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PMC1200429_F1_3033.jpg | What key item or scene is captured in this photo? | Photomicrographs of histopathological and immunohistochemical studies of representative surgical lung biopsy specimens (A-E; idiopathic UIP, F-J; CVD-associated UIP, K-O; idiopathic NSIP, scale bar = 100 μm). Histopathological examination (hematoxylin-eosin staining) revealed fibroblastic foci in both idiopathic UIP (A) and CVD-associated UIP (F), and fibroblast proliferation in idiopathic NSIP (K). Hyperplastic cuboidal epithelial cells were stained with cytokeratin, indicating that these cells were type II pneumocytes (B, G and L). Strong expression of HSP47 was noted predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (C). Weak or no expression of HSP47 was noted in fibroblasts and type II pneumocytes in CVD-associated UIP (H). In idiopathic NSIP, strong expression of HSP47 was noted in fibroblasts, but not in type II pneumocytes (M). Type I procollagen was strongly expressed predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (D), but neither in CVD-associated UIP (I) nor idiopathic NSIP (N). Expression of α-SMA was noted in some of fibroblasts, indicating that these cells were myofibroblasts, in all three diseases (E, J and O). Insets c, d, h, i, m and n are pictures taken at high power magnification (scale bar = 20 μm) of corresponding C, D, H, I, M and N sections to clearly show the phenotypic difference of type II pneumocytes. α-SMA = α-smooth muscle actin; CVD = collagen vascular disease; HSP47 = heat shock protein 47; NSIP = nonspecific interstitial pneumonia; UIP = usual interstitial pneumonia. |
PMC1200429_F1_3025.jpg | What stands out most in this visual? | Photomicrographs of histopathological and immunohistochemical studies of representative surgical lung biopsy specimens (A-E; idiopathic UIP, F-J; CVD-associated UIP, K-O; idiopathic NSIP, scale bar = 100 μm). Histopathological examination (hematoxylin-eosin staining) revealed fibroblastic foci in both idiopathic UIP (A) and CVD-associated UIP (F), and fibroblast proliferation in idiopathic NSIP (K). Hyperplastic cuboidal epithelial cells were stained with cytokeratin, indicating that these cells were type II pneumocytes (B, G and L). Strong expression of HSP47 was noted predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (C). Weak or no expression of HSP47 was noted in fibroblasts and type II pneumocytes in CVD-associated UIP (H). In idiopathic NSIP, strong expression of HSP47 was noted in fibroblasts, but not in type II pneumocytes (M). Type I procollagen was strongly expressed predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (D), but neither in CVD-associated UIP (I) nor idiopathic NSIP (N). Expression of α-SMA was noted in some of fibroblasts, indicating that these cells were myofibroblasts, in all three diseases (E, J and O). Insets c, d, h, i, m and n are pictures taken at high power magnification (scale bar = 20 μm) of corresponding C, D, H, I, M and N sections to clearly show the phenotypic difference of type II pneumocytes. α-SMA = α-smooth muscle actin; CVD = collagen vascular disease; HSP47 = heat shock protein 47; NSIP = nonspecific interstitial pneumonia; UIP = usual interstitial pneumonia. |
PMC1200429_F1_3022.jpg | What is the focal point of this photograph? | Photomicrographs of histopathological and immunohistochemical studies of representative surgical lung biopsy specimens (A-E; idiopathic UIP, F-J; CVD-associated UIP, K-O; idiopathic NSIP, scale bar = 100 μm). Histopathological examination (hematoxylin-eosin staining) revealed fibroblastic foci in both idiopathic UIP (A) and CVD-associated UIP (F), and fibroblast proliferation in idiopathic NSIP (K). Hyperplastic cuboidal epithelial cells were stained with cytokeratin, indicating that these cells were type II pneumocytes (B, G and L). Strong expression of HSP47 was noted predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (C). Weak or no expression of HSP47 was noted in fibroblasts and type II pneumocytes in CVD-associated UIP (H). In idiopathic NSIP, strong expression of HSP47 was noted in fibroblasts, but not in type II pneumocytes (M). Type I procollagen was strongly expressed predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (D), but neither in CVD-associated UIP (I) nor idiopathic NSIP (N). Expression of α-SMA was noted in some of fibroblasts, indicating that these cells were myofibroblasts, in all three diseases (E, J and O). Insets c, d, h, i, m and n are pictures taken at high power magnification (scale bar = 20 μm) of corresponding C, D, H, I, M and N sections to clearly show the phenotypic difference of type II pneumocytes. α-SMA = α-smooth muscle actin; CVD = collagen vascular disease; HSP47 = heat shock protein 47; NSIP = nonspecific interstitial pneumonia; UIP = usual interstitial pneumonia. |
PMC1200429_F1_3027.jpg | What is the central feature of this picture? | Photomicrographs of histopathological and immunohistochemical studies of representative surgical lung biopsy specimens (A-E; idiopathic UIP, F-J; CVD-associated UIP, K-O; idiopathic NSIP, scale bar = 100 μm). Histopathological examination (hematoxylin-eosin staining) revealed fibroblastic foci in both idiopathic UIP (A) and CVD-associated UIP (F), and fibroblast proliferation in idiopathic NSIP (K). Hyperplastic cuboidal epithelial cells were stained with cytokeratin, indicating that these cells were type II pneumocytes (B, G and L). Strong expression of HSP47 was noted predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (C). Weak or no expression of HSP47 was noted in fibroblasts and type II pneumocytes in CVD-associated UIP (H). In idiopathic NSIP, strong expression of HSP47 was noted in fibroblasts, but not in type II pneumocytes (M). Type I procollagen was strongly expressed predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (D), but neither in CVD-associated UIP (I) nor idiopathic NSIP (N). Expression of α-SMA was noted in some of fibroblasts, indicating that these cells were myofibroblasts, in all three diseases (E, J and O). Insets c, d, h, i, m and n are pictures taken at high power magnification (scale bar = 20 μm) of corresponding C, D, H, I, M and N sections to clearly show the phenotypic difference of type II pneumocytes. α-SMA = α-smooth muscle actin; CVD = collagen vascular disease; HSP47 = heat shock protein 47; NSIP = nonspecific interstitial pneumonia; UIP = usual interstitial pneumonia. |
