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PMC1180430_F1_2604.jpg | What does this image primarily show? | Fibreoptic endoscopic image showing a pedunculated mass causing significant lumen obstruction. |
PMC1180430_F3_2606.jpg | What is the dominant medical problem in this image? | One month postoperative CT chest (axial view) showing normal tracheal walls and lumen. |
PMC1180430_F3_2605.jpg | What is the core subject represented in this visual? | One month postoperative CT chest (axial view) showing normal tracheal walls and lumen. |
PMC1180452_F3_2613.jpg | What is the core subject represented in this visual? | Movements of BDNF-GFP puncta in an axon and dendrites of a living neuron. A, Image of a cortical neuron which expressed BDNF-GFP in soma, axon and dendrites. Time-lapse images in each square along an axon and a dendrite are magnified and shown in B and C, respectively. Scale bar, 50 μm. B, Moving (b and c) and non-moving (a) puncta in the axon. Each image was taken at a time point indicated at the top of each figure. Right is the distal side of the axon. Scale bar in the bottom image indicates 5 μm and applies to all the images in B and C. C, Moving (a and b) and non-moving (c) puncta in the dendrite. Right is the distal side of the dendrite. Each image was taken at a time point indicated at the top of each figure. |
PMC1180452_F3_2612.jpg | What stands out most in this visual? | Movements of BDNF-GFP puncta in an axon and dendrites of a living neuron. A, Image of a cortical neuron which expressed BDNF-GFP in soma, axon and dendrites. Time-lapse images in each square along an axon and a dendrite are magnified and shown in B and C, respectively. Scale bar, 50 μm. B, Moving (b and c) and non-moving (a) puncta in the axon. Each image was taken at a time point indicated at the top of each figure. Right is the distal side of the axon. Scale bar in the bottom image indicates 5 μm and applies to all the images in B and C. C, Moving (a and b) and non-moving (c) puncta in the dendrite. Right is the distal side of the dendrite. Each image was taken at a time point indicated at the top of each figure. |
PMC1180452_F3_2609.jpg | What is the principal component of this image? | Movements of BDNF-GFP puncta in an axon and dendrites of a living neuron. A, Image of a cortical neuron which expressed BDNF-GFP in soma, axon and dendrites. Time-lapse images in each square along an axon and a dendrite are magnified and shown in B and C, respectively. Scale bar, 50 μm. B, Moving (b and c) and non-moving (a) puncta in the axon. Each image was taken at a time point indicated at the top of each figure. Right is the distal side of the axon. Scale bar in the bottom image indicates 5 μm and applies to all the images in B and C. C, Moving (a and b) and non-moving (c) puncta in the dendrite. Right is the distal side of the dendrite. Each image was taken at a time point indicated at the top of each figure. |
PMC1180452_F3_2611.jpg | What object or scene is depicted here? | Movements of BDNF-GFP puncta in an axon and dendrites of a living neuron. A, Image of a cortical neuron which expressed BDNF-GFP in soma, axon and dendrites. Time-lapse images in each square along an axon and a dendrite are magnified and shown in B and C, respectively. Scale bar, 50 μm. B, Moving (b and c) and non-moving (a) puncta in the axon. Each image was taken at a time point indicated at the top of each figure. Right is the distal side of the axon. Scale bar in the bottom image indicates 5 μm and applies to all the images in B and C. C, Moving (a and b) and non-moving (c) puncta in the dendrite. Right is the distal side of the dendrite. Each image was taken at a time point indicated at the top of each figure. |
PMC1180452_F3_2608.jpg | What is the core subject represented in this visual? | Movements of BDNF-GFP puncta in an axon and dendrites of a living neuron. A, Image of a cortical neuron which expressed BDNF-GFP in soma, axon and dendrites. Time-lapse images in each square along an axon and a dendrite are magnified and shown in B and C, respectively. Scale bar, 50 μm. B, Moving (b and c) and non-moving (a) puncta in the axon. Each image was taken at a time point indicated at the top of each figure. Right is the distal side of the axon. Scale bar in the bottom image indicates 5 μm and applies to all the images in B and C. C, Moving (a and b) and non-moving (c) puncta in the dendrite. Right is the distal side of the dendrite. Each image was taken at a time point indicated at the top of each figure. |
PMC1180452_F3_2614.jpg | What is the dominant medical problem in this image? | Movements of BDNF-GFP puncta in an axon and dendrites of a living neuron. A, Image of a cortical neuron which expressed BDNF-GFP in soma, axon and dendrites. Time-lapse images in each square along an axon and a dendrite are magnified and shown in B and C, respectively. Scale bar, 50 μm. B, Moving (b and c) and non-moving (a) puncta in the axon. Each image was taken at a time point indicated at the top of each figure. Right is the distal side of the axon. Scale bar in the bottom image indicates 5 μm and applies to all the images in B and C. C, Moving (a and b) and non-moving (c) puncta in the dendrite. Right is the distal side of the dendrite. Each image was taken at a time point indicated at the top of each figure. |
PMC1180459_F5_2616.jpg | What does this image primarily show? | Visualization of marked paths and points on a black carton (a) in the thermogram (b). Note that this visualization was created by a stimulation with a heat source at a distance of 10 cm. |
PMC1180459_F5_2615.jpg | What can you see in this picture? | Visualization of marked paths and points on a black carton (a) in the thermogram (b). Note that this visualization was created by a stimulation with a heat source at a distance of 10 cm. |
PMC1180466_F1_2617.jpg | What can you see in this picture? | CT scan with intravenouse contrast: Free intraperitoneal air and a enlarged jejunum. |
PMC1180478_F3_2618.jpg | What can you see in this picture? | Co-localization of E6s and E6AP in 293T (A) and HaCaT (B). Transiently transfected cells were analyzed for E6 or E6 variants fused to GFP, E6AP (Alexa 568 dye) and nuclear DNA (DAPI) by confocal microscopy. Slides were analyzed by microscopy with 3 lasers excitation lines. The images from the individual channels (DAPI, GFP, Alexa 568) as well as the merged image are shown. P and V represent non-transfected cells and pEGFP-C1 vector transfected cells, respectively. The scale bar represents 20 μm. |
PMC1180478_F3_2619.jpg | What is the principal component of this image? | Co-localization of E6s and E6AP in 293T (A) and HaCaT (B). Transiently transfected cells were analyzed for E6 or E6 variants fused to GFP, E6AP (Alexa 568 dye) and nuclear DNA (DAPI) by confocal microscopy. Slides were analyzed by microscopy with 3 lasers excitation lines. The images from the individual channels (DAPI, GFP, Alexa 568) as well as the merged image are shown. P and V represent non-transfected cells and pEGFP-C1 vector transfected cells, respectively. The scale bar represents 20 μm. |
PMC1180513_pbio-0030268-g003_2624.jpg | What key item or scene is captured in this photo? | Node Cilia Are Posteriorly Tilted and Positioned(A) Scanning electron micrograph of the wild-type node. Note that cilia emanate from the posterior part of the cells. The view angle is about 30° with respect to the horizontal line.(B, C) Scanning electron micrograph of the iv/iv node. (C) is a high-magnification picture of the region in (B) indicated by an arrow.(D) Deduced tilt of iv/iv node cilia after stereography from multiple-tilt scanning electron micrograph images. Yellow lines indicate cilia, red dots their root positions, and a blue square a plane best-fit to the node surface. When we calculated the tilt of the cilia, we separated the tilt into A-P (anterior–posterior) and L-R components. The average tilt was 26.6° in A-P axis (toward the posterior) and 0.06° in L-R axis (towards the right).(E) Immunofluorecence image of node cells shown as projection of 3D confocal data stack. Basal bodies and cell boundaries are shown by immunofluorescence against γ-tubulin (red) and ZO-1 (green), respectively.(F) 3D reconstruction of (E) viewed from ventral side (top) and right side (bottom), showing posterior bias of basal body positions. White lines divide the cells into the anterior and the posterior halves. Basal bodies located in the anterior and the posterior are shown in yellow and red, respectively.(G) Speculative interpretation of posterior bias of basal bodies in orientation and position of the node cilia. Because the node cells are somewhat rounded, if basal bodies were located at the posterior part of these cells, it would result in posteriorly tilted cilia even though the basal bodies remain perpendicular to the plasma membrane. |
