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PMC1044835_pbio-0030079-g005_1496.jpg | Can you identify the primary element in this image? | Significant Signal Changes in Subjects Receiving Explicit Instructions Compared to Subjects Receiving Implicit Instructions in the Three Tasks Versus RestThreshold of Z = 2.3 at voxel level and a cluster level corrected for the whole brain at p < 0.05. The two black arrows indicate two foci of activity in dorsal premotor cortex that are located deep in the sulci and thus not easily visible on the three-dimensional surface rendering. See Tables S3–S5 for coordinates of local maxima. |
PMC1044835_pbio-0030079-g005_1494.jpg | Describe the main subject of this image. | Significant Signal Changes in Subjects Receiving Explicit Instructions Compared to Subjects Receiving Implicit Instructions in the Three Tasks Versus RestThreshold of Z = 2.3 at voxel level and a cluster level corrected for the whole brain at p < 0.05. The two black arrows indicate two foci of activity in dorsal premotor cortex that are located deep in the sulci and thus not easily visible on the three-dimensional surface rendering. See Tables S3–S5 for coordinates of local maxima. |
PMC1064074_F2_1497.jpg | What can you see in this picture? | Role of Na+–H+ exchanger (NHE)1 in serum deprivation-dependent rearrangement of the actin cytoskeleton. (a) To examine the role of NHE1 in serum deprivation-induced reorganization of the actin cytoskeleton underlying motility and invasive ability, MDA-MB-435 cell monolayers were left in fresh whole growth medium (nondeprived [ND]) or were serum deprived (D) in the presence or absence of 2 μmol/l of the specific NHE1 inhibitor 5-(N, N-dimethyl)-amiloride (DMA) for 1 day. The fluorescent photomicrographs show cell groups at a magnification of 40× (bar = 10 μm). (b) typical one-parameter fluorescence distributions of MDA-MB-435 cells labelled with phalloidin–fluorescein isothiocyanate in the above experimental conditions. The lighter coloured curve is from control, ND cells. Cyt B is the fluorescence distribution after treatment with the actin cytoskeleton disruptor cytochalasin B (5 μmol/l for 15 min). (c) Relative intracellular F-actin content measured by flow cytometry in MDA-MB-435 cells in the above experimental conditions. Mean ± standard error. n = 9; **P < 0.001 versus ND cells. |
PMC1064074_F2_1498.jpg | What is the core subject represented in this visual? | Role of Na+–H+ exchanger (NHE)1 in serum deprivation-dependent rearrangement of the actin cytoskeleton. (a) To examine the role of NHE1 in serum deprivation-induced reorganization of the actin cytoskeleton underlying motility and invasive ability, MDA-MB-435 cell monolayers were left in fresh whole growth medium (nondeprived [ND]) or were serum deprived (D) in the presence or absence of 2 μmol/l of the specific NHE1 inhibitor 5-(N, N-dimethyl)-amiloride (DMA) for 1 day. The fluorescent photomicrographs show cell groups at a magnification of 40× (bar = 10 μm). (b) typical one-parameter fluorescence distributions of MDA-MB-435 cells labelled with phalloidin–fluorescein isothiocyanate in the above experimental conditions. The lighter coloured curve is from control, ND cells. Cyt B is the fluorescence distribution after treatment with the actin cytoskeleton disruptor cytochalasin B (5 μmol/l for 15 min). (c) Relative intracellular F-actin content measured by flow cytometry in MDA-MB-435 cells in the above experimental conditions. Mean ± standard error. n = 9; **P < 0.001 versus ND cells. |
PMC1064077_F7_1501.jpg | What stands out most in this visual? | Solid carcinoma from a mouse transgenic for Hras: expression of α-smooth muscle actin in carcinomas is restricted to stromal myofibroblasts and vascular smooth muscle fibers. A similar observation was made for carcinomas arising in mice transgenic for Neu (Erbb2) and Notch 4 and in most mice transgenic for SV40-TAg (not shown). Scale bar, 320 μm. |
PMC1064094_F1_1511.jpg | Can you identify the primary element in this image? | Histological features of the carcinomatous breast (magnification × 100). Detailed histology of (a) is seen in (b–d). AS, anucleate squames; asterisks, interstitial lymphocytic infiltrates; G, galactophore; K, keratin; LS, lactiferous sinus; LD, lactiferous duct; SG, sebaceous gland (tangenial cut); SGD, sweat gland duct; SH, simple epithelial hyperplasia; PH, papillary epithelial hyperplasia. |
PMC1064094_F1_1512.jpg | What is shown in this image? | Histological features of the carcinomatous breast (magnification × 100). Detailed histology of (a) is seen in (b–d). AS, anucleate squames; asterisks, interstitial lymphocytic infiltrates; G, galactophore; K, keratin; LS, lactiferous sinus; LD, lactiferous duct; SG, sebaceous gland (tangenial cut); SGD, sweat gland duct; SH, simple epithelial hyperplasia; PH, papillary epithelial hyperplasia. |
PMC1064094_F1_1513.jpg | What's the most prominent thing you notice in this picture? | Histological features of the carcinomatous breast (magnification × 100). Detailed histology of (a) is seen in (b–d). AS, anucleate squames; asterisks, interstitial lymphocytic infiltrates; G, galactophore; K, keratin; LS, lactiferous sinus; LD, lactiferous duct; SG, sebaceous gland (tangenial cut); SGD, sweat gland duct; SH, simple epithelial hyperplasia; PH, papillary epithelial hyperplasia. |
PMC1064094_F1_1514.jpg | What is the principal component of this image? | Histological features of the carcinomatous breast (magnification × 100). Detailed histology of (a) is seen in (b–d). AS, anucleate squames; asterisks, interstitial lymphocytic infiltrates; G, galactophore; K, keratin; LS, lactiferous sinus; LD, lactiferous duct; SG, sebaceous gland (tangenial cut); SGD, sweat gland duct; SH, simple epithelial hyperplasia; PH, papillary epithelial hyperplasia. |
PMC1064094_F2_1505.jpg | What is the central feature of this picture? | Papillomavirus sequences detected by in situ hybridisation. (a) Case 10012, in the nipple epithelium (magnification × 40). (b) Case 10041, in the nipple epithelium (magnification × 40). (c) Case 10012, in tumour tissue (magnification × 100). (d) Case 10014, in tumour tissue (magnification × 100). |
PMC1064094_F2_1506.jpg | What does this image primarily show? | Papillomavirus sequences detected by in situ hybridisation. (a) Case 10012, in the nipple epithelium (magnification × 40). (b) Case 10041, in the nipple epithelium (magnification × 40). (c) Case 10012, in tumour tissue (magnification × 100). (d) Case 10014, in tumour tissue (magnification × 100). |
PMC1064094_F2_1503.jpg | Describe the main subject of this image. | Papillomavirus sequences detected by in situ hybridisation. (a) Case 10012, in the nipple epithelium (magnification × 40). (b) Case 10041, in the nipple epithelium (magnification × 40). (c) Case 10012, in tumour tissue (magnification × 100). (d) Case 10014, in tumour tissue (magnification × 100). |
PMC1064094_F2_1504.jpg | Describe the main subject of this image. | Papillomavirus sequences detected by in situ hybridisation. (a) Case 10012, in the nipple epithelium (magnification × 40). (b) Case 10041, in the nipple epithelium (magnification × 40). (c) Case 10012, in tumour tissue (magnification × 100). (d) Case 10014, in tumour tissue (magnification × 100). |
PMC1064097_F1_1508.jpg | What is the central feature of this picture? | A 3-cm infiltrating ductal carcinoma of the right breast. Scintimammography, right lateral projection: 99mTc-(V)DMSA at 10 min and 60 min (upper row, i-ii); 99mTc-Sestamibi (99mTc-MIBI) at 13 min and 55 min (bottom row, iii-iv). Focal radiotracer accumulation (arrowhead) in the upper breast hemisphere, corresponding to the invasive tumor, visible in early and late images with both radiotracers. There is no diffuse uptake pattern in the breast; the studies are considered negative for in situ carcinoma. |
PMC1064097_F1_1509.jpg | What is the main focus of this visual representation? | A 3-cm infiltrating ductal carcinoma of the right breast. Scintimammography, right lateral projection: 99mTc-(V)DMSA at 10 min and 60 min (upper row, i-ii); 99mTc-Sestamibi (99mTc-MIBI) at 13 min and 55 min (bottom row, iii-iv). Focal radiotracer accumulation (arrowhead) in the upper breast hemisphere, corresponding to the invasive tumor, visible in early and late images with both radiotracers. There is no diffuse uptake pattern in the breast; the studies are considered negative for in situ carcinoma. |
PMC1064097_F1_1510.jpg | What is being portrayed in this visual content? | A 3-cm infiltrating ductal carcinoma of the right breast. Scintimammography, right lateral projection: 99mTc-(V)DMSA at 10 min and 60 min (upper row, i-ii); 99mTc-Sestamibi (99mTc-MIBI) at 13 min and 55 min (bottom row, iii-iv). Focal radiotracer accumulation (arrowhead) in the upper breast hemisphere, corresponding to the invasive tumor, visible in early and late images with both radiotracers. There is no diffuse uptake pattern in the breast; the studies are considered negative for in situ carcinoma. |
PMC1064097_F1_1507.jpg | What key item or scene is captured in this photo? | A 3-cm infiltrating ductal carcinoma of the right breast. Scintimammography, right lateral projection: 99mTc-(V)DMSA at 10 min and 60 min (upper row, i-ii); 99mTc-Sestamibi (99mTc-MIBI) at 13 min and 55 min (bottom row, iii-iv). Focal radiotracer accumulation (arrowhead) in the upper breast hemisphere, corresponding to the invasive tumor, visible in early and late images with both radiotracers. There is no diffuse uptake pattern in the breast; the studies are considered negative for in situ carcinoma. |
PMC1064097_F2_1515.jpg | What does this image primarily show? | A 5-cm infiltrating ductal carcinoma, grade 2, with 9-cm, comedo-type, ductal carcinoma in situ of the right breast (patient 4). (a) Mammography, medio-lateral projection. Nodule with spiky margins (transparent arrow), close to the chest wall in the upper breast hemisphere. (b) Scintimammography, right lateral projection: 99mTc-Sestamibi (99mTc-MIBI) at 5 min and 60 min (upper row, i-ii); 99mTc-(V)DMSA at 10 min and 60 min (bottom row, iii-iv). Spindle-shaped focal accumulation (arrowhead) in the area corresponding to the radiological abnormality. The 60-min 99mTc-(V)DMSA image additionally reveals an extensive area of diffuse heterogeneous patchy tracer uptake (arrow) extending below and anterior to the margins of the focal accumulation. Lymph node involvement in the axilla is visible (curved arrow). |