PMC1200429_F1_3021.jpg | What key item or scene is captured in this photo? | Photomicrographs of histopathological and immunohistochemical studies of representative surgical lung biopsy specimens (A-E; idiopathic UIP, F-J; CVD-associated UIP, K-O; idiopathic NSIP, scale bar = 100 μm). Histopathological examination (hematoxylin-eosin staining) revealed fibroblastic foci in both idiopathic UIP (A) and CVD-associated UIP (F), and fibroblast proliferation in idiopathic NSIP (K). Hyperplastic cuboidal epithelial cells were stained with cytokeratin, indicating that these cells were type II pneumocytes (B, G and L). Strong expression of HSP47 was noted predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (C). Weak or no expression of HSP47 was noted in fibroblasts and type II pneumocytes in CVD-associated UIP (H). In idiopathic NSIP, strong expression of HSP47 was noted in fibroblasts, but not in type II pneumocytes (M). Type I procollagen was strongly expressed predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (D), but neither in CVD-associated UIP (I) nor idiopathic NSIP (N). Expression of α-SMA was noted in some of fibroblasts, indicating that these cells were myofibroblasts, in all three diseases (E, J and O). Insets c, d, h, i, m and n are pictures taken at high power magnification (scale bar = 20 μm) of corresponding C, D, H, I, M and N sections to clearly show the phenotypic difference of type II pneumocytes. α-SMA = α-smooth muscle actin; CVD = collagen vascular disease; HSP47 = heat shock protein 47; NSIP = nonspecific interstitial pneumonia; UIP = usual interstitial pneumonia. |
PMC1200429_F1_3032.jpg | What key item or scene is captured in this photo? | Photomicrographs of histopathological and immunohistochemical studies of representative surgical lung biopsy specimens (A-E; idiopathic UIP, F-J; CVD-associated UIP, K-O; idiopathic NSIP, scale bar = 100 μm). Histopathological examination (hematoxylin-eosin staining) revealed fibroblastic foci in both idiopathic UIP (A) and CVD-associated UIP (F), and fibroblast proliferation in idiopathic NSIP (K). Hyperplastic cuboidal epithelial cells were stained with cytokeratin, indicating that these cells were type II pneumocytes (B, G and L). Strong expression of HSP47 was noted predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (C). Weak or no expression of HSP47 was noted in fibroblasts and type II pneumocytes in CVD-associated UIP (H). In idiopathic NSIP, strong expression of HSP47 was noted in fibroblasts, but not in type II pneumocytes (M). Type I procollagen was strongly expressed predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (D), but neither in CVD-associated UIP (I) nor idiopathic NSIP (N). Expression of α-SMA was noted in some of fibroblasts, indicating that these cells were myofibroblasts, in all three diseases (E, J and O). Insets c, d, h, i, m and n are pictures taken at high power magnification (scale bar = 20 μm) of corresponding C, D, H, I, M and N sections to clearly show the phenotypic difference of type II pneumocytes. α-SMA = α-smooth muscle actin; CVD = collagen vascular disease; HSP47 = heat shock protein 47; NSIP = nonspecific interstitial pneumonia; UIP = usual interstitial pneumonia. |
PMC1200429_F1_3023.jpg | What is the dominant medical problem in this image? | Photomicrographs of histopathological and immunohistochemical studies of representative surgical lung biopsy specimens (A-E; idiopathic UIP, F-J; CVD-associated UIP, K-O; idiopathic NSIP, scale bar = 100 μm). Histopathological examination (hematoxylin-eosin staining) revealed fibroblastic foci in both idiopathic UIP (A) and CVD-associated UIP (F), and fibroblast proliferation in idiopathic NSIP (K). Hyperplastic cuboidal epithelial cells were stained with cytokeratin, indicating that these cells were type II pneumocytes (B, G and L). Strong expression of HSP47 was noted predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (C). Weak or no expression of HSP47 was noted in fibroblasts and type II pneumocytes in CVD-associated UIP (H). In idiopathic NSIP, strong expression of HSP47 was noted in fibroblasts, but not in type II pneumocytes (M). Type I procollagen was strongly expressed predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (D), but neither in CVD-associated UIP (I) nor idiopathic NSIP (N). Expression of α-SMA was noted in some of fibroblasts, indicating that these cells were myofibroblasts, in all three diseases (E, J and O). Insets c, d, h, i, m and n are pictures taken at high power magnification (scale bar = 20 μm) of corresponding C, D, H, I, M and N sections to clearly show the phenotypic difference of type II pneumocytes. α-SMA = α-smooth muscle actin; CVD = collagen vascular disease; HSP47 = heat shock protein 47; NSIP = nonspecific interstitial pneumonia; UIP = usual interstitial pneumonia. |
PMC1200429_F1_3029.jpg | What is shown in this image? | Photomicrographs of histopathological and immunohistochemical studies of representative surgical lung biopsy specimens (A-E; idiopathic UIP, F-J; CVD-associated UIP, K-O; idiopathic NSIP, scale bar = 100 μm). Histopathological examination (hematoxylin-eosin staining) revealed fibroblastic foci in both idiopathic UIP (A) and CVD-associated UIP (F), and fibroblast proliferation in idiopathic NSIP (K). Hyperplastic cuboidal epithelial cells were stained with cytokeratin, indicating that these cells were type II pneumocytes (B, G and L). Strong expression of HSP47 was noted predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (C). Weak or no expression of HSP47 was noted in fibroblasts and type II pneumocytes in CVD-associated UIP (H). In idiopathic NSIP, strong expression of HSP47 was noted in fibroblasts, but not in type II pneumocytes (M). Type I procollagen was strongly expressed predominantly in fibroblasts and type II pneumocytes in idiopathic UIP (D), but neither in CVD-associated UIP (I) nor idiopathic NSIP (N). Expression of α-SMA was noted in some of fibroblasts, indicating that these cells were myofibroblasts, in all three diseases (E, J and O). Insets c, d, h, i, m and n are pictures taken at high power magnification (scale bar = 20 μm) of corresponding C, D, H, I, M and N sections to clearly show the phenotypic difference of type II pneumocytes. α-SMA = α-smooth muscle actin; CVD = collagen vascular disease; HSP47 = heat shock protein 47; NSIP = nonspecific interstitial pneumonia; UIP = usual interstitial pneumonia. |
PMC1200430_F2_3018.jpg | Can you identify the primary element in this image? | Immunohistochemical staining of ATP-binding cassette proteins in human lung. A. apical expression of P-gp in bronchial epithelium (COPD patient; frozen section, antibody C219), B. basolateral expression of MRP1 in bronchial epithelium (COPD patient; antibody MRPr1), C. MRP1 expression in bronchoalveolar lavage cells (healthy individual; antibody MRPr1). Lu, lumen. Scale bar = 25 μM. |
