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PMC1368963_F2_4550.jpg | What object or scene is depicted here? | Selected imaging studies from the FPLD3 subject. Panel shows computed tomography cross-section of upper thigh of a normal individual and subject II-5, who had markedly decreased subcutaneous fat on both extremities. |
PMC1368969_F3_4552.jpg | Describe the main subject of this image. | Biopsy finding: Well-differentiated squamous cell carcinoma. |
PMC1368985_F1_4557.jpg | What is shown in this image? | (i) Fluid phase uptake monitored using FITC-dextran. 2 mM cycloheximide inhibits fluid phase uptake by >95%, as shown in this time course. The data obtained for each experiment were normalised with respect to the 30 minute time point for Ax2 in the absence of cycloheximide. (ii) Photomicrographs of amoebae incubated with FITC-dextran. Ax2 were preincubated in the absence (A/ B) or presence (C/ D) of 2 mM cycloheximide for 30 minutes, followed by incubation with FITC-dextran. The amoebae were subsequently fixed in 5% formaldehyde and mounted on a coverslip. A, C: Phase-contrast; B, D: Fluorescence. (iii) Time course showing how membrane uptake, as monitored using FM1-43, is unaffected by cycloheximide. FM1-43 was added at a concentration of 5 μM. The data obtained for each experiment were normalised with respect to the 30 minute time point for Ax2 in the absence of cycloheximide. (iv) Internal membrane bound structures stained with FM1-43. Ax2 were preincubated for 30 minutes without (A/B) or with (C/D) 2 mM cycloheximide prior to incubation with FM1-43 for 60 minutes. The cells were subsequently washed and kept on ice before being placed on a coverslip. A, C: Phase-contrast; B, D: Fluorescence. All images are sections taken using a 60× objective lens unless otherwise stated. |
PMC1368985_F1_4554.jpg | Can you identify the primary element in this image? | (i) Fluid phase uptake monitored using FITC-dextran. 2 mM cycloheximide inhibits fluid phase uptake by >95%, as shown in this time course. The data obtained for each experiment were normalised with respect to the 30 minute time point for Ax2 in the absence of cycloheximide. (ii) Photomicrographs of amoebae incubated with FITC-dextran. Ax2 were preincubated in the absence (A/ B) or presence (C/ D) of 2 mM cycloheximide for 30 minutes, followed by incubation with FITC-dextran. The amoebae were subsequently fixed in 5% formaldehyde and mounted on a coverslip. A, C: Phase-contrast; B, D: Fluorescence. (iii) Time course showing how membrane uptake, as monitored using FM1-43, is unaffected by cycloheximide. FM1-43 was added at a concentration of 5 μM. The data obtained for each experiment were normalised with respect to the 30 minute time point for Ax2 in the absence of cycloheximide. (iv) Internal membrane bound structures stained with FM1-43. Ax2 were preincubated for 30 minutes without (A/B) or with (C/D) 2 mM cycloheximide prior to incubation with FM1-43 for 60 minutes. The cells were subsequently washed and kept on ice before being placed on a coverslip. A, C: Phase-contrast; B, D: Fluorescence. All images are sections taken using a 60× objective lens unless otherwise stated. |
PMC1368985_F1_4553.jpg | What is shown in this image? | (i) Fluid phase uptake monitored using FITC-dextran. 2 mM cycloheximide inhibits fluid phase uptake by >95%, as shown in this time course. The data obtained for each experiment were normalised with respect to the 30 minute time point for Ax2 in the absence of cycloheximide. (ii) Photomicrographs of amoebae incubated with FITC-dextran. Ax2 were preincubated in the absence (A/ B) or presence (C/ D) of 2 mM cycloheximide for 30 minutes, followed by incubation with FITC-dextran. The amoebae were subsequently fixed in 5% formaldehyde and mounted on a coverslip. A, C: Phase-contrast; B, D: Fluorescence. (iii) Time course showing how membrane uptake, as monitored using FM1-43, is unaffected by cycloheximide. FM1-43 was added at a concentration of 5 μM. The data obtained for each experiment were normalised with respect to the 30 minute time point for Ax2 in the absence of cycloheximide. (iv) Internal membrane bound structures stained with FM1-43. Ax2 were preincubated for 30 minutes without (A/B) or with (C/D) 2 mM cycloheximide prior to incubation with FM1-43 for 60 minutes. The cells were subsequently washed and kept on ice before being placed on a coverslip. A, C: Phase-contrast; B, D: Fluorescence. All images are sections taken using a 60× objective lens unless otherwise stated. |
PMC1368985_F1_4556.jpg | What object or scene is depicted here? | (i) Fluid phase uptake monitored using FITC-dextran. 2 mM cycloheximide inhibits fluid phase uptake by >95%, as shown in this time course. The data obtained for each experiment were normalised with respect to the 30 minute time point for Ax2 in the absence of cycloheximide. (ii) Photomicrographs of amoebae incubated with FITC-dextran. Ax2 were preincubated in the absence (A/ B) or presence (C/ D) of 2 mM cycloheximide for 30 minutes, followed by incubation with FITC-dextran. The amoebae were subsequently fixed in 5% formaldehyde and mounted on a coverslip. A, C: Phase-contrast; B, D: Fluorescence. (iii) Time course showing how membrane uptake, as monitored using FM1-43, is unaffected by cycloheximide. FM1-43 was added at a concentration of 5 μM. The data obtained for each experiment were normalised with respect to the 30 minute time point for Ax2 in the absence of cycloheximide. (iv) Internal membrane bound structures stained with FM1-43. Ax2 were preincubated for 30 minutes without (A/B) or with (C/D) 2 mM cycloheximide prior to incubation with FM1-43 for 60 minutes. The cells were subsequently washed and kept on ice before being placed on a coverslip. A, C: Phase-contrast; B, D: Fluorescence. All images are sections taken using a 60× objective lens unless otherwise stated. |
PMC1368989_F1_4563.jpg | What is the core subject represented in this visual? | Histological section from lung biopsy material. Metastatic adenocarcinoma to the lung from previous colon cancer (haematoxylin-eosin ×200). |
PMC1369006_F3_4564.jpg | What's the most prominent thing you notice in this picture? | Immmunohistochemical staining of SCC tumors. Immunostaining for HIF-1α (SC10790), (Santa Cruz Biotech., Inc. Santa Cruz, CA, USA) was performed on 5 μM sections. Staining was analyzed with horseradish peroxidase-linked goat antimouse (Santa Cruz Biotechnology, Santa Cruz, CA) Tumors lacking HIF-1α (top panel) and tumors that manifest an exon 12 HIF-1α polymorphism and TSC deletions in exon 36 and 40 (bottom panel). |
PMC1373607_F4_4566.jpg | What's the most prominent thing you notice in this picture? | Cellular localization of transgene expression. Confocal microscopy demonstrated EGFP-expression in the nerve roots. The left panel provides an anatomic overview of a lumbar section through the spinal cord obtained with transmission light at a low magnification. The middle panel shows EGFP fluorescence (excitation wave length 488 nm, emission wave length 505–530 nm). The right image is a fusion of the fluorescence image with a transmission light micrograph of the same area. The insert depicts a detail at higher magnification. Images were obtained on an LSM 510 META confocal microscope. |
PMC1373607_F4_4567.jpg | What is being portrayed in this visual content? | Cellular localization of transgene expression. Confocal microscopy demonstrated EGFP-expression in the nerve roots. The left panel provides an anatomic overview of a lumbar section through the spinal cord obtained with transmission light at a low magnification. The middle panel shows EGFP fluorescence (excitation wave length 488 nm, emission wave length 505–530 nm). The right image is a fusion of the fluorescence image with a transmission light micrograph of the same area. The insert depicts a detail at higher magnification. Images were obtained on an LSM 510 META confocal microscope. |
PMC1373622_F4_4574.jpg | What is being portrayed in this visual content? | CT26 cell morphology during the course of FasL analysis. Cell lines were seeded at ~2 × 105 cells/ml in 6 well plates to achieve 20% confluency 18 hours later. This point was defined as 0 hr. After 72 hrs, cells had reached ~80–90% confluency. |
PMC1373622_F4_4570.jpg | What key item or scene is captured in this photo? | CT26 cell morphology during the course of FasL analysis. Cell lines were seeded at ~2 × 105 cells/ml in 6 well plates to achieve 20% confluency 18 hours later. This point was defined as 0 hr. After 72 hrs, cells had reached ~80–90% confluency. |
PMC1373622_F4_4571.jpg | What stands out most in this visual? | CT26 cell morphology during the course of FasL analysis. Cell lines were seeded at ~2 × 105 cells/ml in 6 well plates to achieve 20% confluency 18 hours later. This point was defined as 0 hr. After 72 hrs, cells had reached ~80–90% confluency. |