PMC1180513_pbio-0030268-g003_2623.jpg | Describe the main subject of this image. | Node Cilia Are Posteriorly Tilted and Positioned(A) Scanning electron micrograph of the wild-type node. Note that cilia emanate from the posterior part of the cells. The view angle is about 30° with respect to the horizontal line.(B, C) Scanning electron micrograph of the iv/iv node. (C) is a high-magnification picture of the region in (B) indicated by an arrow.(D) Deduced tilt of iv/iv node cilia after stereography from multiple-tilt scanning electron micrograph images. Yellow lines indicate cilia, red dots their root positions, and a blue square a plane best-fit to the node surface. When we calculated the tilt of the cilia, we separated the tilt into A-P (anterior–posterior) and L-R components. The average tilt was 26.6° in A-P axis (toward the posterior) and 0.06° in L-R axis (towards the right).(E) Immunofluorecence image of node cells shown as projection of 3D confocal data stack. Basal bodies and cell boundaries are shown by immunofluorescence against γ-tubulin (red) and ZO-1 (green), respectively.(F) 3D reconstruction of (E) viewed from ventral side (top) and right side (bottom), showing posterior bias of basal body positions. White lines divide the cells into the anterior and the posterior halves. Basal bodies located in the anterior and the posterior are shown in yellow and red, respectively.(G) Speculative interpretation of posterior bias of basal bodies in orientation and position of the node cilia. Because the node cells are somewhat rounded, if basal bodies were located at the posterior part of these cells, it would result in posteriorly tilted cilia even though the basal bodies remain perpendicular to the plasma membrane. |
PMC1180513_pbio-0030268-g003_2620.jpg | Can you identify the primary element in this image? | Node Cilia Are Posteriorly Tilted and Positioned(A) Scanning electron micrograph of the wild-type node. Note that cilia emanate from the posterior part of the cells. The view angle is about 30° with respect to the horizontal line.(B, C) Scanning electron micrograph of the iv/iv node. (C) is a high-magnification picture of the region in (B) indicated by an arrow.(D) Deduced tilt of iv/iv node cilia after stereography from multiple-tilt scanning electron micrograph images. Yellow lines indicate cilia, red dots their root positions, and a blue square a plane best-fit to the node surface. When we calculated the tilt of the cilia, we separated the tilt into A-P (anterior–posterior) and L-R components. The average tilt was 26.6° in A-P axis (toward the posterior) and 0.06° in L-R axis (towards the right).(E) Immunofluorecence image of node cells shown as projection of 3D confocal data stack. Basal bodies and cell boundaries are shown by immunofluorescence against γ-tubulin (red) and ZO-1 (green), respectively.(F) 3D reconstruction of (E) viewed from ventral side (top) and right side (bottom), showing posterior bias of basal body positions. White lines divide the cells into the anterior and the posterior halves. Basal bodies located in the anterior and the posterior are shown in yellow and red, respectively.(G) Speculative interpretation of posterior bias of basal bodies in orientation and position of the node cilia. Because the node cells are somewhat rounded, if basal bodies were located at the posterior part of these cells, it would result in posteriorly tilted cilia even though the basal bodies remain perpendicular to the plasma membrane. |
PMC1180513_pbio-0030268-g003_2621.jpg | What's the most prominent thing you notice in this picture? | Node Cilia Are Posteriorly Tilted and Positioned(A) Scanning electron micrograph of the wild-type node. Note that cilia emanate from the posterior part of the cells. The view angle is about 30° with respect to the horizontal line.(B, C) Scanning electron micrograph of the iv/iv node. (C) is a high-magnification picture of the region in (B) indicated by an arrow.(D) Deduced tilt of iv/iv node cilia after stereography from multiple-tilt scanning electron micrograph images. Yellow lines indicate cilia, red dots their root positions, and a blue square a plane best-fit to the node surface. When we calculated the tilt of the cilia, we separated the tilt into A-P (anterior–posterior) and L-R components. The average tilt was 26.6° in A-P axis (toward the posterior) and 0.06° in L-R axis (towards the right).(E) Immunofluorecence image of node cells shown as projection of 3D confocal data stack. Basal bodies and cell boundaries are shown by immunofluorescence against γ-tubulin (red) and ZO-1 (green), respectively.(F) 3D reconstruction of (E) viewed from ventral side (top) and right side (bottom), showing posterior bias of basal body positions. White lines divide the cells into the anterior and the posterior halves. Basal bodies located in the anterior and the posterior are shown in yellow and red, respectively.(G) Speculative interpretation of posterior bias of basal bodies in orientation and position of the node cilia. Because the node cells are somewhat rounded, if basal bodies were located at the posterior part of these cells, it would result in posteriorly tilted cilia even though the basal bodies remain perpendicular to the plasma membrane. |
PMC1180513_pbio-0030268-g003_2622.jpg | What's the most prominent thing you notice in this picture? | Node Cilia Are Posteriorly Tilted and Positioned(A) Scanning electron micrograph of the wild-type node. Note that cilia emanate from the posterior part of the cells. The view angle is about 30° with respect to the horizontal line.(B, C) Scanning electron micrograph of the iv/iv node. (C) is a high-magnification picture of the region in (B) indicated by an arrow.(D) Deduced tilt of iv/iv node cilia after stereography from multiple-tilt scanning electron micrograph images. Yellow lines indicate cilia, red dots their root positions, and a blue square a plane best-fit to the node surface. When we calculated the tilt of the cilia, we separated the tilt into A-P (anterior–posterior) and L-R components. The average tilt was 26.6° in A-P axis (toward the posterior) and 0.06° in L-R axis (towards the right).(E) Immunofluorecence image of node cells shown as projection of 3D confocal data stack. Basal bodies and cell boundaries are shown by immunofluorescence against γ-tubulin (red) and ZO-1 (green), respectively.(F) 3D reconstruction of (E) viewed from ventral side (top) and right side (bottom), showing posterior bias of basal body positions. White lines divide the cells into the anterior and the posterior halves. Basal bodies located in the anterior and the posterior are shown in yellow and red, respectively.(G) Speculative interpretation of posterior bias of basal bodies in orientation and position of the node cilia. Because the node cells are somewhat rounded, if basal bodies were located at the posterior part of these cells, it would result in posteriorly tilted cilia even though the basal bodies remain perpendicular to the plasma membrane. |
PMC1180851_F4_2627.jpg | What is the principal component of this image? | SEM micrograph from F. oxysporum 07 SD strain at ×11000 magnification. |
PMC1180853_F4_2632.jpg | What is the dominant medical problem in this image? | Confocal microscopy of cells co-expressing HIV-1 Gag, Env and SR-protein. Panel A: 293T cells expressing HIV-1 pNL4.3 were subjected to immuno-staining using anti-Map17 (green staining) and anti-Env gp120 (red staining) antibodies and staining was viewed by confocal microscopy as described in methods. Most if not all cells expressed Gag and Env but only partial colocalization was seen (merge picture). Right panel corresponds to the same cells viewed by phase contrast microscopy. Panel B: same as in A except that His tagged-ASF/SF2 SR protein was overexpressed by DNA transfection with about 75% transfection efficiency (see methods). ASF/SF2 protein is localized in the nucleus (blue staining) and its overexpression caused a drastic reduction of Env level while Gag remained well expressed in agreement with the western blot data (Figure 3) but with an heterogenous pattern (first panel). Panel C: same as in A except that His tagged-SC35 SR protein was overexpressed by DNA transfection with about 75% transfection efficiency (see methods). SC35 protein (nuclear blue staining) overexpression caused a reduction of Env level while Gag was still highly expressed in agreement with the western blot data (Figure 2). Note that in all cases examined here (anti-Map17; green staining in panel A to C) Gag was found to accumulate at the plasma membrane and in intracellular compartments corresponding to vesicles [42] (Muriaux et al., unpublished data). |
