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PMC547972_pbio-0030053-g005_1204.jpg | What is the focal point of this photograph? |
fat-7 Is Necessary for Normal Life Span and Inhibits β-Oxidation(A) Nomarski images of WT worms subjected to fat-7 RNAi at days 1 and 3 of adulthood. The arrow in the day 1 image points to vacuole formation in the intestine, and the arrow in the day 3 image points to clearing that results from collapse of the gonad. These characteristics are nearly identical to those observed for nhr-49(nr2041) worms (see Figure 1B).(B) QRT-PCR measurement of acs-2 and ech-1 expression in WT and nhr-49(nr2041) L4 animals grown on control RNAi bacteria (dark gray bars) or on fat-7 RNAi bacteria (blue bars). Error bars represent standard error of measurement.(C) RNAi knockdown of fat-7 expression in WT animals reduced Nile Red fat staining(D) RNAi of fat-7 in nhr-49(nr2041) also decreased fat staining. |
PMC547972_pbio-0030053-g005_1205.jpg | What is being portrayed in this visual content? |
fat-7 Is Necessary for Normal Life Span and Inhibits β-Oxidation(A) Nomarski images of WT worms subjected to fat-7 RNAi at days 1 and 3 of adulthood. The arrow in the day 1 image points to vacuole formation in the intestine, and the arrow in the day 3 image points to clearing that results from collapse of the gonad. These characteristics are nearly identical to those observed for nhr-49(nr2041) worms (see Figure 1B).(B) QRT-PCR measurement of acs-2 and ech-1 expression in WT and nhr-49(nr2041) L4 animals grown on control RNAi bacteria (dark gray bars) or on fat-7 RNAi bacteria (blue bars). Error bars represent standard error of measurement.(C) RNAi knockdown of fat-7 expression in WT animals reduced Nile Red fat staining(D) RNAi of fat-7 in nhr-49(nr2041) also decreased fat staining. |
PMC547972_pbio-0030053-g005_1202.jpg | What is the dominant medical problem in this image? |
fat-7 Is Necessary for Normal Life Span and Inhibits β-Oxidation(A) Nomarski images of WT worms subjected to fat-7 RNAi at days 1 and 3 of adulthood. The arrow in the day 1 image points to vacuole formation in the intestine, and the arrow in the day 3 image points to clearing that results from collapse of the gonad. These characteristics are nearly identical to those observed for nhr-49(nr2041) worms (see Figure 1B).(B) QRT-PCR measurement of acs-2 and ech-1 expression in WT and nhr-49(nr2041) L4 animals grown on control RNAi bacteria (dark gray bars) or on fat-7 RNAi bacteria (blue bars). Error bars represent standard error of measurement.(C) RNAi knockdown of fat-7 expression in WT animals reduced Nile Red fat staining(D) RNAi of fat-7 in nhr-49(nr2041) also decreased fat staining. |
PMC548132_F2_1210.jpg | What is the dominant medical problem in this image? | Apoptosis detected by TUNEL at the implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, G) and D34 (D, E, F, H) of gestation. Apoptotic nuclei were stained dark. Arrowhead and arrow in panel A – D indicated the nuclei of syncytiotrophoblast and villous stromal cells respectively. The insets in C and D showed the positive nuclei under a higher magnification. Note the syncytiotrophoblast layer covering the basal feet of the anchoring villi in E and the cell columns in F. G and H represent the stromal cells and glandular epithelial cells respectively in the endometrium. I was the negative control. St, syncytiotrophoblast; CT, cytotrophoblast; Vi, placental villi. Scale bars represent 50 μm. |
PMC548132_F2_1212.jpg | Describe the main subject of this image. | Apoptosis detected by TUNEL at the implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, G) and D34 (D, E, F, H) of gestation. Apoptotic nuclei were stained dark. Arrowhead and arrow in panel A – D indicated the nuclei of syncytiotrophoblast and villous stromal cells respectively. The insets in C and D showed the positive nuclei under a higher magnification. Note the syncytiotrophoblast layer covering the basal feet of the anchoring villi in E and the cell columns in F. G and H represent the stromal cells and glandular epithelial cells respectively in the endometrium. I was the negative control. St, syncytiotrophoblast; CT, cytotrophoblast; Vi, placental villi. Scale bars represent 50 μm. |
PMC548132_F2_1209.jpg | What is shown in this image? | Apoptosis detected by TUNEL at the implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, G) and D34 (D, E, F, H) of gestation. Apoptotic nuclei were stained dark. Arrowhead and arrow in panel A – D indicated the nuclei of syncytiotrophoblast and villous stromal cells respectively. The insets in C and D showed the positive nuclei under a higher magnification. Note the syncytiotrophoblast layer covering the basal feet of the anchoring villi in E and the cell columns in F. G and H represent the stromal cells and glandular epithelial cells respectively in the endometrium. I was the negative control. St, syncytiotrophoblast; CT, cytotrophoblast; Vi, placental villi. Scale bars represent 50 μm. |
PMC548132_F2_1214.jpg | What is the central feature of this picture? | Apoptosis detected by TUNEL at the implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, G) and D34 (D, E, F, H) of gestation. Apoptotic nuclei were stained dark. Arrowhead and arrow in panel A – D indicated the nuclei of syncytiotrophoblast and villous stromal cells respectively. The insets in C and D showed the positive nuclei under a higher magnification. Note the syncytiotrophoblast layer covering the basal feet of the anchoring villi in E and the cell columns in F. G and H represent the stromal cells and glandular epithelial cells respectively in the endometrium. I was the negative control. St, syncytiotrophoblast; CT, cytotrophoblast; Vi, placental villi. Scale bars represent 50 μm. |
PMC548132_F2_1206.jpg | What is the core subject represented in this visual? | Apoptosis detected by TUNEL at the implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, G) and D34 (D, E, F, H) of gestation. Apoptotic nuclei were stained dark. Arrowhead and arrow in panel A – D indicated the nuclei of syncytiotrophoblast and villous stromal cells respectively. The insets in C and D showed the positive nuclei under a higher magnification. Note the syncytiotrophoblast layer covering the basal feet of the anchoring villi in E and the cell columns in F. G and H represent the stromal cells and glandular epithelial cells respectively in the endometrium. I was the negative control. St, syncytiotrophoblast; CT, cytotrophoblast; Vi, placental villi. Scale bars represent 50 μm. |
PMC548132_F2_1211.jpg | What object or scene is depicted here? | Apoptosis detected by TUNEL at the implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, G) and D34 (D, E, F, H) of gestation. Apoptotic nuclei were stained dark. Arrowhead and arrow in panel A – D indicated the nuclei of syncytiotrophoblast and villous stromal cells respectively. The insets in C and D showed the positive nuclei under a higher magnification. Note the syncytiotrophoblast layer covering the basal feet of the anchoring villi in E and the cell columns in F. G and H represent the stromal cells and glandular epithelial cells respectively in the endometrium. I was the negative control. St, syncytiotrophoblast; CT, cytotrophoblast; Vi, placental villi. Scale bars represent 50 μm. |
PMC548132_F2_1207.jpg | Can you identify the primary element in this image? | Apoptosis detected by TUNEL at the implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, G) and D34 (D, E, F, H) of gestation. Apoptotic nuclei were stained dark. Arrowhead and arrow in panel A – D indicated the nuclei of syncytiotrophoblast and villous stromal cells respectively. The insets in C and D showed the positive nuclei under a higher magnification. Note the syncytiotrophoblast layer covering the basal feet of the anchoring villi in E and the cell columns in F. G and H represent the stromal cells and glandular epithelial cells respectively in the endometrium. I was the negative control. St, syncytiotrophoblast; CT, cytotrophoblast; Vi, placental villi. Scale bars represent 50 μm. |
PMC548132_F2_1208.jpg | Describe the main subject of this image. | Apoptosis detected by TUNEL at the implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, G) and D34 (D, E, F, H) of gestation. Apoptotic nuclei were stained dark. Arrowhead and arrow in panel A – D indicated the nuclei of syncytiotrophoblast and villous stromal cells respectively. The insets in C and D showed the positive nuclei under a higher magnification. Note the syncytiotrophoblast layer covering the basal feet of the anchoring villi in E and the cell columns in F. G and H represent the stromal cells and glandular epithelial cells respectively in the endometrium. I was the negative control. St, syncytiotrophoblast; CT, cytotrophoblast; Vi, placental villi. Scale bars represent 50 μm. |
PMC548132_F3_1215.jpg | What can you see in this picture? | The proliferating activity revealed by Ki-67 immunostaining at implantation sites of the rhesus monkey on D17 (A, E, G), D19 (B), D28 (C) and D34 (D, F, H) of gestation. Panels A-D were under a lower magnification. Ki-67 protein was stained red, and nuclei blue. E and F were the placental villi under a higher magnification. G and H were the anchoring villi under a higher magnification. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cell. En, endometrium. Scale bars represent 100 μm. |
PMC548132_F3_1217.jpg | Describe the main subject of this image. | The proliferating activity revealed by Ki-67 immunostaining at implantation sites of the rhesus monkey on D17 (A, E, G), D19 (B), D28 (C) and D34 (D, F, H) of gestation. Panels A-D were under a lower magnification. Ki-67 protein was stained red, and nuclei blue. E and F were the placental villi under a higher magnification. G and H were the anchoring villi under a higher magnification. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cell. En, endometrium. Scale bars represent 100 μm. |
