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{
"caption": "PA plain radiograph Turner syndrome scoliosis.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808441-1-1748-7161-2-3-2.jpg"
}
|
000700
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "PA plain radiograph Turner syndrome scoliosis.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808441-2-1748-7161-2-3-1.jpg"
}
|
000701
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Fundus of a 34 year-old patient with cone rod dystrophy due to Spinocerebellar Ataxia Type 7 (SCA7). Note that the macular area, and also the mid periphery, are atrophic.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808442-0-1750-1172-2-7-3.jpg"
}
|
000702
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Fundus of a 31 year-old patient with Bardet Biedl syndrome. The peripheral retina does not show any large lesion but the macula is atrophic.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808442-1-1750-1172-2-7-2.jpg"
}
|
000703
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Fundus of a 45 year-old patient with cone rod dystrophy segregating with a loss-of-function mutation (E1087X) in ABCA4. Note the presence of various-shaped pigment deposits in the posterior pole with atrophy of the retina, while the retina appears less damaged in periphery (upper part of the photograph).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808442-2-1750-1172-2-7-1.jpg"
}
|
000704
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Left panel: Type VI AHA. Complex plaque with possible surface defect, hemorrhage (dotted red area) or thrombus near the lipid core (in the center). Mid panel: Type VII AHA. Calcified plaque (purple areas). Right panel: Type VIII AHA. Fibrotic plaque without lipid core (extensive area of fibrosis).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808443-0-1477-9560-5-4-2.jpg"
}
|
000705
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Left panel: Cadaver carotid artery. Type III AHA. Preatheroma with extracellular lipid pools (blue area in the center). Mid panel: Type IV AHA. Atheroma with confluent extracellular lipid core (pink area in the center). Right panel: Type V AHA. Fibroatheroma (clearer pink area – atheroma – surrounded by darker pink area – fibrosis).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808443-1-1477-9560-5-4-1.jpg"
}
|
000706
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "OX-42 immunohistochemistry during symptomatic phase of disease. A, low power view reveals intensified immunoreactivity in spinal cord ventral horns; multiple large, rounded spots are visible. B, higher power view of large immunoreactive spots is suggestive of phagocytic clusters. C, same field as in B; counterstaining with cresyl violet facilitates identification of large immunoreactive spots as multinucleated giant cells. D, E, the same microscopic field prior to and after cresyl violet counterstaining reveals a well-formed multinucleated giant cell of the Langhans type. F, enlargement of framed area in C shows apoptotic microglial nucleus (arrow) within a giant cell. Scale bars: 500 μm (A), 40 μm (B, C), 20 μm (D-F).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808448-0-1742-2094-4-9-2.jpg"
}
|
000707
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Lectin staining of microglia in the brainstem (level of cranial nerve VII) in wildtype animals (A) and in late symptomatic/end stage animals (B-H). Cresyl violet counterstain. A, microglia show normal ramified morphology. B, a large lectin-positive aggregate of fused microglia is evident in severely vacuolated brainstem tissue. Note enlarged perineuronal spaces to the right. C, string-like microglial fusions extend over long distances. D, breakage of neuronal process, probably a dendrite, from cell body within markedly vacuolated space (arrows). E, two multinucleated microglial giant cells are seen below a neuron with broken off process (arrow). F, large multinucleated giant cell displaying vacuolization is present amidst numerous microglial cytoplasmic fragments. G, multinucleated giant cell of the Langhans type displaying characteristic peripheral arrangement of nuclei. H, rounded lectin-positive microglial cell (arrow) within vacuolated space displays nuclear fragmentation indicative of apoptosis. Scale bars: 20 μm (A-H).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808448-2-1742-2094-4-9-4.jpg"
}
|
000708
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "OX-42 immunohistochemistry during end stage disease demonstrates extensive microglial cytoplasmic fragmentation (A-E). A, D, two different views of spinal ventral gray matter demonstrate loss of microglial cell integrity and widespread punctate staining indicative of cytorrhexis. Note that many neurons remain stained with cresyl violet. B, enlargement of framed area in A shows detail of microglial cytorrhexis, including a disintegrating giant cell on the right. E, enlargement of framed area in D shows detail of microglial cytorrhexis. C, motor neuron in SOD1G93A rat reveals intense hyperchromasia with cresyl violet and nuclear cap. F, normal motor neuron and microglia from wild type spinal cord. Scale bars: 40 μm (A, D); 20 μm (B, C, E, F).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808448-3-1742-2094-4-9-3.jpg"
}
|
000709
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Microglial staining with OX-42 immunohistochemistry in the spinal cord during three different stages of motor neuron disease progression. A, presymptomatic stage; inset shows early microglial fusion in spinal cord. B, disease onset; C, end stage; D, wild type control. Note the dramatic increase in microglial staining with OX-42 during onset (B) and its subsequent decline during end stage (C). Scale bar: 200 μm. E, morphometric quantification of microglial immunostaining with OX-42 during disease development; * p < 0.05 and ** p < 0.001 with respect to age-matched controls; # p < 0.05 with respect to onset group.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808448-5-1742-2094-4-9-1.jpg"
}
|
000710
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Histology of the tendinopathic tendon at repair (Transverse plane, × 20 Magnification). Revealing scanty hypocellular degenerate tendon displaying separation of collagen fibrils (solid arrows) and disorganisation. Small pieces of fibrin (hollow arrow) were also present and there was no inflammation or neovascularisation.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808454-0-1471-2474-8-19-1.jpg"
}
|
000711
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "The improved stability of the patella is confirmed.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808455-0-1471-2474-8-22-8.jpg"
}
|
000712
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "The graft is passed through the tunnels, laterally then medially.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808455-5-1471-2474-8-22-4.jpg"
}
|
000713
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Following medial and lateral parapatellar incisions, the patella is stabilised using a large clamp on the right of the figure. Tunnels are produced by sequential drill holes in the superior half of the patella, 1 cm apart.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808455-7-1471-2474-8-22-2.jpg"
}
|
000714
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Photomicrograph of the resected neurofibroma showing spindle cells with characteristic elongated, wavy nuclei. (20× magnification, Haematoxylin and Eosin)",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808458-0-1477-7819-5-23-2.jpg"
}
|
000715
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Cranio-caudal mammograms showing the mass lesion in the central area of the left breast.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808458-1-1477-7819-5-23-1.jpg"
}
|
000716
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Mammographic findings. A bilobed soft tissue lesion measuring about 3.2 × 2.5 cms, suspicious for malignancy, seen in the upper and outer quadrant of the left breast.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808459-0-1477-7819-5-24-1.jpg"
}
|
000717
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "A). Tumor cells exhibiting strong cytokeratin (CK) expression (DAB × 200). Inset showing an occasional clusterof CK positive 'epithelial-like' cells. (DAB × 400). B). Tumor cellsadjacent to the micropapilloma showing positive CK7 expression. Arrow showing a cluster of cells (DAB × 100). C). Strongdiffuse expression for HMWCK. D). Positive vimentin expression. (DAB × 400). E). Focal expression for smooth muscle actin (SMA). A vessel identified in the proximity of tumor cells (DAB × 400). F). Positiveintranuclear p63 expression. (DAB × 400). G). Focal Ki-67 expression(arrows). (DAB × 400).. H). Negative expression for CD34 in the tumorcells. (DAB × 200).I. Negative CerbB-2/HER 2/neu expression. (DAB × 200).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808459-1-1477-7819-5-24-3.jpg"
}
|
000718
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Ultrastructural appearance of the tumor cells. A single cell with peripheral villous processes embedded in a collagenous stroma. Magnification: 4,400×. Inset showing higher magnification of a tumor cell cluster with microvilli and cell junctions. Tumor cell exhibiting intracellular junctions (arrow). Magnification: × 20,000.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808459-2-1477-7819-5-24-4.jpg"
}
|
000719
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "'Fibromatosis-like' carcinoma of the breast associated with a micropapilloma. A) Spindly tumor cells with an occasional cluster (arrow) in the vicinity of a micropapilloma. (H & E × 200). B). Interspersed areas of 'keloid-like' collagen, reminiscent of appearance of a fibromatosis. (H & E × 100). C). A focus of benign ductal hyperplasia amidst tumor cells. (H & E × 100). Inset showing spindle cells with focal cell clusters exhibiting minimal atypia. (H & E × 400). D). Tumor cells infiltrating the fat. (H & E × 100).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808459-3-1477-7819-5-24-2.jpg"
}
|
000720
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Example of immunohistochemical analysis performed on the RST and HNPCC tumors (Amplification 10×). A, Positive expression of HLA class I antigens detected with the HCA2 antibody. The epithelial (large arrow) membranous expression of HLA class I antigens is identical to the lymphocytic infiltrate (small arrow). B, Loss of expression of HLA class I identified with the HCA 2 antibody. The lymphocytic infiltrate (small arrow) was used as a positive control to determine the loss of expression on the epithelial cells. C, Loss of expression of β2m in a HNPCC case. D, Loss of expression of one of the APM members (Tapasin) in a RST case.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808468-0-1471-2407-7-33-1.jpg"