PMC1180853_F4_2628.jpg | What object or scene is depicted here? | Confocal microscopy of cells co-expressing HIV-1 Gag, Env and SR-protein. Panel A: 293T cells expressing HIV-1 pNL4.3 were subjected to immuno-staining using anti-Map17 (green staining) and anti-Env gp120 (red staining) antibodies and staining was viewed by confocal microscopy as described in methods. Most if not all cells expressed Gag and Env but only partial colocalization was seen (merge picture). Right panel corresponds to the same cells viewed by phase contrast microscopy. Panel B: same as in A except that His tagged-ASF/SF2 SR protein was overexpressed by DNA transfection with about 75% transfection efficiency (see methods). ASF/SF2 protein is localized in the nucleus (blue staining) and its overexpression caused a drastic reduction of Env level while Gag remained well expressed in agreement with the western blot data (Figure 3) but with an heterogenous pattern (first panel). Panel C: same as in A except that His tagged-SC35 SR protein was overexpressed by DNA transfection with about 75% transfection efficiency (see methods). SC35 protein (nuclear blue staining) overexpression caused a reduction of Env level while Gag was still highly expressed in agreement with the western blot data (Figure 2). Note that in all cases examined here (anti-Map17; green staining in panel A to C) Gag was found to accumulate at the plasma membrane and in intracellular compartments corresponding to vesicles [42] (Muriaux et al., unpublished data). |
PMC1180853_F4_2630.jpg | What does this image primarily show? | Confocal microscopy of cells co-expressing HIV-1 Gag, Env and SR-protein. Panel A: 293T cells expressing HIV-1 pNL4.3 were subjected to immuno-staining using anti-Map17 (green staining) and anti-Env gp120 (red staining) antibodies and staining was viewed by confocal microscopy as described in methods. Most if not all cells expressed Gag and Env but only partial colocalization was seen (merge picture). Right panel corresponds to the same cells viewed by phase contrast microscopy. Panel B: same as in A except that His tagged-ASF/SF2 SR protein was overexpressed by DNA transfection with about 75% transfection efficiency (see methods). ASF/SF2 protein is localized in the nucleus (blue staining) and its overexpression caused a drastic reduction of Env level while Gag remained well expressed in agreement with the western blot data (Figure 3) but with an heterogenous pattern (first panel). Panel C: same as in A except that His tagged-SC35 SR protein was overexpressed by DNA transfection with about 75% transfection efficiency (see methods). SC35 protein (nuclear blue staining) overexpression caused a reduction of Env level while Gag was still highly expressed in agreement with the western blot data (Figure 2). Note that in all cases examined here (anti-Map17; green staining in panel A to C) Gag was found to accumulate at the plasma membrane and in intracellular compartments corresponding to vesicles [42] (Muriaux et al., unpublished data). |
PMC1180853_F4_2633.jpg | Can you identify the primary element in this image? | Confocal microscopy of cells co-expressing HIV-1 Gag, Env and SR-protein. Panel A: 293T cells expressing HIV-1 pNL4.3 were subjected to immuno-staining using anti-Map17 (green staining) and anti-Env gp120 (red staining) antibodies and staining was viewed by confocal microscopy as described in methods. Most if not all cells expressed Gag and Env but only partial colocalization was seen (merge picture). Right panel corresponds to the same cells viewed by phase contrast microscopy. Panel B: same as in A except that His tagged-ASF/SF2 SR protein was overexpressed by DNA transfection with about 75% transfection efficiency (see methods). ASF/SF2 protein is localized in the nucleus (blue staining) and its overexpression caused a drastic reduction of Env level while Gag remained well expressed in agreement with the western blot data (Figure 3) but with an heterogenous pattern (first panel). Panel C: same as in A except that His tagged-SC35 SR protein was overexpressed by DNA transfection with about 75% transfection efficiency (see methods). SC35 protein (nuclear blue staining) overexpression caused a reduction of Env level while Gag was still highly expressed in agreement with the western blot data (Figure 2). Note that in all cases examined here (anti-Map17; green staining in panel A to C) Gag was found to accumulate at the plasma membrane and in intracellular compartments corresponding to vesicles [42] (Muriaux et al., unpublished data). |
PMC1180859_F1_2634.jpg | Can you identify the primary element in this image? | Microscopic photograph of the biopsied specimen. A. Bland glands mimicking benign foveolar epithelial hyperplasia are noted in the heavy inflammatory backgrounds (hematoxylin and eosin, X400). B. Glands are destructed by inflammatory cell infiltrates and epithelial cells reveal mild atypia (hematoxylin and eosin, X400). |
PMC1180859_F1_2635.jpg | What can you see in this picture? | Microscopic photograph of the biopsied specimen. A. Bland glands mimicking benign foveolar epithelial hyperplasia are noted in the heavy inflammatory backgrounds (hematoxylin and eosin, X400). B. Glands are destructed by inflammatory cell infiltrates and epithelial cells reveal mild atypia (hematoxylin and eosin, X400). |
PMC1181810_F4_2636.jpg | Can you identify the primary element in this image? | Biopsy of the multiple small nodules revealed the haphazard arrangement of uniform spindle cells in a collagenous stroma. (×100, H &E). |
PMC1181820_F1_2637.jpg | What can you see in this picture? | The PA chest X-ray: left-sided pleural effusion and a large mass in anterolateral part of left lung which had overshadowed the left border of the heart. Arrowhead indicates shift of the heart to the right side. |
PMC1181820_F2_2639.jpg | What is the focal point of this photograph? | Chest computed tomography scan with contrast at the level of T7 showing the large pseudoaneurysm. The lesion was a well-defined partially calcified mass with tubular density adjacent to the heart. Arrowheads indicate the calcifications. It was filled with contrast medium concurrently with the heart. This lesion, which was mostly occupied by thrombosis, had a mass effect on heart. |
PMC1181820_F3_2642.jpg | What is the main focus of this visual representation? | The MRI indicated a mass with inhomogeneous signals implying the presence of blood and clots in addition to calcification. (SVC = Superior Vena Cava; IVC = Inferior Vena Cava; LV = Left Ventricle; P = Pseudoaneurysm) |
PMC1181820_F3_2640.jpg | What key item or scene is captured in this photo? | The MRI indicated a mass with inhomogeneous signals implying the presence of blood and clots in addition to calcification. (SVC = Superior Vena Cava; IVC = Inferior Vena Cava; LV = Left Ventricle; P = Pseudoaneurysm) |
PMC1181820_F4_2638.jpg | What does this image primarily show? | Chest computed tomography scan with contrast at T7 level. Arrowhead marks the ostium. |
PMC1182361_F5_2652.jpg | Can you identify the primary element in this image? | Carbohydrate expression as determined by lectin binding using immunocytochemistry. Figure 5A–C shows a hESC colony that represents uniform lectin binding. Ricinus Communis agglutinin (RCA) binding in red (5A) is shown throughout this SSEA-4 positive colony in green (5B). The DAPI nuclear stain image (blue) is also shown (5C). Other lectins showed partial binding patterns, such as Vicia Villosa agglutinin (VVA) binding (red), which is shown in a hESC colony (5D) that has uniform SSEA-4 antibody binding (green) (5E). Arrows denote distinct SSEA-4 positive regions lacking VVA binding. DAPI nuclear staining (blue) is also shown (5F). PHA-E binding is shown in two separate images in Figure 5G–H. In 5G there are two adjacent colonies, one that expresses strong binding of SSEA-4 antibody (green) and weak to no binding of PHA-E (red), and an adjacent colony showing binding of PHA-E without SSEA-4 antibody binding. (DAPI nuclear staining in blue). 5H, shows another colony with a streak of stacked cells (as determined by high DAPI expression, see arrow) in the middle of the colony that are beginning to lose SSEA-4 expression (green), but have strong PHA-E binding (red). However, the rest of the colony adjacent to this streak of cells is uniformly positive for SSEA-4 but is lacking PHA-E binding. 5I shows lack of DBA binding and presence of SSEA-4 and DAPI staining. Images and scale bars: 5A-G) 20× magnification, 100 μm. H-I) 10× magnification, 100 μm. |