PMC548132_F3_1216.jpg | What can you see in this picture? | The proliferating activity revealed by Ki-67 immunostaining at implantation sites of the rhesus monkey on D17 (A, E, G), D19 (B), D28 (C) and D34 (D, F, H) of gestation. Panels A-D were under a lower magnification. Ki-67 protein was stained red, and nuclei blue. E and F were the placental villi under a higher magnification. G and H were the anchoring villi under a higher magnification. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cell. En, endometrium. Scale bars represent 100 μm. |
PMC548132_F3_1221.jpg | What object or scene is depicted here? | The proliferating activity revealed by Ki-67 immunostaining at implantation sites of the rhesus monkey on D17 (A, E, G), D19 (B), D28 (C) and D34 (D, F, H) of gestation. Panels A-D were under a lower magnification. Ki-67 protein was stained red, and nuclei blue. E and F were the placental villi under a higher magnification. G and H were the anchoring villi under a higher magnification. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cell. En, endometrium. Scale bars represent 100 μm. |
PMC548132_F3_1222.jpg | What is the dominant medical problem in this image? | The proliferating activity revealed by Ki-67 immunostaining at implantation sites of the rhesus monkey on D17 (A, E, G), D19 (B), D28 (C) and D34 (D, F, H) of gestation. Panels A-D were under a lower magnification. Ki-67 protein was stained red, and nuclei blue. E and F were the placental villi under a higher magnification. G and H were the anchoring villi under a higher magnification. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cell. En, endometrium. Scale bars represent 100 μm. |
PMC548132_F3_1220.jpg | What is being portrayed in this visual content? | The proliferating activity revealed by Ki-67 immunostaining at implantation sites of the rhesus monkey on D17 (A, E, G), D19 (B), D28 (C) and D34 (D, F, H) of gestation. Panels A-D were under a lower magnification. Ki-67 protein was stained red, and nuclei blue. E and F were the placental villi under a higher magnification. G and H were the anchoring villi under a higher magnification. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cell. En, endometrium. Scale bars represent 100 μm. |
PMC548132_F3_1218.jpg | Can you identify the primary element in this image? | The proliferating activity revealed by Ki-67 immunostaining at implantation sites of the rhesus monkey on D17 (A, E, G), D19 (B), D28 (C) and D34 (D, F, H) of gestation. Panels A-D were under a lower magnification. Ki-67 protein was stained red, and nuclei blue. E and F were the placental villi under a higher magnification. G and H were the anchoring villi under a higher magnification. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cell. En, endometrium. Scale bars represent 100 μm. |
PMC548132_F4_1235.jpg | What can you see in this picture? | Immunohistochemical staining for Bcl-2 at implantation sites of the rhesus monkey. Bcl-2 staining is red, and nuclear counterstain blue. A, villous plancenta on D17. B, villous plancenta on D19. C, extravillous trophoblast cells in the basal plate of D17. D, villous plancenta on D28. E, villous plancenta on D34. F, villous plancenta on D34 under a higher magnification. G, the extravillous endovascular trophoblast cells; in the inset, the fetal origin of these cells was confirmed by anti-cytokeratin antibody (brown), and their position within the vascular wall was confirmed by anti-actin antibody staining (red). H, decidua. I, negative control. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cells. Ge, glandular epithelium. Evc, extravillous cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F4_1238.jpg | Describe the main subject of this image. | Immunohistochemical staining for Bcl-2 at implantation sites of the rhesus monkey. Bcl-2 staining is red, and nuclear counterstain blue. A, villous plancenta on D17. B, villous plancenta on D19. C, extravillous trophoblast cells in the basal plate of D17. D, villous plancenta on D28. E, villous plancenta on D34. F, villous plancenta on D34 under a higher magnification. G, the extravillous endovascular trophoblast cells; in the inset, the fetal origin of these cells was confirmed by anti-cytokeratin antibody (brown), and their position within the vascular wall was confirmed by anti-actin antibody staining (red). H, decidua. I, negative control. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cells. Ge, glandular epithelium. Evc, extravillous cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F4_1233.jpg | What can you see in this picture? | Immunohistochemical staining for Bcl-2 at implantation sites of the rhesus monkey. Bcl-2 staining is red, and nuclear counterstain blue. A, villous plancenta on D17. B, villous plancenta on D19. C, extravillous trophoblast cells in the basal plate of D17. D, villous plancenta on D28. E, villous plancenta on D34. F, villous plancenta on D34 under a higher magnification. G, the extravillous endovascular trophoblast cells; in the inset, the fetal origin of these cells was confirmed by anti-cytokeratin antibody (brown), and their position within the vascular wall was confirmed by anti-actin antibody staining (red). H, decidua. I, negative control. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cells. Ge, glandular epithelium. Evc, extravillous cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F4_1237.jpg | What is being portrayed in this visual content? | Immunohistochemical staining for Bcl-2 at implantation sites of the rhesus monkey. Bcl-2 staining is red, and nuclear counterstain blue. A, villous plancenta on D17. B, villous plancenta on D19. C, extravillous trophoblast cells in the basal plate of D17. D, villous plancenta on D28. E, villous plancenta on D34. F, villous plancenta on D34 under a higher magnification. G, the extravillous endovascular trophoblast cells; in the inset, the fetal origin of these cells was confirmed by anti-cytokeratin antibody (brown), and their position within the vascular wall was confirmed by anti-actin antibody staining (red). H, decidua. I, negative control. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cells. Ge, glandular epithelium. Evc, extravillous cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F4_1234.jpg | What is the core subject represented in this visual? | Immunohistochemical staining for Bcl-2 at implantation sites of the rhesus monkey. Bcl-2 staining is red, and nuclear counterstain blue. A, villous plancenta on D17. B, villous plancenta on D19. C, extravillous trophoblast cells in the basal plate of D17. D, villous plancenta on D28. E, villous plancenta on D34. F, villous plancenta on D34 under a higher magnification. G, the extravillous endovascular trophoblast cells; in the inset, the fetal origin of these cells was confirmed by anti-cytokeratin antibody (brown), and their position within the vascular wall was confirmed by anti-actin antibody staining (red). H, decidua. I, negative control. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cells. Ge, glandular epithelium. Evc, extravillous cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F4_1236.jpg | Describe the main subject of this image. | Immunohistochemical staining for Bcl-2 at implantation sites of the rhesus monkey. Bcl-2 staining is red, and nuclear counterstain blue. A, villous plancenta on D17. B, villous plancenta on D19. C, extravillous trophoblast cells in the basal plate of D17. D, villous plancenta on D28. E, villous plancenta on D34. F, villous plancenta on D34 under a higher magnification. G, the extravillous endovascular trophoblast cells; in the inset, the fetal origin of these cells was confirmed by anti-cytokeratin antibody (brown), and their position within the vascular wall was confirmed by anti-actin antibody staining (red). H, decidua. I, negative control. Vi, placental villi. ST, syncytiotrophoblast. CT, cytotrophoblast. Sc, stromal cells. Ge, glandular epithelium. Evc, extravillous cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F5_1227.jpg | What is the core subject represented in this visual? | Immunohistochemical staining for P53 at implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, H), and D34 (D, E, F, G) of gestation. P53 was stained dark in nuclei. A-D were villous placenta under a lower magnification. The inset of panel A shows the staining in the syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. E, staining in villous placenta under a higher magnification. F, staining in cell columns. G, syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. H, the endometrium with arrows indicating stromal cells. ST, syncytiotrophoblast. CT, cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F5_1226.jpg | What is the central feature of this picture? | Immunohistochemical staining for P53 at implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, H), and D34 (D, E, F, G) of gestation. P53 was stained dark in nuclei. A-D were villous placenta under a lower magnification. The inset of panel A shows the staining in the syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. E, staining in villous placenta under a higher magnification. F, staining in cell columns. G, syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. H, the endometrium with arrows indicating stromal cells. ST, syncytiotrophoblast. CT, cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F5_1225.jpg | Describe the main subject of this image. | Immunohistochemical staining for P53 at implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, H), and D34 (D, E, F, G) of gestation. P53 was stained dark in nuclei. A-D were villous placenta under a lower magnification. The inset of panel A shows the staining in the syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. E, staining in villous placenta under a higher