PMC1373622_F4_4573.jpg | What object or scene is depicted here? | CT26 cell morphology during the course of FasL analysis. Cell lines were seeded at ~2 × 105 cells/ml in 6 well plates to achieve 20% confluency 18 hours later. This point was defined as 0 hr. After 72 hrs, cells had reached ~80–90% confluency. |
PMC1373625_F4_4581.jpg | What is the principal component of this image? | Photomicrographs of histological findings in the animal lungs at 48 h of endotoxin exposure corresponding to 24 h of different gas exposure in control (C) and lipopolysaccharides (LPS)-treated rats. Definition of the subgroups see Fig. 1 legends. All the lungs were fixed by pulmonary arterial perfusion at deflation pressure of 10 cm H2O for 30 min. Definition and characteristics of subset figures: A, C-Air, well aerated alveoli; B C-ONO, nearly normal alveolar structure alternative with over expanded alveoli; C, C-O, mild atelectatic alveoli; D, C-NO, nearly normal alveolar structure alternative with over expanded alveoli; E, LPS-Air, severe inflammation and edema; F LPS-ONO, severe inflammation and collapsed alternative with over expanded alveoli; G, LPS-O, very severe inflammation and collapse of alveoli; H, LPS-NO, mild collapse of alveoli. Hematoxylin and eosin staining; original magnification ×100. |
PMC1373625_F4_4580.jpg | What is the dominant medical problem in this image? | Photomicrographs of histological findings in the animal lungs at 48 h of endotoxin exposure corresponding to 24 h of different gas exposure in control (C) and lipopolysaccharides (LPS)-treated rats. Definition of the subgroups see Fig. 1 legends. All the lungs were fixed by pulmonary arterial perfusion at deflation pressure of 10 cm H2O for 30 min. Definition and characteristics of subset figures: A, C-Air, well aerated alveoli; B C-ONO, nearly normal alveolar structure alternative with over expanded alveoli; C, C-O, mild atelectatic alveoli; D, C-NO, nearly normal alveolar structure alternative with over expanded alveoli; E, LPS-Air, severe inflammation and edema; F LPS-ONO, severe inflammation and collapsed alternative with over expanded alveoli; G, LPS-O, very severe inflammation and collapse of alveoli; H, LPS-NO, mild collapse of alveoli. Hematoxylin and eosin staining; original magnification ×100. |
PMC1373625_F4_4575.jpg | Can you identify the primary element in this image? | Photomicrographs of histological findings in the animal lungs at 48 h of endotoxin exposure corresponding to 24 h of different gas exposure in control (C) and lipopolysaccharides (LPS)-treated rats. Definition of the subgroups see Fig. 1 legends. All the lungs were fixed by pulmonary arterial perfusion at deflation pressure of 10 cm H2O for 30 min. Definition and characteristics of subset figures: A, C-Air, well aerated alveoli; B C-ONO, nearly normal alveolar structure alternative with over expanded alveoli; C, C-O, mild atelectatic alveoli; D, C-NO, nearly normal alveolar structure alternative with over expanded alveoli; E, LPS-Air, severe inflammation and edema; F LPS-ONO, severe inflammation and collapsed alternative with over expanded alveoli; G, LPS-O, very severe inflammation and collapse of alveoli; H, LPS-NO, mild collapse of alveoli. Hematoxylin and eosin staining; original magnification ×100. |
PMC1373625_F4_4579.jpg | Can you identify the primary element in this image? | Photomicrographs of histological findings in the animal lungs at 48 h of endotoxin exposure corresponding to 24 h of different gas exposure in control (C) and lipopolysaccharides (LPS)-treated rats. Definition of the subgroups see Fig. 1 legends. All the lungs were fixed by pulmonary arterial perfusion at deflation pressure of 10 cm H2O for 30 min. Definition and characteristics of subset figures: A, C-Air, well aerated alveoli; B C-ONO, nearly normal alveolar structure alternative with over expanded alveoli; C, C-O, mild atelectatic alveoli; D, C-NO, nearly normal alveolar structure alternative with over expanded alveoli; E, LPS-Air, severe inflammation and edema; F LPS-ONO, severe inflammation and collapsed alternative with over expanded alveoli; G, LPS-O, very severe inflammation and collapse of alveoli; H, LPS-NO, mild collapse of alveoli. Hematoxylin and eosin staining; original magnification ×100. |
PMC1373625_F4_4576.jpg | What can you see in this picture? | Photomicrographs of histological findings in the animal lungs at 48 h of endotoxin exposure corresponding to 24 h of different gas exposure in control (C) and lipopolysaccharides (LPS)-treated rats. Definition of the subgroups see Fig. 1 legends. All the lungs were fixed by pulmonary arterial perfusion at deflation pressure of 10 cm H2O for 30 min. Definition and characteristics of subset figures: A, C-Air, well aerated alveoli; B C-ONO, nearly normal alveolar structure alternative with over expanded alveoli; C, C-O, mild atelectatic alveoli; D, C-NO, nearly normal alveolar structure alternative with over expanded alveoli; E, LPS-Air, severe inflammation and edema; F LPS-ONO, severe inflammation and collapsed alternative with over expanded alveoli; G, LPS-O, very severe inflammation and collapse of alveoli; H, LPS-NO, mild collapse of alveoli. Hematoxylin and eosin staining; original magnification ×100. |
PMC1373625_F4_4577.jpg | What can you see in this picture? | Photomicrographs of histological findings in the animal lungs at 48 h of endotoxin exposure corresponding to 24 h of different gas exposure in control (C) and lipopolysaccharides (LPS)-treated rats. Definition of the subgroups see Fig. 1 legends. All the lungs were fixed by pulmonary arterial perfusion at deflation pressure of 10 cm H2O for 30 min. Definition and characteristics of subset figures: A, C-Air, well aerated alveoli; B C-ONO, nearly normal alveolar structure alternative with over expanded alveoli; C, C-O, mild atelectatic alveoli; D, C-NO, nearly normal alveolar structure alternative with over expanded alveoli; E, LPS-Air, severe inflammation and edema; F LPS-ONO, severe inflammation and collapsed alternative with over expanded alveoli; G, LPS-O, very severe inflammation and collapse of alveoli; H, LPS-NO, mild collapse of alveoli. Hematoxylin and eosin staining; original magnification ×100. |
PMC1373634_F2_4583.jpg | What stands out most in this visual? | PUC cells selected for stem cell-like morphology. The initial population of cells (passage zero, or P0; A) expanded from explants contain many different cell types based on morphology. After one passage (P1) using the described selection technique, the number of round and fibroblast-like cells was significantly increased (B) and was further enhanced after passage 2 (C). Bar = 200 μM. |
PMC1373634_F2_4582.jpg | Can you identify the primary element in this image? | PUC cells selected for stem cell-like morphology. The initial population of cells (passage zero, or P0; A) expanded from explants contain many different cell types based on morphology. After one passage (P1) using the described selection technique, the number of round and fibroblast-like cells was significantly increased (B) and was further enhanced after passage 2 (C). Bar = 200 μM. |
PMC1373642_F1_4586.jpg | What is the main focus of this visual representation? | Activation Maps for fMRI task. Statistical parametric maps of the single-group analyses for ε3/3 homozygotes (panel A) and ε3/4 heterozygotes (panel B), and for regions where the ε3/3 homozygotes activated to a greater extent than the ε3/4 heterozygotes (panel C). The left side of each coronal section represents the left hemisphere. The dark-shaded area represents the MTL region to which the statistical analyses were confined. The lighter-shaded areasrepresent regions outside of the MTL mask. |
PMC1373647_F2_4587.jpg | What's the most prominent thing you notice in this picture? | Anteroposterior digital subtraction arteriography shows a severe right renal artery stenosis. |
PMC1373660_F1_4589.jpg | What key item or scene is captured in this photo? | Computed tomographic scan showing a low-density mass measuring 8 × 7 cm that has destroyed part of the cortical bone of the sternum. |
PMC1373660_F1_4588.jpg | What object or scene is depicted here? | Computed tomographic scan showing a low-density mass measuring 8 × 7 cm that has destroyed part of the cortical bone of the sternum. |
PMC1373662_F1_4592.jpg | What stands out most in this visual? | a) Plain x-ray KUB showing a large left staghorn calculus. b) Intravenous urogram showing non-visualized left kidney & normally functioning right kidney. |
PMC1373662_F1_4591.jpg | What's the most prominent thing you notice in this picture? | a) Plain x-ray KUB showing a large left staghorn calculus. b) Intravenous urogram showing non-visualized left kidney & normally functioning right kidney. |
PMC1373662_F2_4593.jpg | What object or scene is depicted here? | a) Plain x-ray KUB revealing a large right staghorn calculus extending in the upper ureter. b) Intravenous urography showing non-visualized right kidney with normally functioning left kidney. |