}
|
000721
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "The thyroid needle aspirate in patient 4 shows single and loosely clustered polygonal cells with abundant, granular cytoplasm and eccentrically located oval nuclei with prominent nucleoli, suggesting a Hurthle cell carcinoma versus a metastatic amelanotic melanoma (Papanicolaou stain, × 400).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808473-1-1742-6413-4-5-5.jpg"
}
|
000722
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Histology of metastatic amelanotic melanoma to the thyroid in patient 4 shows large malignant polygonal cells with oval nuclei and prominent nucleoli, in solid pattern (hematoxylin and eosin, × 250).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808473-4-1742-6413-4-5-10.jpg"
}
|
000723
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Histology of a moderately differentiated squamous cell carcinoma metastatic to the thyroid in patient 1. Residual thyroid follicles are present elsewhere (hematoxylin and eosin, × 250).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808473-5-1742-6413-4-5-7.jpg"
}
|
000724
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Histology of a renal cell carcinoma, clear cell type, metastatic to the thyroid in patient 3 shows tumor cells with granular cytoplasm, oval nuclei and conspicuous nucleoli arranged in glandular pattern (hematoxylin and eosin, × 250).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808473-6-1742-6413-4-5-9.jpg"
}
|
000725
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Histology of an adenoid cystic carcinoma metastatic to the thyroid in patient 2 shows small cells surrounding round spaces containing pale, slightly basophilic material (hematoxylin and eosin, × 250).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808473-7-1742-6413-4-5-8.jpg"
}
|
000726
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Staining of the aspirated tumor cells from patient 4 with HMB-45 antibody shows strong positive cytoplasmic reaction with this antibody, indicating a metastatic melanoma to his thyroid (avidin-biotin-complex technique, × 400).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808473-8-1742-6413-4-5-6.jpg"
}
|
000727
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "The thyroid needle aspirate in patient 1 yields a sheet of nonkeratinizing malignant squamous cells admixed with several single, keratinizing malignant squamous cells (Papanicolaou stain, × 400).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_104-PMC1808473-9-1742-6413-4-5-1.jpg"
}
|
000728
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Behavioral and Electrophysiological Analyses Reveal That Synaptic Transmission Is Not Blocked in the syx3–69 Mutant Fly at Restrictive Temperatures(A and B) Temperature-sensitive paralysis and recovery of the syx3–69 mutant fly. (A) shows the still image of both wild type (+/+) and the syx3–69 mutant before, during, and after exposure to the restrictive temperature (38 °C). Although the wild-type flies are not paralyzed at 38 °C, the syx3–69 mutant flies are. However, the syx3–69 flies recover rapidly to standing position within 2–3 min once returned to the permissive temperature. The quantification of the recovery kinetics is shown in (B). Error bars in this and all other figures indicate the standard errors.(C) The paralyzed syx3–69 mutant flies remain capable of responding to stimuli via the polysynaptic giant fiber (GF) pathway. The flies are anchored on a glass slide upside down with modeling clay while a stimulating electrode is inserted into one of the compound eyes (arrows). The syx3–69 fly constantly shakes its legs, head, and abdomen while paralyzed at 38 °C. In response to electrical stimulation of the giant fiber neuron, the mutant fly extends its legs phase-locked with each stimulus. However, the Shits1 fly is completely paralyzed and does not respond to the stimuli at the same restrictive temperature. The right-most panels summarize the cumulative spontaneous and electrical stimulation–evoked movements of legs in syx3–69 flies and the lack of leg movement in Shits1 flies. These behavioral observations strongly indicate that exposing the syx3–69 fly to 38 °C does not block synaptic transmission. See also Videos S4 and S5.(D) Recordings from indirect flight muscles confirm that synaptic transmission is not blocked in syx3–69 flies at the restrictive temperature. Action potentials in DLMs driven by polysynaptic stimuli along the giant fiber pathway remain the same in the syx3–69 mutant fly as in the wild-type control fly before, during, and after exposure to the restrictive temperature. Synaptic-induced high-frequency action potentials are often observed in both the wild type and the syx3–69 mutant (unpublished data). These high-frequency action potentials also occur spontaneously in the mutant. (An example is shown in the inset box.)",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808484-3-pbiop0050072pg002.jpg"
}
|
000729
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Histological Characteristics of WBR in B. leachi\nRegenerating vasculature fragments that were sacrificed at sequential daily intervals exhibit cellular events during the regeneration process.(A and B) Phase I events: Haemocytes are attached to vasculature epithelium (A) (arrows). Vascular detachment from the tunic (B) (arrows) enables subsequent relocation of blood vessels.(C–E) Phase II events: 2 d after dissection, aggregated haemocytes of various sizes and shapes were observed in the regeneration niches (C) (arrows). Extensive cell proliferation formed an opaque ball of cells (D) with exclusive PCNA staining (E).(F–L) Phase III events: 1 d later, continuous cell proliferation increased the size of cell aggregates and formed blastula-like structures of different shapes (F and G) (arrowheads). At this stage, multibuds developed simultaneously in various regenerating niches (G) (arrowheads and red arrows, respectively), although separation between compartments had not been completed (G) (arrow). PCNA specifically stained newly formed bud spheres and blastula-like structures inside the regeneration niches (H). As development proceeded, axial polarity was observed with the appearance of differential cell layers (I) (arrowheads). From day 5, two invaginations from both corners of the thick vesicle wall creating two elongated double-walled folds were observed (J) (arrows). Between 10–14 days postseparation, the regeneration process reached the final stages, whereby a fully functional adult zooid was developed, including the formation of palleal buds (K). Only one zooid per regenerating fragment reached this final stage, while the others degenerated (L) (arrow).(M–P) TUNEL analysis clearly shows staining in degenerating buds. Bud that was normally developed did not stain for TUNEL and exhibits a normal blastula-like structure with clear polarization: (M) and enlargement in (O). Bud that failed to develop went through a degenerating process and was stained for TUNEL: (N) and enlargement in (P). Note that it failed to develop a normal blastula structure, and cells started to fall apart. b, bud; i, intestine; ph, pharynx. Scale bar represents 100 μm. In (O) and (P) scale bars represent 30 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808485-0-pbiop0050071pg002.jpg"
}
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000730
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Specific RA Inhibitors, DEAB and Citral, Inhibit Bud RegenerationEarly stages of bud regeneration were blocked by different concentrations of RA inhibitors. With the administration of 100 μM of DEAB, vessel coalescence gradually slowed down and stopped completely after day 2 (A). Similar results were obtained with 60 μM of Citral (B), while with 20 μM of the same inhibitor ampullae changed orientation and migrated within the tunic but never regenerated a functional zooid (C). At the 100 μM DEAB concentration, buds had not developed, and multinucleated giant cells appeared, scattered throughout the vessel lumen (D, arrows). At the 10 μM DEAB concentration, morphologically abnormal buds were formed, which failed to develop organ structures, and retained a simple epithelial morphology (E). In severe cases, masses of undifferentiated aggregated cells occupied the interior of the vessel lumen (F). All malformed buds subsequently degenerated. PCNA immunostaining revealed distinctive proliferations at aggregated masses while no staining was detected in blood vessels (G). Scale bar in (A–C) represents 1 mm. Scale bar in (D–G) represents 100 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808485-1-pbiop0050071pg005.jpg"
}
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000731
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Cloning and Expression Pattern of the Raldh Homologue in Intact Colonies and Regeneration Ampullae(A) A fragment of 110 amino acid exhibiting high homology to the Aldedh domain of the budding ascidian P. misakiensis (Pm) and high sequence similarity to Aldedh2 family members from mouse (Mm), Human (Hs), Xenopus (Xl), chick (Gg), and zebrafish (Dr). A domain search revealed an Aldedh domain conserved in all Aldedh family members (98 amino acid marked by a red line).(B–E) Expression pattern of Bl-Raldh in intact colony and regenerating ampullae. Bl-Raldh is expressed in naïve ampullae, exclusively in a population of circulating macrophage cells (B) (arrows), scattered throughout vasculature. In regenerating ampullae, Bl-Raldh is observed in macrophage cells (C) (arrows) adjacent to aggregates of small cells creating morula-like structures (C) (arrowheads, rectangle), enlargement in (E). In later stages, starting from the blastula-like stage, Bl-Raldh expression appears in developing buds (D) (arrow). Note the staining along the ampullae margins represents nonspecific staining of the tunic matrix. Scale bars in (B) and (D) represent 100 μm. Scale bars in (C) and (E) represent 40 μm and 10 μm, respectively.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808485-4-pbiop0050071pg004.jpg"
}
|
000732
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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{