magnification. F, staining in cell columns. G, syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. H, the endometrium with arrows indicating stromal cells. ST, syncytiotrophoblast. CT, cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F5_1228.jpg | What does this image primarily show? | Immunohistochemical staining for P53 at implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, H), and D34 (D, E, F, G) of gestation. P53 was stained dark in nuclei. A-D were villous placenta under a lower magnification. The inset of panel A shows the staining in the syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. E, staining in villous placenta under a higher magnification. F, staining in cell columns. G, syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. H, the endometrium with arrows indicating stromal cells. ST, syncytiotrophoblast. CT, cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F5_1223.jpg | What stands out most in this visual? | Immunohistochemical staining for P53 at implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, H), and D34 (D, E, F, G) of gestation. P53 was stained dark in nuclei. A-D were villous placenta under a lower magnification. The inset of panel A shows the staining in the syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. E, staining in villous placenta under a higher magnification. F, staining in cell columns. G, syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. H, the endometrium with arrows indicating stromal cells. ST, syncytiotrophoblast. CT, cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F5_1224.jpg | What is being portrayed in this visual content? | Immunohistochemical staining for P53 at implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, H), and D34 (D, E, F, G) of gestation. P53 was stained dark in nuclei. A-D were villous placenta under a lower magnification. The inset of panel A shows the staining in the syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. E, staining in villous placenta under a higher magnification. F, staining in cell columns. G, syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. H, the endometrium with arrows indicating stromal cells. ST, syncytiotrophoblast. CT, cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F5_1231.jpg | What is the dominant medical problem in this image? | Immunohistochemical staining for P53 at implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, H), and D34 (D, E, F, G) of gestation. P53 was stained dark in nuclei. A-D were villous placenta under a lower magnification. The inset of panel A shows the staining in the syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. E, staining in villous placenta under a higher magnification. F, staining in cell columns. G, syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. H, the endometrium with arrows indicating stromal cells. ST, syncytiotrophoblast. CT, cytotrophoblast. Scale bars represent 50 μm. |
PMC548132_F5_1230.jpg | What is the central feature of this picture? | Immunohistochemical staining for P53 at implantation sites of the rhesus monkey on D17 (A), D19 (B), D28 (C, H), and D34 (D, E, F, G) of gestation. P53 was stained dark in nuclei. A-D were villous placenta under a lower magnification. The inset of panel A shows the staining in the syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. E, staining in villous placenta under a higher magnification. F, staining in cell columns. G, syncytiotrophoblast covering the basal feet of the anchoring villi under a higher magnification. H, the endometrium with arrows indicating stromal cells. ST, syncytiotrophoblast. CT, cytotrophoblast. Scale bars represent 50 μm. |
PMC548138_F1_1240.jpg | What is the focal point of this photograph? | Preoperative Sister Mary Joseph's nodule ultrasonography: 4 × 4 cm mass confined below the umbilicus (arrows). The main lesion is partly hyperechoic and partly hypoechoic with a poorly defined edge. |
PMC548138_F1_1239.jpg | What is being portrayed in this visual content? | Preoperative Sister Mary Joseph's nodule ultrasonography: 4 × 4 cm mass confined below the umbilicus (arrows). The main lesion is partly hyperechoic and partly hypoechoic with a poorly defined edge. |
PMC548140_F2_1241.jpg | What is the central feature of this picture? | No significant apoptosis was found in TIIcells upon hyperoxia in vivo for 48 hrs. Lung tissue of normoxic rats (left) and of hyperoxic rats (right) were tested for DNA fragmentation by TUNEL reaction as described in Materials and Methods. The positive TUNEL reaction is represented by green fluorescence. The presence of lamellar bodies is indicated by red fluorescence. Pseudo-colour blue was used to highlight the contours of lung tissue. Bar: 25 μm. |
PMC548304_F1_1246.jpg | Can you identify the primary element in this image? | Colonic mucosal inflammation in ulcerative colitis with loss of goblet cells and neutrophilic infiltrate (magnification ×100) |
PMC548319_F6_1247.jpg | What is shown in this image? | Immunocytochemistry determination of IREG1. Hippocampal neurons and SH-SY5Y cells, labeled with rabbit anti-IREG1 antibody and with Alexa-546-conjugated goat anti-rabbit IgG, were imaged in a confocal microscope. Shown are representative fields of cells cultured at different iron concentrations. Note the preferentially cytosolic distribution of IREG1. |
PMC548319_F6_1251.jpg | What is the main focus of this visual representation? | Immunocytochemistry determination of IREG1. Hippocampal neurons and SH-SY5Y cells, labeled with rabbit anti-IREG1 antibody and with Alexa-546-conjugated goat anti-rabbit IgG, were imaged in a confocal microscope. Shown are representative fields of cells cultured at different iron concentrations. Note the preferentially cytosolic distribution of IREG1. |
PMC548669_F2_1262.jpg | What can you see in this picture? | Clc is expressed in epithelia Transverse sections from E16.5 mouse embryos were hybridized to clc (A, D, G and I), clf (B, E, H and J) or cntfr (C and F). Sections through the kidney (A-C) show that clc is expressed in developing nephrons (arrows), clf in ureteric tips (arrowheads) and cntfr in nephrogenic mesenchyme. Sections through the lung (D-F) show that whereas clf is strongly expressed in both distal (arrowheads) and proximal (arrows) epithelia, clc and cntfr are weakly expressed in distal epithelium. Boxed areas are shown in higher magnification in the corner of each panel. Sections through molar tooth germs (G, H) show that mesenchyma (arrows) surrounding the dental follicle is positive for both clc and clf and that the inner enamel epithelium (arrowheads) expresses only clf. Coronal sections through muzzle (I, J) show that both clc and clf are expressed in the epithelium bordering the mandibles and in between the lips and mandibles (arrow) as well as in follicles of vibrissae (arrowheads); in addition, clf is expressed in mesenchyma (asterisks). a, pulmonary artery; dp, dental papilla; de, dental epithelium; oc, oral cavity; uli, upper lip; lli, lower lip. Bars: 100 μm in A-H, 200 μm in I and J. |
PMC548669_F2_1261.jpg | Can you identify the primary element in this image? | Clc is expressed in epithelia Transverse sections from E16.5 mouse embryos were hybridized to clc (A, D, G and I), clf (B, E, H and J) or cntfr (C and F). Sections through the kidney (A-C) show that clc is expressed in developing nephrons (arrows), clf in ureteric tips (arrowheads) and cntfr in nephrogenic mesenchyme. Sections through the lung (D-F) show that whereas clf is strongly expressed in both distal (arrowheads) and proximal (arrows) epithelia, clc and cntfr are weakly expressed in distal epithelium. Boxed areas are shown in higher magnification in the corner of each panel. Sections through molar tooth germs (G, H) show that mesenchyma (arrows) surrounding the dental follicle is positive for both clc and clf and that the inner enamel epithelium (arrowheads) expresses only clf. Coronal sections through muzzle (I, J) show that both clc and clf are expressed in the epithelium bordering the mandibles and in between the lips and mandibles (arrow) as well as in follicles of vibrissae (arrowheads); in addition, clf is expressed in mesenchyma (asterisks). a, pulmonary artery; dp, dental papilla; de, dental epithelium; oc, oral cavity; uli, upper lip; lli, lower lip. Bars: 100 μm in A-H, 200 μm in I and J. |
PMC548669_F2_1254.jpg | What is the central feature of this picture? | Clc is expressed in epithelia Transverse sections from E16.5 mouse embryos were hybridized to clc (A, D, G and I), clf (B, E, H and J) or cntfr (C and F). Sections through the kidney (A-C) show that clc is expressed in developing nephrons (arrows), clf in ureteric tips (arrowheads) and cntfr in nephrogenic mesenchyme. Sections through the lung (D-F) show that whereas clf is strongly expressed in both distal (arrowheads) and proximal (arrows) epithelia, clc and cntfr are weakly expressed in distal epithelium. Boxed areas are shown in higher magnification in the corner of each panel. Sections through molar tooth germs (G, H) show that mesenchyma (arrows) surrounding the dental follicle is positive for both clc and clf and that the inner enamel epithelium (arrowheads) expresses only clf. Coronal sections through muzzle (I, J) show that both clc and clf are expressed in the epithelium bordering the mandibles and in between the lips and mandibles (arrow) as well as in follicles of vibrissae (arrowheads); in addition, clf is expressed in mesenchyma (asterisks). a, pulmonary artery; dp, dental papilla; de, dental epithelium; oc, oral cavity; uli, upper lip; lli, lower lip. Bars: 100 μm in A-H, 200 μm in I and J. |
