An economy that's more sustainable, in terms of the planet and our own well being. An economy that's more fair, in terms of distribution of income in society.
The income distribution graph, in USA, has gotten out of balance over the past few decades.
Continued below.
Also Occupy Bellingham (the only one I've experienced) is kind of fun. Interesting people. A chance to see friends I haven't run into for a long time.
It's community building that is face to face.
Networking.
The process of culture that's an alternative to other uses of time. Other uses such as shopping, watching TV, fighting traffic and yes, I do spend some of my time at work. I still have a job. I'm not just watching folks on the street playing bongo drums all the time.
Sometimes folks play bongo drums in front of the building my job is in, but that's another story. It's living in Bellingham, our "blue state" (for the most part) city.
Someone on NPR interviewed an employee who works inside a Wall Street firm in New York City. They ask what people's reaction, inside Wall Street, was to the protests on the outside.
Basically, that person said he thought folks were angry at the wrong thing. Rather than Wall Street, they should be angry at the Federal Reserve for printing too much money and devaluing the dollar, he said.
Federal Reserve has been trying to keep the economy going in face of high unemployment. Also to keep the government debt financed so Uncle Sam "appears" solvent, at least.
One can't really blame them for that.
Seems like the blame can just go round and round which is why I see this as a cultural issue.
It's a "paradigm shift" kind of thing.
In that blog post, I suggested other strategies to deal with unemployment, like job sharing and better distribution of the wealth. Maybe that's considered "spreading the misery," but really, we might do better, as a culture, if we used a bit less. If we had a bit less waste.
A somewhat more austere culture could continue to move forward, since new technology is always coming into the picture anyway. We could still progress toward more of a sense of prosperity.
Prosperity can be defined in different ways.
Much of our new technology points us in the direction of "smaller can be better." A big stereo system from the 1960s isn't necessarily better than an Ipod of 2011, just because it's larger. Smaller is sometimes just as good, if not better.
We need paradigm shifts toward an economy that's better than we've got now. Better, but not necessarily larger or more consuming. An economy that offers a fairer deal to more than just it's top people.
Much of it is about our overall sense of well being.
We may not all define our well being in the same way, but there can be some new consensus about what our priorities are.
Some signs from Occupy Wall Street protest in Bellingham, October 14 2011.
Below is compilation from some of my posts about the Occupy Movement. I am consolidating blog entries.
One would think folks with savings accounts would march on banks to protest low interest rates
Protest in front of Bank Of America, Bellingham branch October 14 2011.
One would think savers should be marching on the banks demanding better return on savings; rather than just worrying about a $5 per month debit card fee. Maybe the fee is just a tipping point. People are mad at banks.
When I was a kid, banks often paid 5 1/4 interest on savings. Now, interest rates are rock bottom. Bad for savings, but cheap for borrowing; too cheap.
Of course it isn't really the fault of individual banks, it's the world banking system, and things like the Federal Reserve that set overall interest rates.
Part of the reason for the current financial crisis has been interest rates that are too low. When borrowing becomes too cheap, bubbles, such as the housing bubble, get inflated beyond what the normal economy can sustain. There's a disconnect if jobs don't pay much more then $10 per hour while single family homes sell for well over a quarter million.
Video taste of a People's Mike in Bellingham
Segment a bit over 2 minutes.
I see Occupy Wall Street as just another step in the evolution of society
Occupy Wall Street is not necessarily pivotal in the evolution/revolution of our society. It's just another part of the long term paradigm shift toward what can hopefully be a more equitable economy. Also a more sustainable economy.
Important steps, however.
It's good to see so many folks taking interest in the political process and the well being of the community as a whole. Not just personal profits and shortsighted self interests.
Maybe some key congressional races in 2012 will be another step.
It says People's Bank, but the people are protesting
Another rally of Occupy Bellingham protesters. November 4Th at corner of Magnolia and Cornwall. Rallies have been weekly for the past few weeks.
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