"caption": "All-trans RA Leads to Accelerated Regeneration and Multibud FormationRA-treated regenerating fragments that were sectioned at different final stages of the regeneration process show a remarkable accelerated regeneration. By days 6–7 postseparation, most of the regenerating buds reached these final stages (compared to 10–14 days in control experiments), exhibiting complete organogenesis. The regenerating zooids manifested fully differentiated organ systems such as stigmata with cilia (A, arrows). Different from normal blastogenic buds or control experiments, blood cells extensively colonized these regenerating buds between atrial folds and throughout internal cavities (B, arrows). The acceleration of the process was also exemplified in the subsequent blastogenesis. At day 7, the regenerating bud progressed to the stage where secondary buds were formed on the primary palleal buds (C, arrow and arrowhead, respectively). In marked contrast to control regenerating fragments, where only a single bud was developed, numerous buds at different regeneration niches simultaneously reached the final stages of organogenesis (2–5 functional zooids) (D, arrows, compare to Figure 2G). Scale bar represents 100 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808485-7-pbiop0050071pg007.jpg"
}
|
000733
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hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Disruption of RAR Function during Regeneration Causes Bud MalformationsIn order to verify the efficiency and ability of RAR siRNAs to interact and decrease RAR RNA levels, we added RAR siRNAs and control siRNAs to B. leachi colonies and compared RAR RNA levels to untreated colonies. Control siRNAs and untreated colonies exhibit approximately the same transcripts levels (A) (lanes 1 and 3), while RAR siRNAs show a significant reduction in RAR RNA levels (A) (lane 2). Actin transcript levels remain unchanged, indicating the viability of the tissue. After 6 d, control experiments using the control siRNAs completed vasculature movements, forming opaque vessel masses as specified before (B) (compare to Figure 1F). In contrast, in RNAi-affected experiments, blood vessels remained apart, situated haphazardly within the tunic matrix (C) (compare to Figure 5A). In several experiments, vessel movement halted in an intermediate state (D). A similar phenotypic morphology was observed with the RAR pan-antagonist BMS-493 (E). Histological sections reveal malformation of regenerating buds in RNAi treatments (F, arrow, compared to Figure 5E and 5F). In mild cases, buds reached progressive developmental stages but failed to invaginate properly (G, arrow). A similar histological phenotype is observed in BMS-493-treated fragments exhibiting malformed epithelial spheres (H, arrows). Scale bar in (B–E) represents 1 mm; scale bar in (F–H) represents 100 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808485-8-pbiop0050071pg006.jpg"
}
|
000734
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Morphological Events during WBR in B. leachi\n(A) A colony of B. leachi composed of two systems of genetically identical zooids (yellow arrowheads), each 2–3 mm long, embedded within the tunic. A network of blood vessels connects all zooids within a colony, from which pear-shaped vascular termini (ampullae) extend toward the colony margins (arrows).(B–H) Experimentally induced regeneration. The zooids and palleal buds in the center of the colony were cut out, leaving behind the marginal ampullae (B). Segments of several ampullae, 1–3 d after amputation, created a new blood vessel network (C) and (D), respectively (arrows). Isolated ampullae changed their orientations and shapes 6–7 d postseparation within the tunic matrix and coalesced into each other (E). Vasculature movements were more conspicuous when blood vessels were spaced out, creating a dense mass of vessels on one side of the fragment and a semitransparent gelatinous tunic matrix deprived of blood cells and blood vessels on the other side (F). By days 8–9, an opaque mass of blood vessels was formed, followed by the formation of an internal small transparent vesicle (G) (arrow). By days 10–14, a fully operating filter-feeding zooid equipped with functional atrial and peribranchial siphons, both facing upwards as in normal zooids, developed from the opaque mass of blood vessels (H) (arrows). The scale bar represents 1 mm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808485-9-pbiop0050071pg001.jpg"
}
|
000735
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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{
"caption": "Schematic of the Uncaging Procedure(A) Caged fluorescein is injected into one-cell stage her5pac:egfp embryos. Injected embryos are kept in the dark until the fluorescein is uncaged in 6–10 cells of the diencephalic neural plate at bud stage using a laser beam. After further light-protected incubation, the embryos are fixed at prim5 stage, and the uncaged form of the fluorescein is detected via antibody staining.(B) Transverse section of a neural plate after the uncaging experiment, cells of the whole z-axis are labelled.(C) Result of labelling cells via uncaging in domain I, which correlates mostly with the expression pattern of barhl2 at bud stage.(D) At prim5, labelled areas in the diencephalon resemble the endogenous expression pattern of barhl2.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808486-0-pbiop0050069pg003.jpg"
}
|
000736
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hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Fate of Caudal Forebrain Precursors(A) Schematic showing the four different diencephalic expression domains identified in Figure 1.(B) Arbitrary subdivision grid of the caudal forebrain shown on top of the expression domains plus an additional telencephalic subdomain (orange).(C) Colour code used for the final 12 domains investigated.Embryos in (D, E, F, H′, I, L, M, N′, and P′) show the expression of shh and otx5 in red.(D) Different areas of the rostral brain are labelled on an embryo showing expression of shh (in the ZLI) and otx5 (in the pineal gland) in red.(E) Cells of the bright yellow midline area are found in the hypothalamus.(F) Cells inside the lime midline domain populate the ventral ZLI.(G) The light violet area spans the posterior hypothalamus, the basal ZLI, posterior tuberculum, and some of the anterior tegmentum.(H and H′) Cells of the caudal-most midline domain of the forebrain are detected in the anterior tegmentum.(I) Cells labelled in the dark red domain of the neural plate contribute to the prethalamus.(J) Precursors of the orange area will populate the posterior dorsal-most telencephalon.(K) The light blue includes precursors of the dorsal telencephalon and the epithalamus.(L) The dark blue area marks cells of the dorsal telencephalon, epithalamus, and dorsal pretectum.(M) In the light red area, we found precursors of the thalamus.(N–P) (N and N′) Cells of the dark green domain can be found in the dorsal thalamus and, in some cases, in a stream of cells running down to the posterior hypothalamus (N′). Precursors of the light green area (O) populate parts of the pretectum and the tectum whereas cells of the grey area (P and P′) were detected in cells close to the midbrain.Because of the nature of the experiment (negative landmarks and fast developing embryos), we were not always reproducibly labelling the same cells in each experiment. Therefore, one can find, for each experiment, the number of embryos we labelled per experiment and how many of these result in the shown cell labelling. (For example 8/9 means eight out of nine embryos show the same labelling in the area depicted in the picture).eth, epithalamus + pineal gland; hth, hypothalamus; pte, pretectum; pth, prethalamus; tec, tectum; teg, tegmentum; tel, telencephalon; tha, thalamus.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808486-1-pbiop0050069pg004.jpg"
}
|
000737
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hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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{
"caption": "Cell Movement in the Neural Plate(A and B) Schematic overview of the results obtained by the fate-mapping experiments. Colours at prim5 stage correspond to the territories labelled at bud stage.(C–E) Time-lapse analysis of nuclei (red) movement in the neural plate in her5pac:egfp (green): 3D rendering of a 200-μm z-series done at (C) bud stage and (D) 5-somite stage. (E) Schematic overview of the trajectories of individual nuclei over the recorded time (time-lapse movie can be seen in Video S1), with labelled nuclei in white. Wavy lines and dark to light colours of the lines represent the timeline of nuclei movement. Some lines are shorter because nuclei moved out of or into the observed area over the recorded time. We observed three types of movement: the basal cells move anteriorly (green arrow), posterior alar cells move towards the midline and then anteriorly (yellow arrow), and anterior alar cells move diagonally towards the midline (red arrow).(F–L) Transplantation of basal cells: (F) animal pole view in which labelled cells (green) are transplanted on top of the shield; (G) schematic lateral view of shield stage embryo in which transplanted cells are going to move towards the animal pole during gastrulation; (H) schematic lateral view of bud stage embryo in which transplanted cells are spread along the midline of the embryo; and (I) shhGFP is shown in green, transplanted cells in red, at 22 hpf in a live embryo. (J–L) shh is shown in red, transplanted cells in green; at 30 hpf, basally derived cells form a large proportion of the brain, showing that just the tip of the ZLI is formed by alar plate cells (white arrow), the basal ZLI is composed of basal cells (white double arrow), and the ventral part of the developing thalamus is built by basal cells (yellow arrow). The yellow line in (K) indicates the border between alar and basal plate; the arrowhead in (K) points to a single basal cell moving alar.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808486-2-pbiop0050069pg005.jpg"
}
|
000738
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Expression Profile of the Rostral Neural Plate(A–G) Rostral neural plate, anterior to the left. Embryos at bud stage (A–D, F, G , I, and K) or 100% epiboly (E) are shown.(A) six3 (red), fezl (blue). (B) six3 (red), arx (blue). (C) barhl2 (red), flh (blue). (D) irx7 (red), arx (blue). (E) irx7 (red), wnt8b (blue). (F) irx7 (red), foxb1.2 (blue). (G) foxb1.2 (red), fezl (blue). (H) Scheme of the different expression domains inside the diencephalon anlage shown in (A–G). (I) Sagittal section, anterior left, foxb1.2 (red), fezl (blue). (J) Scheme of (I). (K) Transverse section, fezl (blue). (L) Scheme of (K). The different domains are the presumptive anteromedial (I), anterolateral (II), and posterior (III) diencephalon, hypothalamus (IV), and eye field (V).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808486-4-pbiop0050069pg001.jpg"