PMC548669_F2_1259.jpg | What can you see in this picture? | Clc is expressed in epithelia Transverse sections from E16.5 mouse embryos were hybridized to clc (A, D, G and I), clf (B, E, H and J) or cntfr (C and F). Sections through the kidney (A-C) show that clc is expressed in developing nephrons (arrows), clf in ureteric tips (arrowheads) and cntfr in nephrogenic mesenchyme. Sections through the lung (D-F) show that whereas clf is strongly expressed in both distal (arrowheads) and proximal (arrows) epithelia, clc and cntfr are weakly expressed in distal epithelium. Boxed areas are shown in higher magnification in the corner of each panel. Sections through molar tooth germs (G, H) show that mesenchyma (arrows) surrounding the dental follicle is positive for both clc and clf and that the inner enamel epithelium (arrowheads) expresses only clf. Coronal sections through muzzle (I, J) show that both clc and clf are expressed in the epithelium bordering the mandibles and in between the lips and mandibles (arrow) as well as in follicles of vibrissae (arrowheads); in addition, clf is expressed in mesenchyma (asterisks). a, pulmonary artery; dp, dental papilla; de, dental epithelium; oc, oral cavity; uli, upper lip; lli, lower lip. Bars: 100 μm in A-H, 200 μm in I and J. |
PMC548669_F2_1258.jpg | Describe the main subject of this image. | Clc is expressed in epithelia Transverse sections from E16.5 mouse embryos were hybridized to clc (A, D, G and I), clf (B, E, H and J) or cntfr (C and F). Sections through the kidney (A-C) show that clc is expressed in developing nephrons (arrows), clf in ureteric tips (arrowheads) and cntfr in nephrogenic mesenchyme. Sections through the lung (D-F) show that whereas clf is strongly expressed in both distal (arrowheads) and proximal (arrows) epithelia, clc and cntfr are weakly expressed in distal epithelium. Boxed areas are shown in higher magnification in the corner of each panel. Sections through molar tooth germs (G, H) show that mesenchyma (arrows) surrounding the dental follicle is positive for both clc and clf and that the inner enamel epithelium (arrowheads) expresses only clf. Coronal sections through muzzle (I, J) show that both clc and clf are expressed in the epithelium bordering the mandibles and in between the lips and mandibles (arrow) as well as in follicles of vibrissae (arrowheads); in addition, clf is expressed in mesenchyma (asterisks). a, pulmonary artery; dp, dental papilla; de, dental epithelium; oc, oral cavity; uli, upper lip; lli, lower lip. Bars: 100 μm in A-H, 200 μm in I and J. |
PMC548684_F1_1264.jpg | What is the main focus of this visual representation? | Distribution of CD4+ T helper cells in tonsils. Frozen tonsil sections were stained with anti-IgD (PE, red) or anti-CD57 (FITC, green) and isotype control antibodies in panel group A to show the background staining of the system. In panel group B, sections were stained with anti-CD57 (FITC), anti-IgD (PE) and anti-CD4 (APC). In panel group C, sections were stained with anti-CD57 (FITC), anti-CD69 (PE) and anti-CD4 (APC). Two different sections were shown in each group of panels. Stained sections were analyzed with a confocal microscope. GC-Th cells can be divided into CD57+ and CD57- T cells, both of which are CD69+. A few CD69+ or CD57+ T cells are found outside of GC. Most CD4+ T cells in the interfollicular areas (IFA or T cell-rich zone) are CD57- and CD69-. GCs are surrounded by the ring of mantle zones (MZ) filled with IgD+ cells. A representative set of images from three different specimens are shown. |
PMC548684_F1_1265.jpg | What key item or scene is captured in this photo? | Distribution of CD4+ T helper cells in tonsils. Frozen tonsil sections were stained with anti-IgD (PE, red) or anti-CD57 (FITC, green) and isotype control antibodies in panel group A to show the background staining of the system. In panel group B, sections were stained with anti-CD57 (FITC), anti-IgD (PE) and anti-CD4 (APC). In panel group C, sections were stained with anti-CD57 (FITC), anti-CD69 (PE) and anti-CD4 (APC). Two different sections were shown in each group of panels. Stained sections were analyzed with a confocal microscope. GC-Th cells can be divided into CD57+ and CD57- T cells, both of which are CD69+. A few CD69+ or CD57+ T cells are found outside of GC. Most CD4+ T cells in the interfollicular areas (IFA or T cell-rich zone) are CD57- and CD69-. GCs are surrounded by the ring of mantle zones (MZ) filled with IgD+ cells. A representative set of images from three different specimens are shown. |
PMC548684_F1_1266.jpg | Can you identify the primary element in this image? | Distribution of CD4+ T helper cells in tonsils. Frozen tonsil sections were stained with anti-IgD (PE, red) or anti-CD57 (FITC, green) and isotype control antibodies in panel group A to show the background staining of the system. In panel group B, sections were stained with anti-CD57 (FITC), anti-IgD (PE) and anti-CD4 (APC). In panel group C, sections were stained with anti-CD57 (FITC), anti-CD69 (PE) and anti-CD4 (APC). Two different sections were shown in each group of panels. Stained sections were analyzed with a confocal microscope. GC-Th cells can be divided into CD57+ and CD57- T cells, both of which are CD69+. A few CD69+ or CD57+ T cells are found outside of GC. Most CD4+ T cells in the interfollicular areas (IFA or T cell-rich zone) are CD57- and CD69-. GCs are surrounded by the ring of mantle zones (MZ) filled with IgD+ cells. A representative set of images from three different specimens are shown. |
PMC548684_F1_1267.jpg | What is the main focus of this visual representation? | Distribution of CD4+ T helper cells in tonsils. Frozen tonsil sections were stained with anti-IgD (PE, red) or anti-CD57 (FITC, green) and isotype control antibodies in panel group A to show the background staining of the system. In panel group B, sections were stained with anti-CD57 (FITC), anti-IgD (PE) and anti-CD4 (APC). In panel group C, sections were stained with anti-CD57 (FITC), anti-CD69 (PE) and anti-CD4 (APC). Two different sections were shown in each group of panels. Stained sections were analyzed with a confocal microscope. GC-Th cells can be divided into CD57+ and CD57- T cells, both of which are CD69+. A few CD69+ or CD57+ T cells are found outside of GC. Most CD4+ T cells in the interfollicular areas (IFA or T cell-rich zone) are CD57- and CD69-. GCs are surrounded by the ring of mantle zones (MZ) filled with IgD+ cells. A representative set of images from three different specimens are shown. |
PMC548684_F1_1263.jpg | What is shown in this image? | Distribution of CD4+ T helper cells in tonsils. Frozen tonsil sections were stained with anti-IgD (PE, red) or anti-CD57 (FITC, green) and isotype control antibodies in panel group A to show the background staining of the system. In panel group B, sections were stained with anti-CD57 (FITC), anti-IgD (PE) and anti-CD4 (APC). In panel group C, sections were stained with anti-CD57 (FITC), anti-CD69 (PE) and anti-CD4 (APC). Two different sections were shown in each group of panels. Stained sections were analyzed with a confocal microscope. GC-Th cells can be divided into CD57+ and CD57- T cells, both of which are CD69+. A few CD69+ or CD57+ T cells are found outside of GC. Most CD4+ T cells in the interfollicular areas (IFA or T cell-rich zone) are CD57- and CD69-. GCs are surrounded by the ring of mantle zones (MZ) filled with IgD+ cells. A representative set of images from three different specimens are shown. |
PMC548690_F5_1269.jpg | What stands out most in this visual? | Immunofluorescence detection of GANA-1::GFP. A) A coarsely granular cytoplasmic distribution of immunopositivity (green) in body-wall muscle cells (arrowheads). Two non-transgenic worms are shown in the background (asterisks) for comparison. Nuclei are counterstained in red. B) Detailed view of two body wall muscle cells with coarsely granular cytoplasmic distribution of immunopositivity (arrowheads) and a coelomocyte (asterisk), both pictures were acquired by 3D rendering of initial confocal Z-stacks. Note: compare with figure 6. |
PMC548953_pbio-0030059-g003_1273.jpg | What is the central feature of this picture? | Summary of Phenotypes DeterminedLight (left panels) and scanning electron (right panels) micrographs of mosaic Drosophila eyes. Large homozygous mutant clones are orange (arrowheads); heterozygous tissues are dark red. Examples are shown of lethal mutations that give a (A) wild-type (63.4% of lethal mutations), (B) rough (disordered ommatidia, 18.2%), (C) cell lethal (absence of homozygous mutant tissue, 14.5%), and (D) glossy (loss of lens structure, 3.9%) phenotype. For details on how clones are generated, see http://www.bruinfly.ucla.edu. |
PMC548953_pbio-0030059-g003_1277.jpg | What does this image primarily show? | Summary of Phenotypes DeterminedLight (left panels) and scanning electron (right panels) micrographs of mosaic Drosophila eyes. Large homozygous mutant clones are orange (arrowheads); heterozygous tissues are dark red. Examples are shown of lethal mutations that give a (A) wild-type (63.4% of lethal mutations), (B) rough (disordered ommatidia, 18.2%), (C) cell lethal (absence of homozygous mutant tissue, 14.5%), and (D) glossy (loss of lens structure, 3.9%) phenotype. For details on how clones are generated, see http://www.bruinfly.ucla.edu. |
PMC548953_pbio-0030059-g003_1270.jpg | What is being portrayed in this visual content? | Summary of Phenotypes DeterminedLight (left panels) and scanning electron (right panels) micrographs of mosaic Drosophila eyes. Large homozygous mutant clones are orange (arrowheads); heterozygous tissues are dark red. Examples are shown of lethal mutations that give a (A) wild-type (63.4% of lethal mutations), (B) rough (disordered ommatidia, 18.2%), (C) cell lethal (absence of homozygous mutant tissue, 14.5%), and (D) glossy (loss of lens structure, 3.9%) phenotype. For details on how clones are generated, see http://www.bruinfly.ucla.edu. |