PMC1182361_F5_2651.jpg | What is the principal component of this image? | Carbohydrate expression as determined by lectin binding using immunocytochemistry. Figure 5A–C shows a hESC colony that represents uniform lectin binding. Ricinus Communis agglutinin (RCA) binding in red (5A) is shown throughout this SSEA-4 positive colony in green (5B). The DAPI nuclear stain image (blue) is also shown (5C). Other lectins showed partial binding patterns, such as Vicia Villosa agglutinin (VVA) binding (red), which is shown in a hESC colony (5D) that has uniform SSEA-4 antibody binding (green) (5E). Arrows denote distinct SSEA-4 positive regions lacking VVA binding. DAPI nuclear staining (blue) is also shown (5F). PHA-E binding is shown in two separate images in Figure 5G–H. In 5G there are two adjacent colonies, one that expresses strong binding of SSEA-4 antibody (green) and weak to no binding of PHA-E (red), and an adjacent colony showing binding of PHA-E without SSEA-4 antibody binding. (DAPI nuclear staining in blue). 5H, shows another colony with a streak of stacked cells (as determined by high DAPI expression, see arrow) in the middle of the colony that are beginning to lose SSEA-4 expression (green), but have strong PHA-E binding (red). However, the rest of the colony adjacent to this streak of cells is uniformly positive for SSEA-4 but is lacking PHA-E binding. 5I shows lack of DBA binding and presence of SSEA-4 and DAPI staining. Images and scale bars: 5A-G) 20× magnification, 100 μm. H-I) 10× magnification, 100 μm. |
PMC1182361_F5_2647.jpg | What stands out most in this visual? | Carbohydrate expression as determined by lectin binding using immunocytochemistry. Figure 5A–C shows a hESC colony that represents uniform lectin binding. Ricinus Communis agglutinin (RCA) binding in red (5A) is shown throughout this SSEA-4 positive colony in green (5B). The DAPI nuclear stain image (blue) is also shown (5C). Other lectins showed partial binding patterns, such as Vicia Villosa agglutinin (VVA) binding (red), which is shown in a hESC colony (5D) that has uniform SSEA-4 antibody binding (green) (5E). Arrows denote distinct SSEA-4 positive regions lacking VVA binding. DAPI nuclear staining (blue) is also shown (5F). PHA-E binding is shown in two separate images in Figure 5G–H. In 5G there are two adjacent colonies, one that expresses strong binding of SSEA-4 antibody (green) and weak to no binding of PHA-E (red), and an adjacent colony showing binding of PHA-E without SSEA-4 antibody binding. (DAPI nuclear staining in blue). 5H, shows another colony with a streak of stacked cells (as determined by high DAPI expression, see arrow) in the middle of the colony that are beginning to lose SSEA-4 expression (green), but have strong PHA-E binding (red). However, the rest of the colony adjacent to this streak of cells is uniformly positive for SSEA-4 but is lacking PHA-E binding. 5I shows lack of DBA binding and presence of SSEA-4 and DAPI staining. Images and scale bars: 5A-G) 20× magnification, 100 μm. H-I) 10× magnification, 100 μm. |
PMC1182361_F5_2645.jpg | What is the central feature of this picture? | Carbohydrate expression as determined by lectin binding using immunocytochemistry. Figure 5A–C shows a hESC colony that represents uniform lectin binding. Ricinus Communis agglutinin (RCA) binding in red (5A) is shown throughout this SSEA-4 positive colony in green (5B). The DAPI nuclear stain image (blue) is also shown (5C). Other lectins showed partial binding patterns, such as Vicia Villosa agglutinin (VVA) binding (red), which is shown in a hESC colony (5D) that has uniform SSEA-4 antibody binding (green) (5E). Arrows denote distinct SSEA-4 positive regions lacking VVA binding. DAPI nuclear staining (blue) is also shown (5F). PHA-E binding is shown in two separate images in Figure 5G–H. In 5G there are two adjacent colonies, one that expresses strong binding of SSEA-4 antibody (green) and weak to no binding of PHA-E (red), and an adjacent colony showing binding of PHA-E without SSEA-4 antibody binding. (DAPI nuclear staining in blue). 5H, shows another colony with a streak of stacked cells (as determined by high DAPI expression, see arrow) in the middle of the colony that are beginning to lose SSEA-4 expression (green), but have strong PHA-E binding (red). However, the rest of the colony adjacent to this streak of cells is uniformly positive for SSEA-4 but is lacking PHA-E binding. 5I shows lack of DBA binding and presence of SSEA-4 and DAPI staining. Images and scale bars: 5A-G) 20× magnification, 100 μm. H-I) 10× magnification, 100 μm. |
PMC1182361_F5_2650.jpg | What key item or scene is captured in this photo? | Carbohydrate expression as determined by lectin binding using immunocytochemistry. Figure 5A–C shows a hESC colony that represents uniform lectin binding. Ricinus Communis agglutinin (RCA) binding in red (5A) is shown throughout this SSEA-4 positive colony in green (5B). The DAPI nuclear stain image (blue) is also shown (5C). Other lectins showed partial binding patterns, such as Vicia Villosa agglutinin (VVA) binding (red), which is shown in a hESC colony (5D) that has uniform SSEA-4 antibody binding (green) (5E). Arrows denote distinct SSEA-4 positive regions lacking VVA binding. DAPI nuclear staining (blue) is also shown (5F). PHA-E binding is shown in two separate images in Figure 5G–H. In 5G there are two adjacent colonies, one that expresses strong binding of SSEA-4 antibody (green) and weak to no binding of PHA-E (red), and an adjacent colony showing binding of PHA-E without SSEA-4 antibody binding. (DAPI nuclear staining in blue). 5H, shows another colony with a streak of stacked cells (as determined by high DAPI expression, see arrow) in the middle of the colony that are beginning to lose SSEA-4 expression (green), but have strong PHA-E binding (red). However, the rest of the colony adjacent to this streak of cells is uniformly positive for SSEA-4 but is lacking PHA-E binding. 5I shows lack of DBA binding and presence of SSEA-4 and DAPI staining. Images and scale bars: 5A-G) 20× magnification, 100 μm. H-I) 10× magnification, 100 μm. |
PMC1182361_F5_2646.jpg | What is being portrayed in this visual content? | Carbohydrate expression as determined by lectin binding using immunocytochemistry. Figure 5A–C shows a hESC colony that represents uniform lectin binding. Ricinus Communis agglutinin (RCA) binding in red (5A) is shown throughout this SSEA-4 positive colony in green (5B). The DAPI nuclear stain image (blue) is also shown (5C). Other lectins showed partial binding patterns, such as Vicia Villosa agglutinin (VVA) binding (red), which is shown in a hESC colony (5D) that has uniform SSEA-4 antibody binding (green) (5E). Arrows denote distinct SSEA-4 positive regions lacking VVA binding. DAPI nuclear staining (blue) is also shown (5F). PHA-E binding is shown in two separate images in Figure 5G–H. In 5G there are two adjacent colonies, one that expresses strong binding of SSEA-4 antibody (green) and weak to no binding of PHA-E (red), and an adjacent colony showing binding of PHA-E without SSEA-4 antibody binding. (DAPI nuclear staining in blue). 5H, shows another colony with a streak of stacked cells (as determined by high DAPI expression, see arrow) in the middle of the colony that are beginning to lose SSEA-4 expression (green), but have strong PHA-E binding (red). However, the rest of the colony adjacent to this streak of cells is uniformly positive for SSEA-4 but is lacking PHA-E binding. 5I shows lack of DBA binding and presence of SSEA-4 and DAPI staining. Images and scale bars: 5A-G) 20× magnification, 100 μm. H-I) 10× magnification, 100 μm. |
PMC1183199_F12_2657.jpg | What can you see in this picture? | Ultrastructure of ventral ciliary canal. Diagrams of embryonic (A) and adult (E) zebrafish eye showing the locations of histological insets. Histological section through the central portion of the ventral ciliary canal (B). Low magnification TEM micrograph showing differentiating endothelial cells associated with the sinus (C). High magnification TEM micrograph of the undifferentiated endothelial cell, EN (D). Histological section through the central portion of the ventral ciliary canal (F). Low magnification TEM micrograph showing mature endothelial cells overlying the sinus (G). High magnification TEM micrograph of the mature endothelial cells (H). Note the cytoplasmic extensions and presence of large intracellular vacuoles. |
PMC1183199_F12_2660.jpg | What stands out most in this visual? | Ultrastructure of ventral ciliary canal. Diagrams of embryonic (A) and adult (E) zebrafish eye showing the locations of histological insets. Histological section through the central portion of the ventral ciliary canal (B). Low magnification TEM micrograph showing differentiating endothelial cells associated with the sinus (C). High magnification TEM micrograph of the undifferentiated endothelial cell, EN (D). Histological section through the central portion of the ventral ciliary canal (F). Low magnification TEM micrograph showing mature endothelial cells overlying the sinus (G). High magnification TEM micrograph of the mature endothelial cells (H). Note the cytoplasmic extensions and presence of large intracellular vacuoles. |
PMC1183199_F12_2662.jpg | What is the focal point of this photograph? | Ultrastructure of ventral ciliary canal. Diagrams of embryonic (A) and adult (E) zebrafish eye showing the locations of histological insets. Histological section through the central portion of the ventral ciliary canal (B). Low magnification TEM micrograph showing differentiating endothelial cells associated with the sinus (C). High magnification TEM micrograph of the undifferentiated endothelial cell, EN (D). Histological section through the central portion of the ventral ciliary canal (F). Low magnification TEM micrograph showing mature endothelial cells overlying the sinus (G). High magnification TEM micrograph of the mature endothelial cells (H). Note the cytoplasmic extensions and presence of large intracellular vacuoles. |