PMC1064097_F2_1518.jpg | Can you identify the primary element in this image? | A 5-cm infiltrating ductal carcinoma, grade 2, with 9-cm, comedo-type, ductal carcinoma in situ of the right breast (patient 4). (a) Mammography, medio-lateral projection. Nodule with spiky margins (transparent arrow), close to the chest wall in the upper breast hemisphere. (b) Scintimammography, right lateral projection: 99mTc-Sestamibi (99mTc-MIBI) at 5 min and 60 min (upper row, i-ii); 99mTc-(V)DMSA at 10 min and 60 min (bottom row, iii-iv). Spindle-shaped focal accumulation (arrowhead) in the area corresponding to the radiological abnormality. The 60-min 99mTc-(V)DMSA image additionally reveals an extensive area of diffuse heterogeneous patchy tracer uptake (arrow) extending below and anterior to the margins of the focal accumulation. Lymph node involvement in the axilla is visible (curved arrow). |
PMC1064097_F2_1516.jpg | What is the principal component of this image? | A 5-cm infiltrating ductal carcinoma, grade 2, with 9-cm, comedo-type, ductal carcinoma in situ of the right breast (patient 4). (a) Mammography, medio-lateral projection. Nodule with spiky margins (transparent arrow), close to the chest wall in the upper breast hemisphere. (b) Scintimammography, right lateral projection: 99mTc-Sestamibi (99mTc-MIBI) at 5 min and 60 min (upper row, i-ii); 99mTc-(V)DMSA at 10 min and 60 min (bottom row, iii-iv). Spindle-shaped focal accumulation (arrowhead) in the area corresponding to the radiological abnormality. The 60-min 99mTc-(V)DMSA image additionally reveals an extensive area of diffuse heterogeneous patchy tracer uptake (arrow) extending below and anterior to the margins of the focal accumulation. Lymph node involvement in the axilla is visible (curved arrow). |
PMC1064097_F2_1519.jpg | What is being portrayed in this visual content? | A 5-cm infiltrating ductal carcinoma, grade 2, with 9-cm, comedo-type, ductal carcinoma in situ of the right breast (patient 4). (a) Mammography, medio-lateral projection. Nodule with spiky margins (transparent arrow), close to the chest wall in the upper breast hemisphere. (b) Scintimammography, right lateral projection: 99mTc-Sestamibi (99mTc-MIBI) at 5 min and 60 min (upper row, i-ii); 99mTc-(V)DMSA at 10 min and 60 min (bottom row, iii-iv). Spindle-shaped focal accumulation (arrowhead) in the area corresponding to the radiological abnormality. The 60-min 99mTc-(V)DMSA image additionally reveals an extensive area of diffuse heterogeneous patchy tracer uptake (arrow) extending below and anterior to the margins of the focal accumulation. Lymph node involvement in the axilla is visible (curved arrow). |
PMC1064097_F3_1526.jpg | What object or scene is depicted here? | A 6-cm infiltrating ductal carcinoma, grade 2, with coexistent 5-cm ductal carcinoma in situ, comedo type, of the left breast (patient 1). (a) Mammography, medio-lateral projection. Multinodular opacity with abnormal radiating spicules and clustered microcalcifications (transparent arrow) behind the nipple. (b) Scintimammography, left lateral projection: 99mTc-Sestamibi (99mTc-MIBI) at 10 min and 65 min (upper row, i-ii); 99mTc-(V)DMSA at 15 min and 60 min (bottom row, iii-iv). Increased bifocal 99mTc-Sestamibi uptake (arrowheads) behind the nipple, clearly defining the invasive component of the tumor. Focal 99mTc-(V)DMSA accumulation in the same area (arrowhead), with additional diffuse uptake (arrow) extending inferiorly, more prominent at 60 min and corresponding to the in situ tumor component. No diffuse pattern is imaged with 99mTc-Sestamibi. (c) Scintimammography, left lateral projection: 99mTc-(V)DMSA at 60 min (same as (b) iv), with regions of interest (ROIs) drawn. ROI selection for diffuse uptake with each tracer is based on the comparison between early and late images (see text). |
PMC1064097_F3_1528.jpg | What is the principal component of this image? | A 6-cm infiltrating ductal carcinoma, grade 2, with coexistent 5-cm ductal carcinoma in situ, comedo type, of the left breast (patient 1). (a) Mammography, medio-lateral projection. Multinodular opacity with abnormal radiating spicules and clustered microcalcifications (transparent arrow) behind the nipple. (b) Scintimammography, left lateral projection: 99mTc-Sestamibi (99mTc-MIBI) at 10 min and 65 min (upper row, i-ii); 99mTc-(V)DMSA at 15 min and 60 min (bottom row, iii-iv). Increased bifocal 99mTc-Sestamibi uptake (arrowheads) behind the nipple, clearly defining the invasive component of the tumor. Focal 99mTc-(V)DMSA accumulation in the same area (arrowhead), with additional diffuse uptake (arrow) extending inferiorly, more prominent at 60 min and corresponding to the in situ tumor component. No diffuse pattern is imaged with 99mTc-Sestamibi. (c) Scintimammography, left lateral projection: 99mTc-(V)DMSA at 60 min (same as (b) iv), with regions of interest (ROIs) drawn. ROI selection for diffuse uptake with each tracer is based on the comparison between early and late images (see text). |
PMC1064097_F4_1521.jpg | What is the focal point of this photograph? | A 4.5-cm ductal carcinoma in situ of the left breast, comedo, solid and cribriform type (patient 18). (a) Mammography, medio-lateral projection. Microcalcifications (transparent arrow) behind the nipple. (b) Scintimammography, left lateral projection: 99mTc-(V)DMSA at 10 min and 60 min (i-ii). Diffuse semi-lunar accumulation (arrow) extending behind the nipple, more prominent in the late image. 99mTc-Sestamibi scan was not performed in this patient. |
PMC1064097_F4_1520.jpg | Describe the main subject of this image. | A 4.5-cm ductal carcinoma in situ of the left breast, comedo, solid and cribriform type (patient 18). (a) Mammography, medio-lateral projection. Microcalcifications (transparent arrow) behind the nipple. (b) Scintimammography, left lateral projection: 99mTc-(V)DMSA at 10 min and 60 min (i-ii). Diffuse semi-lunar accumulation (arrow) extending behind the nipple, more prominent in the late image. 99mTc-Sestamibi scan was not performed in this patient. |
PMC1064097_F5_1537.jpg | What's the most prominent thing you notice in this picture? | A 4-cm infiltrating lobular carcinoma, grade 3, associated with 6-cm lobular carcinoma in situ (LCIS) of the left breast in a 65-year-old woman (patient 20). (a) Mammography, cranio-caudal projection. Nodular opacity (asterisk) in the inner hemisphere of the breast. (b) Scintimammography, left lateral projection: 99mTc-Sestamibi (99mTc-MIBI) at 10 min and 60 min (upper row, i-ii); 99mTc-(V)DMSA at 10 min and 60 min (bottom row, iii-iv). Focal increased uptake (arrowhead) between upper and lower breast hemisphere, imaged by both radiotracers, corresponding to an invasive tumor. A diffuse patchy 'V'-shaped tracer accumulation (arrows), surrounding the focal activity and extending anterior to it, is revealed with 99mTc-(V)DMSA at 60 min only (iv). It corresponds to LCIS. |
PMC1064097_F6_1524.jpg | What is the focal point of this photograph? | Atypical epithelial hyperplasia of the right breast in a 41-year-old woman. Scintimammography, right lateral projection: 99mTc-(V)DMSA at 15 min and 75 min (upper row, i-ii); 99mTc-Sestamibi (99mTc-MIBI) at 10 min and 70 min (bottom row, iii-iv). Increased diffuse homogeneous 99mTc-(V)DMSA uptake (arrow) at early and late acquisitions, more prominent in the late image. Very faint (hardly visible) 99mTc-Sestamibi activity (arrow) in the same area. |
PMC1064097_F6_1523.jpg | What's the most prominent thing you notice in this picture? | Atypical epithelial hyperplasia of the right breast in a 41-year-old woman. Scintimammography, right lateral projection: 99mTc-(V)DMSA at 15 min and 75 min (upper row, i-ii); 99mTc-Sestamibi (99mTc-MIBI) at 10 min and 70 min (bottom row, iii-iv). Increased diffuse homogeneous 99mTc-(V)DMSA uptake (arrow) at early and late acquisitions, more prominent in the late image. Very faint (hardly visible) 99mTc-Sestamibi activity (arrow) in the same area. |
PMC1064097_F6_1522.jpg | Describe the main subject of this image. | Atypical epithelial hyperplasia of the right breast in a 41-year-old woman. Scintimammography, right lateral projection: 99mTc-(V)DMSA at 15 min and 75 min (upper row, i-ii); 99mTc-Sestamibi (99mTc-MIBI) at 10 min and 70 min (bottom row, iii-iv). Increased diffuse homogeneous 99mTc-(V)DMSA uptake (arrow) at early and late acquisitions, more prominent in the late image. Very faint (hardly visible) 99mTc-Sestamibi activity (arrow) in the same area. |
PMC1064097_F7_1536.jpg | What is the dominant medical problem in this image? | Ductal carcinoma in situ (DCIS), comedo, solid and cribriform type (patient 18). (a) Tumor section (hematoxylin & eosin, × 25). Regions of DCIS (arrowheads), within normal breast tissue (asterisk). (b) In vitro 99mTc-(V)DMSA autoradiogram of the same section (× 25). Distribution of the radioactivity in the same tumor section. The sites of intense tracer uptake (curved arrow) appear darker. (c) Overlay of stained tumor section and autoradiogram. The histologically detected lesion is well correlated with the tissue sites of intense 99mTc-(V)DMSA uptake. |
PMC1064097_F7_1534.jpg | What object or scene is depicted here? | Ductal carcinoma in situ (DCIS), comedo, solid and cribriform type (patient 18). (a) Tumor section (hematoxylin & eosin, × 25). Regions of DCIS (arrowheads), within normal breast tissue (asterisk). (b) In vitro 99mTc-(V)DMSA autoradiogram of the same section (× 25). Distribution of the radioactivity in the same tumor section. The sites of intense tracer uptake (curved arrow) appear darker. (c) Overlay of stained tumor section and autoradiogram. The histologically detected lesion is well correlated with the tissue sites of intense 99mTc-(V)DMSA uptake. |
PMC1064098_F1_1533.jpg | Can you identify the primary element in this image? | MCF10A cells and MCF10AT cells in monoculture and in co-culture with fibroblasts. (a), (b) MCF10A cells and (c), (d) MCF10AT cells in monoculture initially form a lattice/scaffold arrangement (a, c). After several days of culture, spheroidal structures become more prominent (b, d). (e) MCF10AT cells in co-culture with fibroblasts form three-dimensional rounded structures. Similar structures are formed by MCF10A cells in co-culture with fibroblasts (phase contrast, 100 × magnification; scale bar, 200 μm). |