PMC1373662_F2_4594.jpg | What is the main focus of this visual representation? | a) Plain x-ray KUB revealing a large right staghorn calculus extending in the upper ureter. b) Intravenous urography showing non-visualized right kidney with normally functioning left kidney. |
PMC1382015_pbio-0040069-g003_4601.jpg | What can you see in this picture? | Common Activation for the Illusory-Rabbit and the Veridical-Rabbit versus Control Conditions Embedded in the Localizer Results for Skin-Sites P1, P2, and P3The brain images (A, B, C) again show the common activation (random-effects group analysis) for the veridical-rabbit and illusory-rabbit conditions in orange (peak at X = 36, Y = −32, Z = 66), now projected onto the differential contrasts for the localizer conditions (P1 versus P2 and P3 in bright gray, P2 versus P1 and P3 in intermediate gray, P3 versus P1 and P2 in dark gray) within BAs 3a, 3b, 1, and 2, as defined by the cytoarchitectonic atlas [11]. The differential activations for P1, P2, and P3 show the expected medial-to-lateral ordering for the different forearm positions (B and C). Although there is some spread in these localizer activations (as expected for smoothed fMRI data across a group, but see alsoFigure 4), note that the critical experimental activation for the two rabbit conditions (shown in orange here) clearly falls quite centrally within the localizer activation that corresponds to P2 (see B and C). Moreover, (D) plots the parameter estimates (SPM beta-values and standard errors in red) extracted from the region that was experimentally activated by the rabbit (orange), showing these for each of the separate group-localizer conditions. Note the stronger response to P2 than P3 or P1 here, as shown by the vast majority of individuals (9/10 and 8/10 respectively, see main text). |
PMC1382015_pbio-0040069-g003_4599.jpg | What can you see in this picture? | Common Activation for the Illusory-Rabbit and the Veridical-Rabbit versus Control Conditions Embedded in the Localizer Results for Skin-Sites P1, P2, and P3The brain images (A, B, C) again show the common activation (random-effects group analysis) for the veridical-rabbit and illusory-rabbit conditions in orange (peak at X = 36, Y = −32, Z = 66), now projected onto the differential contrasts for the localizer conditions (P1 versus P2 and P3 in bright gray, P2 versus P1 and P3 in intermediate gray, P3 versus P1 and P2 in dark gray) within BAs 3a, 3b, 1, and 2, as defined by the cytoarchitectonic atlas [11]. The differential activations for P1, P2, and P3 show the expected medial-to-lateral ordering for the different forearm positions (B and C). Although there is some spread in these localizer activations (as expected for smoothed fMRI data across a group, but see alsoFigure 4), note that the critical experimental activation for the two rabbit conditions (shown in orange here) clearly falls quite centrally within the localizer activation that corresponds to P2 (see B and C). Moreover, (D) plots the parameter estimates (SPM beta-values and standard errors in red) extracted from the region that was experimentally activated by the rabbit (orange), showing these for each of the separate group-localizer conditions. Note the stronger response to P2 than P3 or P1 here, as shown by the vast majority of individuals (9/10 and 8/10 respectively, see main text). |
PMC1382015_pbio-0040069-g004_4596.jpg | What is the main focus of this visual representation? | Common Activation for the Illusory-Rabbit and the Veridical-Rabbit versus Control Conditions with Less Spatial SmoothingThe brain images (A, B) show the common activation for the veridical-rabbit and illusory-rabbit in yellow (p < 0.001, uncorrected), from a group analysis using a considerably reduced smoothing kernel (4-mm FWHM). Note that the activation elicited by both the illusory- and veridical-rabbit (relative to the control) conditions is in virtually the identical location within SI (peak at X = 38, Y = −32, Z = 68) as before (seeFigure 3), and at the same threshold. Panel C shows the outcome of single-participant ROI analysis of the mean parameter estimates (SPM beta-values, from the analysis with 4-mm FWHM smoothing), extracted separately for each individual from the participant-specific locations within SI responding maximally to stimulation at P1, P2, or P3 (relative to the other two skin sites from these three) during the individual localizer sessions. The bars show the signal change during illusory- (left bar in each pair) and veridical- (right bar in each pair) rabbit, relative to the control conditions (standard errors indicated in red), for the individually defined cortical ROIs activated by P1, P2, or P3 stimulation (see above). This individual analysis thus confirms that both rabbit conditions led to significant activity increases (relative to control) only within the individual participant-specific cortical representations of P2, but not of P1 or P3. Thus, the rabbit-related activations corresponded to the skin location where stimulation was illusorily felt in the critical rabbit condition. |
PMC1382015_pbio-0040069-g004_4595.jpg | What is the core subject represented in this visual? | Common Activation for the Illusory-Rabbit and the Veridical-Rabbit versus Control Conditions with Less Spatial SmoothingThe brain images (A, B) show the common activation for the veridical-rabbit and illusory-rabbit in yellow (p < 0.001, uncorrected), from a group analysis using a considerably reduced smoothing kernel (4-mm FWHM). Note that the activation elicited by both the illusory- and veridical-rabbit (relative to the control) conditions is in virtually the identical location within SI (peak at X = 38, Y = −32, Z = 68) as before (seeFigure 3), and at the same threshold. Panel C shows the outcome of single-participant ROI analysis of the mean parameter estimates (SPM beta-values, from the analysis with 4-mm FWHM smoothing), extracted separately for each individual from the participant-specific locations within SI responding maximally to stimulation at P1, P2, or P3 (relative to the other two skin sites from these three) during the individual localizer sessions. The bars show the signal change during illusory- (left bar in each pair) and veridical- (right bar in each pair) rabbit, relative to the control conditions (standard errors indicated in red), for the individually defined cortical ROIs activated by P1, P2, or P3 stimulation (see above). This individual analysis thus confirms that both rabbit conditions led to significant activity increases (relative to control) only within the individual participant-specific cortical representations of P2, but not of P1 or P3. Thus, the rabbit-related activations corresponded to the skin location where stimulation was illusorily felt in the critical rabbit condition. |
PMC1382020_pbio-0040067-g001_4605.jpg | What's the most prominent thing you notice in this picture? | Severe Reorganization of Chromatin Territories in Rod Photoreceptors from SCA7 Mice(A) Ultrastructure of rod nuclei in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a) and two distinct R7E (panels b and c) animals are shown. In R7N mice, rod nuclei are characterized by a large territory of centrally located heterochromatin. In R7E mice, rod nuclei were bigger and rounder, and displayed much more euchromatin, which appears lightly stained by electrons. Arrows indicate pale grey structures likely resulting from aggregation of mutant ATXN7 in rods from R7E mice. Scale bar represents 1 μm.(B) Ultrastructure of photoreceptor nuclei during disease progression in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a), 2-mo-old R7E (panel b), and 2-y-old R7E (panel c) animals are shown. This time-course analysis revealed that alterations of rod nuclear architecture progressively worsened as retinopathy progressed in R7E mice. Cone photoreceptor nuclei (c), which are found in the outermost part of the ONL adjacent to inner segments (is), present a different architecture with several heterochromatin clumps surrounded by more euchromatin. As evidenced in panel c, rod nuclei in R7E mice look highly similar to cone nuclei. Scale bar represents 5 μm.(C) Ultrastructure of photoreceptor nuclei in SCA7 knock-in mice. Electron microsocopy micrographs from 3-mo-old WT (panels a and d) and two distinct age-matched SCA7266Q/5Q (panels b, c, e, and f) animals are shown. Morphological appearance of the central densely stained heterochromatin territory is altered in mutant mice. At higher magnification (lower panels [e–f]), rod nuclei from heterozygous knock-in animals are slightly larger and contain more euchromatin than nuclei from control mice. Cone nuclei (c) and photoreceptor inner segments (is) are depicted. Scale bars represent 2 μm in upper panels (a–c) and 0.5 μm in lower panels (e–f). |