PMC1183199_F12_2661.jpg | What is the dominant medical problem in this image? | Ultrastructure of ventral ciliary canal. Diagrams of embryonic (A) and adult (E) zebrafish eye showing the locations of histological insets. Histological section through the central portion of the ventral ciliary canal (B). Low magnification TEM micrograph showing differentiating endothelial cells associated with the sinus (C). High magnification TEM micrograph of the undifferentiated endothelial cell, EN (D). Histological section through the central portion of the ventral ciliary canal (F). Low magnification TEM micrograph showing mature endothelial cells overlying the sinus (G). High magnification TEM micrograph of the mature endothelial cells (H). Note the cytoplasmic extensions and presence of large intracellular vacuoles. |
PMC1183199_F12_2659.jpg | What is the principal component of this image? | Ultrastructure of ventral ciliary canal. Diagrams of embryonic (A) and adult (E) zebrafish eye showing the locations of histological insets. Histological section through the central portion of the ventral ciliary canal (B). Low magnification TEM micrograph showing differentiating endothelial cells associated with the sinus (C). High magnification TEM micrograph of the undifferentiated endothelial cell, EN (D). Histological section through the central portion of the ventral ciliary canal (F). Low magnification TEM micrograph showing mature endothelial cells overlying the sinus (G). High magnification TEM micrograph of the mature endothelial cells (H). Note the cytoplasmic extensions and presence of large intracellular vacuoles. |
PMC1183199_F12_2658.jpg | What stands out most in this visual? | Ultrastructure of ventral ciliary canal. Diagrams of embryonic (A) and adult (E) zebrafish eye showing the locations of histological insets. Histological section through the central portion of the ventral ciliary canal (B). Low magnification TEM micrograph showing differentiating endothelial cells associated with the sinus (C). High magnification TEM micrograph of the undifferentiated endothelial cell, EN (D). Histological section through the central portion of the ventral ciliary canal (F). Low magnification TEM micrograph showing mature endothelial cells overlying the sinus (G). High magnification TEM micrograph of the mature endothelial cells (H). Note the cytoplasmic extensions and presence of large intracellular vacuoles. |
PMC1183220_F2_2667.jpg | What can you see in this picture? | Immunoreactive nerve fibres in non-painful (left column) and painful (right column) human tooth pulp sections, in pulp from painful teeth within the subontoblastic plexus region 'boxed' in Figure 1. Staining with antibodies to Nav1.8 (A and C) and neurofilament (B and D). Arrows indicate Nav1.8 immunoreactive nerve fibres. Magnification × 40 |
PMC1183220_F2_2665.jpg | What is the principal component of this image? | Immunoreactive nerve fibres in non-painful (left column) and painful (right column) human tooth pulp sections, in pulp from painful teeth within the subontoblastic plexus region 'boxed' in Figure 1. Staining with antibodies to Nav1.8 (A and C) and neurofilament (B and D). Arrows indicate Nav1.8 immunoreactive nerve fibres. Magnification × 40 |
PMC1183220_F2_2664.jpg | What is being portrayed in this visual content? | Immunoreactive nerve fibres in non-painful (left column) and painful (right column) human tooth pulp sections, in pulp from painful teeth within the subontoblastic plexus region 'boxed' in Figure 1. Staining with antibodies to Nav1.8 (A and C) and neurofilament (B and D). Arrows indicate Nav1.8 immunoreactive nerve fibres. Magnification × 40 |
PMC1183220_F2_2666.jpg | What can you see in this picture? | Immunoreactive nerve fibres in non-painful (left column) and painful (right column) human tooth pulp sections, in pulp from painful teeth within the subontoblastic plexus region 'boxed' in Figure 1. Staining with antibodies to Nav1.8 (A and C) and neurofilament (B and D). Arrows indicate Nav1.8 immunoreactive nerve fibres. Magnification × 40 |
PMC1183227_F1_2668.jpg | What is the main focus of this visual representation? | CT scan of chest of showing communication between the right main bronchus and the gastric conduit. |
PMC1183227_F1_2669.jpg | What is being portrayed in this visual content? | CT scan of chest of showing communication between the right main bronchus and the gastric conduit. |
PMC1183249_F7_2671.jpg | What can you see in this picture? | Representative photomicrograph of an intact (A) and epithelium-denuded (B) tracheal preparation. The photographs were taken at 100 × magnification. |
PMC1183249_F7_2670.jpg | What is the dominant medical problem in this image? | Representative photomicrograph of an intact (A) and epithelium-denuded (B) tracheal preparation. The photographs were taken at 100 × magnification. |
PMC1183253_F2_2672.jpg | What's the most prominent thing you notice in this picture? | Expression of E-Cadherin in the normal endocervix (2a, hematoxylin and eosin, original magnification ×100; 2b: hematoxylin and eosin, original magnification ×200), ectocervix (2c: hematoxylin and eosin, original magnification ×100) and squamous metaplastic epithelium at the transformation zone (2d) (hematoxylin and eosin, original magnification ×200). |
PMC1183253_F2_2674.jpg | What is the central feature of this picture? | Expression of E-Cadherin in the normal endocervix (2a, hematoxylin and eosin, original magnification ×100; 2b: hematoxylin and eosin, original magnification ×200), ectocervix (2c: hematoxylin and eosin, original magnification ×100) and squamous metaplastic epithelium at the transformation zone (2d) (hematoxylin and eosin, original magnification ×200). |
PMC1183253_F2_2673.jpg | What is shown in this image? | Expression of E-Cadherin in the normal endocervix (2a, hematoxylin and eosin, original magnification ×100; 2b: hematoxylin and eosin, original magnification ×200), ectocervix (2c: hematoxylin and eosin, original magnification ×100) and squamous metaplastic epithelium at the transformation zone (2d) (hematoxylin and eosin, original magnification ×200). |
PMC1184062_F4_2680.jpg | What is the dominant medical problem in this image? | RNA in situ hybridization and IHC analysis of colorectal cancer cases. Sections from sporadic/familial colorectal cancer and placenta (as positive control) were hybridised with Dig-labelled PSG9 RNA probes. Both PSG2 (b) and PSG9 (c) were expressed at a high level in placental tissue. Sense-probes were used as a negative control on placental tissue (a). In microscopic normal epithelial cells from FAP cases, PSG9 expression was detected at the top of crypt (d) (see discussion). PSG9 transcripts (shown as dark blue) were detected at very low levels in normal mucosa (e), adenomas (f), while high expression was detected in tumour cells from the same FAP case (g). In contrast to sporadic cases, PSG9 was detected in normal appearing mucosa in some FAP cases with APC germline mutations, suggesting that dose and level of APC have an impact on PSG9 levels in cells (e, i). A high level of PSG9 was detected in a sporadic case (k), while corresponding normal tissue was negative (i). Tumours and corresponding normal tissue were also examined for β-catenin stabilization by immunostaining (h, j, l). As expected, high levels of β-catenin were detected in all sporadic colorectal tumours (l), while the protein level was less intense in FAP cases (h) where PSG9 up-regulation could be measured (g). |
PMC1184062_F4_2677.jpg | What does this image primarily show? | RNA in situ hybridization and IHC analysis of colorectal cancer cases. Sections from sporadic/familial colorectal cancer and placenta (as positive control) were hybridised with Dig-labelled PSG9 RNA probes. Both PSG2 (b) and PSG9 (c) were expressed at a high level in placental tissue. Sense-probes were used as a negative control on placental tissue (a). In microscopic normal epithelial cells from FAP cases, PSG9 expression was detected at the top of crypt (d) (see discussion). PSG9 transcripts (shown as dark blue) were detected at very low levels in normal mucosa (e), adenomas (f), while high expression was detected in tumour cells from the same FAP case (g). In contrast to sporadic cases, PSG9 was detected in normal appearing mucosa in some FAP cases with APC germline mutations, suggesting that dose and level of APC have an impact on PSG9 levels in cells (e, i). A high level of PSG9 was detected in a sporadic case (k), while corresponding normal tissue was negative (i). Tumours and corresponding normal tissue were also examined for β-catenin stabilization by immunostaining (h, j, l). As expected, high levels of β-catenin were detected in all sporadic colorectal tumours (l), while the protein level was less intense in FAP cases (h) where PSG9 up-regulation could be measured (g). |