PMC1064098_F1_1529.jpg | Describe the main subject of this image. | MCF10A cells and MCF10AT cells in monoculture and in co-culture with fibroblasts. (a), (b) MCF10A cells and (c), (d) MCF10AT cells in monoculture initially form a lattice/scaffold arrangement (a, c). After several days of culture, spheroidal structures become more prominent (b, d). (e) MCF10AT cells in co-culture with fibroblasts form three-dimensional rounded structures. Similar structures are formed by MCF10A cells in co-culture with fibroblasts (phase contrast, 100 × magnification; scale bar, 200 μm). |
PMC1064098_F1_1530.jpg | What is the main focus of this visual representation? | MCF10A cells and MCF10AT cells in monoculture and in co-culture with fibroblasts. (a), (b) MCF10A cells and (c), (d) MCF10AT cells in monoculture initially form a lattice/scaffold arrangement (a, c). After several days of culture, spheroidal structures become more prominent (b, d). (e) MCF10AT cells in co-culture with fibroblasts form three-dimensional rounded structures. Similar structures are formed by MCF10A cells in co-culture with fibroblasts (phase contrast, 100 × magnification; scale bar, 200 μm). |
PMC1064098_F1_1531.jpg | What stands out most in this visual? | MCF10A cells and MCF10AT cells in monoculture and in co-culture with fibroblasts. (a), (b) MCF10A cells and (c), (d) MCF10AT cells in monoculture initially form a lattice/scaffold arrangement (a, c). After several days of culture, spheroidal structures become more prominent (b, d). (e) MCF10AT cells in co-culture with fibroblasts form three-dimensional rounded structures. Similar structures are formed by MCF10A cells in co-culture with fibroblasts (phase contrast, 100 × magnification; scale bar, 200 μm). |
PMC1064098_F2_1540.jpg | What does this image primarily show? | H&E-stained histologic sections of MCF10A cell and MCF10AT cell monocultures and co-cultures with fibroblasts. (a) MCF10A cells form small spheroids. (b) MCF10A cells in co-culture with fibroblasts are located adjacent to the fibroblast aggregate (F) and maintain smaller spheroids. (c) In monoculture, MCF10AT cells form larger rounded three-dimensional structures. (d) In co-culture, MCF10AT cells form solid sheets and rounded groups of cells located adjacent to the fibroblasts (F). The occurrence of squamous metaplasia (SM) is more evident in MCF10AT monocultures, while it is suppressed in co-cultures. Overall, MCF10A cells have less squamous metaplasia than MCF10AT cultures (400 × magnification; scale bar, 50 μm). |
PMC1064098_F2_1542.jpg | What is the principal component of this image? | H&E-stained histologic sections of MCF10A cell and MCF10AT cell monocultures and co-cultures with fibroblasts. (a) MCF10A cells form small spheroids. (b) MCF10A cells in co-culture with fibroblasts are located adjacent to the fibroblast aggregate (F) and maintain smaller spheroids. (c) In monoculture, MCF10AT cells form larger rounded three-dimensional structures. (d) In co-culture, MCF10AT cells form solid sheets and rounded groups of cells located adjacent to the fibroblasts (F). The occurrence of squamous metaplasia (SM) is more evident in MCF10AT monocultures, while it is suppressed in co-cultures. Overall, MCF10A cells have less squamous metaplasia than MCF10AT cultures (400 × magnification; scale bar, 50 μm). |
PMC1064098_F2_1543.jpg | What is the dominant medical problem in this image? | H&E-stained histologic sections of MCF10A cell and MCF10AT cell monocultures and co-cultures with fibroblasts. (a) MCF10A cells form small spheroids. (b) MCF10A cells in co-culture with fibroblasts are located adjacent to the fibroblast aggregate (F) and maintain smaller spheroids. (c) In monoculture, MCF10AT cells form larger rounded three-dimensional structures. (d) In co-culture, MCF10AT cells form solid sheets and rounded groups of cells located adjacent to the fibroblasts (F). The occurrence of squamous metaplasia (SM) is more evident in MCF10AT monocultures, while it is suppressed in co-cultures. Overall, MCF10A cells have less squamous metaplasia than MCF10AT cultures (400 × magnification; scale bar, 50 μm). |
PMC1064098_F3_1546.jpg | What is the core subject represented in this visual? | Distribution and relative quantities of fibroblasts and epithelial cells in a normal terminal duct-lobular unit, hyperplasia and ductal carcinoma in situ (DCIS). (a) A terminal duct-lobular unit with epithelial cells (arrowheads) arranged in acini and intralobular terminal ducts separated by stroma-containing fibroblasts (arrows) in a ratio of epithelial cells to fibroblasts (E:F) of 2.7:1. (b) Ductal hyperplasia with a proliferation of epithelial cells (arrowheads) filling and expanding terminal ducts separated by reactive stroma including fibroblasts (arrows) in an E:F of 3.3:1. (c) High-grade DCIS, with epithelial cells (arrowheads) demonstrating markedly atypical nuclei, involving terminal ducts separated by reactive stroma including fibroblasts (arrows) in an E:F of 2:1 (200 × magnification; scale bar, 50 μm). |
PMC1064098_F3_1545.jpg | What can you see in this picture? | Distribution and relative quantities of fibroblasts and epithelial cells in a normal terminal duct-lobular unit, hyperplasia and ductal carcinoma in situ (DCIS). (a) A terminal duct-lobular unit with epithelial cells (arrowheads) arranged in acini and intralobular terminal ducts separated by stroma-containing fibroblasts (arrows) in a ratio of epithelial cells to fibroblasts (E:F) of 2.7:1. (b) Ductal hyperplasia with a proliferation of epithelial cells (arrowheads) filling and expanding terminal ducts separated by reactive stroma including fibroblasts (arrows) in an E:F of 3.3:1. (c) High-grade DCIS, with epithelial cells (arrowheads) demonstrating markedly atypical nuclei, involving terminal ducts separated by reactive stroma including fibroblasts (arrows) in an E:F of 2:1 (200 × magnification; scale bar, 50 μm). |
PMC1064114_F1_1549.jpg | What is the focal point of this photograph? | Histopathology of tumours in (BALB/cHeA × MSM/Ms)F1 mice with genotypes p53+/- Atm+/-, p53+/- Atm+/+ or p53+/+ Atm+/-. (a, b) Spontaneously developing mammary adenocarcinoma from p53+/- Atm+/- mouse. (c, d) Mammary adenocarcinoma from X-irradiated p53+/- Atm+/- mouse. (e, f) Mammary adenocarcinoma from X-irradiated p53+/- Atm+/+ mouse. (g) Osteosarcoma observed in nonirradiated p53+/- Atm+/- mouse. (h) Thymic lymphoma from p53+/+ Atm+/- mouse exposed to X-rays. Panels a, c and e: 40×. Panels b, d, f, g and h: 100×. |
PMC1064114_F1_1552.jpg | What key item or scene is captured in this photo? | Histopathology of tumours in (BALB/cHeA × MSM/Ms)F1 mice with genotypes p53+/- Atm+/-, p53+/- Atm+/+ or p53+/+ Atm+/-. (a, b) Spontaneously developing mammary adenocarcinoma from p53+/- Atm+/- mouse. (c, d) Mammary adenocarcinoma from X-irradiated p53+/- Atm+/- mouse. (e, f) Mammary adenocarcinoma from X-irradiated p53+/- Atm+/+ mouse. (g) Osteosarcoma observed in nonirradiated p53+/- Atm+/- mouse. (h) Thymic lymphoma from p53+/+ Atm+/- mouse exposed to X-rays. Panels a, c and e: 40×. Panels b, d, f, g and h: 100×. |
PMC1064114_F1_1547.jpg | What object or scene is depicted here? | Histopathology of tumours in (BALB/cHeA × MSM/Ms)F1 mice with genotypes p53+/- Atm+/-, p53+/- Atm+/+ or p53+/+ Atm+/-. (a, b) Spontaneously developing mammary adenocarcinoma from p53+/- Atm+/- mouse. (c, d) Mammary adenocarcinoma from X-irradiated p53+/- Atm+/- mouse. (e, f) Mammary adenocarcinoma from X-irradiated p53+/- Atm+/+ mouse. (g) Osteosarcoma observed in nonirradiated p53+/- Atm+/- mouse. (h) Thymic lymphoma from p53+/+ Atm+/- mouse exposed to X-rays. Panels a, c and e: 40×. Panels b, d, f, g and h: 100×. |
PMC1064114_F1_1550.jpg | What is the core subject represented in this visual? | Histopathology of tumours in (BALB/cHeA × MSM/Ms)F1 mice with genotypes p53+/- Atm+/-, p53+/- Atm+/+ or p53+/+ Atm+/-. (a, b) Spontaneously developing mammary adenocarcinoma from p53+/- Atm+/- mouse. (c, d) Mammary adenocarcinoma from X-irradiated p53+/- Atm+/- mouse. (e, f) Mammary adenocarcinoma from X-irradiated p53+/- Atm+/+ mouse. (g) Osteosarcoma observed in nonirradiated p53+/- Atm+/- mouse. (h) Thymic lymphoma from p53+/+ Atm+/- mouse exposed to X-rays. Panels a, c and e: 40×. Panels b, d, f, g and h: 100×. |
PMC1064114_F1_1551.jpg | What is shown in this image? | Histopathology of tumours in (BALB/cHeA × MSM/Ms)F1 mice with genotypes p53+/- Atm+/-, p53+/- Atm+/+ or p53+/+ Atm+/-. (a, b) Spontaneously developing mammary adenocarcinoma from p53+/- Atm+/- mouse. (c, d) Mammary adenocarcinoma from X-irradiated p53+/- Atm+/- mouse. (e, f) Mammary adenocarcinoma from X-irradiated p53+/- Atm+/+ mouse. (g) Osteosarcoma observed in nonirradiated p53+/- Atm+/- mouse. (h) Thymic lymphoma from p53+/+ Atm+/- mouse exposed to X-rays. Panels a, c and e: 40×. Panels b, d, f, g and h: 100×. |
PMC1064136_F2_1566.jpg | What is the main focus of this visual representation? | Claudin (CLDN)1 positivity in normal breast epithelium, tumour cell membranes and intraductal papilloma. (a) CLDN1 positivity in normal breast epithelium. Normal epithelial cells exhibit intensive CLDN1 positivity in the cell membrane. Image obtained using laser scanning confocal microscopy (MRC 1024; Bio-Rad). Primary antibody was CLDN1 polyclonal antibody (Zymed); secondary antibody was IgG conjugated to Alexafluor 488 (Molecular Probes). Cell nuclei were counter-stained with propidium iodide. Green fluorescence along the cell membranes corresponds to CLDN1; the nuclei are seen in red. (Original magnification: 400×.) (b) CLDN1 positivity in tumour cell membranes. Shown is the immunohistochemical reaction of invasive ductal carcinoma of the breast using polyclonal CLDN-1 antibody. Note the membrane staining only in some scattered tumour cells, as compared with normal epithelial cells (panel a). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 600×.) (c) CLDN1 positivity in tumour cell membranes. Shown is the immunohistochemical reaction of invasive ductal carcinoma using polyclonal CLDN1 antibody. There is scattered membrane staining in some tumour cells. The secondary antibody is IgG conjugated to Alexafluor 488. Cell nuclei were counter-stained with propidium iodide. The image was obtained using laser scanning confocal microscopy (MRC 1024; Bio-Rad). (Original magnification: 400×.) (d) CLDN1 positivity in intraductal papilloma. Shown is the immunohistochemical reaction of a breast papilloma with an area of apocrine metaplasia. There is increased CLDN1 positivity in apocrine cells and negative staining in the surrounding papilloma. Sections were counter-stained with Mayer's hemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 200×.) |