PMC548953_pbio-0030059-g003_1274.jpg | What does this image primarily show? | Summary of Phenotypes DeterminedLight (left panels) and scanning electron (right panels) micrographs of mosaic Drosophila eyes. Large homozygous mutant clones are orange (arrowheads); heterozygous tissues are dark red. Examples are shown of lethal mutations that give a (A) wild-type (63.4% of lethal mutations), (B) rough (disordered ommatidia, 18.2%), (C) cell lethal (absence of homozygous mutant tissue, 14.5%), and (D) glossy (loss of lens structure, 3.9%) phenotype. For details on how clones are generated, see http://www.bruinfly.ucla.edu. |
PMC548953_pbio-0030059-g003_1276.jpg | Describe the main subject of this image. | Summary of Phenotypes DeterminedLight (left panels) and scanning electron (right panels) micrographs of mosaic Drosophila eyes. Large homozygous mutant clones are orange (arrowheads); heterozygous tissues are dark red. Examples are shown of lethal mutations that give a (A) wild-type (63.4% of lethal mutations), (B) rough (disordered ommatidia, 18.2%), (C) cell lethal (absence of homozygous mutant tissue, 14.5%), and (D) glossy (loss of lens structure, 3.9%) phenotype. For details on how clones are generated, see http://www.bruinfly.ucla.edu. |
PMC548953_pbio-0030059-g003_1271.jpg | What is shown in this image? | Summary of Phenotypes DeterminedLight (left panels) and scanning electron (right panels) micrographs of mosaic Drosophila eyes. Large homozygous mutant clones are orange (arrowheads); heterozygous tissues are dark red. Examples are shown of lethal mutations that give a (A) wild-type (63.4% of lethal mutations), (B) rough (disordered ommatidia, 18.2%), (C) cell lethal (absence of homozygous mutant tissue, 14.5%), and (D) glossy (loss of lens structure, 3.9%) phenotype. For details on how clones are generated, see http://www.bruinfly.ucla.edu. |
PMC548953_pbio-0030059-g003_1275.jpg | Describe the main subject of this image. | Summary of Phenotypes DeterminedLight (left panels) and scanning electron (right panels) micrographs of mosaic Drosophila eyes. Large homozygous mutant clones are orange (arrowheads); heterozygous tissues are dark red. Examples are shown of lethal mutations that give a (A) wild-type (63.4% of lethal mutations), (B) rough (disordered ommatidia, 18.2%), (C) cell lethal (absence of homozygous mutant tissue, 14.5%), and (D) glossy (loss of lens structure, 3.9%) phenotype. For details on how clones are generated, see http://www.bruinfly.ucla.edu. |
PMC549033_F1_1278.jpg | What is the focal point of this photograph? | Immunohistochemical analysis of metastatic tumor tissue from responder patient 1 and non-responder patient 7. A; H-E stain and B; anti-HLA-A24 MoAb from patient 1. C; anti-HLA-A2 MoAb before DC vaccination and D; anti-HLA-A2 MoAb after 4 DC injections from patient 7. Magnification × 200. |
PMC549033_F1_1280.jpg | What can you see in this picture? | Immunohistochemical analysis of metastatic tumor tissue from responder patient 1 and non-responder patient 7. A; H-E stain and B; anti-HLA-A24 MoAb from patient 1. C; anti-HLA-A2 MoAb before DC vaccination and D; anti-HLA-A2 MoAb after 4 DC injections from patient 7. Magnification × 200. |
PMC549033_F1_1279.jpg | What is the central feature of this picture? | Immunohistochemical analysis of metastatic tumor tissue from responder patient 1 and non-responder patient 7. A; H-E stain and B; anti-HLA-A24 MoAb from patient 1. C; anti-HLA-A2 MoAb before DC vaccination and D; anti-HLA-A2 MoAb after 4 DC injections from patient 7. Magnification × 200. |
PMC549033_F1_1281.jpg | What is shown in this image? | Immunohistochemical analysis of metastatic tumor tissue from responder patient 1 and non-responder patient 7. A; H-E stain and B; anti-HLA-A24 MoAb from patient 1. C; anti-HLA-A2 MoAb before DC vaccination and D; anti-HLA-A2 MoAb after 4 DC injections from patient 7. Magnification × 200. |
PMC549033_F3_1288.jpg | What can you see in this picture? | Impact of DC vaccines on metastatic lesions of the lung in responder patient 1. Upper and lower panels show a lung and hilar lymph node metastatic lesion (arrow), respectively. The CT scan was made before therapy and after 4, 7 and 10 DC vaccinations. |
PMC549033_F3_1286.jpg | Can you identify the primary element in this image? | Impact of DC vaccines on metastatic lesions of the lung in responder patient 1. Upper and lower panels show a lung and hilar lymph node metastatic lesion (arrow), respectively. The CT scan was made before therapy and after 4, 7 and 10 DC vaccinations. |
PMC549033_F3_1289.jpg | What is the focal point of this photograph? | Impact of DC vaccines on metastatic lesions of the lung in responder patient 1. Upper and lower panels show a lung and hilar lymph node metastatic lesion (arrow), respectively. The CT scan was made before therapy and after 4, 7 and 10 DC vaccinations. |
PMC549033_F3_1282.jpg | What is the core subject represented in this visual? | Impact of DC vaccines on metastatic lesions of the lung in responder patient 1. Upper and lower panels show a lung and hilar lymph node metastatic lesion (arrow), respectively. The CT scan was made before therapy and after 4, 7 and 10 DC vaccinations. |
PMC549033_F3_1285.jpg | Describe the main subject of this image. | Impact of DC vaccines on metastatic lesions of the lung in responder patient 1. Upper and lower panels show a lung and hilar lymph node metastatic lesion (arrow), respectively. The CT scan was made before therapy and after 4, 7 and 10 DC vaccinations. |
PMC549033_F3_1283.jpg | Can you identify the primary element in this image? | Impact of DC vaccines on metastatic lesions of the lung in responder patient 1. Upper and lower panels show a lung and hilar lymph node metastatic lesion (arrow), respectively. The CT scan was made before therapy and after 4, 7 and 10 DC vaccinations. |
PMC549033_F4_1290.jpg | What key item or scene is captured in this photo? | Phenotype analysis of lymphocytes infiltrating the tumor site in responder patient 1. Obvious infiltration of a larger number of CD4+ or CD8+ T cells and a small number of CD20+ B cells is shown. Indirect staining using anti-CD4, CD8, CD20 or CD56 MoAb as primary Ab and goat anti-mouse Ab as secondary Ab was performed. Magnification × 200. |
PMC549033_F4_1292.jpg | What is the main focus of this visual representation? | Phenotype analysis of lymphocytes infiltrating the tumor site in responder patient 1. Obvious infiltration of a larger number of CD4+ or CD8+ T cells and a small number of CD20+ B cells is shown. Indirect staining using anti-CD4, CD8, CD20 or CD56 MoAb as primary Ab and goat anti-mouse Ab as secondary Ab was performed. Magnification × 200. |
PMC549044_F2_1295.jpg | What is the focal point of this photograph? | (A) BAL cell differential of RSV-infected mice. Mice were treated with cyclophosphamide (CYP) or vehicle 5 days before infection with RSV. Animals were sacrificed on day 4 postinfection and BAL was performed. Following cytocentrifugation, BAL cells were stained with Leukostat and counted from 4 different slides from each group in a blinded fashion. Cell counts as percentage of total were plotted. (B) Measurement of airway hyperrresponsiveness (AHR). Mice treated as above were tested for AHR by methacholine challenge in a plethysmograph. AHR is expressed as PENH, percent of control. (C) Lung histopathology. Mice were infected with RSV alone (C and D) or treated with cyclophosphamide (A and B) prior to RSV infection. The third group of mice was not exposed to RSV (E and F). Animals were sacrificed on day 5 and their lungs removed and sectioned. Paraffin-embedded lung sections were stained with hematoxylin-eosin. |
PMC549044_F2_1297.jpg | What is the dominant medical problem in this image? | (A) BAL cell differential of RSV-infected mice. Mice were treated with cyclophosphamide (CYP) or vehicle 5 days before infection with RSV. Animals were sacrificed on day 4 postinfection and BAL was performed. Following cytocentrifugation, BAL cells were stained with Leukostat and counted from 4 different slides from each group in a blinded fashion. Cell counts as percentage of total were plotted. (B) Measurement of airway hyperrresponsiveness (AHR). Mice treated as above were tested for AHR by methacholine challenge in a plethysmograph. AHR is expressed as PENH, percent of control. (C) Lung histopathology. Mice were infected with RSV alone (C and D) or treated with cyclophosphamide (A and B) prior to RSV infection. The third group of mice was not exposed to RSV (E and F). Animals were sacrificed on day 5 and their lungs removed and sectioned. Paraffin-embedded lung sections were stained with hematoxylin-eosin. |
PMC549044_F2_1299.jpg | What is the principal component of this image? | (A) BAL cell differential of RSV-infected mice. Mice were treated with cyclophosphamide (CYP) or vehicle 5 days before infection with RSV. Animals were sacrificed on day 4 postinfection and BAL was performed. Following cytocentrifugation, BAL cells were stained with Leukostat and counted from 4 different slides from each group in a blinded fashion. Cell counts as percentage of total were plotted. (B) Measurement of airway hyperrresponsiveness (AHR). Mice treated as above were tested for AHR by methacholine challenge in a plethysmograph. AHR is expressed as PENH, percent of control. (C) Lung histopathology. Mice were infected with RSV alone (C and D) or treated with cyclophosphamide (A and B) prior to RSV infection. The third group of mice was not exposed to RSV (E and F). Animals were sacrificed on day 5 and their lungs removed and sectioned. Paraffin-embedded lung sections were stained with hematoxylin-eosin. |
PMC549065_F2_1303.jpg | What object or scene is depicted here? | Cartoon representations of ACHB. (a) The ligand-binding dimer of ACHB; (b) the pentamer of ACHB. The representations were derived from the crystal structure of the snail acetylcholine-binding protein (PDB 1UV6). Residues forming the ligand-binding box are shaded orange. The chain of residues that could potentially act as a conduit for transmission of conformational changes is colored green and the prominent conserved ones among them have been labeled. |