PMC1184062_F4_2679.jpg | What is the core subject represented in this visual? | RNA in situ hybridization and IHC analysis of colorectal cancer cases. Sections from sporadic/familial colorectal cancer and placenta (as positive control) were hybridised with Dig-labelled PSG9 RNA probes. Both PSG2 (b) and PSG9 (c) were expressed at a high level in placental tissue. Sense-probes were used as a negative control on placental tissue (a). In microscopic normal epithelial cells from FAP cases, PSG9 expression was detected at the top of crypt (d) (see discussion). PSG9 transcripts (shown as dark blue) were detected at very low levels in normal mucosa (e), adenomas (f), while high expression was detected in tumour cells from the same FAP case (g). In contrast to sporadic cases, PSG9 was detected in normal appearing mucosa in some FAP cases with APC germline mutations, suggesting that dose and level of APC have an impact on PSG9 levels in cells (e, i). A high level of PSG9 was detected in a sporadic case (k), while corresponding normal tissue was negative (i). Tumours and corresponding normal tissue were also examined for β-catenin stabilization by immunostaining (h, j, l). As expected, high levels of β-catenin were detected in all sporadic colorectal tumours (l), while the protein level was less intense in FAP cases (h) where PSG9 up-regulation could be measured (g). |
PMC1184062_F4_2685.jpg | What is the dominant medical problem in this image? | RNA in situ hybridization and IHC analysis of colorectal cancer cases. Sections from sporadic/familial colorectal cancer and placenta (as positive control) were hybridised with Dig-labelled PSG9 RNA probes. Both PSG2 (b) and PSG9 (c) were expressed at a high level in placental tissue. Sense-probes were used as a negative control on placental tissue (a). In microscopic normal epithelial cells from FAP cases, PSG9 expression was detected at the top of crypt (d) (see discussion). PSG9 transcripts (shown as dark blue) were detected at very low levels in normal mucosa (e), adenomas (f), while high expression was detected in tumour cells from the same FAP case (g). In contrast to sporadic cases, PSG9 was detected in normal appearing mucosa in some FAP cases with APC germline mutations, suggesting that dose and level of APC have an impact on PSG9 levels in cells (e, i). A high level of PSG9 was detected in a sporadic case (k), while corresponding normal tissue was negative (i). Tumours and corresponding normal tissue were also examined for β-catenin stabilization by immunostaining (h, j, l). As expected, high levels of β-catenin were detected in all sporadic colorectal tumours (l), while the protein level was less intense in FAP cases (h) where PSG9 up-regulation could be measured (g). |
PMC1184062_F4_2681.jpg | What is the principal component of this image? | RNA in situ hybridization and IHC analysis of colorectal cancer cases. Sections from sporadic/familial colorectal cancer and placenta (as positive control) were hybridised with Dig-labelled PSG9 RNA probes. Both PSG2 (b) and PSG9 (c) were expressed at a high level in placental tissue. Sense-probes were used as a negative control on placental tissue (a). In microscopic normal epithelial cells from FAP cases, PSG9 expression was detected at the top of crypt (d) (see discussion). PSG9 transcripts (shown as dark blue) were detected at very low levels in normal mucosa (e), adenomas (f), while high expression was detected in tumour cells from the same FAP case (g). In contrast to sporadic cases, PSG9 was detected in normal appearing mucosa in some FAP cases with APC germline mutations, suggesting that dose and level of APC have an impact on PSG9 levels in cells (e, i). A high level of PSG9 was detected in a sporadic case (k), while corresponding normal tissue was negative (i). Tumours and corresponding normal tissue were also examined for β-catenin stabilization by immunostaining (h, j, l). As expected, high levels of β-catenin were detected in all sporadic colorectal tumours (l), while the protein level was less intense in FAP cases (h) where PSG9 up-regulation could be measured (g). |
PMC1184062_F4_2678.jpg | What object or scene is depicted here? | RNA in situ hybridization and IHC analysis of colorectal cancer cases. Sections from sporadic/familial colorectal cancer and placenta (as positive control) were hybridised with Dig-labelled PSG9 RNA probes. Both PSG2 (b) and PSG9 (c) were expressed at a high level in placental tissue. Sense-probes were used as a negative control on placental tissue (a). In microscopic normal epithelial cells from FAP cases, PSG9 expression was detected at the top of crypt (d) (see discussion). PSG9 transcripts (shown as dark blue) were detected at very low levels in normal mucosa (e), adenomas (f), while high expression was detected in tumour cells from the same FAP case (g). In contrast to sporadic cases, PSG9 was detected in normal appearing mucosa in some FAP cases with APC germline mutations, suggesting that dose and level of APC have an impact on PSG9 levels in cells (e, i). A high level of PSG9 was detected in a sporadic case (k), while corresponding normal tissue was negative (i). Tumours and corresponding normal tissue were also examined for β-catenin stabilization by immunostaining (h, j, l). As expected, high levels of β-catenin were detected in all sporadic colorectal tumours (l), while the protein level was less intense in FAP cases (h) where PSG9 up-regulation could be measured (g). |
PMC1184062_F4_2682.jpg | What is the main focus of this visual representation? | RNA in situ hybridization and IHC analysis of colorectal cancer cases. Sections from sporadic/familial colorectal cancer and placenta (as positive control) were hybridised with Dig-labelled PSG9 RNA probes. Both PSG2 (b) and PSG9 (c) were expressed at a high level in placental tissue. Sense-probes were used as a negative control on placental tissue (a). In microscopic normal epithelial cells from FAP cases, PSG9 expression was detected at the top of crypt (d) (see discussion). PSG9 transcripts (shown as dark blue) were detected at very low levels in normal mucosa (e), adenomas (f), while high expression was detected in tumour cells from the same FAP case (g). In contrast to sporadic cases, PSG9 was detected in normal appearing mucosa in some FAP cases with APC germline mutations, suggesting that dose and level of APC have an impact on PSG9 levels in cells (e, i). A high level of PSG9 was detected in a sporadic case (k), while corresponding normal tissue was negative (i). Tumours and corresponding normal tissue were also examined for β-catenin stabilization by immunostaining (h, j, l). As expected, high levels of β-catenin were detected in all sporadic colorectal tumours (l), while the protein level was less intense in FAP cases (h) where PSG9 up-regulation could be measured (g). |
PMC1184062_F4_2683.jpg | What does this image primarily show? | RNA in situ hybridization and IHC analysis of colorectal cancer cases. Sections from sporadic/familial colorectal cancer and placenta (as positive control) were hybridised with Dig-labelled PSG9 RNA probes. Both PSG2 (b) and PSG9 (c) were expressed at a high level in placental tissue. Sense-probes were used as a negative control on placental tissue (a). In microscopic normal epithelial cells from FAP cases, PSG9 expression was detected at the top of crypt (d) (see discussion). PSG9 transcripts (shown as dark blue) were detected at very low levels in normal mucosa (e), adenomas (f), while high expression was detected in tumour cells from the same FAP case (g). In contrast to sporadic cases, PSG9 was detected in normal appearing mucosa in some FAP cases with APC germline mutations, suggesting that dose and level of APC have an impact on PSG9 levels in cells (e, i). A high level of PSG9 was detected in a sporadic case (k), while corresponding normal tissue was negative (i). Tumours and corresponding normal tissue were also examined for β-catenin stabilization by immunostaining (h, j, l). As expected, high levels of β-catenin were detected in all sporadic colorectal tumours (l), while the protein level was less intense in FAP cases (h) where PSG9 up-regulation could be measured (g). |