PMC1064136_F2_1565.jpg | What is the focal point of this photograph? | Claudin (CLDN)1 positivity in normal breast epithelium, tumour cell membranes and intraductal papilloma. (a) CLDN1 positivity in normal breast epithelium. Normal epithelial cells exhibit intensive CLDN1 positivity in the cell membrane. Image obtained using laser scanning confocal microscopy (MRC 1024; Bio-Rad). Primary antibody was CLDN1 polyclonal antibody (Zymed); secondary antibody was IgG conjugated to Alexafluor 488 (Molecular Probes). Cell nuclei were counter-stained with propidium iodide. Green fluorescence along the cell membranes corresponds to CLDN1; the nuclei are seen in red. (Original magnification: 400×.) (b) CLDN1 positivity in tumour cell membranes. Shown is the immunohistochemical reaction of invasive ductal carcinoma of the breast using polyclonal CLDN-1 antibody. Note the membrane staining only in some scattered tumour cells, as compared with normal epithelial cells (panel a). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 600×.) (c) CLDN1 positivity in tumour cell membranes. Shown is the immunohistochemical reaction of invasive ductal carcinoma using polyclonal CLDN1 antibody. There is scattered membrane staining in some tumour cells. The secondary antibody is IgG conjugated to Alexafluor 488. Cell nuclei were counter-stained with propidium iodide. The image was obtained using laser scanning confocal microscopy (MRC 1024; Bio-Rad). (Original magnification: 400×.) (d) CLDN1 positivity in intraductal papilloma. Shown is the immunohistochemical reaction of a breast papilloma with an area of apocrine metaplasia. There is increased CLDN1 positivity in apocrine cells and negative staining in the surrounding papilloma. Sections were counter-stained with Mayer's hemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 200×.) |
PMC1064136_F3_1561.jpg | What is the core subject represented in this visual? | Claudin (CLDN)3 positivity in benign breast tissue and invasive ductal breast carcinoma. (a) CLDN3 positivity in benign breast tissue. Regular immunohistochemical reaction of benign breast epithelial cells using polyclonal CLDN3 antibody. Continous membrane staining characterizes most of the luminal epithelial cells. Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) (b) CLDN3 positivity in invasive ductal breast carcinoma. CLDN3 positivity is apparent in the membranes of some carcinoma cells. Sections were counter-stained with Mayer's hemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 600×.) (c) CLDN3 positivity in benign breast epithelium. CLDN3 positivity is seen in the majority of the membranes of benign epithelial cells. CLDN3 appeared to be localized in normal breast close to the apical end of the cell membranes or in the basolateral membranes of the epithelial cells. The primary antibody was CLDN3 polyclonal antibody (Zymed); the secondary antibody was IgG conjugated to Alexafluor 488 (Molecular Probes). Cell nuclei were counter-stained with propidium iodide. The image was obtained using laser scanning confocal microscopy (MRC 1024; Bio-Rad). (Original magnification: 400×.) (d) CLDN3 positivity in benign breast epithelium. CLDN3 positivity is seen in the membranes of the majority of breast epithelial cells. The positive membrane reaction is incomplete in most of the cells. The primary antibody was CLDN3 polyclonal antibody (Zymed). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) |
PMC1064136_F3_1559.jpg | What's the most prominent thing you notice in this picture? | Claudin (CLDN)3 positivity in benign breast tissue and invasive ductal breast carcinoma. (a) CLDN3 positivity in benign breast tissue. Regular immunohistochemical reaction of benign breast epithelial cells using polyclonal CLDN3 antibody. Continous membrane staining characterizes most of the luminal epithelial cells. Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) (b) CLDN3 positivity in invasive ductal breast carcinoma. CLDN3 positivity is apparent in the membranes of some carcinoma cells. Sections were counter-stained with Mayer's hemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 600×.) (c) CLDN3 positivity in benign breast epithelium. CLDN3 positivity is seen in the majority of the membranes of benign epithelial cells. CLDN3 appeared to be localized in normal breast close to the apical end of the cell membranes or in the basolateral membranes of the epithelial cells. The primary antibody was CLDN3 polyclonal antibody (Zymed); the secondary antibody was IgG conjugated to Alexafluor 488 (Molecular Probes). Cell nuclei were counter-stained with propidium iodide. The image was obtained using laser scanning confocal microscopy (MRC 1024; Bio-Rad). (Original magnification: 400×.) (d) CLDN3 positivity in benign breast epithelium. CLDN3 positivity is seen in the membranes of the majority of breast epithelial cells. The positive membrane reaction is incomplete in most of the cells. The primary antibody was CLDN3 polyclonal antibody (Zymed). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) |
PMC1064136_F3_1560.jpg | What is being portrayed in this visual content? | Claudin (CLDN)3 positivity in benign breast tissue and invasive ductal breast carcinoma. (a) CLDN3 positivity in benign breast tissue. Regular immunohistochemical reaction of benign breast epithelial cells using polyclonal CLDN3 antibody. Continous membrane staining characterizes most of the luminal epithelial cells. Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) (b) CLDN3 positivity in invasive ductal breast carcinoma. CLDN3 positivity is apparent in the membranes of some carcinoma cells. Sections were counter-stained with Mayer's hemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 600×.) (c) CLDN3 positivity in benign breast epithelium. CLDN3 positivity is seen in the majority of the membranes of benign epithelial cells. CLDN3 appeared to be localized in normal breast close to the apical end of the cell membranes or in the basolateral membranes of the epithelial cells. The primary antibody was CLDN3 polyclonal antibody (Zymed); the secondary antibody was IgG conjugated to Alexafluor 488 (Molecular Probes). Cell nuclei were counter-stained with propidium iodide. The image was obtained using laser scanning confocal microscopy (MRC 1024; Bio-Rad). (Original magnification: 400×.) (d) CLDN3 positivity in benign breast epithelium. CLDN3 positivity is seen in the membranes of the majority of breast epithelial cells. The positive membrane reaction is incomplete in most of the cells. The primary antibody was CLDN3 polyclonal antibody (Zymed). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) |
PMC1064136_F3_1562.jpg | What does this image primarily show? | Claudin (CLDN)3 positivity in benign breast tissue and invasive ductal breast carcinoma. (a) CLDN3 positivity in benign breast tissue. Regular immunohistochemical reaction of benign breast epithelial cells using polyclonal CLDN3 antibody. Continous membrane staining characterizes most of the luminal epithelial cells. Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) (b) CLDN3 positivity in invasive ductal breast carcinoma. CLDN3 positivity is apparent in the membranes of some carcinoma cells. Sections were counter-stained with Mayer's hemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 600×.) (c) CLDN3 positivity in benign breast epithelium. CLDN3 positivity is seen in the majority of the membranes of benign epithelial cells. CLDN3 appeared to be localized in normal breast close to the apical end of the cell membranes or in the basolateral membranes of the epithelial cells. The primary antibody was CLDN3 polyclonal antibody (Zymed); the secondary antibody was IgG conjugated to Alexafluor 488 (Molecular Probes). Cell nuclei were counter-stained with propidium iodide. The image was obtained using laser scanning confocal microscopy (MRC 1024; Bio-Rad). (Original magnification: 400×.) (d) CLDN3 positivity in benign breast epithelium. CLDN3 positivity is seen in the membranes of the majority of breast epithelial cells. The positive membrane reaction is incomplete in most of the cells. The primary antibody was CLDN3 polyclonal antibody (Zymed). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) |
PMC1064136_F4_1558.jpg | What is the principal component of this image? | Claudin (CLDN)4 expression in benign breast epithelium, in invasive ductal carcinomas and in intraductal papilloma. (a) Intense CLDN4 positivity in benign breast epithelium. Shown is the immunohistochemical reaction of benign breast using monoclonal CLDN4 antibody (Zymed). Strong positivity is seen in epithelial cell membranes. Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) (b) CLDN4 positivity in invasive ductal breast carcinoma. CLDN4 is expressed in invasive ductal breast carcinoma of grade 3. Positive reaction is evident in the membranes of the tumour cells. Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 600×.) (c) CLDN4 expression in invasive ductal carcinoma of the breast. Shown is complete loss of CLDN4 expression in invasive ductal breast carcinoma of grade 1 as compared with grade 3 (panel b). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) (d) CLDN4 positivity in intraductal papilloma. Shown is the immunohistochemical reaction of breast papilloma with an area of apocrine metaplasia. The loss of CLDN4 positivity in apocrine cells and the positive staining of other epithelial cells is a 'mirror image' of that seen in the CLDN1 reaction (Fig. 2d). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) |