}
|
000739
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hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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{
"caption": "Transplantation of Prethalamic Precursors(A) Schematic overview of the transplantation experiment putting prethalamic precursors in ectopic regions of the neural plate.(B–D and H–J) shows dlx2a (blue), tbr1 (red), and transplanted cells in green; (E–G and K–P) shows lhx5 (blue), irx1b (red), and transplanted cells in green.(B–G) Transplanted cells located in the hindbrain show ectopic expression of the prethalamus markers dlx2a (B–D) or lhx5 (E–G); no expression of the telencephalon marker tbr1 (see inset in [B]) could be found in the clone. Cells do not exhibit expression of irx1b (arrow in [F]) in the transplanted cells.(H–P) After transplantation into the forebrain, ectopic cell–non-autonomous expression of dlx2a (arrow in [J]) could be seen (probably resulting in the split of the telencephalon, arrow in [I]) as well as of lhx5 in the thalamus (arrow in [M]). Cells did not switch on the expression of thalamic irx1b (arrow in [O]) in the thalamus.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808486-6-pbiop0050069pg007.jpg"
}
|
000740
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hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Voltage-Induced Intracellular Calcium Signals Occur in the Absence of Calcium Inward Current(A–C) Simultaneous patch clamp recording (lower traces) and calcium imaging (upper traces) from a representative, acutely isolated DUM neuron under different conditions. (A) In TEA- and TTX-containing saline, a voltage step from −90 mV holding to 0 mV test potential causes a calcium inward current followed by a calcium-activated potassium outward current. This is accompanied by a large elevation in internal calcium. (B) No membrane currents are observed in the same neuron after 3 min in calcium-free saline, but a slow elevation in intracellular calcium occurs in response to a similar voltage step as in (A). (C) Switching back to calcium-containing extracellular saline restores membrane currents and intracellular calcium signals as observed in (A).(D) Following depletion of intracellular calcium stores by extracellular application of CPA, no calcium elevation is recorded in zero-calcium saline in response to the step depolarization.(E and F) Average amplitudes (E) and average times to peak (F) of the calcium signals are shown for six neurons (mean and standard deviation) that were recorded continuously in calcium-containing control saline (left bars), zero-calcium saline (middle bars), and calcium-containing saline (right bars).(G) Photograph of a representative neuron just prior to recording demonstrates that isolated neurons are not in contact with each other or with neighboring glia cells.(H) This lack of contact is further supported by immunocytochemical labeling of the same neuron after the physiological experiments. Anti HRP (red) is used as a general neuronal marker, and a DNA stain (propidium iodide and RNAse [green]; see Materials and Methods) is used to depict nuclei. No nuclei of glia cells or neurons are detected in proximity to the recorded neuron.(I) SEM picture of a recorded soma with its primary neurite shows no contact with other neighboring cells.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808487-4-pbiop0050066pg001.jpg"
}
|
000741
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "DHPG Enhances APP Translation in WT but Not fmr-1 KO Neurons(A) Immunofluorescent confocal images of WT (top) and KO (bottom) neuronal cells treated with or without DHPG (0, 10, and 20 min) and hybridized with anti-22C11 APP primary and anti-mouse rhodamine-conjugated secondary antibodies. The dashed yellow rectangles encompass segments of dendrites, which are enlarged and displayed below the photos.(B) Dendritic APP levels were quantitated with ImageJ software and plotted as a percentage of untreated WT samples. Asterisks indicate significant differences, with p < 0.001 between the pairs.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808499-6-pbiop0050052pg005.jpg"
}
|
000742
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Inflammation in SNpc of DAT-Retlx/lx Mice(A, B, D–I, K, and L) Immunohistochemical stainings of dorsal striatum (A and B) and SNpc (D–I, K, and L) of 24-mo-old control (A, D, E, H, and K) and DAT-Retlx/lx mice (B, F, G, I, and L) for Iba-1 (A, B, E, G, H, and I), TH (D and F), and MAC1 (K and L). To localize microglial cells in SNpc, adjacent sections were stained for TH, and the area of the SNpc was marked and copied to the adjacent section stained for macrophages.(C, J, and M) Histograms showing the number of Iba-1–positive (C and J) and MAC1-positive (M) cells in the striatum (C) and SNpc (J and M) of 24-mo-old (C and J) DAT-Retlx/lx mice and controls. No significant alterations in the numbers of Iba-1–positive cells were observed in the striatum of 24-mo-old mutants and controls ([C] n = 4, p = 0.065). A significant increase in the numbers of Iba-1–positive cells was observed in the SNpc of 24-mo-old DAT-Retlx/lx mice compared to controls (J) (n = 5, p < 0.05). The same result was obtained using MAC1 as a second independent microglial marker (M) (n = 3, p < 0.05). *, p < 0.05 (Student t-test). Scale bars indicate 100 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808500-1-pbiop0050039pg006.jpg"
}
|
000743
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Conditional Ablation of Ret Expression in the Nigrostriatal System(A–D) Recombination efficiency of DAT-Cre mice crossed with Rosa26R lacZ reporter mice (DAT-Rosa26R). β-galactosidase (X-Gal) activity (blue) in coronal brain sections of DAT-Rosa26R transgenic mice at embryonic day E15.5 (A) and at 3-mo postnatal (B). Anti- TH (C) and anti–β-galactosidase (β-Gal) (D) immunostaining in adjacent brain sections of 2-y-old DAT-Rosa26R mice. Cre activity is restricted to SNpc and VTA.(E–J) Immunohistochemical detection of TH (E, G, and I) and Ret (F, H, and J) in adjacent coronal brain sections of 3-mo-old wild-type (wt), DAT-Retlx/lx, and Nes-Retlx/lx mice. Note the nearly complete removal of Ret immunoreactivity in SNpc and VTA of DAT-Retlx/lx and Nes-Retlx/lx mice.(K and L) Western blot analysis of Ret protein levels in protein lysates from SNpc (K) and striatum (L) of 3-mo-old control (Retlx/+and DAT-Retlx/+) and DAT-Retlx/lx mutant mice. Immunoblots were reprobed with anti–α-tubulin antibodies as loading controls.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808500-2-pbiop0050039pg001.jpg"
}
|
000744
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Progressive Loss of Nigral DA Neurons in DAT-Retlx/lx Mice(A) Coronal brain section of a 3-mo-old wild-type mouse showing DA neurons in the SNpc and the VTA stained with an antibody against TH. The inset shows a higher magnification view of the stippled area.(B and C) Stereological quantification of TH-positive DA neurons in the SNpc of 3-, 12-, and 24-mo-old control, DAT-TrkBlx/lx, DAT-Retlx/lx, and double homozygous Dat-Ret/TrkB mice (C) (n = 3 mice per genotype), Nes-Retlx/lx mutant mice and littermate controls (D) (n = 4 mice per genotype). *, p < 0.05 (Student t-test).(D) Double immunostaining for NeuN and TH (very mild staining protocol to outline the SNpc [stippled area]). The inset shows a higher magnification view of the stippled box, displaying nuclear localization for NeuN and cytoplasmic immunoreactivity for TH.(E) Stereological quantification of NeuN-positive neurons in the SNpc of 12- and 24-mo-old control and DAT-Retlx/lx mice (n = 5 mice per genotype at 12 mo, and n = 4 mice per genotype at 24 mo). *, p < 0.0001 and p < 0.001 for 12- and 24-mo-old DAT-Retlx/lx mice, respectively (Student t-test).(F–H) Adjacent sections of SNpc and VTA of a 1-y-old wild-type mouse stained for TH (F), dopa-decarboxylase (G), and Pitx3 (H). Insets show higher magnification images.(I and J) Stereological quantification of DDC-positive (I) and Pitx3-positive (J) cells in the SNpc of 12-mo-old littermate control and DAT-Retlx/lx mice (n = 3 mice per genotype). *, p < 0.05 (Student t-test).(K and L) Stereological quantification of TH-positive cells in the VTA region of 1-y-old control and DAT-Ret/TrkB mutant mice (K) (n = 3 mice per genotype; p > 0.5; Student t-test) and in the LC of 12-mo-old control and Nes-Retlx/lx mutant mice (L) (n = 4 mice per genotype; p >0.5; Student t-test). Scale bar indicates 250 μm and, in insets, 100 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808500-3-pbiop0050039pg002.jpg"
}
|
000745
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Gliosis in Dorsal Striatum of DAT-Retlx/lx Mice(A, B, D, E, G, and H) Bright-field photomicrographs of dorsal striatum (A, B, D, and E) and SNpc (G and H) of 12-mo-old (A and B) and 24-mo-old (D, E, G, and H) control (A, D, and G) and DAT-Retlx/lx mutants (B, E, and H) stained for GFAP.(C, F, and I) Histograms showing the number of GFAP-positive reactive astrocytes (n = 3–5 per genotype). There is a 2-fold increase in the number of reactive astrocytes in the striatum of 2-y-old DAT-Retlx/lx mutants as compared to wild-type controls and DAT-TrkBlx/lx mutants (F) (p < 0.0001), whereas no difference is seen in 12-mo-old DAT-Retlx/lx mutants compared to controls (C) (p = 0.9). No significant increase in the number of reactive astrocytes is seen in the SNpc of 24-mo-old DAT-Retlx/lx mutants compared to controls (I) (p = 0.24). **, p < 0.01 (Student t-test). Scale bars indicate 50 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808500-4-pbiop0050039pg005.jpg"
}
|
000746
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hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Loss of Postsynaptic Target Cells but Not Local Striatal Interneurons in DAT-Retlx/lx MiceImmunohistochemical stainings of dorsal striatum of 2-y-old control (A, D, and G) and DAT-Retlx/lx mutants (B, E, and H) for NeuN (A and B), DARPP-32 (D and E), or parvalbumin (G and H). Histograms showing the number of NeuN-positive (C), DARPP-32–positive (F), and parvalbumin-positive cells (I) in DAT-Retlx/lx mutants and age-matched controls (n = 3–5 each genotype). Note also the reduced staining intensities for NeuN and DARPP-32 in DAT-Retlx/lx compared to control mice. *, p < 0.05; **, p < 0.01 (Student t-test). Scale bars indicate 50 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808500-5-pbiop0050039pg004.jpg"