PMC1184065_F4_2688.jpg | What does this image primarily show? | Enhanced or abrogated FGF10/FGFR2b signaling modulates embryonic SMG branching morphogenesis in vitro. A-B. Enhanced signaling. Paired E13 SMG primordia were cultured for 3 days in the absence (A) or presence (B) of 500 ng/ml FGF10 peptide supplementation. FGF10 induced a significant increase in branching compared to control (CONT). C-D. Abrogated signaling. Paired E13 SMG primordia were cultured for 3 days in 10 ng/ml IgG-Fc (C) or FGFR2b-Fc chimera (D). FGFR2b-Fc chimera treated explant exhibits a significant decrease in branching compared to IgG-Fc control. Bar, 30 μm. E. Comparison of mean Spooner ratios in E13 + 3 and E14 + 2 explants. Exogenous FGF10 peptide supplementation induced a significant 81% increase in E13 +3 explants [200 ng/ml (P < 0.01); 500 ng/ml (P < 0.001)] and a significant 46% increase in E 14 + 2 explants (P < 0.0001) compared to controls. FGFR2b-Fc chimera-mediated interruption of E13 + 3 and E 14 + 2 SMGs significantly reduced branching morphogenesis by 22% [E13 +3: 10 ng/ml (P < 0.01); E 14 + 2: 5 ng/ml (P > 0.0001); 10 ng/ml (P < 0.01)] compared to controls. |
PMC1184065_F4_2690.jpg | What is the main focus of this visual representation? | Enhanced or abrogated FGF10/FGFR2b signaling modulates embryonic SMG branching morphogenesis in vitro. A-B. Enhanced signaling. Paired E13 SMG primordia were cultured for 3 days in the absence (A) or presence (B) of 500 ng/ml FGF10 peptide supplementation. FGF10 induced a significant increase in branching compared to control (CONT). C-D. Abrogated signaling. Paired E13 SMG primordia were cultured for 3 days in 10 ng/ml IgG-Fc (C) or FGFR2b-Fc chimera (D). FGFR2b-Fc chimera treated explant exhibits a significant decrease in branching compared to IgG-Fc control. Bar, 30 μm. E. Comparison of mean Spooner ratios in E13 + 3 and E14 + 2 explants. Exogenous FGF10 peptide supplementation induced a significant 81% increase in E13 +3 explants [200 ng/ml (P < 0.01); 500 ng/ml (P < 0.001)] and a significant 46% increase in E 14 + 2 explants (P < 0.0001) compared to controls. FGFR2b-Fc chimera-mediated interruption of E13 + 3 and E 14 + 2 SMGs significantly reduced branching morphogenesis by 22% [E13 +3: 10 ng/ml (P < 0.01); E 14 + 2: 5 ng/ml (P > 0.0001); 10 ng/ml (P < 0.01)] compared to controls. |
PMC1184065_F4_2691.jpg | Describe the main subject of this image. | Enhanced or abrogated FGF10/FGFR2b signaling modulates embryonic SMG branching morphogenesis in vitro. A-B. Enhanced signaling. Paired E13 SMG primordia were cultured for 3 days in the absence (A) or presence (B) of 500 ng/ml FGF10 peptide supplementation. FGF10 induced a significant increase in branching compared to control (CONT). C-D. Abrogated signaling. Paired E13 SMG primordia were cultured for 3 days in 10 ng/ml IgG-Fc (C) or FGFR2b-Fc chimera (D). FGFR2b-Fc chimera treated explant exhibits a significant decrease in branching compared to IgG-Fc control. Bar, 30 μm. E. Comparison of mean Spooner ratios in E13 + 3 and E14 + 2 explants. Exogenous FGF10 peptide supplementation induced a significant 81% increase in E13 +3 explants [200 ng/ml (P < 0.01); 500 ng/ml (P < 0.001)] and a significant 46% increase in E 14 + 2 explants (P < 0.0001) compared to controls. FGFR2b-Fc chimera-mediated interruption of E13 + 3 and E 14 + 2 SMGs significantly reduced branching morphogenesis by 22% [E13 +3: 10 ng/ml (P < 0.01); E 14 + 2: 5 ng/ml (P > 0.0001); 10 ng/ml (P < 0.01)] compared to controls. |
PMC1184092_F1_2693.jpg | What object or scene is depicted here? | Thick, deep blue colloid material with cracking pattern in FNA of a benign colloid nodule (Diff-Quik stain, × 250). |
PMC1184092_F7_2695.jpg | What is the principal component of this image? | Hurthle cells in loose, monolayered sheet and singly in FNA of a Hurthle cell lesion (Diff-Quik stain, × 400). |
PMC1184092_F8_2699.jpg | Describe the main subject of this image. | Thick branching papillary tissue fragment with fibrovascular core in FNA of a conventional papillary carcinoma (Papanicolaou stain, × 100). |
PMC1184092_F9_2696.jpg | What key item or scene is captured in this photo? | Thin branching papillary tissue fragment with fibrovascular core in FNA of a conventional papillary carcinoma (Papanicolaou stain, × 100). |
PMC1184092_F9_2697.jpg | What does this image primarily show? | Thin branching papillary tissue fragment with fibrovascular core in FNA of a conventional papillary carcinoma (Papanicolaou stain, × 100). |
PMC1184092_F10_2698.jpg | What key item or scene is captured in this photo? | A sheet of tumor cells showing focal nuclear crowding with several cells displaying nuclear grooves in FNA of a conventional papillary carcinoma (Papanicolaou stain, × 400). |
PMC1184092_F11_2701.jpg | What key item or scene is captured in this photo? | A loose sheet of tumor cells showing minimal nuclear crowding and two cells with intranuclear cytoplasmic inclusions in FNA of a conventional papillary carcinoma (Diff-Quik stain, × 400). |
PMC1184092_F13_2702.jpg | What is the main focus of this visual representation? | A loose cluster of metaplastic squamous cells seen in FNA of a conventional papillary carcinoma (Papanicolaou stain, × 400). |
PMC1184092_F14_2703.jpg | What is the central feature of this picture? | Papillary carcinoma, microfollicular variant showing in FNA cells in acinar arrangement. A tumor cell with an intranuclear cytoplasmic inclusion is noted (Papanicolaou stain, × 400). |
PMC1184092_F15_2707.jpg | What is the principal component of this image? | Papillary carcinoma, tall-cell variant showing in FNA a sheet of pleomorphic cells with some cells with elongated configuration and cytoplasmic tails. A tumor cell with intranuclear cytoplasmic inclusion is present (Diff-Quik stain, × 400). |
PMC1184092_F17_2705.jpg | What is shown in this image? | Medullary carcinoma showing in FNA dyshesive plasmacytoid tumor cells with eccentrically located round nuclei and intracytoplasmic azurophil granules (Diff-Quik stain, × 400). |
PMC1184092_F18_2706.jpg | What is the core subject represented in this visual? | Medullary carcinoma showing in FNA loosely clustered spindle-shaped tumor cells with scanty, ill-defined cytoplasm (Papanicolaou stain, × 400). |
PMC1184092_F20_2708.jpg | What is the central feature of this picture? | Anaplastic carcinoma, giant-cell type showing in FNA single and clustered large, bizarre malignant cells with pleomorphic nuclei and prominent nucleoli (Papanicolaou stain, × 400). |
PMC1184092_F24_2711.jpg | What is the dominant medical problem in this image? | Hashimoto thyroiditis showing in FNA numerous lymphoid cells admixed with a sheet of follicular epithelial cells (Papanicolaou stain, × 100). |
PMC1184092_F25_2710.jpg | What is the main focus of this visual representation? | A sheet of follicular epithelial cells with oncocytic change admixed with benign lymphoid cells seen in FNA of a Hashimoto thyroiditis (Papanicolaou stain, × 400). |
PMC1184092_F26_2712.jpg | What key item or scene is captured in this photo? | A syncytial cluster of epithelioid cells with carrot-shaped nuclei seen in FNA of a subacute thyroiditis (Diff-Quik stain, × 400). |
PMC1184093_F1_2714.jpg | What is shown in this image? | Endoscopic ultrasound image of a 52 x 39 mm hypoechoic mass in the upper mediastinum (Olympus UC-30P). |
PMC1184097_F4_2731.jpg | What can you see in this picture? | Enlargement and contrast of selected regions after 2-DE of mouse brain membranes (see areas defined in Fig 3). Areas i-vi show selective increases in spot number, resolution, and density. Samples were extracted with A) 4% CHAPS, B) 3% CHAPS : 1% LPC, C) 3% CHAPS : 1% MEGA 10, D) 3% CHAPS : 0.5% LPC : 0.5% MEGA 10. Results are representative of three independent experiments. Green arrows indicate spots showing increased volume and density, red arrows indicate decrease, blue arrows indicate novel spots. |
PMC1184097_F4_2718.jpg | What is shown in this image? | Enlargement and contrast of selected regions after 2-DE of mouse brain membranes (see areas defined in Fig 3). Areas i-vi show selective increases in spot number, resolution, and density. Samples were extracted with A) 4% CHAPS, B) 3% CHAPS : 1% LPC, C) 3% CHAPS : 1% MEGA 10, D) 3% CHAPS : 0.5% LPC : 0.5% MEGA 10. Results are representative of three independent experiments. Green arrows indicate spots showing increased volume and density, red arrows indicate decrease, blue arrows indicate novel spots. |
PMC1184102_F2_2740.jpg | What key item or scene is captured in this photo? | Histological appearance of C57 BI/6 mouse lungs 3 and 7 days following bleomycin challenge. (A) Histologic section from the lung of a C57 Bl/6 mouse treated with saline showing a normal parenchyma. Representative histologic sections of C57 Bl/6 mice at 3 (B) and 7 (C and D) days after bleomycin treatment showing appreciable morphologic emphysema but not fibrosis. Scattered inflammatory cells are present through lung parenchyma (E). (E) Shows a higher magnification of (D). (A-C): Hematoxylin-eosin stain, scale bar represents 400 μm. (D) and (E): Masson's trichrome stain, original magnification × 40 and × 100, respectively. Scale bars represent 400 μm and 100 μm, respectively. |