PMC549065_F2_1302.jpg | What key item or scene is captured in this photo? | Cartoon representations of ACHB. (a) The ligand-binding dimer of ACHB; (b) the pentamer of ACHB. The representations were derived from the crystal structure of the snail acetylcholine-binding protein (PDB 1UV6). Residues forming the ligand-binding box are shaded orange. The chain of residues that could potentially act as a conduit for transmission of conformational changes is colored green and the prominent conserved ones among them have been labeled. |
PMC549083_F1_1310.jpg | What is the core subject represented in this visual? | 1A: Pre-surgical T2-weighted STIR-sequence, axial section: in right ventral chest wall bright superficial thickening of cutis and subcutis without involvement of muscles. 1B: Pre-surgical T2-weighted STIR-sequence, axial section: very bright, flat superficial cutaneous PNF in proximal part of right upper arm. 1C: Pre-surgical clinical frontal view of both PNF on right upper arm and thorax wall. 1D: Post-surgical T1-weighted sequence, axial section: small defect in cutis and subcutis, no PNF visible anymore. 1E: Post-surgical T2-weighted STIR-sequence, axial section: complete removal of tumor with hypointensive induration. 1F: Post-surgical clinical frontal view of both scars on right upper arm and thorax wall. |
PMC549083_F1_1312.jpg | What key item or scene is captured in this photo? | 1A: Pre-surgical T2-weighted STIR-sequence, axial section: in right ventral chest wall bright superficial thickening of cutis and subcutis without involvement of muscles. 1B: Pre-surgical T2-weighted STIR-sequence, axial section: very bright, flat superficial cutaneous PNF in proximal part of right upper arm. 1C: Pre-surgical clinical frontal view of both PNF on right upper arm and thorax wall. 1D: Post-surgical T1-weighted sequence, axial section: small defect in cutis and subcutis, no PNF visible anymore. 1E: Post-surgical T2-weighted STIR-sequence, axial section: complete removal of tumor with hypointensive induration. 1F: Post-surgical clinical frontal view of both scars on right upper arm and thorax wall. |
PMC549083_F1_1311.jpg | What can you see in this picture? | 1A: Pre-surgical T2-weighted STIR-sequence, axial section: in right ventral chest wall bright superficial thickening of cutis and subcutis without involvement of muscles. 1B: Pre-surgical T2-weighted STIR-sequence, axial section: very bright, flat superficial cutaneous PNF in proximal part of right upper arm. 1C: Pre-surgical clinical frontal view of both PNF on right upper arm and thorax wall. 1D: Post-surgical T1-weighted sequence, axial section: small defect in cutis and subcutis, no PNF visible anymore. 1E: Post-surgical T2-weighted STIR-sequence, axial section: complete removal of tumor with hypointensive induration. 1F: Post-surgical clinical frontal view of both scars on right upper arm and thorax wall. |
PMC549083_F1_1309.jpg | What can you see in this picture? | 1A: Pre-surgical T2-weighted STIR-sequence, axial section: in right ventral chest wall bright superficial thickening of cutis and subcutis without involvement of muscles. 1B: Pre-surgical T2-weighted STIR-sequence, axial section: very bright, flat superficial cutaneous PNF in proximal part of right upper arm. 1C: Pre-surgical clinical frontal view of both PNF on right upper arm and thorax wall. 1D: Post-surgical T1-weighted sequence, axial section: small defect in cutis and subcutis, no PNF visible anymore. 1E: Post-surgical T2-weighted STIR-sequence, axial section: complete removal of tumor with hypointensive induration. 1F: Post-surgical clinical frontal view of both scars on right upper arm and thorax wall. |
PMC549083_F2_1306.jpg | Describe the main subject of this image. | 2A: Pre-surgical T2-weighted STIR-sequence, axial section: superficial tumor covering the laryngeal prominence. 2B: Pre-surgical clinical frontal view of PNF of ventral neck. 2C: Post-surgical T2-weighted STIR-sequence, axial section: scar tissue praelaryngeal visible. 2D: Post-surgical clinical frontal view of laryngeal scar. |
PMC549083_F2_1304.jpg | What is the main focus of this visual representation? | 2A: Pre-surgical T2-weighted STIR-sequence, axial section: superficial tumor covering the laryngeal prominence. 2B: Pre-surgical clinical frontal view of PNF of ventral neck. 2C: Post-surgical T2-weighted STIR-sequence, axial section: scar tissue praelaryngeal visible. 2D: Post-surgical clinical frontal view of laryngeal scar. |
PMC549083_F2_1305.jpg | What's the most prominent thing you notice in this picture? | 2A: Pre-surgical T2-weighted STIR-sequence, axial section: superficial tumor covering the laryngeal prominence. 2B: Pre-surgical clinical frontal view of PNF of ventral neck. 2C: Post-surgical T2-weighted STIR-sequence, axial section: scar tissue praelaryngeal visible. 2D: Post-surgical clinical frontal view of laryngeal scar. |
PMC549083_F3_1318.jpg | What stands out most in this visual? | 3A: Pre-surgical T2-weighted STIR sequence of left ventral abdominal wall, paraumbilical. Bright plexiform neurofibroma with thickening of cutis without involvement of muscle. 3B: Pre-surgical T2-weighted STIR sequence, axial section of left ventral abdominal wall, costal margin. Small bright plexiform neurofibroma in cutis and subcutis ventral left. 3C: Pre-surgical clinical frontal view of abdomen with both superficial plexiform neurofibromas visible. 3D: Post-surgical MRI control from A. Complete removal of plexiform neurofibroma. 3E: Post-surgical MRI control from B. Complete removal of plexiform neurofibroma. 3F: Post-surgical clinical frontal view of abdomen. Only two visible scars left after surgery. |
PMC549083_F3_1320.jpg | What is being portrayed in this visual content? | 3A: Pre-surgical T2-weighted STIR sequence of left ventral abdominal wall, paraumbilical. Bright plexiform neurofibroma with thickening of cutis without involvement of muscle. 3B: Pre-surgical T2-weighted STIR sequence, axial section of left ventral abdominal wall, costal margin. Small bright plexiform neurofibroma in cutis and subcutis ventral left. 3C: Pre-surgical clinical frontal view of abdomen with both superficial plexiform neurofibromas visible. 3D: Post-surgical MRI control from A. Complete removal of plexiform neurofibroma. 3E: Post-surgical MRI control from B. Complete removal of plexiform neurofibroma. 3F: Post-surgical clinical frontal view of abdomen. Only two visible scars left after surgery. |
PMC549083_F3_1323.jpg | What key item or scene is captured in this photo? | 3A: Pre-surgical T2-weighted STIR sequence of left ventral abdominal wall, paraumbilical. Bright plexiform neurofibroma with thickening of cutis without involvement of muscle. 3B: Pre-surgical T2-weighted STIR sequence, axial section of left ventral abdominal wall, costal margin. Small bright plexiform neurofibroma in cutis and subcutis ventral left. 3C: Pre-surgical clinical frontal view of abdomen with both superficial plexiform neurofibromas visible. 3D: Post-surgical MRI control from A. Complete removal of plexiform neurofibroma. 3E: Post-surgical MRI control from B. Complete removal of plexiform neurofibroma. 3F: Post-surgical clinical frontal view of abdomen. Only two visible scars left after surgery. |
PMC549083_F4_1315.jpg | What is the focal point of this photograph? | 4A: Pre-surgical T2-weighted STIR-sequence, axial section: discrete signs of flat funicular, cutaneous and subcutaneous PNF near the left iliac crest with involvement of soft tissue, but without visible infiltration of abdominal muscles. 4B: Pre-surgical clinical view of PNF in the left flank. 4C: Post-surgical T2-weighted Haste-sequence: complete resection of tumor, only a smooth fibrous post-surgical induration and small scar can be identified. 4D: Post-surgical clinical view of hypertrophic scar. |
PMC549083_F6_1324.jpg | What is the core subject represented in this visual? | 6A: Pre-surgical T2-weighted STIR-sequence, transversal section: bright, flat cutaneous and subcutaneous PNF of right back without involvement of abdominal wall and muscles. 6B: Pre-surgical clinical view of PNF on right back with hypertrichosis. 6C: Post-surgical T2-weighted Turbo Spin Echo-sequence, axial section: complete removal of PNF, thin scar, no subcutaneous fatty tissue visible in scan. 6D: Post-surgical clinical view of scar after tumor removal on back. |
PMC549083_F6_1325.jpg | What object or scene is depicted here? | 6A: Pre-surgical T2-weighted STIR-sequence, transversal section: bright, flat cutaneous and subcutaneous PNF of right back without involvement of abdominal wall and muscles. 6B: Pre-surgical clinical view of PNF on right back with hypertrichosis. 6C: Post-surgical T2-weighted Turbo Spin Echo-sequence, axial section: complete removal of PNF, thin scar, no subcutaneous fatty tissue visible in scan. 6D: Post-surgical clinical view of scar after tumor removal on back. |
PMC549083_F7_1328.jpg | What is the main focus of this visual representation? | 7A: Pre-surgical T2-weighted STIR-sequence, transversal section: Cutaneous and subcutaneous PNF of forearm, bright signal without involvement of muscles or fascia. 7B: Pre-surigcal clinical view of hyperpigmented PNF of left forearm. 7C: Post-surgical T2-weighted STIR-sequence, axial section: complete removal of tumor. 7D: Post-surgical clinical view of scar on left forearm. |
PMC549083_F7_1327.jpg | What is being portrayed in this visual content? | 7A: Pre-surgical T2-weighted STIR-sequence, transversal section: Cutaneous and subcutaneous PNF of forearm, bright signal without involvement of muscles or fascia. 7B: Pre-surigcal clinical view of hyperpigmented PNF of left forearm. 7C: Post-surgical T2-weighted STIR-sequence, axial section: complete removal of tumor. 7D: Post-surgical clinical view of scar on left forearm. |