}
|
000747
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Progressive Loss of Striatal Innervation in DAT-Retlx/lx, but Not DAT-TrkBlx/lx Mice(A–D, F, and G) Representative images of dorsal striatum stained by immunofluorescence using antibodies against TH (A–D) and DAT (F and G) of control (A, B, and F) and DAT-Retlx/lx mutants (C, D, and G) at 12 (A, C, F, and G) and 24 mo of age (B and D).(E) The innervation density based on anti-TH immunofluorescence was quantified in dorsal versus ventral striatum of 12-mo-old controls (n = 16) versus DAT-TrkBlx/lx (n = 4), DAT-Retlx/lx (n = 6), double DAT-Ret/TrkB (n = 5), and Nes-Retlx/lx mutants (n = 7). DAT-Retlx/lx, double DAT-Ret/TrkB, and Nes-Retlx/lx mutants showed significant reductions in TH fiber density in dorsal (p < 0.001) and ventral striatum (p < 0.001, p < 0.01, and p < 0.01 for DAT-Retlx/lx, double DAT-Ret/TrkB, and Nes-Retlx/lx mutants, respectively). **, p < 0.01 (Student t-test).(H) The innervation density based on anti-DAT immunofluorescence was quantified in 12-mo-old Nes-Retlx/lx mutants compared to age-matched controls (n = 4 per genotype; p < 0.001, Student t-test).(I) Time course of TH-positive fiber loss from 3 to 24 mo of age. DAT-Retlx/lx mutant mice show a progressive fiber loss, starting at 6 to 9 mo (p = 0.09 and p < 0.05 at 6 mo and 9 mo, respectively) and maximizing at 24 mo (p < 0.0001). DAT-TrkBlx/lx mutant mice do not show any signs of fiber loss even at 24 mo of age (p = 0.13). *, p < 0.05; **, p < 0.01 (Student t-test). Scale bar indicates 25 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1808500-6-pbiop0050039pg003.jpg"
}
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000748
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hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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{
"caption": "The photo shows the 3D hologram of the ventricular septal defect repaired with a patch.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810238-1-1476-7120-5-8-1.jpg"
}
|
000749
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Visual scoring compared to CMYK analysis. (A) Representative images of 256 NSCLC biopsies show plasma membrane specific EGFR-NovaRed labeling with visual scores ranging from 0–3. (B) A box and whiskers graph (median, 25% to 75% box range, min and max whiskers) representation of mean Yellow intensity of specimens shows a direct relationship with the categorical visual scores.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810239-2-1746-1596-2-8-5.jpg"
}
|
000750
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Thymus atrophy in mice infected with WR and Wyeth strains. (A) Pictures of the thymus in mice infected intranasally with 106 p.f.u. or 104 p.f.u. of WR or 106 p.f.u. of Wyeth at 5 days post-infection. Arrows indicate the thymi. (B) The numbers of thymocytes from mice infected with WR and Wyeth strains at 3 (white bar), 5 (light gray bar), 10 (dark gray bar) and 18 (black bar) days post-infection. Thymocyets were pooled from groups of three mice and counted. Data are shown as the average numbers of thymocytes per mouse. The dotted line is the average number of thymocytes from uninfected mice. ND; not determined. (C) Virus titers in thymus of mice infected with WR and Wyeth strains at 3 (white bar), 5 (light gray bar), and 10 (dark gray bar) days post-infection. Titers are shown as p.f.u. per organ in log scale. The error bars indicate the standard deviations in triplicate samples. The dotted line indicates the detection limit. ND; not determined. (D) CD4 and CD8 expressions of thymocyets from mice infected with WR and Wyeth strains at 5 (upper five panels) and 10 (lower two panels) days post-infection.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810241-4-1743-422X-4-22-7.jpg"
}
|
000751
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Astrocytic staining (8 months). Astrocytic staining (8 months) in WT and TG mice. At 8 months staining is more patchy and less uniform in the TG/DSP-4 compared with TG/VEH group. Scale bar represents 200 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810243-3-1742-2094-4-8-5.jpg"
}
|
000752
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Amyloid histology – representative sections (11 months). Sagittal sections across cortex and hippocampus for amyloid staining (11 months) in WT and TG mice. At 11 months staining is of a similar level in TG/DSP-4 and TG/VEH groups. Scale bar represents 1 mm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810243-4-1742-2094-4-8-6.jpg"
}
|
000753
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Astrocytic staining (11 months). Astrocytic staining (11 months) in WT and TG mice. At 11 months the staining pattern is similar in TG/DSP-4 and TG/VEH groups. Scale bar represents 200 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810243-9-1742-2094-4-8-7.jpg"
}
|
000754
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "TLR9 immunoreactivity in the nasal mucosa. Immunohistochemical localization of TLR9 in biopsies of nasal mucosa is depicted in (B-F) whereas (A) illustrates a representative picture of a control slide. A) No immunoreactivity was observed in control sections where an isotype-matched control antibody was used. B) In an adjacent section, immunoreactivity for TLR9 is seen in the apical part of the epithelial lining, in scattered intra- and subepithelial leukocytes and in elongated fibroblast-like cells in the subepithelial tissue (arrow). The epithelial TLR9 immunoreactivity varied from being foremost present within the apical region of the epithelium (B) to a more even distribution (C). D) A distinct TLR9 immunoreactivity was also present in endothelial cells (arrowhead). E) Bright field micrographs demonstrating TLR9-positive large non-granulated mononuclear cells (arrowhead) and mast cells (inset). F) TLR9-positive intraepithelial lymphocytes (arrows E-F). Scale bars: A-C = 50 μm, D-E = 20 μm, and F = 350 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810251-4-1465-9921-8-17-2.jpg"
}
|
000755
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "34-year old male patient with confirmed AS (duration of inflammatory back pain 13 years, BASDAI 4.9, HLA B27 positive). Inflammatory lesions of the anterior chest wall are shown in the manubriosternal joint (curved arrows) on coronal (left) and sagittal (right) STIR images. Inflammatory changes are seen in the lower thoracic spine and L1 (arrows).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810253-0-1471-2474-8-20-5.jpg"
}
|
000756
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "28-year old male patient with suspected early AS (duration of inflammatory back pain 7 months, BASDAI 3.7, BASDAI 2 5, HLA B27 positive). Coronal (left) and sagittal (right) STIR images show the most commonly seen signal abnormalities in suspected early AS. Inflammatory changes (open arrows) are seen in the lower aspects of the SI joints and subtle abnormalities in the anterior corner of the endplates in the thoracic spine (arrows).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810253-1-1471-2474-8-20-2.jpg"
}
|
000757
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "30-year old male patient with confirmed AS (duration of inflammatory back pain 7 years, BASDAI 4.8, HLA B27 positive). Sagittal STIR images show inflammatory lesions in the thoracic and lumbar spine (arrows). Inflammatory lesions of the spinous process are shown at L4 (curved arrow)",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810253-2-1471-2474-8-20-3.jpg"
}
|
000758
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "47-year old male patient with confirmed AS (duration of inflammatory back pain 13 years, BASDAI 7.0, HLA B27 positive). Fatty replacement of subchondral bone marrow is shown in the lower sacral quadrant (arrows) on the coronal T1-weighted image.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810253-3-1471-2474-8-20-4.jpg"
}
|
000759
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "30-year old male patient with confirmed AS (duration of inflammatory back pain 7 years, BASDAI 4.8, HLA B27 positive). Two coronal STIR images demonstrate inflammatory lesions in the thoracic spine (solid arrows), in the sacroiliac joint (sacral side) (open arrows), and in the left hip. Extensive bone marrow changes in the acetabulum (curved arrow) and an effusion of the hip joint are shown (arrowheads).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810253-6-1471-2474-8-20-6.jpg"
}
|
000760
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Effect of Z-Phe-Ala-CHN2 on the size of the lysosome of T. brucei bloodstream forms in vivo. Mice were infected and treated as described in the legend to Fig. 1. On day 5 p.i., trypanosomes were purified and processed for electron microscopy. Ultrathin sections of representative cells purified from mice treated with Z-Phe-Ala-CHN2 (a) and vehicle alone (b) are shown. Note the enlarged lysosome in the trypanosome exposed to Z-Phe-Ala-CHN2 compared with that in the short-stumpy form from control mice. fl, flagellum; fp, flagellar pocket; ly, lysosome, m, mitochondrion. Bar, 0.5 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810305-0-1475-9292-6-2-2.jpg"
}
|
000761
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Effect of Z-Phe-Ala-CHN2 on the morphology of T. brucei bloodstream forms in vivo. Mice that had been infected with the pleomorphic variant clone AnTat 1.1 were injected intraperitoneally with 250 mg kg-1 of Z-Phe-Ala-CHN2 or vehicle alone on days 3 and 4 p.i. On day 5 p.i., blood smears were prepared and stained with May-Grünwald's stain solution. Representative examples from Z-Phe-Ala-CHN2-treated mice (a) and control mice (b) are shown. Trypanosomes exposed to the inhibitor appeared stumpy-like with a blue-stained region (arrowhead) between the kinetoplast and the nucleus, a location that is consistent with that of the lysosome in bloodstream forms. k, kinetoplast; n, nucleus; LS, long-slender forms; SS, short-stumpy forms.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810305-1-1475-9292-6-2-1.jpg"
}
|
000762