PMC1382020_pbio-0040067-g001_4612.jpg | What is the principal component of this image? | Severe Reorganization of Chromatin Territories in Rod Photoreceptors from SCA7 Mice(A) Ultrastructure of rod nuclei in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a) and two distinct R7E (panels b and c) animals are shown. In R7N mice, rod nuclei are characterized by a large territory of centrally located heterochromatin. In R7E mice, rod nuclei were bigger and rounder, and displayed much more euchromatin, which appears lightly stained by electrons. Arrows indicate pale grey structures likely resulting from aggregation of mutant ATXN7 in rods from R7E mice. Scale bar represents 1 μm.(B) Ultrastructure of photoreceptor nuclei during disease progression in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a), 2-mo-old R7E (panel b), and 2-y-old R7E (panel c) animals are shown. This time-course analysis revealed that alterations of rod nuclear architecture progressively worsened as retinopathy progressed in R7E mice. Cone photoreceptor nuclei (c), which are found in the outermost part of the ONL adjacent to inner segments (is), present a different architecture with several heterochromatin clumps surrounded by more euchromatin. As evidenced in panel c, rod nuclei in R7E mice look highly similar to cone nuclei. Scale bar represents 5 μm.(C) Ultrastructure of photoreceptor nuclei in SCA7 knock-in mice. Electron microsocopy micrographs from 3-mo-old WT (panels a and d) and two distinct age-matched SCA7266Q/5Q (panels b, c, e, and f) animals are shown. Morphological appearance of the central densely stained heterochromatin territory is altered in mutant mice. At higher magnification (lower panels [e–f]), rod nuclei from heterozygous knock-in animals are slightly larger and contain more euchromatin than nuclei from control mice. Cone nuclei (c) and photoreceptor inner segments (is) are depicted. Scale bars represent 2 μm in upper panels (a–c) and 0.5 μm in lower panels (e–f). |
PMC1382020_pbio-0040067-g001_4610.jpg | What is the focal point of this photograph? | Severe Reorganization of Chromatin Territories in Rod Photoreceptors from SCA7 Mice(A) Ultrastructure of rod nuclei in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a) and two distinct R7E (panels b and c) animals are shown. In R7N mice, rod nuclei are characterized by a large territory of centrally located heterochromatin. In R7E mice, rod nuclei were bigger and rounder, and displayed much more euchromatin, which appears lightly stained by electrons. Arrows indicate pale grey structures likely resulting from aggregation of mutant ATXN7 in rods from R7E mice. Scale bar represents 1 μm.(B) Ultrastructure of photoreceptor nuclei during disease progression in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a), 2-mo-old R7E (panel b), and 2-y-old R7E (panel c) animals are shown. This time-course analysis revealed that alterations of rod nuclear architecture progressively worsened as retinopathy progressed in R7E mice. Cone photoreceptor nuclei (c), which are found in the outermost part of the ONL adjacent to inner segments (is), present a different architecture with several heterochromatin clumps surrounded by more euchromatin. As evidenced in panel c, rod nuclei in R7E mice look highly similar to cone nuclei. Scale bar represents 5 μm.(C) Ultrastructure of photoreceptor nuclei in SCA7 knock-in mice. Electron microsocopy micrographs from 3-mo-old WT (panels a and d) and two distinct age-matched SCA7266Q/5Q (panels b, c, e, and f) animals are shown. Morphological appearance of the central densely stained heterochromatin territory is altered in mutant mice. At higher magnification (lower panels [e–f]), rod nuclei from heterozygous knock-in animals are slightly larger and contain more euchromatin than nuclei from control mice. Cone nuclei (c) and photoreceptor inner segments (is) are depicted. Scale bars represent 2 μm in upper panels (a–c) and 0.5 μm in lower panels (e–f). |
PMC1382020_pbio-0040067-g001_4603.jpg | What is the central feature of this picture? | Severe Reorganization of Chromatin Territories in Rod Photoreceptors from SCA7 Mice(A) Ultrastructure of rod nuclei in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a) and two distinct R7E (panels b and c) animals are shown. In R7N mice, rod nuclei are characterized by a large territory of centrally located heterochromatin. In R7E mice, rod nuclei were bigger and rounder, and displayed much more euchromatin, which appears lightly stained by electrons. Arrows indicate pale grey structures likely resulting from aggregation of mutant ATXN7 in rods from R7E mice. Scale bar represents 1 μm.(B) Ultrastructure of photoreceptor nuclei during disease progression in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a), 2-mo-old R7E (panel b), and 2-y-old R7E (panel c) animals are shown. This time-course analysis revealed that alterations of rod nuclear architecture progressively worsened as retinopathy progressed in R7E mice. Cone photoreceptor nuclei (c), which are found in the outermost part of the ONL adjacent to inner segments (is), present a different architecture with several heterochromatin clumps surrounded by more euchromatin. As evidenced in panel c, rod nuclei in R7E mice look highly similar to cone nuclei. Scale bar represents 5 μm.(C) Ultrastructure of photoreceptor nuclei in SCA7 knock-in mice. Electron microsocopy micrographs from 3-mo-old WT (panels a and d) and two distinct age-matched SCA7266Q/5Q (panels b, c, e, and f) animals are shown. Morphological appearance of the central densely stained heterochromatin territory is altered in mutant mice. At higher magnification (lower panels [e–f]), rod nuclei from heterozygous knock-in animals are slightly larger and contain more euchromatin than nuclei from control mice. Cone nuclei (c) and photoreceptor inner segments (is) are depicted. Scale bars represent 2 μm in upper panels (a–c) and 0.5 μm in lower panels (e–f). |
PMC1382020_pbio-0040067-g001_4613.jpg | What key item or scene is captured in this photo? | Severe Reorganization of Chromatin Territories in Rod Photoreceptors from SCA7 Mice(A) Ultrastructure of rod nuclei in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a) and two distinct R7E (panels b and c) animals are shown. In R7N mice, rod nuclei are characterized by a large territory of centrally located heterochromatin. In R7E mice, rod nuclei were bigger and rounder, and displayed much more euchromatin, which appears lightly stained by electrons. Arrows indicate pale grey structures likely resulting from aggregation of mutant ATXN7 in rods from R7E mice. Scale bar represents 1 μm.(B) Ultrastructure of photoreceptor nuclei during disease progression in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a), 2-mo-old R7E (panel b), and 2-y-old R7E (panel c) animals are shown. This time-course analysis revealed that alterations of rod nuclear architecture progressively worsened as retinopathy progressed in R7E mice. Cone photoreceptor nuclei (c), which are found in the outermost part of the ONL adjacent to inner segments (is), present a different architecture with several heterochromatin clumps surrounded by more euchromatin. As evidenced in panel c, rod nuclei in R7E mice look highly similar to cone nuclei. Scale bar represents 5 μm.(C) Ultrastructure of photoreceptor nuclei in SCA7 knock-in mice. Electron microsocopy micrographs from 3-mo-old WT (panels a and d) and two distinct age-matched SCA7266Q/5Q (panels b, c, e, and f) animals are shown. Morphological appearance of the central densely stained heterochromatin territory is altered in mutant mice. At higher magnification (lower panels [e–f]), rod nuclei from heterozygous knock-in animals are slightly larger and contain more euchromatin than nuclei from control mice. Cone nuclei (c) and photoreceptor inner segments (is) are depicted. Scale bars represent 2 μm in upper panels (a–c) and 0.5 μm in lower panels (e–f). |
PMC1382020_pbio-0040067-g001_4607.jpg | What can you see in this picture? | Severe Reorganization of Chromatin Territories in Rod Photoreceptors from SCA7 Mice(A) Ultrastructure of rod nuclei in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a) and two distinct R7E (panels b and c) animals are shown. In R7N mice, rod nuclei are characterized by a large territory of centrally located heterochromatin. In R7E mice, rod nuclei were bigger and rounder, and displayed much more euchromatin, which appears lightly stained by electrons. Arrows indicate pale grey structures likely resulting from aggregation of mutant ATXN7 in rods from R7E mice. Scale bar represents 1 μm.(B) Ultrastructure of photoreceptor nuclei during disease progression in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a), 2-mo-old R7E (panel b), and 2-y-old R7E (panel c) animals are shown. This time-course analysis revealed that alterations of rod nuclear architecture progressively worsened as retinopathy progressed in R7E mice. Cone photoreceptor nuclei (c), which are found in the outermost part of the ONL adjacent to inner segments (is), present a different architecture with several heterochromatin clumps surrounded by more euchromatin. As evidenced in panel c, rod nuclei in R7E mice look highly similar to cone nuclei. Scale bar represents 5 μm.(C) Ultrastructure of photoreceptor nuclei in SCA7 knock-in mice. Electron microsocopy micrographs from 3-mo-old WT (panels a and d) and two distinct age-matched SCA7266Q/5Q (panels b, c, e, and f) animals are shown. Morphological appearance of the central densely stained heterochromatin territory is altered in mutant mice. At higher magnification (lower panels [e–f]), rod nuclei from heterozygous knock-in animals are slightly larger and contain more euchromatin than nuclei from control mice. Cone nuclei (c) and photoreceptor inner segments (is) are depicted. Scale bars represent 2 μm in upper panels (a–c) and 0.5 μm in lower panels (e–f). |