PMC1184102_F2_2736.jpg | What is shown in this image? | Histological appearance of C57 BI/6 mouse lungs 3 and 7 days following bleomycin challenge. (A) Histologic section from the lung of a C57 Bl/6 mouse treated with saline showing a normal parenchyma. Representative histologic sections of C57 Bl/6 mice at 3 (B) and 7 (C and D) days after bleomycin treatment showing appreciable morphologic emphysema but not fibrosis. Scattered inflammatory cells are present through lung parenchyma (E). (E) Shows a higher magnification of (D). (A-C): Hematoxylin-eosin stain, scale bar represents 400 μm. (D) and (E): Masson's trichrome stain, original magnification × 40 and × 100, respectively. Scale bars represent 400 μm and 100 μm, respectively. |
PMC1184102_F2_2737.jpg | What is the dominant medical problem in this image? | Histological appearance of C57 BI/6 mouse lungs 3 and 7 days following bleomycin challenge. (A) Histologic section from the lung of a C57 Bl/6 mouse treated with saline showing a normal parenchyma. Representative histologic sections of C57 Bl/6 mice at 3 (B) and 7 (C and D) days after bleomycin treatment showing appreciable morphologic emphysema but not fibrosis. Scattered inflammatory cells are present through lung parenchyma (E). (E) Shows a higher magnification of (D). (A-C): Hematoxylin-eosin stain, scale bar represents 400 μm. (D) and (E): Masson's trichrome stain, original magnification × 40 and × 100, respectively. Scale bars represent 400 μm and 100 μm, respectively. |
PMC1184102_F2_2738.jpg | What is the focal point of this photograph? | Histological appearance of C57 BI/6 mouse lungs 3 and 7 days following bleomycin challenge. (A) Histologic section from the lung of a C57 Bl/6 mouse treated with saline showing a normal parenchyma. Representative histologic sections of C57 Bl/6 mice at 3 (B) and 7 (C and D) days after bleomycin treatment showing appreciable morphologic emphysema but not fibrosis. Scattered inflammatory cells are present through lung parenchyma (E). (E) Shows a higher magnification of (D). (A-C): Hematoxylin-eosin stain, scale bar represents 400 μm. (D) and (E): Masson's trichrome stain, original magnification × 40 and × 100, respectively. Scale bars represent 400 μm and 100 μm, respectively. |
PMC1184102_F5_2743.jpg | What does this image primarily show? | Histological appearance of pallid and C57 Bl/6 mouse lungs 14 days following bleomycin challenge. Representative lung histologic sections of a pallid (A) and a C57BI/6 (B) mouse at 14 days after bleomycin. Fibrotic and emphysematous areas are widely spread and intermixed. Emphysema is often located quite distant from the fibrotic reaction (A-B).(C) shows a higher magnification of (B). (A): Hematoxylin-eosin stain, scale bar represents 400 μm. (B) and (C): Masson's trichrome stain, scale bars represent 400 μm and 100 μm, respectively. |
PMC1184102_F5_2742.jpg | What is the dominant medical problem in this image? | Histological appearance of pallid and C57 Bl/6 mouse lungs 14 days following bleomycin challenge. Representative lung histologic sections of a pallid (A) and a C57BI/6 (B) mouse at 14 days after bleomycin. Fibrotic and emphysematous areas are widely spread and intermixed. Emphysema is often located quite distant from the fibrotic reaction (A-B).(C) shows a higher magnification of (B). (A): Hematoxylin-eosin stain, scale bar represents 400 μm. (B) and (C): Masson's trichrome stain, scale bars represent 400 μm and 100 μm, respectively. |
PMC1184102_F7_2744.jpg | What is being portrayed in this visual content? | Immunohistochemical reaction for TGF-β and TGF-α 7 days following bleomycin challenge. Lung parenchyma of a C57BI/6 mouse at 7 days after bleomycin treatment. (A) Immunohistochemical reaction for TGF-β. Counterstained with hematoxylin, scale bar represents 40 μm. (B) Immunohistochemical reaction for TGF-α. Counterstained with hematoxylin, scale bar represents 25 μm. |
PMC1184102_F8_2746.jpg | What is being portrayed in this visual content? | Histological appearance of C57 BI/6 lung receiving 4-(2-aminoethyl)-benzenesulfonyl fluoride hydrochloride 21 days after bleomycin challenge. Representative histological section of a C57BI/6 mouse, receiving 4-(2-aminoethyl)-benzenesulfonyl fluoride hydrochloride and bleomycin, at 14 days after the treatment. No appreciable areas of emphysema are detectable in the lung parenchyma (A). Few trivial foci of fibrosis can be appreciated in some areas (B). (B) shows a higher magnification of (A). (A) and (B): Masson's trichrome stain, scale bars represent 400 μm and 50 μm, respectively. |
PMC1184102_F8_2747.jpg | What is the focal point of this photograph? | Histological appearance of C57 BI/6 lung receiving 4-(2-aminoethyl)-benzenesulfonyl fluoride hydrochloride 21 days after bleomycin challenge. Representative histological section of a C57BI/6 mouse, receiving 4-(2-aminoethyl)-benzenesulfonyl fluoride hydrochloride and bleomycin, at 14 days after the treatment. No appreciable areas of emphysema are detectable in the lung parenchyma (A). Few trivial foci of fibrosis can be appreciated in some areas (B). (B) shows a higher magnification of (A). (A) and (B): Masson's trichrome stain, scale bars represent 400 μm and 50 μm, respectively. |
PMC1184591_pbio-0030283-g002_2750.jpg | What does this image primarily show? | Clonal NS Cells Generated through Sox1 Neural Lineage Selection(A) Phase image of neural precursors at passage 1 (a) and 5 (c), with (b) and (d) showing corresponding Sox1-GFP fluorescence. Image (e) shows a single cell, 1 h after plating in Terasaki well, and (f) shows a phase-contrast image of clonal cell line at passage 20.(B) Differentiation of NS-5 cells into astrocytes (g,h) and neurons (j,k) with loss of nestin immunoreactivity (i,l).(C) These NS-5 cells are immunoreactive for neural precursor cell/radial glia markers (m–o,q,r) and negative for GFAP (p).(D) Clones of NS-5 cells exhibit homogenous expression of BLBP with no immunoreactivity for GFAP in the presence of EGF/FGF (s), and generate neurons upon growth factor withdrawal (t).(E) Metaphase spread of NS-5 (passage 31). |
PMC1184591_pbio-0030283-g002_2752.jpg | What does this image primarily show? | Clonal NS Cells Generated through Sox1 Neural Lineage Selection(A) Phase image of neural precursors at passage 1 (a) and 5 (c), with (b) and (d) showing corresponding Sox1-GFP fluorescence. Image (e) shows a single cell, 1 h after plating in Terasaki well, and (f) shows a phase-contrast image of clonal cell line at passage 20.(B) Differentiation of NS-5 cells into astrocytes (g,h) and neurons (j,k) with loss of nestin immunoreactivity (i,l).(C) These NS-5 cells are immunoreactive for neural precursor cell/radial glia markers (m–o,q,r) and negative for GFAP (p).(D) Clones of NS-5 cells exhibit homogenous expression of BLBP with no immunoreactivity for GFAP in the presence of EGF/FGF (s), and generate neurons upon growth factor withdrawal (t).(E) Metaphase spread of NS-5 (passage 31). |
PMC1184591_pbio-0030283-g002_2748.jpg | What object or scene is depicted here? | Clonal NS Cells Generated through Sox1 Neural Lineage Selection(A) Phase image of neural precursors at passage 1 (a) and 5 (c), with (b) and (d) showing corresponding Sox1-GFP fluorescence. Image (e) shows a single cell, 1 h after plating in Terasaki well, and (f) shows a phase-contrast image of clonal cell line at passage 20.(B) Differentiation of NS-5 cells into astrocytes (g,h) and neurons (j,k) with loss of nestin immunoreactivity (i,l).(C) These NS-5 cells are immunoreactive for neural precursor cell/radial glia markers (m–o,q,r) and negative for GFAP (p).(D) Clones of NS-5 cells exhibit homogenous expression of BLBP with no immunoreactivity for GFAP in the presence of EGF/FGF (s), and generate neurons upon growth factor withdrawal (t).(E) Metaphase spread of NS-5 (passage 31). |
PMC1185534_F3_2755.jpg | What is being portrayed in this visual content? | FISH analysis of BAC clones RP11-573E11 (panel A), RP11-51B23 and RP11-47J17 (not shown) in parental cells NGP.1A.TR1 (with a derivative chromosome 11, due to an unbalanced translocation between chromosomes 11 and 2) confirms the existence of a small deletion in 11p15.3. The breakpoint of the distal 11q25->11qter deletion of the transferred chromosome in subclone MCH574c3 was mapped between BAC clones RP11-340L13 (not shown) and RP11-697E14 (panel B). |
PMC1185534_F3_2754.jpg | What is the focal point of this photograph? | FISH analysis of BAC clones RP11-573E11 (panel A), RP11-51B23 and RP11-47J17 (not shown) in parental cells NGP.1A.TR1 (with a derivative chromosome 11, due to an unbalanced translocation between chromosomes 11 and 2) confirms the existence of a small deletion in 11p15.3. The breakpoint of the distal 11q25->11qter deletion of the transferred chromosome in subclone MCH574c3 was mapped between BAC clones RP11-340L13 (not shown) and RP11-697E14 (panel B). |
PMC1185555_F2_2758.jpg | Describe the main subject of this image. | In normal pancreas, only the intercalated duct cells were positive for MUC1. (Left: HE, Right: MUC1, original magnification × 400) |
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