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Representative SEM images of the different particle sizing preparations of beryllium metal and beryllium oxide evaluated in the study. (A1) shows the dry metal powder illustrating compact morphology with smaller sub-micrometer size particles attached to the surface of larger particles; (A2) metal powder suspended in liquid for sizing with a LPC illustrating detachment of smaller submicrometer size metal particles from the surface of larger particles and/or detachment of particle agglomerates; and (A3) metal powder suspended in liquid for sizing with CCSEM illustrating similar morphology as observed for the LPC suspension. Similarly, (B1) shows the dry oxide powder having cluster morphology; (B2) oxide powder suspended in liquid for LPC analysis illustrating similar morphology to dry oxide powder; and (B3) oxide powder suspended in liquid for CCSEM analysis illustrating similar morphology to dry oxide powder and powder for LPC analysis.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810321-0-1743-8977-4-3-1.jpg"
}
|
000763
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Adrenal gland morphology is unchanged by the electroporation protocol. A panel-40×, B panel-100×, of representative animals that had nothing done-(left panels, control), had Sry delivered by electroporation (middle panels, Sry/electro) or empty vector delivered (right panels). The lighter color purple in the middle of the tissue is the medulla. The holes or cracks in the medulla are not defects but tears in the tissue from processing. Gene or empty vector delivery did not disrupt tissue morphology.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810322-2-1471-2261-7-6-4.jpg"
}
|
000764
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Dissection of the Function of foxi3a and foxi3b in X-Su(H)/Ank mRNA-Injected Embryos or bmp7 Morphants.(A) Schematic diagram showing the role of Bmp and Delta-Notch signaling in specifying the epidermal ectoderm (gray) and singling-out epidermal ionocytes (yellow) from the epidermal stem cell pool (blue). (B) Normal Na+,K+-ATPase rich cell (NaRC) and H+-ATPase rich cell (HRC) differentiation in wild-type embryos aged at 24 hours post-fertilization (hpf). In wild-type embryos, a few IC progenitors were selected from the epidermal stem cell pool within the epidermal ionocyte domain by Delta-Notch-mediated lateral inhibition, and then differentiated into NaRCs (green, detected by atp1b1b in situ) or HRCs (red, detected by ca2a in situ) which are scattered on the epidermal layer. (C) For X-Su(H)/Ank mRNA-injected embryos (500 pg/embryo), the foxi3a and foxi3b expressions were inhibited due to the elevated Notch activity in the epidermal ionocyte domain. In such a condition, all epidermal ionocyte progenitors adopted the epidermal stem cell fate; therefore, subsequent NaRC and HRC differentiation was completely abolished. (D) When foxi3a mRNA (50 pg/embryo) and X-Su(H)/Ank mRNA (500 pg/embryo) were co-injected, high levels of exogenous foxi3a expression could compensate for the elevated Notch activity and restore both NaRC and HRC differentiation. (E) When foxi3b mRNA (50 pg/embryo) and X-Su(H)/Ank mRNA (500 pg/embryo) were co-injected, a high level of exogenous foxi3b expression was also sufficient to compensate for the elevated Notch activity to restore NaRC and partially restore HRC differentiation. (F) In bmp7 morphants (0.1 mM/embryo), although the low level of Bmp signals was still sufficient to promote P63 expression, it was insufficient to drive either foxi3a or foxi3b expression and finally the epidermal ionocytes lost their identity. (G) When foxi3a mRNA (50 pg/embryo) and bmp7 MO (0.1 mM/embryo) were co-injected, a high level of exogenous foxi3a expression could compensate for the low Bmp activity and restore both NaRC and HRC differentiation. (H) When foxi3b mRNA (50 pg/embryo) and bmp7 MO (0.1 mM/embryo) were co-injected, a high level of exogenous foxi3b expression could compensate for the low Bmp activity to restore NaRC and partial HRC differentiation. All embryos were scored at 24 hpf.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810426-1-ponep0000302pg008.jpg"
}
|
000765
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "deltaC is Positively Regulated by ascl1a and Receives Negative Feedback by notch.\n(A) Misexpression of VP16:ascl1a mRNA was sufficient to generate ectopic deltaC expression outside the epidermal ionocyte domain. foxi3a expression, on the contrary, was not affected by VP16:ascl1a mRNA misexpression. (B–F) Evaluation of deltaC expression by genetic mutants or mRNA-injected embryos with enhanced or reduced Notch activity. Compared to the wild-type (B), deltaC expression in the epidermal ionocyte domain was more homogeneous in mibta52b (C), beatit446 (D), and X-Su(H)DBM mRNA-injected embryos (E). On the contrary, deltaC expression in the epidermal ionocyte domain was completely abolished in X-Su(H)/Ank mRNA-injected embryos (F). Embryos in the upper panel of all photos are oriented in ventral view, with the anterior to the top, while in the lower panel, all are oriented in lateral view, with the anterior to the left. Epidermal ionocyte domains are highlighted by dotted lines. hpf, hour post-fertilization; tb, tail bud.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810426-10-ponep0000302pg005.jpg"
}
|
000766
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Early Development of Epidermal Ionocytes in Zebrafish Embryos.(A–D) Detection of atp1b1b (green) and ca2a (red) expression in differentiating epidermal ionocytes by fluorescent double in situ hybridization from the 18-somite (18-s) to 72-hour post fertilization (hpf) stage. Note that ca2a is also expressed on spinal cord neurons (sn) and the pronephric duct (pd) in A and B. In A, some epidermal ionocytes which were double-positive for both ca2a and atp1b1b are highlighted with asterisks. (C, D) High-magnification view of ca2a and atp1b1b expressions in the yolk extension region of 72-hpf embryos. Differentiating H+-ATPase rich-cells cells (HRCs) (labeled by asterisks) express a high level of ca2a and a low level of atp1b1b, while differentiating Na+,K+-ATPase-rich cells (NaRCs) are positive for only atp1b1b. (E–M) Dynamic expression of foxi3a (red) and foxi3b (green) in epidermal ionocyte progenitors and differentiating epidermal ionocytes from the 5-s to the 72-hpf stage. Whole-mount in situ hybridization of 72-hpf embryos show that the expression patterns between foxi3a (I) and foxi3b (J) are distinct in the cephalic domain. (K) In the yolk extension region, some cells express a high level of foxi3a (red) and a low level of foxi3b (green), while others are positive only for foxi3b (green). Immunodetection of Na+,K+-ATPase (green) and H+-ATPase (red) in 72-hpf embryos which were in situ-stained with either foxi3a (L) or foxi3b (M). Results showed that foxi3a was only expressed in HRCs (red arrow), while foxi3b was expressed by both HRCs (red arrow) and NaRCs (green arrow). (N) Schematic diagram showing the major events of epidermal ionocyte development in zebrafish embryos at the progenitor stage (the 90% epiboly to 14-s stages), differentiation stage (the 14-s stage to 36 hpf), and maturation stage (from 36 hpf onwards). The developmental stage is indicated in the left lower corner of each panel.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810426-3-ponep0000302pg001.jpg"
}
|
000767
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Knock-down \nfoxi3a Expression Severely Reduces Epidermal Ionocyte Progenitor Number and Abolishes the Later Differentiation Program.(A–G) Interfering with foxi3a and foxi3b functions of epidermal ionocyte differentiation by a morpholino (0.5 mM/embryo) injection. Morphants were fixed at 24 hours post fertilization (hpf) and stained with atp1b1b (green), ca2a (red), and P63 (blue) to detect Na+,K+-ATPase rich cells (NaRCs), H+-ATPase rich cells (HRCs), and epidermal stem cells, respectively. (H–I) A rescue experiment to show the specificity of foxi3a morpholinos. The foxi3a mRNA used for the rescue experiment does not contain a binding site for MO2. (J–L) Comparison of the vital dye uptake ability between the wild type (wt), foxi3a morphants, and foxi3b morphants. NaRCs and HRCs in either wild-types or foxi3b morphants can absorb MitoTracker (red) and Con-A (green) through to their apical openings. For foxi3a morphants, no MitoTracker or Con-A staining was detected due to blockage of the entire differentiation program. (M–O) Detection of the apical opening of epidermal ionocytes in wild-types, foxi3a morphants, and foxi3b morphants by scanning electron microscopy. The apical openings of NaRCs and HRCs in wild-types are shaped as deep holes (green box) or a mesh (red box), respectively. The apical openings were totally undetected in foxi3a morphants due to blockage of the entire differentiation program. For foxi3b morphants, the apical openings for both NaRCs and HRCs were reduced. Embryos in (A–I) were scored at 24 hpf, while in (J–O), they were scored at 72 hpf. In I, embryos are orientated in a dorsal-up and anterior-top position.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810426-5-ponep0000302pg009.jpg"
}
|
000768
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810426-7-ponep0000302pg004.jpg"
}
|
000769
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Excess Epidermal Ionocytes Detected in mibta52b Occur at the Expanse of Epidermal Stem Cell Fate.(A–C) Detection of the cell proliferation activity within the epidermal ionocyte domain between mibta52b and siblings at the tail bud (tb) stage. For mibta52b embryos (B) or their siblings (A), epidermal ionocyte progenitors were labeled with foxi3a (black), and mitotic cells were labeled with phosphor-histone 3 (pH3) antibody staining (green). Cells which were double positive for foxi3a and pH3 are highlighted by asterisks. (C) Quantitative comparison of the epidermal ionocyte progenitor number, mitotic divided cell number, and mitotic divided epidermal ionocytes between mibta52b embryos and siblings. (D–I) The excess epidermal ionocytes in mibta52b embryos occur at the expense of the epidermal stem cell fate. For 24-hour post-fertilization (hpf) mibta52b embryos (D–F) and siblings (G–I), differentiating Na+,K+-ATPase-rich cells (NaRCs), H+-ATPase-rich cells (HRCs), and epidermal stem cells were labeled with atp1b1b (green), ca2a, (red), and P63 (blue) staining, respectively. (J) Quantitative comparison of NaRC, HRC, and epidermal stem cell numbers between mibta52b embryos and siblings. The cell number in (C and J) is presented as the mean±S.D. *, p<0.05, compared with siblings, as determined by Student's t-test.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810426-8-ponep0000302pg003.jpg"