PMC1382020_pbio-0040067-g001_4602.jpg | What is the focal point of this photograph? | Severe Reorganization of Chromatin Territories in Rod Photoreceptors from SCA7 Mice(A) Ultrastructure of rod nuclei in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a) and two distinct R7E (panels b and c) animals are shown. In R7N mice, rod nuclei are characterized by a large territory of centrally located heterochromatin. In R7E mice, rod nuclei were bigger and rounder, and displayed much more euchromatin, which appears lightly stained by electrons. Arrows indicate pale grey structures likely resulting from aggregation of mutant ATXN7 in rods from R7E mice. Scale bar represents 1 μm.(B) Ultrastructure of photoreceptor nuclei during disease progression in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a), 2-mo-old R7E (panel b), and 2-y-old R7E (panel c) animals are shown. This time-course analysis revealed that alterations of rod nuclear architecture progressively worsened as retinopathy progressed in R7E mice. Cone photoreceptor nuclei (c), which are found in the outermost part of the ONL adjacent to inner segments (is), present a different architecture with several heterochromatin clumps surrounded by more euchromatin. As evidenced in panel c, rod nuclei in R7E mice look highly similar to cone nuclei. Scale bar represents 5 μm.(C) Ultrastructure of photoreceptor nuclei in SCA7 knock-in mice. Electron microsocopy micrographs from 3-mo-old WT (panels a and d) and two distinct age-matched SCA7266Q/5Q (panels b, c, e, and f) animals are shown. Morphological appearance of the central densely stained heterochromatin territory is altered in mutant mice. At higher magnification (lower panels [e–f]), rod nuclei from heterozygous knock-in animals are slightly larger and contain more euchromatin than nuclei from control mice. Cone nuclei (c) and photoreceptor inner segments (is) are depicted. Scale bars represent 2 μm in upper panels (a–c) and 0.5 μm in lower panels (e–f). |
PMC1382020_pbio-0040067-g001_4608.jpg | What can you see in this picture? | Severe Reorganization of Chromatin Territories in Rod Photoreceptors from SCA7 Mice(A) Ultrastructure of rod nuclei in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a) and two distinct R7E (panels b and c) animals are shown. In R7N mice, rod nuclei are characterized by a large territory of centrally located heterochromatin. In R7E mice, rod nuclei were bigger and rounder, and displayed much more euchromatin, which appears lightly stained by electrons. Arrows indicate pale grey structures likely resulting from aggregation of mutant ATXN7 in rods from R7E mice. Scale bar represents 1 μm.(B) Ultrastructure of photoreceptor nuclei during disease progression in R7E mice. Electron microscopy micrographs from 2-y-old R7N (panel a), 2-mo-old R7E (panel b), and 2-y-old R7E (panel c) animals are shown. This time-course analysis revealed that alterations of rod nuclear architecture progressively worsened as retinopathy progressed in R7E mice. Cone photoreceptor nuclei (c), which are found in the outermost part of the ONL adjacent to inner segments (is), present a different architecture with several heterochromatin clumps surrounded by more euchromatin. As evidenced in panel c, rod nuclei in R7E mice look highly similar to cone nuclei. Scale bar represents 5 μm.(C) Ultrastructure of photoreceptor nuclei in SCA7 knock-in mice. Electron microsocopy micrographs from 3-mo-old WT (panels a and d) and two distinct age-matched SCA7266Q/5Q (panels b, c, e, and f) animals are shown. Morphological appearance of the central densely stained heterochromatin territory is altered in mutant mice. At higher magnification (lower panels [e–f]), rod nuclei from heterozygous knock-in animals are slightly larger and contain more euchromatin than nuclei from control mice. Cone nuclei (c) and photoreceptor inner segments (is) are depicted. Scale bars represent 2 μm in upper panels (a–c) and 0.5 μm in lower panels (e–f). |
PMC1382229_F2_4614.jpg | What object or scene is depicted here? | Immunohistochemical staining of primary Merkel cell carcinoma for differential diagnosis and neuroendocrine differentiation. A. Hematoxylin-eosin staining, the tumour cells have round nuclei, original magnification 200×. B. Positive cytokeratin-20 staining, showing typical punctate pattern of immunostaining, original magnification 400×. C. Negative staining for Thyroid-transcriptor factor-1, original magnification 400×. D. chromogranin -A staining, original magnification 400× and E. synaptophysin staining, original magnification 400×. |
PMC1382278_F1_4615.jpg | Describe the main subject of this image. | Parasternal long axis two-dimensional echocardiographic view showing dilated coronary sinus. (LA = left atrium, LV = left ventricle, CS = coronary sinus). |
PMC1382278_F4_4618.jpg | What does this image primarily show? | Transesophageal echocardiography in right atrial long axis two-dimensional echocardiographic view demonstrates absence of right vena cava superior (black star) (LA = left atrium, RA= right atrium). |
PMC1382278_F5_4620.jpg | What can you see in this picture? | Upper venous digital subtraction cavography which indicates absence of the right superior vena cava and a persistent left superior vena cava (PLSVC) in the left lateral part of the thorax (white arrow). |
PMC1383487_ppat-0020012-g003_4626.jpg | Describe the main subject of this image. | Regional Distribution of Protease-Resistant PrPSc in Voles following Transmission of sCJD and gCJDPET blots of coronal sections of the forebrain (telencephalon in [A] and diencephalon in [B]), midbrain (C), and hindbrain (D) in voles infected with MM2 sCJD, MM1 sCJD, MV1 sCJD, V210I gCJD, and E200K gCJD. At the lower part of the figure, the labeled coronal sections of a negative control brain are shown. NC, neocortex; Sp, septum; St, striatum; Hp, hippocampus; Th, thalamus; Hy, hypothalamus; SC, superior colliculus; GN, geniculate nuclei; SN, substantia nigra; Cb, cerebellum; MO, medulla oblongata. |
PMC1383487_ppat-0020012-g003_4621.jpg | What is the core subject represented in this visual? | Regional Distribution of Protease-Resistant PrPSc in Voles following Transmission of sCJD and gCJDPET blots of coronal sections of the forebrain (telencephalon in [A] and diencephalon in [B]), midbrain (C), and hindbrain (D) in voles infected with MM2 sCJD, MM1 sCJD, MV1 sCJD, V210I gCJD, and E200K gCJD. At the lower part of the figure, the labeled coronal sections of a negative control brain are shown. NC, neocortex; Sp, septum; St, striatum; Hp, hippocampus; Th, thalamus; Hy, hypothalamus; SC, superior colliculus; GN, geniculate nuclei; SN, substantia nigra; Cb, cerebellum; MO, medulla oblongata. |
PMC1383487_ppat-0020012-g003_4624.jpg | What is being portrayed in this visual content? | Regional Distribution of Protease-Resistant PrPSc in Voles following Transmission of sCJD and gCJDPET blots of coronal sections of the forebrain (telencephalon in [A] and diencephalon in [B]), midbrain (C), and hindbrain (D) in voles infected with MM2 sCJD, MM1 sCJD, MV1 sCJD, V210I gCJD, and E200K gCJD. At the lower part of the figure, the labeled coronal sections of a negative control brain are shown. NC, neocortex; Sp, septum; St, striatum; Hp, hippocampus; Th, thalamus; Hy, hypothalamus; SC, superior colliculus; GN, geniculate nuclei; SN, substantia nigra; Cb, cerebellum; MO, medulla oblongata. |
PMC1383487_ppat-0020012-g003_4623.jpg | What is the principal component of this image? | Regional Distribution of Protease-Resistant PrPSc in Voles following Transmission of sCJD and gCJDPET blots of coronal sections of the forebrain (telencephalon in [A] and diencephalon in [B]), midbrain (C), and hindbrain (D) in voles infected with MM2 sCJD, MM1 sCJD, MV1 sCJD, V210I gCJD, and E200K gCJD. At the lower part of the figure, the labeled coronal sections of a negative control brain are shown. NC, neocortex; Sp, septum; St, striatum; Hp, hippocampus; Th, thalamus; Hy, hypothalamus; SC, superior colliculus; GN, geniculate nuclei; SN, substantia nigra; Cb, cerebellum; MO, medulla oblongata. |