PMC1064136_F4_1557.jpg | What's the most prominent thing you notice in this picture? | Claudin (CLDN)4 expression in benign breast epithelium, in invasive ductal carcinomas and in intraductal papilloma. (a) Intense CLDN4 positivity in benign breast epithelium. Shown is the immunohistochemical reaction of benign breast using monoclonal CLDN4 antibody (Zymed). Strong positivity is seen in epithelial cell membranes. Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) (b) CLDN4 positivity in invasive ductal breast carcinoma. CLDN4 is expressed in invasive ductal breast carcinoma of grade 3. Positive reaction is evident in the membranes of the tumour cells. Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 600×.) (c) CLDN4 expression in invasive ductal carcinoma of the breast. Shown is complete loss of CLDN4 expression in invasive ductal breast carcinoma of grade 1 as compared with grade 3 (panel b). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) (d) CLDN4 positivity in intraductal papilloma. Shown is the immunohistochemical reaction of breast papilloma with an area of apocrine metaplasia. The loss of CLDN4 positivity in apocrine cells and the positive staining of other epithelial cells is a 'mirror image' of that seen in the CLDN1 reaction (Fig. 2d). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) |
PMC1064136_F4_1556.jpg | What is the main focus of this visual representation? | Claudin (CLDN)4 expression in benign breast epithelium, in invasive ductal carcinomas and in intraductal papilloma. (a) Intense CLDN4 positivity in benign breast epithelium. Shown is the immunohistochemical reaction of benign breast using monoclonal CLDN4 antibody (Zymed). Strong positivity is seen in epithelial cell membranes. Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) (b) CLDN4 positivity in invasive ductal breast carcinoma. CLDN4 is expressed in invasive ductal breast carcinoma of grade 3. Positive reaction is evident in the membranes of the tumour cells. Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 600×.) (c) CLDN4 expression in invasive ductal carcinoma of the breast. Shown is complete loss of CLDN4 expression in invasive ductal breast carcinoma of grade 1 as compared with grade 3 (panel b). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) (d) CLDN4 positivity in intraductal papilloma. Shown is the immunohistochemical reaction of breast papilloma with an area of apocrine metaplasia. The loss of CLDN4 positivity in apocrine cells and the positive staining of other epithelial cells is a 'mirror image' of that seen in the CLDN1 reaction (Fig. 2d). Sections were counter-stained with Mayer's haemalaun. The chromogen substrate was aminoethylcarbazol. (Original magnification: 400×.) |
PMC1064138_F3_1569.jpg | What is being portrayed in this visual content? | Immunolocalization of claudin 7 (Cy3, red) in cultured mammary epithelial cells, epididymis, lung, kidney, and liver. ZO-1 is stained with fluorescein isothiocyanate to demonstrate location of the tight junctions. (a) Eph4 cells. Claudin 7 is found with a patchy distribution at the tight junctions with ZO1. Vesicular stain can also be seen in the cytoplasm. The inset at the top shows the z axis across the xy view of the section at the level of the arrow. The overlap of ZO1 and claudin indicates colocalization at the level of resolution of the light microscope. (b) Mouse epididymis. Claudin 7 stain colocalizes with ZO-1 in most, but not all, tight junctions. Lu, lumen. Small arrowheads in this and subsequent panels denote the apical border of the epithelium. (c) Lung. The luminal cells of the bronchiole show heavy staining for claudin 7 in a punctate distribution at the basolateral surface of the cell; however, some claudin 7 colocalizes with ZO-1 (see black-and-white inset). (d) Kidney. Some of the tubules of the renal cortex stain as observed by Li and colleagues [7]. Claudin 7 shows a punctate distribution that is heaviest in the basal portion of the cells. (e) Liver. Tight junctions at the bile canaliculi are stained with ZO-1. However, no stain for claudin 7 is apparent. The magnification for each figure is indicated by the label (u, μm) above the scale bar. |
PMC1064138_F3_1571.jpg | What is the principal component of this image? | Immunolocalization of claudin 7 (Cy3, red) in cultured mammary epithelial cells, epididymis, lung, kidney, and liver. ZO-1 is stained with fluorescein isothiocyanate to demonstrate location of the tight junctions. (a) Eph4 cells. Claudin 7 is found with a patchy distribution at the tight junctions with ZO1. Vesicular stain can also be seen in the cytoplasm. The inset at the top shows the z axis across the xy view of the section at the level of the arrow. The overlap of ZO1 and claudin indicates colocalization at the level of resolution of the light microscope. (b) Mouse epididymis. Claudin 7 stain colocalizes with ZO-1 in most, but not all, tight junctions. Lu, lumen. Small arrowheads in this and subsequent panels denote the apical border of the epithelium. (c) Lung. The luminal cells of the bronchiole show heavy staining for claudin 7 in a punctate distribution at the basolateral surface of the cell; however, some claudin 7 colocalizes with ZO-1 (see black-and-white inset). (d) Kidney. Some of the tubules of the renal cortex stain as observed by Li and colleagues [7]. Claudin 7 shows a punctate distribution that is heaviest in the basal portion of the cells. (e) Liver. Tight junctions at the bile canaliculi are stained with ZO-1. However, no stain for claudin 7 is apparent. The magnification for each figure is indicated by the label (u, μm) above the scale bar. |
PMC1064138_F3_1575.jpg | What key item or scene is captured in this photo? | Immunolocalization of claudin 7 (Cy3, red) in cultured mammary epithelial cells, epididymis, lung, kidney, and liver. ZO-1 is stained with fluorescein isothiocyanate to demonstrate location of the tight junctions. (a) Eph4 cells. Claudin 7 is found with a patchy distribution at the tight junctions with ZO1. Vesicular stain can also be seen in the cytoplasm. The inset at the top shows the z axis across the xy view of the section at the level of the arrow. The overlap of ZO1 and claudin indicates colocalization at the level of resolution of the light microscope. (b) Mouse epididymis. Claudin 7 stain colocalizes with ZO-1 in most, but not all, tight junctions. Lu, lumen. Small arrowheads in this and subsequent panels denote the apical border of the epithelium. (c) Lung. The luminal cells of the bronchiole show heavy staining for claudin 7 in a punctate distribution at the basolateral surface of the cell; however, some claudin 7 colocalizes with ZO-1 (see black-and-white inset). (d) Kidney. Some of the tubules of the renal cortex stain as observed by Li and colleagues [7]. Claudin 7 shows a punctate distribution that is heaviest in the basal portion of the cells. (e) Liver. Tight junctions at the bile canaliculi are stained with ZO-1. However, no stain for claudin 7 is apparent. The magnification for each figure is indicated by the label (u, μm) above the scale bar. |
PMC1064138_F3_1570.jpg | What's the most prominent thing you notice in this picture? | Immunolocalization of claudin 7 (Cy3, red) in cultured mammary epithelial cells, epididymis, lung, kidney, and liver. ZO-1 is stained with fluorescein isothiocyanate to demonstrate location of the tight junctions. (a) Eph4 cells. Claudin 7 is found with a patchy distribution at the tight junctions with ZO1. Vesicular stain can also be seen in the cytoplasm. The inset at the top shows the z axis across the xy view of the section at the level of the arrow. The overlap of ZO1 and claudin indicates colocalization at the level of resolution of the light microscope. (b) Mouse epididymis. Claudin 7 stain colocalizes with ZO-1 in most, but not all, tight junctions. Lu, lumen. Small arrowheads in this and subsequent panels denote the apical border of the epithelium. (c) Lung. The luminal cells of the bronchiole show heavy staining for claudin 7 in a punctate distribution at the basolateral surface of the cell; however, some claudin 7 colocalizes with ZO-1 (see black-and-white inset). (d) Kidney. Some of the tubules of the renal cortex stain as observed by Li and colleagues [7]. Claudin 7 shows a punctate distribution that is heaviest in the basal portion of the cells. (e) Liver. Tight junctions at the bile canaliculi are stained with ZO-1. However, no stain for claudin 7 is apparent. The magnification for each figure is indicated by the label (u, μm) above the scale bar. |
PMC1064138_F3_1572.jpg | What is the main focus of this visual representation? | Immunolocalization of claudin 7 (Cy3, red) in cultured mammary epithelial cells, epididymis, lung, kidney, and liver. ZO-1 is stained with fluorescein isothiocyanate to demonstrate location of the tight junctions. (a) Eph4 cells. Claudin 7 is found with a patchy distribution at the tight junctions with ZO1. Vesicular stain can also be seen in the cytoplasm. The inset at the top shows the z axis across the xy view of the section at the level of the arrow. The overlap of ZO1 and claudin indicates colocalization at the level of resolution of the light microscope. (b) Mouse epididymis. Claudin 7 stain colocalizes with ZO-1 in most, but not all, tight junctions. Lu, lumen. Small arrowheads in this and subsequent panels denote the apical border of the epithelium. (c) Lung. The luminal cells of the bronchiole show heavy staining for claudin 7 in a punctate distribution at the basolateral surface of the cell; however, some claudin 7 colocalizes with ZO-1 (see black-and-white inset). (d) Kidney. Some of the tubules of the renal cortex stain as observed by Li and colleagues [7]. Claudin 7 shows a punctate distribution that is heaviest in the basal portion of the cells. (e) Liver. Tight junctions at the bile canaliculi are stained with ZO-1. However, no stain for claudin 7 is apparent. The magnification for each figure is indicated by the label (u, μm) above the scale bar. |
PMC1064138_F3_1573.jpg | What is the principal component of this image? | Immunolocalization of claudin 7 (Cy3, red) in cultured mammary epithelial cells, epididymis, lung, kidney, and liver. ZO-1 is stained with fluorescein isothiocyanate to demonstrate location of the tight junctions. (a) Eph4 cells. Claudin 7 is found with a patchy distribution at the tight junctions with ZO1. Vesicular stain can also be seen in the cytoplasm. The inset at the top shows the z axis across the xy view of the section at the level of the arrow. The overlap of ZO1 and claudin indicates colocalization at the level of resolution of the light microscope. (b) Mouse epididymis. Claudin 7 stain colocalizes with ZO-1 in most, but not all, tight junctions. Lu, lumen. Small arrowheads in this and subsequent panels denote the apical border of the epithelium. (c) Lung. The luminal cells of the bronchiole show heavy staining for claudin 7 in a punctate distribution at the basolateral surface of the cell; however, some claudin 7 colocalizes with ZO-1 (see black-and-white inset). (d) Kidney. Some of the tubules of the renal cortex stain as observed by Li and colleagues [7]. Claudin 7 shows a punctate distribution that is heaviest in the basal portion of the cells. (e) Liver. Tight junctions at the bile canaliculi are stained with ZO-1. However, no stain for claudin 7 is apparent. The magnification for each figure is indicated by the label (u, μm) above the scale bar. |