}
|
000770
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "Electron density maps confirming the molecular replacement solution. (A) Superposition of the anomalous difference Fourier map calculated using Cys426 data collected on the chromium edge contoured at 3.5σ with the final refined model of ParC55. Panels were rendered using Coot [46]. (B) Stereo view of a region of the 2Fobs-Fcalc electron density map from wild-type ParC55 data contoured at 1.5σ with the final refined model superimposed.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810434-2-ponep0000301pg006.jpg"
}
|
000771
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
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|
{
"caption": "IBV field isolates efficiently infect primary chicken kidney cells. Monolayers of CK cells were separately infected with IBV strain Ark99, Ark_DPI, CA99, Conn46, H52, Iowa97, and Mass41 for 12 h. Cell monolayers were labeled with monoclonal α-S1 or M (15:88, 13:18, or 9:19) antibodies to detect viral infection.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810517-0-1743-422X-4-20-5.jpg"
}
|
000772
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "fAPN expression rescues FIPV-1146 and TGEV infection in non-permissive BHK-21 cells. A) CRFK, BHK, or BHK cells transfected with fAPN/pcDNA3.1D/TOPO were separately infected with FIPV-1146 for 9 h. Monolayers were stained with 17B71 monoclonal antibody to detect FIPV-1146 infections. B) A72, BHK, or BHK cells transfected with fAPN/pcDNA3.1D/TOPO were separated infected with TGEV for 8 h. Monolayers were labeled with rabbit polyclonal antibody 367 to detect TGEV infections. C) BHK and BHK transfected with fAPN/pcDNA3.1D/TOPO cells were separately infected with FIPV-1146 or TGEV. Viral infectivity was determined by counting >300 cells in three separate experiments. Error bars represent the standard deviation from the mean.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810517-1-1743-422X-4-20-2.jpg"
}
|
000773
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "IBV strain Mass41 can infect feline cells at low levels. A & B) Primary CK or CRFK, cells were infected with IBV_Mass41 for 12 h and labeled with monoclonal α-S1(15:88) antibody to detect viral infection in three independent experiments. Viral infectivity was determined by counting >300 cells. Error bars represent the standard deviation from the mean.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810517-2-1743-422X-4-20-3.jpg"
}
|
000774
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "fAPN is not a functional receptor for field strains of IBV. BHKexp.pCiNeo (A) or BHKexp.fAPN (B) cells were independently infected with IBV strain Ark99, Ark_DPI, CA99, Iowa97, Conn46, H52, and Mass41 for 12 h. Cell monolayers were labeled with monoclonal α-S1 or M (15:88, 13:18, or 9:19) antibodies to detect and determine viral infections. Viral infectivity was determined by counting approximately 106 cells in three separate experiments.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810517-5-1743-422X-4-20-6.jpg"
}
|
000775
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "AP radiograph of the upper limb showing absent radius with radially deviated hand.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810518-0-1471-2369-8-5-1.jpg"
}
|
000776
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "MRI Scan showing a crossed fused kidney on the left side.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810518-2-1471-2369-8-5-4.jpg"
}
|
000777
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Intravenous Urogram showing crossed fused renal ectopia.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810518-3-1471-2369-8-5-2.jpg"
}
|
000778
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Light microscopy of haemangiomatous vessels of the face stained with haematoxyline-eosine revealing micro-anatomical details. A = artery; V = vein; N = nerve. Both the endothelial and medium layers of the artery wall are uneven discontinuous and non homogeneous (magnification 100×; bar 100 μm).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810521-0-1746-160X-3-12-1.jpg"
}
|
000779
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "A and B. Light microscopy of total nerve fibers in a normal (A) and haemangiomatous (B) artery of the face stained using Bodian's method. The adventitia was separated from other layers of the artery wall and stretched on a slice. As can be seen, there are fewer nerve fibers in the haemangiomatous artery (B) than in the normal artery (A) (magnification 400×; bar 100 μm).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810521-1-1746-160X-3-12-2.jpg"
}
|
000780
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "A and B. Fluorescent light microscopy of beta-adrenergic receptors contained in a transversal section of a normal (A) and an haemangioma-tous (B) artery of the face stained with fluorescent pindolole. The beta adrenergic receptors in the haemangiomatous arteries are located exclusively in the adventitia, while they lack in other layers. A = adventitia; L = lumen(magnification 800×; bar 100 μm).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810521-2-1746-160X-3-12-5.jpg"
}
|
000781
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "A and B. Fluorescent light microscopy of a transversal section of a normal (A) artery of the face stained using Qayyum's method, which stains the catecholaminergic nerve fibers. Results are compared with an analogue image from an haemangiomatous artery (B) A = adventitia; M = medium layer; L = lumen (magnification 400×; bar 100 μm).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810521-3-1746-160X-3-12-4.jpg"
}
|
000782
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "A and B. Fluorescent light microscopy of a transversal section of a normal (A) artery of the face stained using Falck's method for the staining of adrenergic nerve fibers compared with a haemangiomatous artery (B). A = adventitia; M = medium layer; E = endothelial layer; L = lumen (magnification 400×; bar 100 μm).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810521-4-1746-160X-3-12-3.jpg"
}
|
000783
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "AM-hMSCs multi-lineage differentiations in vitro: chondrogenic (A), osteogenic (B), adipogenic (C-H) commitments. Chondrogenic differentiation revealed by immunohistochemical stain for collagen II in induced AM-hMSCs. Original magnification ×40 (A). Osteogenic differentiation evidenced by the formation of mineralized matrix as shown by von Kossa staining. Original magnification ×10 (B).Small colonies with lipid secretion during the first week of adipogenic induction as highlighted by Red Oil staining for neutral lipids. Magnification ×4 (C); at higher magnification, multivacuolar adipogenic cells. Magnification ×10 and ×25 respectively (D, E). Big aggregates with intensive and massive lipid secretion at the third week of adipogenic induction. Magnification ×10, ×10 and ×40 respectively (F, G, H).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810523-0-1471-213X-7-11-5.jpg"
}
|
000784
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Angiogenic commitment: light microscopic analysis of AM-hMSCs after incubation on Matrigel. (A) Spontaneous organization in capillary-like structures on semisolid medium after 2 (A1), 4 (A2) and 20 (A3) hours of incubation. (B) Increased capillary-like structure formation in AM-hMSCs cultured in angiogenic medium supplemented by VEGF 50 ng/mL after 2 (B1), 4 (B2) and 20 (B3) hours' incubation. Within 4 hours of incubation on semisolid medium, cells preserve a round shape and homogeneous distribution (A1 and B1).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810523-4-1471-213X-7-11-7.jpg"
}
|
000785
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Immunofluorescence detection of vWF, FLT-1 and KDR expression. AM-hMSCs cultured in standard medium for 7 days did not show vWF expression (A, Magnification ×40). AM-hMSCs stimulated with medium containing 50 ng/ml of VEGF for 7 days showed vWF expression (B, Magnification ×40); the immunostaining revealed a cytoplasmatic granular positivity at higher magnification (C, Magnification ×100). FLT-1 and KDR expression in induced AM-hMSCs (D, E, Magnification ×40). Nuclei are stained with DAPI (blue).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810523-5-1471-213X-7-11-9.jpg"
}
|
000786
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Human amniotic membrane. Amniotic membrane sheet as seen by light microscopy. The sample has been stained with Mallory's stain to highlight the connective tissue elements (stained red) as indicated by the arrows (A). Morphology of AM-hMSCs subconfluent at third passage. Magnification ×40. Arrows indicate mitotic figures (B).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810523-7-1471-213X-7-11-1.jpg"
}
|
000787
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Skeletal muscle differentiation of AM-hMSCs. RT-PCR for skeletal muscle transcription factors MyoD and Myogenin. MyoD appears after 1 week of induction while Myogenin is expressed in the second week of induction. Samples are as follows: lane 1: AM-hMSCs cultured in control medium; lane 2: induced AM-hMSCs after 7 days; lane 3: induced AM-hMSCs after 14 days; lane 4: positive control (RD18 cell line); lane 5: reagent control. Beta-actin was used as a house-keeping gene (A). Immunocytochemical staining for Desmin after 3 weeks' induction: uninduced AM-hMSCs (B) and Desmin positive induced cells (C).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810523-8-1471-213X-7-11-6.jpg"
}
|
000788