PMC1383488_ppat-0020013-g004_4630.jpg | What is the dominant medical problem in this image? | Localization of T. gondii IMC4, TgCAM1, and TgCAM2(A) LM localization of a T. gondii protein (TgIMC4) with weak similarity to articulin family members, and weaker similarity to TgIMC1. Fluorescence LM images of living transgenic parasites expressing TgIMC4 fused to the C-terminus of EGFP. Fluorescence is observed on both the mother and daughter IMC. FRAP reveals significant differences in the turnover of TgIMC1 and TgIMC4 (unpublished data).(B and C) Fluorescence LM images of living transgenic parasites expressing GFP-CAM1 (B) and GFP-CAM2 (C). Bright fluorescence is observed in the conoid region of both mother and daughters (arrows).(D and E) EM images of T. gondii cytoskeletons from the same two lines of transgenic parasites as in (B) and (C [immunogold-labeled with anti-GFP antibody and negatively stained with phosphotungstic acid]). Specific staining occurs over the conoid itself, and lightly over the subpellicular MTs. In (D), diagonal lines of gold particles are visible, tracing the conoid fibers. |
PMC1383488_ppat-0020013-g004_4629.jpg | What is the principal component of this image? | Localization of T. gondii IMC4, TgCAM1, and TgCAM2(A) LM localization of a T. gondii protein (TgIMC4) with weak similarity to articulin family members, and weaker similarity to TgIMC1. Fluorescence LM images of living transgenic parasites expressing TgIMC4 fused to the C-terminus of EGFP. Fluorescence is observed on both the mother and daughter IMC. FRAP reveals significant differences in the turnover of TgIMC1 and TgIMC4 (unpublished data).(B and C) Fluorescence LM images of living transgenic parasites expressing GFP-CAM1 (B) and GFP-CAM2 (C). Bright fluorescence is observed in the conoid region of both mother and daughters (arrows).(D and E) EM images of T. gondii cytoskeletons from the same two lines of transgenic parasites as in (B) and (C [immunogold-labeled with anti-GFP antibody and negatively stained with phosphotungstic acid]). Specific staining occurs over the conoid itself, and lightly over the subpellicular MTs. In (D), diagonal lines of gold particles are visible, tracing the conoid fibers. |
PMC1383488_ppat-0020013-g004_4632.jpg | What can you see in this picture? | Localization of T. gondii IMC4, TgCAM1, and TgCAM2(A) LM localization of a T. gondii protein (TgIMC4) with weak similarity to articulin family members, and weaker similarity to TgIMC1. Fluorescence LM images of living transgenic parasites expressing TgIMC4 fused to the C-terminus of EGFP. Fluorescence is observed on both the mother and daughter IMC. FRAP reveals significant differences in the turnover of TgIMC1 and TgIMC4 (unpublished data).(B and C) Fluorescence LM images of living transgenic parasites expressing GFP-CAM1 (B) and GFP-CAM2 (C). Bright fluorescence is observed in the conoid region of both mother and daughters (arrows).(D and E) EM images of T. gondii cytoskeletons from the same two lines of transgenic parasites as in (B) and (C [immunogold-labeled with anti-GFP antibody and negatively stained with phosphotungstic acid]). Specific staining occurs over the conoid itself, and lightly over the subpellicular MTs. In (D), diagonal lines of gold particles are visible, tracing the conoid fibers. |
PMC1383488_ppat-0020013-g004_4628.jpg | What key item or scene is captured in this photo? | Localization of T. gondii IMC4, TgCAM1, and TgCAM2(A) LM localization of a T. gondii protein (TgIMC4) with weak similarity to articulin family members, and weaker similarity to TgIMC1. Fluorescence LM images of living transgenic parasites expressing TgIMC4 fused to the C-terminus of EGFP. Fluorescence is observed on both the mother and daughter IMC. FRAP reveals significant differences in the turnover of TgIMC1 and TgIMC4 (unpublished data).(B and C) Fluorescence LM images of living transgenic parasites expressing GFP-CAM1 (B) and GFP-CAM2 (C). Bright fluorescence is observed in the conoid region of both mother and daughters (arrows).(D and E) EM images of T. gondii cytoskeletons from the same two lines of transgenic parasites as in (B) and (C [immunogold-labeled with anti-GFP antibody and negatively stained with phosphotungstic acid]). Specific staining occurs over the conoid itself, and lightly over the subpellicular MTs. In (D), diagonal lines of gold particles are visible, tracing the conoid fibers. |
PMC1383488_ppat-0020013-g004_4631.jpg | What is the main focus of this visual representation? | Localization of T. gondii IMC4, TgCAM1, and TgCAM2(A) LM localization of a T. gondii protein (TgIMC4) with weak similarity to articulin family members, and weaker similarity to TgIMC1. Fluorescence LM images of living transgenic parasites expressing TgIMC4 fused to the C-terminus of EGFP. Fluorescence is observed on both the mother and daughter IMC. FRAP reveals significant differences in the turnover of TgIMC1 and TgIMC4 (unpublished data).(B and C) Fluorescence LM images of living transgenic parasites expressing GFP-CAM1 (B) and GFP-CAM2 (C). Bright fluorescence is observed in the conoid region of both mother and daughters (arrows).(D and E) EM images of T. gondii cytoskeletons from the same two lines of transgenic parasites as in (B) and (C [immunogold-labeled with anti-GFP antibody and negatively stained with phosphotungstic acid]). Specific staining occurs over the conoid itself, and lightly over the subpellicular MTs. In (D), diagonal lines of gold particles are visible, tracing the conoid fibers. |
PMC1383488_ppat-0020013-g006_4641.jpg | What object or scene is depicted here? | LM Localization of a T. gondii MORN Domain Protein, TgMORN1(A–C) Single optical section of living transgenic parasites expressing YFP-α-tubulin (green) and mRFP-TgMORN1 (red). Bright red fluorescence is observed at the spindle poles (yellow arrows), near the ends of the growing IMC in developing daughters (pink arrowheads), and in a conical patch at the basal end of the mature parasite. Weaker fluorescence is observed in the region of the conoids of both mother and daughters (blue arrows). Note in (B), showing YFP-tubulin only, that two small green dots are seen in each daughter. The more apical dot is the centriole, the more basal dot (yellow arrow) is the spindle pole [7,9].(C) TgMORN1 accumulates at the basal dot (spindle pole, yellow arrow) but not the centriole.(D–F) Double transgenic parasites expressing IMC1-YFP (green) and mRFP-TgMORN1 (red).(D) Projection of a deconvolved 3D stack of images. MORN1 is clearly seen to form a ring around the basal end of the developing daughter scaffold.(E) Projection of a deconvolved 3D stack of images of an extracellular parasite, showing a cytoplasmic fiber of TgMORN1. No daughters are present. Same scale as (D).(F) Parasite culture treated with oryzalin for 24 h before imaging. A vacuole containing four grossly distorted parasites. IMC1 accumulates as large shells and smaller blobs. f′ & f′′: higher magnification views (rotated 90°) of IMC1 blobs from (F) revealing a core of TgMORN1. |
PMC1383488_ppat-0020013-g006_4642.jpg | What key item or scene is captured in this photo? | LM Localization of a T. gondii MORN Domain Protein, TgMORN1(A–C) Single optical section of living transgenic parasites expressing YFP-α-tubulin (green) and mRFP-TgMORN1 (red). Bright red fluorescence is observed at the spindle poles (yellow arrows), near the ends of the growing IMC in developing daughters (pink arrowheads), and in a conical patch at the basal end of the mature parasite. Weaker fluorescence is observed in the region of the conoids of both mother and daughters (blue arrows). Note in (B), showing YFP-tubulin only, that two small green dots are seen in each daughter. The more apical dot is the centriole, the more basal dot (yellow arrow) is the spindle pole [7,9].(C) TgMORN1 accumulates at the basal dot (spindle pole, yellow arrow) but not the centriole.(D–F) Double transgenic parasites expressing IMC1-YFP (green) and mRFP-TgMORN1 (red).(D) Projection of a deconvolved 3D stack of images. MORN1 is clearly seen to form a ring around the basal end of the developing daughter scaffold.(E) Projection of a deconvolved 3D stack of images of an extracellular parasite, showing a cytoplasmic fiber of TgMORN1. No daughters are present. Same scale as (D).(F) Parasite culture treated with oryzalin for 24 h before imaging. A vacuole containing four grossly distorted parasites. IMC1 accumulates as large shells and smaller blobs. f′ & f′′: higher magnification views (rotated 90°) of IMC1 blobs from (F) revealing a core of TgMORN1. |
PMC1383488_ppat-0020013-g006_4639.jpg | What is being portrayed in this visual content? | LM Localization of a T. gondii MORN Domain Protein, TgMORN1(A–C) Single optical section of living transgenic parasites expressing YFP-α-tubulin (green) and mRFP-TgMORN1 (red). Bright red fluorescence is observed at the spindle poles (yellow arrows), near the ends of the growing IMC in developing daughters (pink arrowheads), and in a conical patch at the basal end of the mature parasite. Weaker fluorescence is observed in the region of the conoids of both mother and daughters (blue arrows). Note in (B), showing YFP-tubulin only, that two small green dots are seen in each daughter. The more apical dot is the centriole, the more basal dot (yellow arrow) is the spindle pole [7,9].(C) TgMORN1 accumulates at the basal dot (spindle pole, yellow arrow) but not the centriole.(D–F) Double transgenic parasites expressing IMC1-YFP (green) and mRFP-TgMORN1 (red).(D) Projection of a deconvolved 3D stack of images. MORN1 is clearly seen to form a ring around the basal end of the developing daughter scaffold.(E) Projection of a deconvolved 3D stack of images of an extracellular parasite, showing a cytoplasmic fiber of TgMORN1. No daughters are present. Same scale as (D).(F) Parasite culture treated with oryzalin for 24 h before imaging. A vacuole containing four grossly distorted parasites. IMC1 accumulates as large shells and smaller blobs. f′ & f′′: higher magnification views (rotated 90°) of IMC1 blobs from (F) revealing a core of TgMORN1. |