PMC1200430_F2_3019.jpg | What is being portrayed in this visual content? | Immunohistochemical staining of ATP-binding cassette proteins in human lung. A. apical expression of P-gp in bronchial epithelium (COPD patient; frozen section, antibody C219), B. basolateral expression of MRP1 in bronchial epithelium (COPD patient; antibody MRPr1), C. MRP1 expression in bronchoalveolar lavage cells (healthy individual; antibody MRPr1). Lu, lumen. Scale bar = 25 μM. |
PMC1201156_F5_3035.jpg | Can you identify the primary element in this image? | The results of MCE and CFR in a patient with Group B. 1) HPDI showing resting apical perfusion defect (A) and without improvement of perfusion during ATP stress (B) in the anteroseptal and apical lesion. 2) PDV in the infarct-related artery slightly increased during ATP stress (D) compared with baseline (C) by TTDE |
PMC1201156_F5_3037.jpg | What is the principal component of this image? | The results of MCE and CFR in a patient with Group B. 1) HPDI showing resting apical perfusion defect (A) and without improvement of perfusion during ATP stress (B) in the anteroseptal and apical lesion. 2) PDV in the infarct-related artery slightly increased during ATP stress (D) compared with baseline (C) by TTDE |
PMC1201156_F5_3036.jpg | What is the core subject represented in this visual? | The results of MCE and CFR in a patient with Group B. 1) HPDI showing resting apical perfusion defect (A) and without improvement of perfusion during ATP stress (B) in the anteroseptal and apical lesion. 2) PDV in the infarct-related artery slightly increased during ATP stress (D) compared with baseline (C) by TTDE |
PMC1201156_F5_3038.jpg | What does this image primarily show? | The results of MCE and CFR in a patient with Group B. 1) HPDI showing resting apical perfusion defect (A) and without improvement of perfusion during ATP stress (B) in the anteroseptal and apical lesion. 2) PDV in the infarct-related artery slightly increased during ATP stress (D) compared with baseline (C) by TTDE |
PMC1201157_F3_3050.jpg | What is the dominant medical problem in this image? | Tumor endothelium express LPP3 protein alongside VEGF. Paraffin-embedded angioma (A-C) and hemangioma (D-I) tumor tissue sections (4 μm) were subjected to antigen retrieval, and sequentially incubated with the indicated antibodies. After washing with PBS, sections were incubated with donkey anti-goat/rabbit IgG conjugated to Texas-red (red) and goat anti-mouse IgG conjugated to FITC (green). C, F, and I images represent overlays of A, B; D, E; and G, H respectively. Images were captured below saturation level. Merged yellow represents co-expression. Data shown are representative of those obtained in at least three separate experiments, with similar results. (L, lumen; Magnification, 100×; Bars, 50 μM). |
PMC1201157_F3_3052.jpg | What key item or scene is captured in this photo? | Tumor endothelium express LPP3 protein alongside VEGF. Paraffin-embedded angioma (A-C) and hemangioma (D-I) tumor tissue sections (4 μm) were subjected to antigen retrieval, and sequentially incubated with the indicated antibodies. After washing with PBS, sections were incubated with donkey anti-goat/rabbit IgG conjugated to Texas-red (red) and goat anti-mouse IgG conjugated to FITC (green). C, F, and I images represent overlays of A, B; D, E; and G, H respectively. Images were captured below saturation level. Merged yellow represents co-expression. Data shown are representative of those obtained in at least three separate experiments, with similar results. (L, lumen; Magnification, 100×; Bars, 50 μM). |
PMC1201157_F3_3053.jpg | Can you identify the primary element in this image? | Tumor endothelium express LPP3 protein alongside VEGF. Paraffin-embedded angioma (A-C) and hemangioma (D-I) tumor tissue sections (4 μm) were subjected to antigen retrieval, and sequentially incubated with the indicated antibodies. After washing with PBS, sections were incubated with donkey anti-goat/rabbit IgG conjugated to Texas-red (red) and goat anti-mouse IgG conjugated to FITC (green). C, F, and I images represent overlays of A, B; D, E; and G, H respectively. Images were captured below saturation level. Merged yellow represents co-expression. Data shown are representative of those obtained in at least three separate experiments, with similar results. (L, lumen; Magnification, 100×; Bars, 50 μM). |
PMC1201157_F3_3049.jpg | What is the principal component of this image? | Tumor endothelium express LPP3 protein alongside VEGF. Paraffin-embedded angioma (A-C) and hemangioma (D-I) tumor tissue sections (4 μm) were subjected to antigen retrieval, and sequentially incubated with the indicated antibodies. After washing with PBS, sections were incubated with donkey anti-goat/rabbit IgG conjugated to Texas-red (red) and goat anti-mouse IgG conjugated to FITC (green). C, F, and I images represent overlays of A, B; D, E; and G, H respectively. Images were captured below saturation level. Merged yellow represents co-expression. Data shown are representative of those obtained in at least three separate experiments, with similar results. (L, lumen; Magnification, 100×; Bars, 50 μM). |
PMC1201157_F3_3057.jpg | What is the focal point of this photograph? | Tumor endothelium express LPP3 protein alongside VEGF. Paraffin-embedded angioma (A-C) and hemangioma (D-I) tumor tissue sections (4 μm) were subjected to antigen retrieval, and sequentially incubated with the indicated antibodies. After washing with PBS, sections were incubated with donkey anti-goat/rabbit IgG conjugated to Texas-red (red) and goat anti-mouse IgG conjugated to FITC (green). C, F, and I images represent overlays of A, B; D, E; and G, H respectively. Images were captured below saturation level. Merged yellow represents co-expression. Data shown are representative of those obtained in at least three separate experiments, with similar results. (L, lumen; Magnification, 100×; Bars, 50 μM). |
PMC1201157_F3_3056.jpg | What stands out most in this visual? | Tumor endothelium express LPP3 protein alongside VEGF. Paraffin-embedded angioma (A-C) and hemangioma (D-I) tumor tissue sections (4 μm) were subjected to antigen retrieval, and sequentially incubated with the indicated antibodies. After washing with PBS, sections were incubated with donkey anti-goat/rabbit IgG conjugated to Texas-red (red) and goat anti-mouse IgG conjugated to FITC (green). C, F, and I images represent overlays of A, B; D, E; and G, H respectively. Images were captured below saturation level. Merged yellow represents co-expression. Data shown are representative of those obtained in at least three separate experiments, with similar results. (L, lumen; Magnification, 100×; Bars, 50 μM). |