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Pattern of proliferation and G1 arrest in the eye. (A) Projection of several confocal sections of a WT eye disc showing Armadillo (green), Elav (red) and Ato (blue) localization. The morphogenetic furrow (MF, arrowhead in all figures) is highlighted by accumulation of Armadillo (β-catenin), which outlines cell membranes. Ato expression appears between 6–8 cells anterior to the MF and becomes limited to the R8 photoreceptor just posterior to the furrow. Elav is expressed in all the photoreceptor cells posterior to the Ato expressing R8. In this and all subsequent figures, anterior is to the left. (B) WT eye disc showing the incorporation of BrdU (red) and the expression of PCNA-GFP reporter (indicating dE2F1 activation, green) and Ato protein (blue). Anterior to the furrow there is a non-proliferative region, without BrdU incorporation (white bar). The pattern of PCNA-GFP expression coincides with the regions of proliferation. (C) Scheme showing the different proliferating regions of the eye disc. The panel shows a drawing of the disc in 1B. The inset shows a picture of the whole disc. From anterior to posterior: orange marks the region of undifferentiated cells that proliferate randomly; the NPR is marked in blue (its extent is marked by the white bar), with the darker zone showing the morphogenetic furrow (also marked by an arrowhead); finally, the red band marks the region of the second mitotic wave. (D) Z-axis reconstruction of a WT eye disc. The outlines of the cells are shown by Armadillo (Arm) expression (green). The peripodial membrane appears at the top with some BrdU positive cells (red). In the disc proper there is a high accumulation of Arm protein in the apical part of the MF (arrowhead). S-phase nuclei in the SMW are basally located (arrow), whereas anterior to the NPR, BrdU positive nuclei are more apical. The NPR includes the furrow cells (that accumulate high apical levels of Arm) and between 4–6 rows of more anterior cells. Ato expressing cells (blue) are restricted to the disc proper. (E) The cytoplasmic expression of PCNA-GFP reporter (blue) is seen in cells that are completing the cell cycle in the most anterior part of the NPR, but is not expressed in the cells of the MF (that accumulate E-cadherin in the apical region, in green). In the SMW the cells with BrdU positive nuclei also express the PCNA-GFP.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810524-0-1471-213X-7-13-1.jpg"
}
|
000789
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Dpp and Hh control G1 arrest primarily in the anterior of the NPR. (A) WT eye disc showing the cells in mitosis as marked by phosphohistone H3 antibody (PH3, in red) and the Ato pattern of expression (blue). The white arrow marks the line of synchronized mitosis anterior to the NPR in A and B. In the region anterior to this line the frequency of phosphohistone H3 positive cells is very low (asterisk) (B) Eye disc with a large smo3 tkva12 M+ clone (absence of green). The yellow arrow marks the region where the distinct line of mitosis (pH3, red; the so-called first mitotic wave) is lost. (C) tkva12 clones (absence of green) showing some BrdU positive cells (red) in the anterior part but not in the posterior (arrows). (D) Similarly, in tkva12 ci94 clones (marked by the absence of Ci antibody in green) there are no BrdU positive cells in the posterior region of the NPR (red). The arrows mark some BrdU cells in the anterior part of the NPR. (E-F) Mad12 ci94 clones (marked by absence of Ci, green) stained for BrdU (E) and CycB (F) in red. The arrows mark clones in the posterior part of the NPR where there is no ectopic BrdU incorporation or CycB accumulation. (G) smo3 tkva12 clones (arrows) marked by absence of β-gal, in green (arrows). The picture shows a representative clone in the lower part of the panel with no ectopic BrdU positive cells (red) (H) Ectopic CycB (red) accumulates only in the anterior region of the NPR in smo3 tkva12 clones (absence of green). This is highlighted in clones that span the whole NPR, where there is clear CycB accumulation that does not reach the most posterior cells (arrows).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810524-1-1471-213X-7-13-3.jpg"
}
|
000790
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Factors contributing to G1 arrest. (A-B) PCNA-GFP expression (green) in discs with tkva12 (A) and smo3 tkva12 (B) clones. Upregulation in the posterior part of the NPR only occurs in the smo3 tkva12 clones. (C-D) Eye disc with smo3 (C) and tkva12 (D) clones (absence of GFP in red), stained for Dap antibody in green. The loss of smo, but not tkv, causes the loss of Dap in the furrow (arrows). (E) Eye disc with ato1 M+ clones (absence of green) showing no ectopic BrdU incorporation (red) in the NPR. (F) UAS-ato overexpression clones (marked by GFP in green) can inhibit CycB accumulation (red) close to the anterior part of the NPR (arrow in F').",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810524-2-1471-213X-7-13-4.jpg"
}
|
000791
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Rux is necessary to maintain G1 arrest in the posterior of the NPR. (A-B) rux8 clones (absence of β-galactosidase in green) stained for BrdU (A) and CycB (B) in red. Both ectopic BrdU incorporation and CycB accumulation lie predominantly in the posterior part of the NPR, although occasional BrdU positive cells are also seen more anteriorly. (C-D) PCNA-GFP reporter expression (green in C and D, and white in C' and D') in discs with rux8 clones (absence of red in C) and CycA overexpression clones (marked by presence of β-galactosidase (red in D). The PCNA-GFP reporter is slightly activated in the rux clone in the NPR (arrow in C') and in cells overexpressing CycA in the NPR (arrow in D'). (F-G) rux-lacZ transgene expression (red) in a WT disc (F) and in a disc harbouring smo3 tkva12 double mutant clones. The transgene is expressed in the NPR, the position of which is localised by the expression of Ato (blue in F), and its levels decreases just posterior to the MF. The levels of rux-lacZ increase in the double mutant cells for smo and tkv (marked by absence of green in G). The bar indicates the width of the NPR.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810524-3-1471-213X-7-13-5.jpg"
}
|
000792
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Effect of overexpression of cyclins in the NPR. All panels except B show BrdU staining (red) of eye disc harbouring different overexpression clones marked with GFP (green). (A) The overexpression of CycE is able to induce ectopic BrdU incorporation with a high efficiency in the anterior part of the NPR, but less so the posterior, where only a few cells enter S phase. (B) The PCNA-GFP reporter (green) is active (arrows) in the CycE overexpression clones (marked by presence of β-gal in red) within the NPR. (C) In dE2F1 overexpression clones there is BrdU incorporation only in the anterior part of the NPR. (D) The overexpression of CycE and dE2F1 can induce incorporation of BrdU in anterior and posterior cells of the NPR. (E) CycA overexpressing cells incorporate BrdU in any part of the NPR, but with a higher efficiency in the posterior part, where most cells are BrdU positive. (F) Simultaneous overexpression of CycE and CycA induces a high proportion of BrdU incorporation in any part of the NPR.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810524-4-1471-213X-7-13-2.jpg"
}
|
000793
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "CRTH2 antagonism in vivo attenuates airway tissue eosinophilia and mucus cell hyperplasia. Above (A): OVA challenge produced marked eosinophilia and mucus cell hyperplasia (***, p < 0.001 compared to saline control). Treatment with ramatroban or the specific CRTH2 antagonist TM30089 significantly reduced airway tissue eosinophilia (black bars) and mucus production (white bars); #, p < 0.05 compared to vehicle treatment. Below (B-G): Light micrographs showing effects in particularly well-responding animals. Lung tissue eosinophilia in normal saline treated lung (B), OVA/vehicle treated lung (C), and OVA/TM30089 treated lung (D). Airway mucus cells are shown in normal saline treated lung (E), OVA/vehicle treated lung (F), and OVA/TM30089 treated lung (G). Scale bar = 100 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810525-1-1465-9921-8-16-2.jpg"
}
|
000794
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "PrPsc immunolabelling in the spinal tract nucleus of the trigeminal nerve (case 06/008). Fine granular staining of PrPsc in the neuropil with the rat monoclonal antibody R145 [37].",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810526-0-1746-6148-3-2-1.jpg"
}
|
000795
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Cross sectional cut of CT scan of abdomen at the time of clinical presentation. Multiple hypoechoic densities are present in the spleen (arrows).",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810538-0-1471-2334-7-8-1.jpg"
}
|
000796
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Hematoxylin and eosin stain of lymph node biopsy showing a stellate granuloma and microabscesses.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810538-1-1471-2334-7-8-2.jpg"
}
|
000797
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Cytological staining of normal and GAN fibroblasts grown under low-serum conditions. (A) Percentage of cells containing Red-Oil-O-positive droplets. (B-D) Fibroblasts MCH070 (B), WG0791 (C) and WG0321 (D) were stained with Oil Red O and Hematoxylin dyes. Lipid droplets were stained in red and nuclei were stained in blue. Lipid droplets accumulated in WG0791 and WG0321 cells but not in MCH070 cells. (E-G) Fibroblasts MCH070 (E), WG0791 (F) and WG0321 (G) were immunostained with monoclonal anti-vimentin V9 antibody and Oil Red O. Vimentin filaments were stained in green and lipid droplets were stained in red. Scale bars, 10 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810559-2-1471-2156-8-6-4.jpg"
}
|
000798
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
|
{
"caption": "Cytological analysis of normal and GAN fibroblasts. (A) Fractions of wild-type and GAN cells containing vimentin aggregates in normal and low-serum media. Upon low-serum treatment, there was a dramatic increase of vimentin aggregates in GAN cells, from 12% to 43% for WG0791 cells and from 19% to 89% for WG0321 cells. Vimentin did not form aggregates in normal cells under any culture conditions. (B and C) Immunostaining of MCH070 (wild-type) cells with a polyclonal anti-vimentin antibody (B) and a monoclonal anti-pan-keratin antibody (C). A small percentage of MCH070 fibroblasts expressed both vimentin and keratins. Both of these intermediate filament proteins could form an extensive filament network. (D and E) Immunostaining of WG0321 (GAN) cells with a polyclonal anti-vimentin antibody (D) and a monoclonal anti-pan-keratin antibody (E). Similar to MCH070, a small percentage of WG0321 fibroblasts expressed vimentin and keratins. Both proteins could be found in the aggregates (white arrows). Note that some vimentin aggregates did not contain keratins (arrowheads in D). Scale bar, 10 μm.",
"subfigure_path": "/datasets/PMC-15M/filtered_biomedica/filtered_v4/subfigures_final/subfig_0_filelist_commercial_batch_0_105-PMC1810559-3-1471-2156-8-6-2.jpg"
}
|
000799
|
hf://datasets/vector-institute/open-pmc-18m@b5bf5b815f7ed24176e14a861ca062afe8d8775d/data_00000.tar
|
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