PMC1064849_pbio-0030087-g004_1578.jpg | What key item or scene is captured in this photo? | Transmission EMs Show the Post-Replating Progression of CPS Cells(A) Round, day 3 cells contain disordered myosin filaments. Some of these cells beat while still floating (see Video S1) and typically have APs as shown in Figure 6A.(B) Upper box is a blowup taken from lower panel, showing myosin filaments of characteristic 1.6-μm length radiating outward from dense body.(C) Day 14 cell with a single, central nucleus shows a stretching out of the dense bodies into an organizing sarcomere.(D) Day 3 round cells containing copious mitochondria (inset).(E) Elongated day 7 cell containing a dense body (arrowhead).(F) Uninucleate day 14 cell, same cell as in (C).(G) By day 56, a well-defined sarcomere is present, with identifiable A- and I-bands and M- and Z-lines.(H) Sarcomere from a fetal cardiomyocyte is shown for comparison. |
PMC1064849_pbio-0030087-g004_1582.jpg | What can you see in this picture? | Transmission EMs Show the Post-Replating Progression of CPS Cells(A) Round, day 3 cells contain disordered myosin filaments. Some of these cells beat while still floating (see Video S1) and typically have APs as shown in Figure 6A.(B) Upper box is a blowup taken from lower panel, showing myosin filaments of characteristic 1.6-μm length radiating outward from dense body.(C) Day 14 cell with a single, central nucleus shows a stretching out of the dense bodies into an organizing sarcomere.(D) Day 3 round cells containing copious mitochondria (inset).(E) Elongated day 7 cell containing a dense body (arrowhead).(F) Uninucleate day 14 cell, same cell as in (C).(G) By day 56, a well-defined sarcomere is present, with identifiable A- and I-bands and M- and Z-lines.(H) Sarcomere from a fetal cardiomyocyte is shown for comparison. |
PMC1064849_pbio-0030087-g004_1583.jpg | What is the dominant medical problem in this image? | Transmission EMs Show the Post-Replating Progression of CPS Cells(A) Round, day 3 cells contain disordered myosin filaments. Some of these cells beat while still floating (see Video S1) and typically have APs as shown in Figure 6A.(B) Upper box is a blowup taken from lower panel, showing myosin filaments of characteristic 1.6-μm length radiating outward from dense body.(C) Day 14 cell with a single, central nucleus shows a stretching out of the dense bodies into an organizing sarcomere.(D) Day 3 round cells containing copious mitochondria (inset).(E) Elongated day 7 cell containing a dense body (arrowhead).(F) Uninucleate day 14 cell, same cell as in (C).(G) By day 56, a well-defined sarcomere is present, with identifiable A- and I-bands and M- and Z-lines.(H) Sarcomere from a fetal cardiomyocyte is shown for comparison. |
PMC1064849_pbio-0030087-g004_1577.jpg | What stands out most in this visual? | Transmission EMs Show the Post-Replating Progression of CPS Cells(A) Round, day 3 cells contain disordered myosin filaments. Some of these cells beat while still floating (see Video S1) and typically have APs as shown in Figure 6A.(B) Upper box is a blowup taken from lower panel, showing myosin filaments of characteristic 1.6-μm length radiating outward from dense body.(C) Day 14 cell with a single, central nucleus shows a stretching out of the dense bodies into an organizing sarcomere.(D) Day 3 round cells containing copious mitochondria (inset).(E) Elongated day 7 cell containing a dense body (arrowhead).(F) Uninucleate day 14 cell, same cell as in (C).(G) By day 56, a well-defined sarcomere is present, with identifiable A- and I-bands and M- and Z-lines.(H) Sarcomere from a fetal cardiomyocyte is shown for comparison. |
PMC1064849_pbio-0030087-g004_1579.jpg | What stands out most in this visual? | Transmission EMs Show the Post-Replating Progression of CPS Cells(A) Round, day 3 cells contain disordered myosin filaments. Some of these cells beat while still floating (see Video S1) and typically have APs as shown in Figure 6A.(B) Upper box is a blowup taken from lower panel, showing myosin filaments of characteristic 1.6-μm length radiating outward from dense body.(C) Day 14 cell with a single, central nucleus shows a stretching out of the dense bodies into an organizing sarcomere.(D) Day 3 round cells containing copious mitochondria (inset).(E) Elongated day 7 cell containing a dense body (arrowhead).(F) Uninucleate day 14 cell, same cell as in (C).(G) By day 56, a well-defined sarcomere is present, with identifiable A- and I-bands and M- and Z-lines.(H) Sarcomere from a fetal cardiomyocyte is shown for comparison. |
PMC1064849_pbio-0030087-g004_1580.jpg | What is the dominant medical problem in this image? | Transmission EMs Show the Post-Replating Progression of CPS Cells(A) Round, day 3 cells contain disordered myosin filaments. Some of these cells beat while still floating (see Video S1) and typically have APs as shown in Figure 6A.(B) Upper box is a blowup taken from lower panel, showing myosin filaments of characteristic 1.6-μm length radiating outward from dense body.(C) Day 14 cell with a single, central nucleus shows a stretching out of the dense bodies into an organizing sarcomere.(D) Day 3 round cells containing copious mitochondria (inset).(E) Elongated day 7 cell containing a dense body (arrowhead).(F) Uninucleate day 14 cell, same cell as in (C).(G) By day 56, a well-defined sarcomere is present, with identifiable A- and I-bands and M- and Z-lines.(H) Sarcomere from a fetal cardiomyocyte is shown for comparison. |
PMC1064851_pbio-0030093-g001_1591.jpg | What is the principal component of this image? | Expression of eve
(A–D) Embryos of four Drosophila species at early cellular blastoderm stage. EVE stained with immunoperoxidase DAB reaction enhanced by nickel.(E–H) Df(eve) D. melanogaster embryos with two copies of transgenes containing eve S2E from four species fused to D. melanogaster eve coding region (−0.9 to +1.85 kb) at blastoderm stage. Immunofluorescence-labeled EVE. The S2Eere-EVE (G) produces consistently weaker stripes than lines carrying S2Es from the other three species. (A and E) D. melanogaster, (B and F) D. yakuba, (C and G) D. erecta, and (D and H) D. pseudoobscura.
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PMC1064851_pbio-0030093-g001_1586.jpg | What is being portrayed in this visual content? | Expression of eve
(A–D) Embryos of four Drosophila species at early cellular blastoderm stage. EVE stained with immunoperoxidase DAB reaction enhanced by nickel.(E–H) Df(eve) D. melanogaster embryos with two copies of transgenes containing eve S2E from four species fused to D. melanogaster eve coding region (−0.9 to +1.85 kb) at blastoderm stage. Immunofluorescence-labeled EVE. The S2Eere-EVE (G) produces consistently weaker stripes than lines carrying S2Es from the other three species. (A and E) D. melanogaster, (B and F) D. yakuba, (C and G) D. erecta, and (D and H) D. pseudoobscura.
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PMC1064851_pbio-0030093-g001_1590.jpg | What is the dominant medical problem in this image? | Expression of eve
(A–D) Embryos of four Drosophila species at early cellular blastoderm stage. EVE stained with immunoperoxidase DAB reaction enhanced by nickel.(E–H) Df(eve) D. melanogaster embryos with two copies of transgenes containing eve S2E from four species fused to D. melanogaster eve coding region (−0.9 to +1.85 kb) at blastoderm stage. Immunofluorescence-labeled EVE. The S2Eere-EVE (G) produces consistently weaker stripes than lines carrying S2Es from the other three species. (A and E) D. melanogaster, (B and F) D. yakuba, (C and G) D. erecta, and (D and H) D. pseudoobscura.
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PMC1064851_pbio-0030093-g001_1584.jpg | What is shown in this image? | Expression of eve
(A–D) Embryos of four Drosophila species at early cellular blastoderm stage. EVE stained with immunoperoxidase DAB reaction enhanced by nickel.(E–H) Df(eve) D. melanogaster embryos with two copies of transgenes containing eve S2E from four species fused to D. melanogaster eve coding region (−0.9 to +1.85 kb) at blastoderm stage. Immunofluorescence-labeled EVE. The S2Eere-EVE (G) produces consistently weaker stripes than lines carrying S2Es from the other three species. (A and E) D. melanogaster, (B and F) D. yakuba, (C and G) D. erecta, and (D and H) D. pseudoobscura.
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PMC1064851_pbio-0030093-g001_1588.jpg | What is the main focus of this visual representation? | Expression of eve
(A–D) Embryos of four Drosophila species at early cellular blastoderm stage. EVE stained with immunoperoxidase DAB reaction enhanced by nickel.(E–H) Df(eve) D. melanogaster embryos with two copies of transgenes containing eve S2E from four species fused to D. melanogaster eve coding region (−0.9 to +1.85 kb) at blastoderm stage. Immunofluorescence-labeled EVE. The S2Eere-EVE (G) produces consistently weaker stripes than lines carrying S2Es from the other three species. (A and E) D. melanogaster, (B and F) D. yakuba, (C and G) D. erecta, and (D and H) D. pseudoobscura.
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PMC1064851_pbio-0030093-g001_1589.jpg | What is the core subject represented in this visual? | Expression of eve
(A–D) Embryos of four Drosophila species at early cellular blastoderm stage. EVE stained with immunoperoxidase DAB reaction enhanced by nickel.(E–H) Df(eve) D. melanogaster embryos with two copies of transgenes containing eve S2E from four species fused to D. melanogaster eve coding region (−0.9 to +1.85 kb) at blastoderm stage. Immunofluorescence-labeled EVE. The S2Eere-EVE (G) produces consistently weaker stripes than lines carrying S2Es from the other three species. (A and E) D. melanogaster, (B and F) D. yakuba, (C and G) D. erecta, and (D and H) D. pseudoobscura.