PMC1201157_F3_3051.jpg | What can you see in this picture? | Tumor endothelium express LPP3 protein alongside VEGF. Paraffin-embedded angioma (A-C) and hemangioma (D-I) tumor tissue sections (4 μm) were subjected to antigen retrieval, and sequentially incubated with the indicated antibodies. After washing with PBS, sections were incubated with donkey anti-goat/rabbit IgG conjugated to Texas-red (red) and goat anti-mouse IgG conjugated to FITC (green). C, F, and I images represent overlays of A, B; D, E; and G, H respectively. Images were captured below saturation level. Merged yellow represents co-expression. Data shown are representative of those obtained in at least three separate experiments, with similar results. (L, lumen; Magnification, 100×; Bars, 50 μM). |
PMC1201157_F3_3054.jpg | What is being portrayed in this visual content? | Tumor endothelium express LPP3 protein alongside VEGF. Paraffin-embedded angioma (A-C) and hemangioma (D-I) tumor tissue sections (4 μm) were subjected to antigen retrieval, and sequentially incubated with the indicated antibodies. After washing with PBS, sections were incubated with donkey anti-goat/rabbit IgG conjugated to Texas-red (red) and goat anti-mouse IgG conjugated to FITC (green). C, F, and I images represent overlays of A, B; D, E; and G, H respectively. Images were captured below saturation level. Merged yellow represents co-expression. Data shown are representative of those obtained in at least three separate experiments, with similar results. (L, lumen; Magnification, 100×; Bars, 50 μM). |
PMC1201157_F5_3040.jpg | Describe the main subject of this image. | Inhibition of bFGF and VEGF induced capillary morphogenesis of ECs in 3D type I collagen matrix. The samples shown in the upper panels (A-E) were treated with anti-MHC class II mAbs, whereas those in the lower panels (F-J) with anti-αvβ3 integrin antibodies. Cross sections were stained with acidified eosin as described in methods. Magnification, 100×. Bar, 200 μM. |
PMC1201157_F5_3039.jpg | What is the focal point of this photograph? | Inhibition of bFGF and VEGF induced capillary morphogenesis of ECs in 3D type I collagen matrix. The samples shown in the upper panels (A-E) were treated with anti-MHC class II mAbs, whereas those in the lower panels (F-J) with anti-αvβ3 integrin antibodies. Cross sections were stained with acidified eosin as described in methods. Magnification, 100×. Bar, 200 μM. |
PMC1201157_F5_3042.jpg | What is the core subject represented in this visual? | Inhibition of bFGF and VEGF induced capillary morphogenesis of ECs in 3D type I collagen matrix. The samples shown in the upper panels (A-E) were treated with anti-MHC class II mAbs, whereas those in the lower panels (F-J) with anti-αvβ3 integrin antibodies. Cross sections were stained with acidified eosin as described in methods. Magnification, 100×. Bar, 200 μM. |
PMC1201157_F5_3043.jpg | What stands out most in this visual? | Inhibition of bFGF and VEGF induced capillary morphogenesis of ECs in 3D type I collagen matrix. The samples shown in the upper panels (A-E) were treated with anti-MHC class II mAbs, whereas those in the lower panels (F-J) with anti-αvβ3 integrin antibodies. Cross sections were stained with acidified eosin as described in methods. Magnification, 100×. Bar, 200 μM. |
PMC1201157_F5_3048.jpg | What object or scene is depicted here? | Inhibition of bFGF and VEGF induced capillary morphogenesis of ECs in 3D type I collagen matrix. The samples shown in the upper panels (A-E) were treated with anti-MHC class II mAbs, whereas those in the lower panels (F-J) with anti-αvβ3 integrin antibodies. Cross sections were stained with acidified eosin as described in methods. Magnification, 100×. Bar, 200 μM. |
PMC1201157_F5_3046.jpg | What is being portrayed in this visual content? | Inhibition of bFGF and VEGF induced capillary morphogenesis of ECs in 3D type I collagen matrix. The samples shown in the upper panels (A-E) were treated with anti-MHC class II mAbs, whereas those in the lower panels (F-J) with anti-αvβ3 integrin antibodies. Cross sections were stained with acidified eosin as described in methods. Magnification, 100×. Bar, 200 μM. |
PMC1201170_F4_3061.jpg | What is the main focus of this visual representation? | Spam1 transcripts which are compartmentalized are absent from the bridges and are associated with the cytoskeleton. a) EM autoradiography of seminiferous tubules after in situ hybridization with a tritiated (3H-labeled) Spam-1 antisense RNA probe. Note that silver grains are associated with the ER (arrowheads) but not with any other major spermatid structures such as the chromatoid bodies (A), the radial bodies (B) or the microtubules of the manchette (C). D is an intercellular bridge where the curvatures at the top and bottom represent the outer limits of the bridge. While some grains are seen in association with the ER in the vicinity, they are absent from the bridge. The circles centered over the silver grains include profiles of ER (arrowheads). (E) Late spermatids (S) and Sertoli cells (Se) are unreactive. (F) Shows the cytoplasm of round spermatid (RS) step 8 of a control section hybridized to a sense probe. Co, chromatoid body; Rb, radial body; M, manchette. X19,000 b. Northern hybridization of Spam1 and β-actin mRNAs in free cytosolic-, cytoskeletal-, and membrane-bound testicular RNA fractions. The fractions were separated by subcellular fractionation techniques. A) shows Northern blotting, while B) shows total RNA as a loading control with ethidium bromide staining. The presence of cytoskeletal-bound β-actin RNA in the free cytosolic fraction suggests that Spam1 in the latter could be present as a contaminant due to the preparation procedure. |
PMC1201170_F4_3065.jpg | What does this image primarily show? | Spam1 transcripts which are compartmentalized are absent from the bridges and are associated with the cytoskeleton. a) EM autoradiography of seminiferous tubules after in situ hybridization with a tritiated (3H-labeled) Spam-1 antisense RNA probe. Note that silver grains are associated with the ER (arrowheads) but not with any other major spermatid structures such as the chromatoid bodies (A), the radial bodies (B) or the microtubules of the manchette (C). D is an intercellular bridge where the curvatures at the top and bottom represent the outer limits of the bridge. While some grains are seen in association with the ER in the vicinity, they are absent from the bridge. The circles centered over the silver grains include profiles of ER (arrowheads). (E) Late spermatids (S) and Sertoli cells (Se) are unreactive. (F) Shows the cytoplasm of round spermatid (RS) step 8 of a control section hybridized to a sense probe. Co, chromatoid body; Rb, radial body; M, manchette. X19,000 b. Northern hybridization of Spam1 and β-actin mRNAs in free cytosolic-, cytoskeletal-, and membrane-bound testicular RNA fractions. The fractions were separated by subcellular fractionation techniques. A) shows Northern blotting, while B) shows total RNA as a loading control with ethidium bromide staining. The presence of cytoskeletal-bound β-actin RNA in the free cytosolic fraction suggests that Spam1 in the latter could be present as a contaminant due to the preparation procedure. |