PMC549193_F8_1333.jpg | What is the main focus of this visual representation? | Light and electron microscopy revealed an exclusively anterograde gradient of axon degeneration in transected and crushed WldS sciatic/tibial nerves after prolonged lesion times A, F: Quantification of axon preservation at proximal and distal ends of the peripheral nerve stump after transection (A) and crush (F) injury exposed exclusively anterograde gradients of axon degeneration after 15 to 30 days following injury (15 d lesion time-point only after transection injury). Differences in the number of protected axons between the proximal and distal end of the stump were maximum after 20 days and more moderate prior or later to that, correspondingly. Remarkably, after 30 days following crush lesion considerable numbers of totally intact axons could be counted (63.5 % in distal tibial nerve) pointing to a weaker effect of compression over transection and generally to the longevity of distal WldS axons. B-E: Light microscopic images (B, D) and corresponding electron micrographs (C, E) taken from the proximal (B, C) and distal (D, E) end of the peripheral nerve stump after 20 days following transection lesion. At the proximal end (sciatic nerve) 28.1 % myelinated axons were structurally preserved while at the distal end (tibial nerve) we could observe 85.0 % preserved axons pointing to an anterograde gradient of axon degeneration. G-J: Light microscopic images (G, I) and corresponding electron micrographs (H, J) taken from the proximal (G, H) and distal (I, J) end of the peripheral nerve stump after 20 days following compression lesion. Similar to the transection lesion also here we identified a clear anterograde degeneration gradient with 70.0 % intact axons at the proximal end and 94.8 % preserved axons at the distal end of the nerve stump. Magnification of light microscopy is 630 × and electron microscopy is 3400 × |
PMC549193_F8_1331.jpg | What object or scene is depicted here? | Light and electron microscopy revealed an exclusively anterograde gradient of axon degeneration in transected and crushed WldS sciatic/tibial nerves after prolonged lesion times A, F: Quantification of axon preservation at proximal and distal ends of the peripheral nerve stump after transection (A) and crush (F) injury exposed exclusively anterograde gradients of axon degeneration after 15 to 30 days following injury (15 d lesion time-point only after transection injury). Differences in the number of protected axons between the proximal and distal end of the stump were maximum after 20 days and more moderate prior or later to that, correspondingly. Remarkably, after 30 days following crush lesion considerable numbers of totally intact axons could be counted (63.5 % in distal tibial nerve) pointing to a weaker effect of compression over transection and generally to the longevity of distal WldS axons. B-E: Light microscopic images (B, D) and corresponding electron micrographs (C, E) taken from the proximal (B, C) and distal (D, E) end of the peripheral nerve stump after 20 days following transection lesion. At the proximal end (sciatic nerve) 28.1 % myelinated axons were structurally preserved while at the distal end (tibial nerve) we could observe 85.0 % preserved axons pointing to an anterograde gradient of axon degeneration. G-J: Light microscopic images (G, I) and corresponding electron micrographs (H, J) taken from the proximal (G, H) and distal (I, J) end of the peripheral nerve stump after 20 days following compression lesion. Similar to the transection lesion also here we identified a clear anterograde degeneration gradient with 70.0 % intact axons at the proximal end and 94.8 % preserved axons at the distal end of the nerve stump. Magnification of light microscopy is 630 × and electron microscopy is 3400 × |
PMC549193_F8_1335.jpg | What is the dominant medical problem in this image? | Light and electron microscopy revealed an exclusively anterograde gradient of axon degeneration in transected and crushed WldS sciatic/tibial nerves after prolonged lesion times A, F: Quantification of axon preservation at proximal and distal ends of the peripheral nerve stump after transection (A) and crush (F) injury exposed exclusively anterograde gradients of axon degeneration after 15 to 30 days following injury (15 d lesion time-point only after transection injury). Differences in the number of protected axons between the proximal and distal end of the stump were maximum after 20 days and more moderate prior or later to that, correspondingly. Remarkably, after 30 days following crush lesion considerable numbers of totally intact axons could be counted (63.5 % in distal tibial nerve) pointing to a weaker effect of compression over transection and generally to the longevity of distal WldS axons. B-E: Light microscopic images (B, D) and corresponding electron micrographs (C, E) taken from the proximal (B, C) and distal (D, E) end of the peripheral nerve stump after 20 days following transection lesion. At the proximal end (sciatic nerve) 28.1 % myelinated axons were structurally preserved while at the distal end (tibial nerve) we could observe 85.0 % preserved axons pointing to an anterograde gradient of axon degeneration. G-J: Light microscopic images (G, I) and corresponding electron micrographs (H, J) taken from the proximal (G, H) and distal (I, J) end of the peripheral nerve stump after 20 days following compression lesion. Similar to the transection lesion also here we identified a clear anterograde degeneration gradient with 70.0 % intact axons at the proximal end and 94.8 % preserved axons at the distal end of the nerve stump. Magnification of light microscopy is 630 × and electron microscopy is 3400 × |
PMC549193_F8_1338.jpg | What is shown in this image? | Light and electron microscopy revealed an exclusively anterograde gradient of axon degeneration in transected and crushed WldS sciatic/tibial nerves after prolonged lesion times A, F: Quantification of axon preservation at proximal and distal ends of the peripheral nerve stump after transection (A) and crush (F) injury exposed exclusively anterograde gradients of axon degeneration after 15 to 30 days following injury (15 d lesion time-point only after transection injury). Differences in the number of protected axons between the proximal and distal end of the stump were maximum after 20 days and more moderate prior or later to that, correspondingly. Remarkably, after 30 days following crush lesion considerable numbers of totally intact axons could be counted (63.5 % in distal tibial nerve) pointing to a weaker effect of compression over transection and generally to the longevity of distal WldS axons. B-E: Light microscopic images (B, D) and corresponding electron micrographs (C, E) taken from the proximal (B, C) and distal (D, E) end of the peripheral nerve stump after 20 days following transection lesion. At the proximal end (sciatic nerve) 28.1 % myelinated axons were structurally preserved while at the distal end (tibial nerve) we could observe 85.0 % preserved axons pointing to an anterograde gradient of axon degeneration. G-J: Light microscopic images (G, I) and corresponding electron micrographs (H, J) taken from the proximal (G, H) and distal (I, J) end of the peripheral nerve stump after 20 days following compression lesion. Similar to the transection lesion also here we identified a clear anterograde degeneration gradient with 70.0 % intact axons at the proximal end and 94.8 % preserved axons at the distal end of the nerve stump. Magnification of light microscopy is 630 × and electron microscopy is 3400 × |
PMC549193_F8_1337.jpg | What is the focal point of this photograph? | Light and electron microscopy revealed an exclusively anterograde gradient of axon degeneration in transected and crushed WldS sciatic/tibial nerves after prolonged lesion times A, F: Quantification of axon preservation at proximal and distal ends of the peripheral nerve stump after transection (A) and crush (F) injury exposed exclusively anterograde gradients of axon degeneration after 15 to 30 days following injury (15 d lesion time-point only after transection injury). Differences in the number of protected axons between the proximal and distal end of the stump were maximum after 20 days and more moderate prior or later to that, correspondingly. Remarkably, after 30 days following crush lesion considerable numbers of totally intact axons could be counted (63.5 % in distal tibial nerve) pointing to a weaker effect of compression over transection and generally to the longevity of distal WldS axons. B-E: Light microscopic images (B, D) and corresponding electron micrographs (C, E) taken from the proximal (B, C) and distal (D, E) end of the peripheral nerve stump after 20 days following transection lesion. At the proximal end (sciatic nerve) 28.1 % myelinated axons were structurally preserved while at the distal end (tibial nerve) we could observe 85.0 % preserved axons pointing to an anterograde gradient of axon degeneration. G-J: Light microscopic images (G, I) and corresponding electron micrographs (H, J) taken from the proximal (G, H) and distal (I, J) end of the peripheral nerve stump after 20 days following compression lesion. Similar to the transection lesion also here we identified a clear anterograde degeneration gradient with 70.0 % intact axons at the proximal end and 94.8 % preserved axons at the distal end of the nerve stump. Magnification of light microscopy is 630 × and electron microscopy is 3400 × |