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PMC1064851_pbio-0030093-g003_1595.jpg | What is shown in this image? | Developmental Series of EVE Abundance(A–E) Immunofluorescence labeling of time-staged early EVEΔS2E homozygous embryos. This developmental sequence, which corresponds roughly from the initialization of cellularization (A) to its completion (E), takes approximately 45 min at 25 oC in wild-type flies [41].(F) Expression of en in same genotype at stage 10. Arrows mark third and fourth en stripes. Note the short interval between en stripes 3 and 4 (parasegment 3) and the reduced fourth stripe.(G) EVE expression in stripe 2 during the developmental series around cellularization, where times 1–5 correspond to pictures in A–E. Stage 1 is early cellularization, while the process has been completed for embryos in class 5. The series is comparable to time classes 4–8 on the FlyEx Web site (http://flyex.ams.sunysb.edu/flyex/) [34]. Estimated least square means (± SE) for EVEΔS2E/Cy stock and wild-type line w1118; note the Cy/Cy homozygote is essentially wild-type. Early eve pair-rule expression is not known to be autoregulated (as occurs in postcellularization stages), and we observe a 2-fold difference in early stripe expression, with an additive component (a) of 0.62 and negligible dominance deviation (d/a) = 0.01, for the first two stages. This dosage dependency is lost after the cellularization stage (3), presumably because all embryos carry two copies of the autoregulatory element. |
PMC1064851_pbio-0030093-g003_1593.jpg | What object or scene is depicted here? | Developmental Series of EVE Abundance(A–E) Immunofluorescence labeling of time-staged early EVEΔS2E homozygous embryos. This developmental sequence, which corresponds roughly from the initialization of cellularization (A) to its completion (E), takes approximately 45 min at 25 oC in wild-type flies [41].(F) Expression of en in same genotype at stage 10. Arrows mark third and fourth en stripes. Note the short interval between en stripes 3 and 4 (parasegment 3) and the reduced fourth stripe.(G) EVE expression in stripe 2 during the developmental series around cellularization, where times 1–5 correspond to pictures in A–E. Stage 1 is early cellularization, while the process has been completed for embryos in class 5. The series is comparable to time classes 4–8 on the FlyEx Web site (http://flyex.ams.sunysb.edu/flyex/) [34]. Estimated least square means (± SE) for EVEΔS2E/Cy stock and wild-type line w1118; note the Cy/Cy homozygote is essentially wild-type. Early eve pair-rule expression is not known to be autoregulated (as occurs in postcellularization stages), and we observe a 2-fold difference in early stripe expression, with an additive component (a) of 0.62 and negligible dominance deviation (d/a) = 0.01, for the first two stages. This dosage dependency is lost after the cellularization stage (3), presumably because all embryos carry two copies of the autoregulatory element. |
PMC1064851_pbio-0030093-g003_1598.jpg | What is the dominant medical problem in this image? | Developmental Series of EVE Abundance(A–E) Immunofluorescence labeling of time-staged early EVEΔS2E homozygous embryos. This developmental sequence, which corresponds roughly from the initialization of cellularization (A) to its completion (E), takes approximately 45 min at 25 oC in wild-type flies [41].(F) Expression of en in same genotype at stage 10. Arrows mark third and fourth en stripes. Note the short interval between en stripes 3 and 4 (parasegment 3) and the reduced fourth stripe.(G) EVE expression in stripe 2 during the developmental series around cellularization, where times 1–5 correspond to pictures in A–E. Stage 1 is early cellularization, while the process has been completed for embryos in class 5. The series is comparable to time classes 4–8 on the FlyEx Web site (http://flyex.ams.sunysb.edu/flyex/) [34]. Estimated least square means (± SE) for EVEΔS2E/Cy stock and wild-type line w1118; note the Cy/Cy homozygote is essentially wild-type. Early eve pair-rule expression is not known to be autoregulated (as occurs in postcellularization stages), and we observe a 2-fold difference in early stripe expression, with an additive component (a) of 0.62 and negligible dominance deviation (d/a) = 0.01, for the first two stages. This dosage dependency is lost after the cellularization stage (3), presumably because all embryos carry two copies of the autoregulatory element. |
PMC1064851_pbio-0030093-g003_1597.jpg | What can you see in this picture? | Developmental Series of EVE Abundance(A–E) Immunofluorescence labeling of time-staged early EVEΔS2E homozygous embryos. This developmental sequence, which corresponds roughly from the initialization of cellularization (A) to its completion (E), takes approximately 45 min at 25 oC in wild-type flies [41].(F) Expression of en in same genotype at stage 10. Arrows mark third and fourth en stripes. Note the short interval between en stripes 3 and 4 (parasegment 3) and the reduced fourth stripe.(G) EVE expression in stripe 2 during the developmental series around cellularization, where times 1–5 correspond to pictures in A–E. Stage 1 is early cellularization, while the process has been completed for embryos in class 5. The series is comparable to time classes 4–8 on the FlyEx Web site (http://flyex.ams.sunysb.edu/flyex/) [34]. Estimated least square means (± SE) for EVEΔS2E/Cy stock and wild-type line w1118; note the Cy/Cy homozygote is essentially wild-type. Early eve pair-rule expression is not known to be autoregulated (as occurs in postcellularization stages), and we observe a 2-fold difference in early stripe expression, with an additive component (a) of 0.62 and negligible dominance deviation (d/a) = 0.01, for the first two stages. This dosage dependency is lost after the cellularization stage (3), presumably because all embryos carry two copies of the autoregulatory element. |
PMC1064897_F2_1600.jpg | Can you identify the primary element in this image? | Histological assessment of synovial inflammation and joint destruction. No signs of arthritis are seen in the tarsal joints of wild-type (wt) and JNK1 (c-Jun N-terminal kinase 1) knockout (JNK1-/-) mice, whereas severe inflammation (I) and numerous erosions (E) are observed in human TNF transgenic (hTNFtg) and intercrossed (JNK1-/-hTNFtg) mice. H-&-E-stained sections; magnification 50×. |
PMC1064897_F2_1601.jpg | Describe the main subject of this image. | Histological assessment of synovial inflammation and joint destruction. No signs of arthritis are seen in the tarsal joints of wild-type (wt) and JNK1 (c-Jun N-terminal kinase 1) knockout (JNK1-/-) mice, whereas severe inflammation (I) and numerous erosions (E) are observed in human TNF transgenic (hTNFtg) and intercrossed (JNK1-/-hTNFtg) mice. H-&-E-stained sections; magnification 50×. |
PMC1064897_F2_1602.jpg | Describe the main subject of this image. | Histological assessment of synovial inflammation and joint destruction. No signs of arthritis are seen in the tarsal joints of wild-type (wt) and JNK1 (c-Jun N-terminal kinase 1) knockout (JNK1-/-) mice, whereas severe inflammation (I) and numerous erosions (E) are observed in human TNF transgenic (hTNFtg) and intercrossed (JNK1-/-hTNFtg) mice. H-&-E-stained sections; magnification 50×. |
PMC1064897_F4_1603.jpg | What stands out most in this visual? | Synovial osteoclasts in human tumour necrosis factor transgenic (hTNFtg) and JNK1-/-hTNFtg mice. As demonstrated by staining with tartrate-resistant acid phosphatase (a), there are abundant osteoclasts (OC) at the site of erosions in hTNFtg and intercrossed (JNK1-/-hTNFtg) mice, which all developed arthritis (magnification 100×). The number of osteoclasts was similar in the two animal groups (b). Vertical bars indicate standard deviation. JNK, c-Jun N-terminal kinase. |
PMC1064897_F5_1608.jpg | What is the main focus of this visual representation? | Evaluation of proteoglycan loss in human tumour necrosis factor transgenic (hTNFtg) and JNK1-/-hTNFtg mice. As shown by toluidine blue staining (a), arthritis leads to loss of proteoglycan (arrows) in the cartilage of hTNFtg and intercrossed JNK1-/-hTNFtg mice (magnification 100×). The area of early cartilage damage (b) was similar in the two groups with arthritis, whereas the joints of wild-type (wt) and JNK1 knockout (JNK1-/-) animals were unaffected. Vertical bars indicate standard deviation. JNK, c-Jun N-terminal kinase. |
PMC1064897_F5_1610.jpg | What object or scene is depicted here? | Evaluation of proteoglycan loss in human tumour necrosis factor transgenic (hTNFtg) and JNK1-/-hTNFtg mice. As shown by toluidine blue staining (a), arthritis leads to loss of proteoglycan (arrows) in the cartilage of hTNFtg and intercrossed JNK1-/-hTNFtg mice (magnification 100×). The area of early cartilage damage (b) was similar in the two groups with arthritis, whereas the joints of wild-type (wt) and JNK1 knockout (JNK1-/-) animals were unaffected. Vertical bars indicate standard deviation. JNK, c-Jun N-terminal kinase. |
PMC1064897_F5_1612.jpg | What is the dominant medical problem in this image? | Evaluation of proteoglycan loss in human tumour necrosis factor transgenic (hTNFtg) and JNK1-/-hTNFtg mice. As shown by toluidine blue staining (a), arthritis leads to loss of proteoglycan (arrows) in the cartilage of hTNFtg and intercrossed JNK1-/-hTNFtg mice (magnification 100×). The area of early cartilage damage (b) was similar in the two groups with arthritis, whereas the joints of wild-type (wt) and JNK1 knockout (JNK1-/-) animals were unaffected. Vertical bars indicate standard deviation. JNK, c-Jun N-terminal kinase. |
PMC1065025_F1_1607.jpg | What is the focal point of this photograph? | The girl: cranial computed tomography, done 7 hours after admission, showing cerebral oedema. |
PMC1065025_F2_1613.jpg | What is the central feature of this picture? | The girl: computed tomography of the thorax, done shortly after admission to hospital, showing infiltrations in the basal dorsal thorax following aspiration. |
PMC1065049_F3_1616.jpg | What is shown in this image? | Cross-section of a nerve biopsy specimen from patient 4 exhibiting severe axonal neuropathy. There is loss of myelinated nerve fibres. Some large myelinated fibres show degenerating myelin ovoids. Secondary demyelination is seen in rare nerve fibres. Clusters of Schwann cells without nerve fibres are increased. Resin section, stained with paraphenylene diamine, magnification 115×. |
PMC1065316_F4_1622.jpg | What is the dominant medical problem in this image? | Immunohistochemistry of CXCR5 in the intima and postcapillary venules in rheumatoid arthritis synovia. (a) CD68+ cells in the intima. (b) Serial section to (a) stained for CXCR5. Note the colocalization of CXCR5 and CD68 to the same group of cells. (c) and (d) Sections from the same region as (a) and (b), treated with isotype-matched control immunoglobulin instead of CD68 and CXCR5 antibodies, respectively. (e) Postcapillary venule positive for CXCR5 within a lymphoid aggregate. Labelling was revealed using 3,3'-diaminobenzidine substrate. (f) Isotype control for (e). (a), (b), (e) and (f) Original magnification, 420 ×; (c) and (d) original magnification, 350 ×. |