PMC1383488_ppat-0020013-g006_4646.jpg | What object or scene is depicted here? | LM Localization of a T. gondii MORN Domain Protein, TgMORN1(A–C) Single optical section of living transgenic parasites expressing YFP-α-tubulin (green) and mRFP-TgMORN1 (red). Bright red fluorescence is observed at the spindle poles (yellow arrows), near the ends of the growing IMC in developing daughters (pink arrowheads), and in a conical patch at the basal end of the mature parasite. Weaker fluorescence is observed in the region of the conoids of both mother and daughters (blue arrows). Note in (B), showing YFP-tubulin only, that two small green dots are seen in each daughter. The more apical dot is the centriole, the more basal dot (yellow arrow) is the spindle pole [7,9].(C) TgMORN1 accumulates at the basal dot (spindle pole, yellow arrow) but not the centriole.(D–F) Double transgenic parasites expressing IMC1-YFP (green) and mRFP-TgMORN1 (red).(D) Projection of a deconvolved 3D stack of images. MORN1 is clearly seen to form a ring around the basal end of the developing daughter scaffold.(E) Projection of a deconvolved 3D stack of images of an extracellular parasite, showing a cytoplasmic fiber of TgMORN1. No daughters are present. Same scale as (D).(F) Parasite culture treated with oryzalin for 24 h before imaging. A vacuole containing four grossly distorted parasites. IMC1 accumulates as large shells and smaller blobs. f′ & f′′: higher magnification views (rotated 90°) of IMC1 blobs from (F) revealing a core of TgMORN1. |
PMC1383488_ppat-0020013-g006_4644.jpg | What's the most prominent thing you notice in this picture? | LM Localization of a T. gondii MORN Domain Protein, TgMORN1(A–C) Single optical section of living transgenic parasites expressing YFP-α-tubulin (green) and mRFP-TgMORN1 (red). Bright red fluorescence is observed at the spindle poles (yellow arrows), near the ends of the growing IMC in developing daughters (pink arrowheads), and in a conical patch at the basal end of the mature parasite. Weaker fluorescence is observed in the region of the conoids of both mother and daughters (blue arrows). Note in (B), showing YFP-tubulin only, that two small green dots are seen in each daughter. The more apical dot is the centriole, the more basal dot (yellow arrow) is the spindle pole [7,9].(C) TgMORN1 accumulates at the basal dot (spindle pole, yellow arrow) but not the centriole.(D–F) Double transgenic parasites expressing IMC1-YFP (green) and mRFP-TgMORN1 (red).(D) Projection of a deconvolved 3D stack of images. MORN1 is clearly seen to form a ring around the basal end of the developing daughter scaffold.(E) Projection of a deconvolved 3D stack of images of an extracellular parasite, showing a cytoplasmic fiber of TgMORN1. No daughters are present. Same scale as (D).(F) Parasite culture treated with oryzalin for 24 h before imaging. A vacuole containing four grossly distorted parasites. IMC1 accumulates as large shells and smaller blobs. f′ & f′′: higher magnification views (rotated 90°) of IMC1 blobs from (F) revealing a core of TgMORN1. |
PMC1383488_ppat-0020013-g006_4640.jpg | What is being portrayed in this visual content? | LM Localization of a T. gondii MORN Domain Protein, TgMORN1(A–C) Single optical section of living transgenic parasites expressing YFP-α-tubulin (green) and mRFP-TgMORN1 (red). Bright red fluorescence is observed at the spindle poles (yellow arrows), near the ends of the growing IMC in developing daughters (pink arrowheads), and in a conical patch at the basal end of the mature parasite. Weaker fluorescence is observed in the region of the conoids of both mother and daughters (blue arrows). Note in (B), showing YFP-tubulin only, that two small green dots are seen in each daughter. The more apical dot is the centriole, the more basal dot (yellow arrow) is the spindle pole [7,9].(C) TgMORN1 accumulates at the basal dot (spindle pole, yellow arrow) but not the centriole.(D–F) Double transgenic parasites expressing IMC1-YFP (green) and mRFP-TgMORN1 (red).(D) Projection of a deconvolved 3D stack of images. MORN1 is clearly seen to form a ring around the basal end of the developing daughter scaffold.(E) Projection of a deconvolved 3D stack of images of an extracellular parasite, showing a cytoplasmic fiber of TgMORN1. No daughters are present. Same scale as (D).(F) Parasite culture treated with oryzalin for 24 h before imaging. A vacuole containing four grossly distorted parasites. IMC1 accumulates as large shells and smaller blobs. f′ & f′′: higher magnification views (rotated 90°) of IMC1 blobs from (F) revealing a core of TgMORN1. |
PMC1383488_ppat-0020013-g008_4636.jpg | What is the principal component of this image? | Colocalization of T. gondii Centrin-2 and DLCFluorescence images (projections of a deconvolved 3D stack) of two different vacuoles (A–C) (D–F), each containing four parasites expressing both EGFP–TgDLC and mRFP–TgCentrin2. Blue brackets in (A–C) mark the position of the apical cap of dynein. Note that the ring of TgCentrin2 spots is always positioned at the lower border of this cap. The arrowheads in (D–F) indicate the faint basal ring of dynein that lies adjacent to the basal spot of centrin2. |
PMC1383488_ppat-0020013-g008_4637.jpg | What is the focal point of this photograph? | Colocalization of T. gondii Centrin-2 and DLCFluorescence images (projections of a deconvolved 3D stack) of two different vacuoles (A–C) (D–F), each containing four parasites expressing both EGFP–TgDLC and mRFP–TgCentrin2. Blue brackets in (A–C) mark the position of the apical cap of dynein. Note that the ring of TgCentrin2 spots is always positioned at the lower border of this cap. The arrowheads in (D–F) indicate the faint basal ring of dynein that lies adjacent to the basal spot of centrin2. |
PMC1383488_ppat-0020013-g008_4634.jpg | Describe the main subject of this image. | Colocalization of T. gondii Centrin-2 and DLCFluorescence images (projections of a deconvolved 3D stack) of two different vacuoles (A–C) (D–F), each containing four parasites expressing both EGFP–TgDLC and mRFP–TgCentrin2. Blue brackets in (A–C) mark the position of the apical cap of dynein. Note that the ring of TgCentrin2 spots is always positioned at the lower border of this cap. The arrowheads in (D–F) indicate the faint basal ring of dynein that lies adjacent to the basal spot of centrin2. |
PMC1386654_F1_4650.jpg | What key item or scene is captured in this photo? | A montage of the panoramic radiographs of the four patients showing in each case the close spatial relationship between the mandibular third molar teeth and the IAN. |
PMC1386654_F1_4647.jpg | What key item or scene is captured in this photo? | A montage of the panoramic radiographs of the four patients showing in each case the close spatial relationship between the mandibular third molar teeth and the IAN. |
PMC1386654_F1_4649.jpg | What is the core subject represented in this visual? | A montage of the panoramic radiographs of the four patients showing in each case the close spatial relationship between the mandibular third molar teeth and the IAN. |
PMC1386654_F1_4648.jpg | What is the core subject represented in this visual? | A montage of the panoramic radiographs of the four patients showing in each case the close spatial relationship between the mandibular third molar teeth and the IAN. |