PMC1201170_F4_3060.jpg | What is the principal component of this image? | Spam1 transcripts which are compartmentalized are absent from the bridges and are associated with the cytoskeleton. a) EM autoradiography of seminiferous tubules after in situ hybridization with a tritiated (3H-labeled) Spam-1 antisense RNA probe. Note that silver grains are associated with the ER (arrowheads) but not with any other major spermatid structures such as the chromatoid bodies (A), the radial bodies (B) or the microtubules of the manchette (C). D is an intercellular bridge where the curvatures at the top and bottom represent the outer limits of the bridge. While some grains are seen in association with the ER in the vicinity, they are absent from the bridge. The circles centered over the silver grains include profiles of ER (arrowheads). (E) Late spermatids (S) and Sertoli cells (Se) are unreactive. (F) Shows the cytoplasm of round spermatid (RS) step 8 of a control section hybridized to a sense probe. Co, chromatoid body; Rb, radial body; M, manchette. X19,000 b. Northern hybridization of Spam1 and β-actin mRNAs in free cytosolic-, cytoskeletal-, and membrane-bound testicular RNA fractions. The fractions were separated by subcellular fractionation techniques. A) shows Northern blotting, while B) shows total RNA as a loading control with ethidium bromide staining. The presence of cytoskeletal-bound β-actin RNA in the free cytosolic fraction suggests that Spam1 in the latter could be present as a contaminant due to the preparation procedure. |
PMC1201170_F4_3059.jpg | What is the main focus of this visual representation? | Spam1 transcripts which are compartmentalized are absent from the bridges and are associated with the cytoskeleton. a) EM autoradiography of seminiferous tubules after in situ hybridization with a tritiated (3H-labeled) Spam-1 antisense RNA probe. Note that silver grains are associated with the ER (arrowheads) but not with any other major spermatid structures such as the chromatoid bodies (A), the radial bodies (B) or the microtubules of the manchette (C). D is an intercellular bridge where the curvatures at the top and bottom represent the outer limits of the bridge. While some grains are seen in association with the ER in the vicinity, they are absent from the bridge. The circles centered over the silver grains include profiles of ER (arrowheads). (E) Late spermatids (S) and Sertoli cells (Se) are unreactive. (F) Shows the cytoplasm of round spermatid (RS) step 8 of a control section hybridized to a sense probe. Co, chromatoid body; Rb, radial body; M, manchette. X19,000 b. Northern hybridization of Spam1 and β-actin mRNAs in free cytosolic-, cytoskeletal-, and membrane-bound testicular RNA fractions. The fractions were separated by subcellular fractionation techniques. A) shows Northern blotting, while B) shows total RNA as a loading control with ethidium bromide staining. The presence of cytoskeletal-bound β-actin RNA in the free cytosolic fraction suggests that Spam1 in the latter could be present as a contaminant due to the preparation procedure. |
PMC1201178_F1_3066.jpg | What object or scene is depicted here? | Sonographic examination: 15 mm hypoechoic solid, non-calcified circumscribed mass, with a thin echoic rim, benign in appearance, located in subcutaneous fat at 9 o'clock in the left breast. |
PMC1201178_F2_3067.jpg | What's the most prominent thing you notice in this picture? | photomicrograph 2A) Invasive ductal carcinoma, apocrine type: tumor exhibits an irregular invasive border and forms glandular structures. Hematoxylin and eosin stain, original magnification × 40. 2B) Invasive ductal carcinoma, apocrine type: cytological characteristics of intermediate nuclear grade, prominent nucleoli, and eosinophilic granular cytoplasm. Hematoxylin and eosin stain, original magnification × 100. |
PMC1201178_F2_3068.jpg | What is the dominant medical problem in this image? | photomicrograph 2A) Invasive ductal carcinoma, apocrine type: tumor exhibits an irregular invasive border and forms glandular structures. Hematoxylin and eosin stain, original magnification × 40. 2B) Invasive ductal carcinoma, apocrine type: cytological characteristics of intermediate nuclear grade, prominent nucleoli, and eosinophilic granular cytoplasm. Hematoxylin and eosin stain, original magnification × 100. |
PMC1208873_F4_3083.jpg | What does this image primarily show? | Normal expression of extraembryonic markers in huntingtin deficient embryos. Whole mount in situ hybridization analysis at E7.5 of markers of the extraembryonic tissues reveals grossly normal expression in the absence of huntingtin. Hnf4, expressed in the visceral endoderm at the junction of embryonic-ectoderm junction (A), is normal in mutant embryos, although the signal is slightly higher (B). Similarly, the expression of Pem transcripts is maintained in mutant embryos (D) similar to normal embryos (C), although Pem is expressed in the abnormal lopsided overhang of visceral endoderm over the anterior of the mutant embryos. Expression of extraembryonic signaling molecules is unaffected by the loss of huntingtin, as evidenced by the expression of Bmp4 (E,F) in the extraembryonic ectoderm, and Lefty1 and Dkk1 (I-L) in the AVE in mutant embryos. Bmp4 is not localized, however, to a ring of extraembryonic ectoderm in mutant embryos (F) as in normal embryos (E). Primitive germ cells (PCGs) are induced normally in both wild-type (G) and mutant embryos (H), suggesting the Bmp4 signaling from the extraembryonic ectoderm to the epiblast is normal. Lefty1 expression appears disorganized in mutant embryos (I) compared to wild-type embryos (J). In contrast, the anterior expression of Dkk1 in the AVE in mutant embryos (L) matches the wild-type expression pattern (K). Despite normal AVE formation, head folds fail to form in mutant embryos, even when cultured in nutrient rich media for 24 hours. Wild-type E7.5 embryos, when cultured in 75% rat serum, develop somites (M), heart (white arrow, N) and head folds (blue arrow head, N) in culture. In contrast, huntingtin deficient embryos continue to live in culture but do not form headfolds, heart or somites (O). Embryos are shown in a lateral view (A-F, I-J) with anterior oriented to the left. Embryos in (G,H,K,L) are shown in an anterior view with proximal oriented up. |