PMC549193_F8_1336.jpg | What is the dominant medical problem in this image? | Light and electron microscopy revealed an exclusively anterograde gradient of axon degeneration in transected and crushed WldS sciatic/tibial nerves after prolonged lesion times A, F: Quantification of axon preservation at proximal and distal ends of the peripheral nerve stump after transection (A) and crush (F) injury exposed exclusively anterograde gradients of axon degeneration after 15 to 30 days following injury (15 d lesion time-point only after transection injury). Differences in the number of protected axons between the proximal and distal end of the stump were maximum after 20 days and more moderate prior or later to that, correspondingly. Remarkably, after 30 days following crush lesion considerable numbers of totally intact axons could be counted (63.5 % in distal tibial nerve) pointing to a weaker effect of compression over transection and generally to the longevity of distal WldS axons. B-E: Light microscopic images (B, D) and corresponding electron micrographs (C, E) taken from the proximal (B, C) and distal (D, E) end of the peripheral nerve stump after 20 days following transection lesion. At the proximal end (sciatic nerve) 28.1 % myelinated axons were structurally preserved while at the distal end (tibial nerve) we could observe 85.0 % preserved axons pointing to an anterograde gradient of axon degeneration. G-J: Light microscopic images (G, I) and corresponding electron micrographs (H, J) taken from the proximal (G, H) and distal (I, J) end of the peripheral nerve stump after 20 days following compression lesion. Similar to the transection lesion also here we identified a clear anterograde degeneration gradient with 70.0 % intact axons at the proximal end and 94.8 % preserved axons at the distal end of the nerve stump. Magnification of light microscopy is 630 × and electron microscopy is 3400 × |
PMC549205_F4_1339.jpg | What is the principal component of this image? | Computer-aided estimate of the surface fractal dimension (Ds) of a vascular network in 2-D biopsy sections. A. Hepatocellular carcinoma section stained with antibodies raised against CD31 (Dako, Milan, Italy) that specifically react with vessels. B. Image segmentation: immunopositive vessels are specifically selected on the basis of the similarity of the color of adjacent pixels. C. Determination of Ds using the box-counting algorithm. Briefly, the method counts the number of boxes of length ε required to cover the object being measured, indicated as N(ε). D. Prototypical curve obtainable using the box-counting method that highlights the so-called fractal windows ranged by box size ε1 and ε2, and represents the appropriate region in which to estimate the dimension. Box sizes of more than ε2 approach the size of the image until one box covers it completely, at which point N(ε) = 1 and the slope = 0. Box sizes smaller than ε1 approach a single pixel or the resolution of the image: in this region, box counting simply gives the area of the image. |
PMC549541_F3_1344.jpg | What key item or scene is captured in this photo? | Photomicrograph showing upper endoscopy biopsy specimen of gastric GIST showing multiple spindle cells with eosinophilic cytoplasm and ovoid to elongated nuclei |
PMC549593_pmed-0020045-g001_1354.jpg | What is the main focus of this visual representation? | Differential Localization and Expression of CD36 Protein in Kidneys of Diabetic Mice with Glomerulopathy and of Humans with DNP(A and B) Indirect double-immunofluorescence labeling of kidney sections from non-diabetic control (A) and diabetic (B) mice with anti-CD36 (green) and proximal tubular marker anti-aquaporin1 (red).(C and D) Double labeling of non-diabetic control mice with anti-CD36 (green) and loop-of-Henle marker sodium potassium chloride cotransporter anti-NKCC (red) (C) and collecting duct marker aquaporin2 (red) (D) (arrow depicts colocalization of anti-CD36 and anti-aquaporin2 staining).(E and F) Double labeling of human kidney sections from control individuals (E) and individuals with diabetes with DNP (F) using anti-CD36 (green) and anti-aquaporin1 (red).(G) Higher-magnification image of (F) with arrows depicting colocalization of anti-CD36 and anti-aquaporin1. (Note that anti-CD36 labeling is heterogeneous: staining is isolated proximal tubular cells.)(H–J) Representative images of anti-CD36 immunoperoxidase staining of sections of normal human kidney (H), human kidney with DNP (I), and human kidney with FSGS (J). Arrow in (I) depicts proximal tubular epithelial staining.(K) CD36 PTEC expression score derived from blinded, semi-quantitative analysis of distribution and intensity of proximal tubular CD36 staining of human biopsy samples from ten normal control, ten DNP, and ten FSGS kidneys and the result shown on a dot plot. Significance was calculated by Wilcoxon Rank Sum Test, and PTEC scores for DNP kidneys were significantly different from those of FSGS kidneys and normal human kidneys. |
PMC549593_pmed-0020045-g001_1353.jpg | What does this image primarily show? | Differential Localization and Expression of CD36 Protein in Kidneys of Diabetic Mice with Glomerulopathy and of Humans with DNP(A and B) Indirect double-immunofluorescence labeling of kidney sections from non-diabetic control (A) and diabetic (B) mice with anti-CD36 (green) and proximal tubular marker anti-aquaporin1 (red).(C and D) Double labeling of non-diabetic control mice with anti-CD36 (green) and loop-of-Henle marker sodium potassium chloride cotransporter anti-NKCC (red) (C) and collecting duct marker aquaporin2 (red) (D) (arrow depicts colocalization of anti-CD36 and anti-aquaporin2 staining).(E and F) Double labeling of human kidney sections from control individuals (E) and individuals with diabetes with DNP (F) using anti-CD36 (green) and anti-aquaporin1 (red).(G) Higher-magnification image of (F) with arrows depicting colocalization of anti-CD36 and anti-aquaporin1. (Note that anti-CD36 labeling is heterogeneous: staining is isolated proximal tubular cells.)(H–J) Representative images of anti-CD36 immunoperoxidase staining of sections of normal human kidney (H), human kidney with DNP (I), and human kidney with FSGS (J). Arrow in (I) depicts proximal tubular epithelial staining.(K) CD36 PTEC expression score derived from blinded, semi-quantitative analysis of distribution and intensity of proximal tubular CD36 staining of human biopsy samples from ten normal control, ten DNP, and ten FSGS kidneys and the result shown on a dot plot. Significance was calculated by Wilcoxon Rank Sum Test, and PTEC scores for DNP kidneys were significantly different from those of FSGS kidneys and normal human kidneys. |
PMC549593_pmed-0020045-g001_1346.jpg | What does this image primarily show? | Differential Localization and Expression of CD36 Protein in Kidneys of Diabetic Mice with Glomerulopathy and of Humans with DNP(A and B) Indirect double-immunofluorescence labeling of kidney sections from non-diabetic control (A) and diabetic (B) mice with anti-CD36 (green) and proximal tubular marker anti-aquaporin1 (red).(C and D) Double labeling of non-diabetic control mice with anti-CD36 (green) and loop-of-Henle marker sodium potassium chloride cotransporter anti-NKCC (red) (C) and collecting duct marker aquaporin2 (red) (D) (arrow depicts colocalization of anti-CD36 and anti-aquaporin2 staining).(E and F) Double labeling of human kidney sections from control individuals (E) and individuals with diabetes with DNP (F) using anti-CD36 (green) and anti-aquaporin1 (red).(G) Higher-magnification image of (F) with arrows depicting colocalization of anti-CD36 and anti-aquaporin1. (Note that anti-CD36 labeling is heterogeneous: staining is isolated proximal tubular cells.)(H–J) Representative images of anti-CD36 immunoperoxidase staining of sections of normal human kidney (H), human kidney with DNP (I), and human kidney with FSGS (J). Arrow in (I) depicts proximal tubular epithelial staining.(K) CD36 PTEC expression score derived from blinded, semi-quantitative analysis of distribution and intensity of proximal tubular CD36 staining of human biopsy samples from ten normal control, ten DNP, and ten FSGS kidneys and the result shown on a dot plot. Significance was calculated by Wilcoxon Rank Sum Test, and PTEC scores for DNP kidneys were significantly different from those of FSGS kidneys and normal human kidneys. |
PMC549593_pmed-0020045-g001_1349.jpg | What is being portrayed in this visual content? | Differential Localization and Expression of CD36 Protein in Kidneys of Diabetic Mice with Glomerulopathy and of Humans with DNP(A and B) Indirect double-immunofluorescence labeling of kidney sections from non-diabetic control (A) and diabetic (B) mice with anti-CD36 (green) and proximal tubular marker anti-aquaporin1 (red).(C and D) Double labeling of non-diabetic control mice with anti-CD36 (green) and loop-of-Henle marker sodium potassium chloride cotransporter anti-NKCC (red) (C) and collecting duct marker aquaporin2 (red) (D) (arrow depicts colocalization of anti-CD36 and anti-aquaporin2 staining).(E and F) Double labeling of human kidney sections from control individuals (E) and individuals with diabetes with DNP (F) using anti-CD36 (green) and anti-aquaporin1 (red).(G) Higher-magnification image of (F) with arrows depicting colocalization of anti-CD36 and anti-aquaporin1. (Note that anti-CD36 labeling is heterogeneous: staining is isolated proximal tubular cells.)(H–J) Representative images of anti-CD36 immunoperoxidase staining of sections of normal human kidney (H), human kidney with DNP (I), and human kidney with FSGS (J). Arrow in (I) depicts proximal tubular epithelial staining.(K) CD36 PTEC expression score derived from blinded, semi-quantitative analysis of distribution and intensity of proximal tubular CD36 staining of human biopsy samples from ten normal control, ten DNP, and ten FSGS kidneys and the result shown on a dot plot. Significance was calculated by Wilcoxon Rank Sum Test, and PTEC scores for DNP kidneys were significantly different from those of FSGS kidneys and normal human kidneys. |
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