PMC1065316_F4_1619.jpg | What is the main focus of this visual representation? | Immunohistochemistry of CXCR5 in the intima and postcapillary venules in rheumatoid arthritis synovia. (a) CD68+ cells in the intima. (b) Serial section to (a) stained for CXCR5. Note the colocalization of CXCR5 and CD68 to the same group of cells. (c) and (d) Sections from the same region as (a) and (b), treated with isotype-matched control immunoglobulin instead of CD68 and CXCR5 antibodies, respectively. (e) Postcapillary venule positive for CXCR5 within a lymphoid aggregate. Labelling was revealed using 3,3'-diaminobenzidine substrate. (f) Isotype control for (e). (a), (b), (e) and (f) Original magnification, 420 ×; (c) and (d) original magnification, 350 ×. |
PMC1065316_F4_1618.jpg | What is being portrayed in this visual content? | Immunohistochemistry of CXCR5 in the intima and postcapillary venules in rheumatoid arthritis synovia. (a) CD68+ cells in the intima. (b) Serial section to (a) stained for CXCR5. Note the colocalization of CXCR5 and CD68 to the same group of cells. (c) and (d) Sections from the same region as (a) and (b), treated with isotype-matched control immunoglobulin instead of CD68 and CXCR5 antibodies, respectively. (e) Postcapillary venule positive for CXCR5 within a lymphoid aggregate. Labelling was revealed using 3,3'-diaminobenzidine substrate. (f) Isotype control for (e). (a), (b), (e) and (f) Original magnification, 420 ×; (c) and (d) original magnification, 350 ×. |
PMC1065316_F4_1620.jpg | What is being portrayed in this visual content? | Immunohistochemistry of CXCR5 in the intima and postcapillary venules in rheumatoid arthritis synovia. (a) CD68+ cells in the intima. (b) Serial section to (a) stained for CXCR5. Note the colocalization of CXCR5 and CD68 to the same group of cells. (c) and (d) Sections from the same region as (a) and (b), treated with isotype-matched control immunoglobulin instead of CD68 and CXCR5 antibodies, respectively. (e) Postcapillary venule positive for CXCR5 within a lymphoid aggregate. Labelling was revealed using 3,3'-diaminobenzidine substrate. (f) Isotype control for (e). (a), (b), (e) and (f) Original magnification, 420 ×; (c) and (d) original magnification, 350 ×. |
PMC1065316_F4_1621.jpg | What key item or scene is captured in this photo? | Immunohistochemistry of CXCR5 in the intima and postcapillary venules in rheumatoid arthritis synovia. (a) CD68+ cells in the intima. (b) Serial section to (a) stained for CXCR5. Note the colocalization of CXCR5 and CD68 to the same group of cells. (c) and (d) Sections from the same region as (a) and (b), treated with isotype-matched control immunoglobulin instead of CD68 and CXCR5 antibodies, respectively. (e) Postcapillary venule positive for CXCR5 within a lymphoid aggregate. Labelling was revealed using 3,3'-diaminobenzidine substrate. (f) Isotype control for (e). (a), (b), (e) and (f) Original magnification, 420 ×; (c) and (d) original magnification, 350 ×. |
PMC1065316_F5_1623.jpg | What can you see in this picture? | Immunohistochemistry of CXCR5 in non-rheumatoid arthritis synovia. (a) CD68 staining in the intimal layer. (b) Serial section to (a) treated with anti-CXCR5, showing that CXCR5+ cells in the intimal layer included those also positive for CD68. (c) and (d) Sections from the same region as (a) and (b), treated with isotype-matched control immunoglobulin instead of CD68 and CXCR5 antibodies, respectively. (e) Subintimal postcapillary venule stains for CXCR5 expression (arrow). (f) Isotype-matched control for (e). Labelling was revealed using 3,3'-diaminobenzidine substrate. (a), (b), (e) and (f) Original magnification, 420 ×; (c) and (d) original magnification, 350 ×. |
PMC1065316_F5_1626.jpg | What can you see in this picture? | Immunohistochemistry of CXCR5 in non-rheumatoid arthritis synovia. (a) CD68 staining in the intimal layer. (b) Serial section to (a) treated with anti-CXCR5, showing that CXCR5+ cells in the intimal layer included those also positive for CD68. (c) and (d) Sections from the same region as (a) and (b), treated with isotype-matched control immunoglobulin instead of CD68 and CXCR5 antibodies, respectively. (e) Subintimal postcapillary venule stains for CXCR5 expression (arrow). (f) Isotype-matched control for (e). Labelling was revealed using 3,3'-diaminobenzidine substrate. (a), (b), (e) and (f) Original magnification, 420 ×; (c) and (d) original magnification, 350 ×. |
PMC1065316_F5_1625.jpg | What can you see in this picture? | Immunohistochemistry of CXCR5 in non-rheumatoid arthritis synovia. (a) CD68 staining in the intimal layer. (b) Serial section to (a) treated with anti-CXCR5, showing that CXCR5+ cells in the intimal layer included those also positive for CD68. (c) and (d) Sections from the same region as (a) and (b), treated with isotype-matched control immunoglobulin instead of CD68 and CXCR5 antibodies, respectively. (e) Subintimal postcapillary venule stains for CXCR5 expression (arrow). (f) Isotype-matched control for (e). Labelling was revealed using 3,3'-diaminobenzidine substrate. (a), (b), (e) and (f) Original magnification, 420 ×; (c) and (d) original magnification, 350 ×. |
PMC1065316_F5_1628.jpg | What key item or scene is captured in this photo? | Immunohistochemistry of CXCR5 in non-rheumatoid arthritis synovia. (a) CD68 staining in the intimal layer. (b) Serial section to (a) treated with anti-CXCR5, showing that CXCR5+ cells in the intimal layer included those also positive for CD68. (c) and (d) Sections from the same region as (a) and (b), treated with isotype-matched control immunoglobulin instead of CD68 and CXCR5 antibodies, respectively. (e) Subintimal postcapillary venule stains for CXCR5 expression (arrow). (f) Isotype-matched control for (e). Labelling was revealed using 3,3'-diaminobenzidine substrate. (a), (b), (e) and (f) Original magnification, 420 ×; (c) and (d) original magnification, 350 ×. |
PMC1065321_F2_1638.jpg | What does this image primarily show? | In vivo near-infrared fluorescent (NIRF) imaging of inflammatory joints in the lipopolysaccharide (LPS) induction model. The NIR2-folate probe was intravenously injected 2 days after LPS intra-articular injection. (a) White-light images obtained 48 hours after intra-articular LPS injection at the right ankle joint; soft tissue swelling was noted at the affected joint. (b) NIRF images obtained 24 hours after NIR2-folate injection. Note the strong fluorescence signal in the LPS-treated ankle compared with the opposite control side (enhancement ratio = 2.31). (c) A merged NIRF signal with a white-light image showing specific increased fluorescence signal intensity at the affected joint. (d) H&E-stain section of the right ankle joint showing abundant inflammatory cell infiltration at subsynovial tissues. Original magnification, 100 ×. (e) NIRF images of a longitudinal section of the LPS-treated ankles. Pseudo-color coding was used to demonstrate the stronger fluorescence signal surrounding the ankle joint. |
PMC1065321_F2_1637.jpg | What can you see in this picture? | In vivo near-infrared fluorescent (NIRF) imaging of inflammatory joints in the lipopolysaccharide (LPS) induction model. The NIR2-folate probe was intravenously injected 2 days after LPS intra-articular injection. (a) White-light images obtained 48 hours after intra-articular LPS injection at the right ankle joint; soft tissue swelling was noted at the affected joint. (b) NIRF images obtained 24 hours after NIR2-folate injection. Note the strong fluorescence signal in the LPS-treated ankle compared with the opposite control side (enhancement ratio = 2.31). (c) A merged NIRF signal with a white-light image showing specific increased fluorescence signal intensity at the affected joint. (d) H&E-stain section of the right ankle joint showing abundant inflammatory cell infiltration at subsynovial tissues. Original magnification, 100 ×. (e) NIRF images of a longitudinal section of the LPS-treated ankles. Pseudo-color coding was used to demonstrate the stronger fluorescence signal surrounding the ankle joint. |
PMC1065321_F2_1640.jpg | What does this image primarily show? | In vivo near-infrared fluorescent (NIRF) imaging of inflammatory joints in the lipopolysaccharide (LPS) induction model. The NIR2-folate probe was intravenously injected 2 days after LPS intra-articular injection. (a) White-light images obtained 48 hours after intra-articular LPS injection at the right ankle joint; soft tissue swelling was noted at the affected joint. (b) NIRF images obtained 24 hours after NIR2-folate injection. Note the strong fluorescence signal in the LPS-treated ankle compared with the opposite control side (enhancement ratio = 2.31). (c) A merged NIRF signal with a white-light image showing specific increased fluorescence signal intensity at the affected joint. (d) H&E-stain section of the right ankle joint showing abundant inflammatory cell infiltration at subsynovial tissues. Original magnification, 100 ×. (e) NIRF images of a longitudinal section of the LPS-treated ankles. Pseudo-color coding was used to demonstrate the stronger fluorescence signal surrounding the ankle joint. |
PMC1065321_F2_1642.jpg | What is the focal point of this photograph? | In vivo near-infrared fluorescent (NIRF) imaging of inflammatory joints in the lipopolysaccharide (LPS) induction model. The NIR2-folate probe was intravenously injected 2 days after LPS intra-articular injection. (a) White-light images obtained 48 hours after intra-articular LPS injection at the right ankle joint; soft tissue swelling was noted at the affected joint. (b) NIRF images obtained 24 hours after NIR2-folate injection. Note the strong fluorescence signal in the LPS-treated ankle compared with the opposite control side (enhancement ratio = 2.31). (c) A merged NIRF signal with a white-light image showing specific increased fluorescence signal intensity at the affected joint. (d) H&E-stain section of the right ankle joint showing abundant inflammatory cell infiltration at subsynovial tissues. Original magnification, 100 ×. (e) NIRF images of a longitudinal section of the LPS-treated ankles. Pseudo-color coding was used to demonstrate the stronger fluorescence signal surrounding the ankle joint. |
PMC1065321_F2_1641.jpg | Can you identify the primary element in this image? | In vivo near-infrared fluorescent (NIRF) imaging of inflammatory joints in the lipopolysaccharide (LPS) induction model. The NIR2-folate probe was intravenously injected 2 days after LPS intra-articular injection. (a) White-light images obtained 48 hours after intra-articular LPS injection at the right ankle joint; soft tissue swelling was noted at the affected joint. (b) NIRF images obtained 24 hours after NIR2-folate injection. Note the strong fluorescence signal in the LPS-treated ankle compared with the opposite control side (enhancement ratio = 2.31). (c) A merged NIRF signal with a white-light image showing specific increased fluorescence signal intensity at the affected joint. (d) H&E-stain section of the right ankle joint showing abundant inflammatory cell infiltration at subsynovial tissues. Original magnification, 100 ×. (e) NIRF images of a longitudinal section of the LPS-treated ankles. Pseudo-color coding was used to demonstrate the stronger fluorescence signal surrounding the ankle joint. |
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