PMC1208873_F4_3086.jpg | What is the principal component of this image? | Normal expression of extraembryonic markers in huntingtin deficient embryos. Whole mount in situ hybridization analysis at E7.5 of markers of the extraembryonic tissues reveals grossly normal expression in the absence of huntingtin. Hnf4, expressed in the visceral endoderm at the junction of embryonic-ectoderm junction (A), is normal in mutant embryos, although the signal is slightly higher (B). Similarly, the expression of Pem transcripts is maintained in mutant embryos (D) similar to normal embryos (C), although Pem is expressed in the abnormal lopsided overhang of visceral endoderm over the anterior of the mutant embryos. Expression of extraembryonic signaling molecules is unaffected by the loss of huntingtin, as evidenced by the expression of Bmp4 (E,F) in the extraembryonic ectoderm, and Lefty1 and Dkk1 (I-L) in the AVE in mutant embryos. Bmp4 is not localized, however, to a ring of extraembryonic ectoderm in mutant embryos (F) as in normal embryos (E). Primitive germ cells (PCGs) are induced normally in both wild-type (G) and mutant embryos (H), suggesting the Bmp4 signaling from the extraembryonic ectoderm to the epiblast is normal. Lefty1 expression appears disorganized in mutant embryos (I) compared to wild-type embryos (J). In contrast, the anterior expression of Dkk1 in the AVE in mutant embryos (L) matches the wild-type expression pattern (K). Despite normal AVE formation, head folds fail to form in mutant embryos, even when cultured in nutrient rich media for 24 hours. Wild-type E7.5 embryos, when cultured in 75% rat serum, develop somites (M), heart (white arrow, N) and head folds (blue arrow head, N) in culture. In contrast, huntingtin deficient embryos continue to live in culture but do not form headfolds, heart or somites (O). Embryos are shown in a lateral view (A-F, I-J) with anterior oriented to the left. Embryos in (G,H,K,L) are shown in an anterior view with proximal oriented up. |
PMC1208873_F4_3090.jpg | Describe the main subject of this image. | Normal expression of extraembryonic markers in huntingtin deficient embryos. Whole mount in situ hybridization analysis at E7.5 of markers of the extraembryonic tissues reveals grossly normal expression in the absence of huntingtin. Hnf4, expressed in the visceral endoderm at the junction of embryonic-ectoderm junction (A), is normal in mutant embryos, although the signal is slightly higher (B). Similarly, the expression of Pem transcripts is maintained in mutant embryos (D) similar to normal embryos (C), although Pem is expressed in the abnormal lopsided overhang of visceral endoderm over the anterior of the mutant embryos. Expression of extraembryonic signaling molecules is unaffected by the loss of huntingtin, as evidenced by the expression of Bmp4 (E,F) in the extraembryonic ectoderm, and Lefty1 and Dkk1 (I-L) in the AVE in mutant embryos. Bmp4 is not localized, however, to a ring of extraembryonic ectoderm in mutant embryos (F) as in normal embryos (E). Primitive germ cells (PCGs) are induced normally in both wild-type (G) and mutant embryos (H), suggesting the Bmp4 signaling from the extraembryonic ectoderm to the epiblast is normal. Lefty1 expression appears disorganized in mutant embryos (I) compared to wild-type embryos (J). In contrast, the anterior expression of Dkk1 in the AVE in mutant embryos (L) matches the wild-type expression pattern (K). Despite normal AVE formation, head folds fail to form in mutant embryos, even when cultured in nutrient rich media for 24 hours. Wild-type E7.5 embryos, when cultured in 75% rat serum, develop somites (M), heart (white arrow, N) and head folds (blue arrow head, N) in culture. In contrast, huntingtin deficient embryos continue to live in culture but do not form headfolds, heart or somites (O). Embryos are shown in a lateral view (A-F, I-J) with anterior oriented to the left. Embryos in (G,H,K,L) are shown in an anterior view with proximal oriented up. |
PMC1208873_F4_3080.jpg | What stands out most in this visual? | Normal expression of extraembryonic markers in huntingtin deficient embryos. Whole mount in situ hybridization analysis at E7.5 of markers of the extraembryonic tissues reveals grossly normal expression in the absence of huntingtin. Hnf4, expressed in the visceral endoderm at the junction of embryonic-ectoderm junction (A), is normal in mutant embryos, although the signal is slightly higher (B). Similarly, the expression of Pem transcripts is maintained in mutant embryos (D) similar to normal embryos (C), although Pem is expressed in the abnormal lopsided overhang of visceral endoderm over the anterior of the mutant embryos. Expression of extraembryonic signaling molecules is unaffected by the loss of huntingtin, as evidenced by the expression of Bmp4 (E,F) in the extraembryonic ectoderm, and Lefty1 and Dkk1 (I-L) in the AVE in mutant embryos. Bmp4 is not localized, however, to a ring of extraembryonic ectoderm in mutant embryos (F) as in normal embryos (E). Primitive germ cells (PCGs) are induced normally in both wild-type (G) and mutant embryos (H), suggesting the Bmp4 signaling from the extraembryonic ectoderm to the epiblast is normal. Lefty1 expression appears disorganized in mutant embryos (I) compared to wild-type embryos (J). In contrast, the anterior expression of Dkk1 in the AVE in mutant embryos (L) matches the wild-type expression pattern (K). Despite normal AVE formation, head folds fail to form in mutant embryos, even when cultured in nutrient rich media for 24 hours. Wild-type E7.5 embryos, when cultured in 75% rat serum, develop somites (M), heart (white arrow, N) and head folds (blue arrow head, N) in culture. In contrast, huntingtin deficient embryos continue to live in culture but do not form headfolds, heart or somites (O). Embryos are shown in a lateral view (A-F, I-J) with anterior oriented to the left. Embryos in (G,H,K,L) are shown in an anterior view with proximal oriented up. |