PMC1386658_F4_4669.jpg | What object or scene is depicted here? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4653.jpg | Describe the main subject of this image. | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4652.jpg | What is the dominant medical problem in this image? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4667.jpg | What is the central feature of this picture? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4654.jpg | What is shown in this image? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4658.jpg | What is being portrayed in this visual content? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4651.jpg | What is the main focus of this visual representation? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4660.jpg | What does this image primarily show? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4670.jpg | What is the main focus of this visual representation? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4666.jpg | What is the principal component of this image? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4655.jpg | What is the focal point of this photograph? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4659.jpg | What is the central feature of this picture? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4657.jpg | What is the core subject represented in this visual? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4662.jpg | What is being portrayed in this visual content? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386658_F4_4668.jpg | What's the most prominent thing you notice in this picture? | Detailed imaging of full-length GFP-APC in living COS-7 cells. Panel A. In subconfluent cells GFP-APC decorates the distal tips of microtubules at cell vertices (arrows, additional file 1, 5s time lapse). Panels B-D. GFP-APC clusters decorating distal tips of microtubules in fixed GFP-APC expressing cells. GFP-APC green, tubulin red and DAPI blue, panel D is a merged image. Panels E-H. GFP-APC puncta can be deposited at the cell cortex (arrows, additional file 2). Panels I-L. GFP-APC puncta could be seen undergoing retrograde movements at the cell periphery (arrowhead, additional file 3). Panels M-P. Part of an original GFP-APC puncta is lost from a shrinking tip while the remaining attached portion continues retrograde movement (arrowheads, additional file 4). Panels Q-T. Some shrinking microtubules tipped with GFP-APC puncta undergo re-growth after periods of shrinkage (arrowhead, move 5). Bars = 10 μm. |
PMC1386661_F6_4671.jpg | What is the central feature of this picture? | Actin expression in fibroblasts from BALF and bronchial biopsies from patients with SSc and mild asthma are arranged into stress fibers. Fibroblasts were cultured from bronchial biopsies and BALF from patients with SSc and mild asthma. Cells were seeded on four-well chamber slides (5000 cells/well), stained with Alexa Fluor™ 488 phalloidin showing stress fibers and analyzed using a fluorescence microscope. |
PMC1386661_F6_4674.jpg | What is the central feature of this picture? | Actin expression in fibroblasts from BALF and bronchial biopsies from patients with SSc and mild asthma are arranged into stress fibers. Fibroblasts were cultured from bronchial biopsies and BALF from patients with SSc and mild asthma. Cells were seeded on four-well chamber slides (5000 cells/well), stained with Alexa Fluor™ 488 phalloidin showing stress fibers and analyzed using a fluorescence microscope. |
PMC1386661_F6_4672.jpg | Describe the main subject of this image. | Actin expression in fibroblasts from BALF and bronchial biopsies from patients with SSc and mild asthma are arranged into stress fibers. Fibroblasts were cultured from bronchial biopsies and BALF from patients with SSc and mild asthma. Cells were seeded on four-well chamber slides (5000 cells/well), stained with Alexa Fluor™ 488 phalloidin showing stress fibers and analyzed using a fluorescence microscope. |
PMC1386678_F1_4678.jpg | Can you identify the primary element in this image? | Chest X-ray (CXR) and high-resolution computed tomography (CT) findings on admission, and again at five months following combined treatment. Top (on admission): (A) Posterior-anterior chest radiograph (P-A CXR) shows multiple tiny reticular nodules on both lungs; (B) Tiny centrilobular and subpleural nodules are evident in both lungs on the chest CT. Bottom (five months after combined treatment): (C) A follow-up CXR shows improvement in the multiple reticular nodules; (D) A follow-up CT scan reveals the improvement of the residual nodules. |
PMC1386678_F1_4676.jpg | What key item or scene is captured in this photo? | Chest X-ray (CXR) and high-resolution computed tomography (CT) findings on admission, and again at five months following combined treatment. Top (on admission): (A) Posterior-anterior chest radiograph (P-A CXR) shows multiple tiny reticular nodules on both lungs; (B) Tiny centrilobular and subpleural nodules are evident in both lungs on the chest CT. Bottom (five months after combined treatment): (C) A follow-up CXR shows improvement in the multiple reticular nodules; (D) A follow-up CT scan reveals the improvement of the residual nodules. |
PMC1386678_F1_4677.jpg | What key item or scene is captured in this photo? | Chest X-ray (CXR) and high-resolution computed tomography (CT) findings on admission, and again at five months following combined treatment. Top (on admission): (A) Posterior-anterior chest radiograph (P-A CXR) shows multiple tiny reticular nodules on both lungs; (B) Tiny centrilobular and subpleural nodules are evident in both lungs on the chest CT. Bottom (five months after combined treatment): (C) A follow-up CXR shows improvement in the multiple reticular nodules; (D) A follow-up CT scan reveals the improvement of the residual nodules. |
PMC1386683_F4_4680.jpg | What stands out most in this visual? | Immunohistochemical detection of E-cadherin in monolayers of NMuMG cells after treatment with LT and hemolytic proteins (1 μg/ml each for 16 h). Nuclei are stained blue with DAPI, and E-cadherin is stained green with FITC-conjugated anti-E-cadherin antibody. In the case of AnlO and AnlB, arrows indicate some of the most damaged areas. 40× magnification. |
PMC1386683_F4_4682.jpg | What key item or scene is captured in this photo? | Immunohistochemical detection of E-cadherin in monolayers of NMuMG cells after treatment with LT and hemolytic proteins (1 μg/ml each for 16 h). Nuclei are stained blue with DAPI, and E-cadherin is stained green with FITC-conjugated anti-E-cadherin antibody. In the case of AnlO and AnlB, arrows indicate some of the most damaged areas. 40× magnification. |
PMC1386683_F4_4683.jpg | What is the dominant medical problem in this image? | Immunohistochemical detection of E-cadherin in monolayers of NMuMG cells after treatment with LT and hemolytic proteins (1 μg/ml each for 16 h). Nuclei are stained blue with DAPI, and E-cadherin is stained green with FITC-conjugated anti-E-cadherin antibody. In the case of AnlO and AnlB, arrows indicate some of the most damaged areas. 40× magnification. |
PMC1386683_F5_4684.jpg | Can you identify the primary element in this image? | Immunohistochemical detection of Synd1 in monolayers of NMuMG cells after treatment with LT and hemolytic proteins (1 μg/ml each for 16 h). Nuclei are stained blue with DAPI, and Synd1 is stained green with FITC-conjugated anti-Synd1 antibody. 40× magnification. |
PMC1386683_F5_4686.jpg | Describe the main subject of this image. | Immunohistochemical detection of Synd1 in monolayers of NMuMG cells after treatment with LT and hemolytic proteins (1 μg/ml each for 16 h). Nuclei are stained blue with DAPI, and Synd1 is stained green with FITC-conjugated anti-Synd1 antibody. 40× magnification. |
PMC1386683_F5_4685.jpg | What is the main focus of this visual representation? | Immunohistochemical detection of Synd1 in monolayers of NMuMG cells after treatment with LT and hemolytic proteins (1 μg/ml each for 16 h). Nuclei are stained blue with DAPI, and Synd1 is stained green with FITC-conjugated anti-Synd1 antibody. 40× magnification. |
PMC1386689_F3_4689.jpg | Describe the main subject of this image. | Immunohistochemistry of Sp17 in nervous system neoplasms: a-c. glioblastomas; d. astrocytoma; e. meningioma; f. ependimoma. In all cases, Sp 17 was localised in the cytoplasm of a few isolated and scattered tumoral cells. (a-d, 40× original magnification, 100× insets; e-f, 100× original magnification). |
PMC1386689_F3_4693.jpg | Describe the main subject of this image. | Immunohistochemistry of Sp17 in nervous system neoplasms: a-c. glioblastomas; d. astrocytoma; e. meningioma; f. ependimoma. In all cases, Sp 17 was localised in the cytoplasm of a few isolated and scattered tumoral cells. (a-d, 40× original magnification, 100× insets; e-f, 100× original magnification). |
PMC1386689_F3_4694.jpg | What object or scene is depicted here? | Immunohistochemistry of Sp17 in nervous system neoplasms: a-c. glioblastomas; d. astrocytoma; e. meningioma; f. ependimoma. In all cases, Sp 17 was localised in the cytoplasm of a few isolated and scattered tumoral cells. (a-d, 40× original magnification, 100× insets; e-f, 100× original magnification). |
PMC1386689_F3_4691.jpg | What is shown in this image? | Immunohistochemistry of Sp17 in nervous system neoplasms: a-c. glioblastomas; d. astrocytoma; e. meningioma; f. ependimoma. In all cases, Sp 17 was localised in the cytoplasm of a few isolated and scattered tumoral cells. (a-d, 40× original magnification, 100× insets; e-f, 100× original magnification). |
PMC1386689_F3_4692.jpg | What is shown in this image? | Immunohistochemistry of Sp17 in nervous system neoplasms: a-c. glioblastomas; d. astrocytoma; e. meningioma; f. ependimoma. In all cases, Sp 17 was localised in the cytoplasm of a few isolated and scattered tumoral cells. (a-d, 40× original magnification, 100× insets; e-f, 100× original magnification). |
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