PMC1208873_F4_3087.jpg | What object or scene is depicted here? | Normal expression of extraembryonic markers in huntingtin deficient embryos. Whole mount in situ hybridization analysis at E7.5 of markers of the extraembryonic tissues reveals grossly normal expression in the absence of huntingtin. Hnf4, expressed in the visceral endoderm at the junction of embryonic-ectoderm junction (A), is normal in mutant embryos, although the signal is slightly higher (B). Similarly, the expression of Pem transcripts is maintained in mutant embryos (D) similar to normal embryos (C), although Pem is expressed in the abnormal lopsided overhang of visceral endoderm over the anterior of the mutant embryos. Expression of extraembryonic signaling molecules is unaffected by the loss of huntingtin, as evidenced by the expression of Bmp4 (E,F) in the extraembryonic ectoderm, and Lefty1 and Dkk1 (I-L) in the AVE in mutant embryos. Bmp4 is not localized, however, to a ring of extraembryonic ectoderm in mutant embryos (F) as in normal embryos (E). Primitive germ cells (PCGs) are induced normally in both wild-type (G) and mutant embryos (H), suggesting the Bmp4 signaling from the extraembryonic ectoderm to the epiblast is normal. Lefty1 expression appears disorganized in mutant embryos (I) compared to wild-type embryos (J). In contrast, the anterior expression of Dkk1 in the AVE in mutant embryos (L) matches the wild-type expression pattern (K). Despite normal AVE formation, head folds fail to form in mutant embryos, even when cultured in nutrient rich media for 24 hours. Wild-type E7.5 embryos, when cultured in 75% rat serum, develop somites (M), heart (white arrow, N) and head folds (blue arrow head, N) in culture. In contrast, huntingtin deficient embryos continue to live in culture but do not form headfolds, heart or somites (O). Embryos are shown in a lateral view (A-F, I-J) with anterior oriented to the left. Embryos in (G,H,K,L) are shown in an anterior view with proximal oriented up. |
PMC1208873_F4_3084.jpg | What is shown in this image? | Normal expression of extraembryonic markers in huntingtin deficient embryos. Whole mount in situ hybridization analysis at E7.5 of markers of the extraembryonic tissues reveals grossly normal expression in the absence of huntingtin. Hnf4, expressed in the visceral endoderm at the junction of embryonic-ectoderm junction (A), is normal in mutant embryos, although the signal is slightly higher (B). Similarly, the expression of Pem transcripts is maintained in mutant embryos (D) similar to normal embryos (C), although Pem is expressed in the abnormal lopsided overhang of visceral endoderm over the anterior of the mutant embryos. Expression of extraembryonic signaling molecules is unaffected by the loss of huntingtin, as evidenced by the expression of Bmp4 (E,F) in the extraembryonic ectoderm, and Lefty1 and Dkk1 (I-L) in the AVE in mutant embryos. Bmp4 is not localized, however, to a ring of extraembryonic ectoderm in mutant embryos (F) as in normal embryos (E). Primitive germ cells (PCGs) are induced normally in both wild-type (G) and mutant embryos (H), suggesting the Bmp4 signaling from the extraembryonic ectoderm to the epiblast is normal. Lefty1 expression appears disorganized in mutant embryos (I) compared to wild-type embryos (J). In contrast, the anterior expression of Dkk1 in the AVE in mutant embryos (L) matches the wild-type expression pattern (K). Despite normal AVE formation, head folds fail to form in mutant embryos, even when cultured in nutrient rich media for 24 hours. Wild-type E7.5 embryos, when cultured in 75% rat serum, develop somites (M), heart (white arrow, N) and head folds (blue arrow head, N) in culture. In contrast, huntingtin deficient embryos continue to live in culture but do not form headfolds, heart or somites (O). Embryos are shown in a lateral view (A-F, I-J) with anterior oriented to the left. Embryos in (G,H,K,L) are shown in an anterior view with proximal oriented up. |
PMC1208873_F4_3091.jpg | What is the dominant medical problem in this image? | Normal expression of extraembryonic markers in huntingtin deficient embryos. Whole mount in situ hybridization analysis at E7.5 of markers of the extraembryonic tissues reveals grossly normal expression in the absence of huntingtin. Hnf4, expressed in the visceral endoderm at the junction of embryonic-ectoderm junction (A), is normal in mutant embryos, although the signal is slightly higher (B). Similarly, the expression of Pem transcripts is maintained in mutant embryos (D) similar to normal embryos (C), although Pem is expressed in the abnormal lopsided overhang of visceral endoderm over the anterior of the mutant embryos. Expression of extraembryonic signaling molecules is unaffected by the loss of huntingtin, as evidenced by the expression of Bmp4 (E,F) in the extraembryonic ectoderm, and Lefty1 and Dkk1 (I-L) in the AVE in mutant embryos. Bmp4 is not localized, however, to a ring of extraembryonic ectoderm in mutant embryos (F) as in normal embryos (E). Primitive germ cells (PCGs) are induced normally in both wild-type (G) and mutant embryos (H), suggesting the Bmp4 signaling from the extraembryonic ectoderm to the epiblast is normal. Lefty1 expression appears disorganized in mutant embryos (I) compared to wild-type embryos (J). In contrast, the anterior expression of Dkk1 in the AVE in mutant embryos (L) matches the wild-type expression pattern (K). Despite normal AVE formation, head folds fail to form in mutant embryos, even when cultured in nutrient rich media for 24 hours. Wild-type E7.5 embryos, when cultured in 75% rat serum, develop somites (M), heart (white arrow, N) and head folds (blue arrow head, N) in culture. In contrast, huntingtin deficient embryos continue to live in culture but do not form headfolds, heart or somites (O). Embryos are shown in a lateral view (A-F, I-J) with anterior oriented to the left. Embryos in (G,H,K,L) are shown in an anterior view with proximal oriented up. |
PMC1208873_F4_3085.jpg | What is the principal component of this image? | Normal expression of extraembryonic markers in huntingtin deficient embryos. Whole mount in situ hybridization analysis at E7.5 of markers of the extraembryonic tissues reveals grossly normal expression in the absence of huntingtin. Hnf4, expressed in the visceral endoderm at the junction of embryonic-ectoderm junction (A), is normal in mutant embryos, although the signal is slightly higher (B). Similarly, the expression of Pem transcripts is maintained in mutant embryos (D) similar to normal embryos (C), although Pem is expressed in the abnormal lopsided overhang of visceral endoderm over the anterior of the mutant embryos. Expression of extraembryonic signaling molecules is unaffected by the loss of huntingtin, as evidenced by the expression of Bmp4 (E,F) in the extraembryonic ectoderm, and Lefty1 and Dkk1 (I-L) in the AVE in mutant embryos. Bmp4 is not localized, however, to a ring of extraembryonic ectoderm in mutant embryos (F) as in normal embryos (E). Primitive germ cells (PCGs) are induced normally in both wild-type (G) and mutant embryos (H), suggesting the Bmp4 signaling from the extraembryonic ectoderm to the epiblast is normal. Lefty1 expression appears disorganized in mutant embryos (I) compared to wild-type embryos (J). In contrast, the anterior expression of Dkk1 in the AVE in mutant embryos (L) matches the wild-type expression pattern (K). Despite normal AVE formation, head folds fail to form in mutant embryos, even when cultured in nutrient rich media for 24 hours. Wild-type E7.5 embryos, when cultured in 75% rat serum, develop somites (M), heart (white arrow, N) and head folds (blue arrow head, N) in culture. In contrast, huntingtin deficient embryos continue to live in culture but do not form headfolds, heart or somites (O). Embryos are shown in a lateral view (A-F, I-J) with anterior oriented to the left. Embryos in (G,H,K,L) are shown in an anterior view with proximal oriented up. |
PMC1208874_F1_3076.jpg | Can you identify the primary element in this image? | Subcellular localisation of Dnmt1 isoforms in mouse somatic cells and preimplantation embryos. A) Schematic representation of GFP-Dnmt1 fusion proteins. The start codons of the long (ATGL) and the short (ATGS) isoforms are indicated. The catalytic domain of Dnmt1 is in black. Subcellular localisation of GFP-Dnmt1 fusions in somatic cells (B) and 2-cell embryos (C). In B mouse C2C12 myoblasts were transfected with either the GFP-Dnmt1S (left pair of panels) or the GFP-Dnmt1L expression constructs (right pair of panels) and imaged by confocal microscopy. The left panel in each pair shows the phase contrast image, while the right panel shows GFP fluorescence (scale bars = 5 μm). In C the same expression constructs were microinjected in pronuclei at the 1-cell stage and embryos were further cultured until the 2-cell stage (scale bars = 20 μm). Both the short and the long isoforms of Dnmt1 are localised in the nucleus of myoblasts and in the cytoplasm of 2-cell embryos. Small amounts of fusion proteins in embryonic nuclei (arrowheads) are due to overexpression of Dnmt1 and consequent saturation of the cytoplasmic retention mechanism. |
PMC1208874_F1_3075.jpg | What object or scene is depicted here? | Subcellular localisation of Dnmt1 isoforms in mouse somatic cells and preimplantation embryos. A) Schematic representation of GFP-Dnmt1 fusion proteins. The start codons of the long (ATGL) and the short (ATGS) isoforms are indicated. The catalytic domain of Dnmt1 is in black. Subcellular localisation of GFP-Dnmt1 fusions in somatic cells (B) and 2-cell embryos (C). In B mouse C2C12 myoblasts were transfected with either the GFP-Dnmt1S (left pair of panels) or the GFP-Dnmt1L expression constructs (right pair of panels) and imaged by confocal microscopy. The left panel in each pair shows the phase contrast image, while the right panel shows GFP fluorescence (scale bars = 5 μm). In C the same expression constructs were microinjected in pronuclei at the 1-cell stage and embryos were further cultured until the 2-cell stage (scale bars = 20 μm). Both the short and the long isoforms of Dnmt1 are localised in the nucleus of myoblasts and in the cytoplasm of 2-cell embryos. Small amounts of fusion proteins in embryonic nuclei (arrowheads) are due to overexpression of Dnmt1 and consequent saturation of the cytoplasmic retention mechanism. |
PMC1208874_F2_3070.jpg | What is the central feature of this picture? | Dnmt1S localisation is independent of phosphorylation. A) Schematic representation of GFP-Dnmt1S phosphorylation mutants. B) Western blot of transfected Cos-7 cells probed with an antibody against the N-terminal domain of Dnmt1 [25] showing expression of GFP-Dnmt1s wild type (wt) and phosphorylation mutants S396A and S396D with the expected molecular mass. Weak bands at 190 kDa representing endogenous Dnmt1L are indicated. C) and D) localisation of GFP-Dnmt1S phosphorylation mutants in mouse somatic cells and preimplantation embryos, respectively. Both mutant proteins localise to the nucleus of somatic cells and to the cytoplasm of preimplantation embryos like wild type GFP-Dnmt1S (Fig. 1B and C). In D embryos were fixed and immunostained with an anti-GFP antibody detected with a red fluorescent secondary antibody. The upper row shows GFP fluorescence and the lower row shows the immunofluorescent signal (IF). The IF gradient from the periphery to the centre of some embryos is an optical artefact depending on signal intensity [15]. |
PMC1208874_F2_3071.jpg | What key item or scene is captured in this photo? | Dnmt1S localisation is independent of phosphorylation. A) Schematic representation of GFP-Dnmt1S phosphorylation mutants. B) Western blot of transfected Cos-7 cells probed with an antibody against the N-terminal domain of Dnmt1 [25] showing expression of GFP-Dnmt1s wild type (wt) and phosphorylation mutants S396A and S396D with the expected molecular mass. Weak bands at 190 kDa representing endogenous Dnmt1L are indicated. C) and D) localisation of GFP-Dnmt1S phosphorylation mutants in mouse somatic cells and preimplantation embryos, respectively. Both mutant proteins localise to the nucleus of somatic cells and to the cytoplasm of preimplantation embryos like wild type GFP-Dnmt1S (Fig. 1B and C). In D embryos were fixed and immunostained with an anti-GFP antibody detected with a red fluorescent secondary antibody. The upper row shows GFP fluorescence and the lower row shows the immunofluorescent signal (IF). The IF gradient from the periphery to the centre of some embryos is an optical artefact depending on signal intensity [15]. |
PMC1208874_F2_3072.jpg | What can you see in this picture? | Dnmt1S localisation is independent of phosphorylation. A) Schematic representation of GFP-Dnmt1S phosphorylation mutants. B) Western blot of transfected Cos-7 cells probed with an antibody against the N-terminal domain of Dnmt1 [25] showing expression of GFP-Dnmt1s wild type (wt) and phosphorylation mutants S396A and S396D with the expected molecular mass. Weak bands at 190 kDa representing endogenous Dnmt1L are indicated. C) and D) localisation of GFP-Dnmt1S phosphorylation mutants in mouse somatic cells and preimplantation embryos, respectively. Both mutant proteins localise to the nucleus of somatic cells and to the cytoplasm of preimplantation embryos like wild type GFP-Dnmt1S (Fig. 1B and C). In D embryos were fixed and immunostained with an anti-GFP antibody detected with a red fluorescent secondary antibody. The upper row shows GFP fluorescence and the lower row shows the immunofluorescent signal (IF). The IF gradient from the periphery to the centre of some embryos is an optical artefact depending on signal intensity [15]. |
PMC1208874_F2_3073.jpg | Describe the main subject of this image. | Dnmt1S localisation is independent of phosphorylation. A) Schematic representation of GFP-Dnmt1S phosphorylation mutants. B) Western blot of transfected Cos-7 cells probed with an antibody against the N-terminal domain of Dnmt1 [25] showing expression of GFP-Dnmt1s wild type (wt) and phosphorylation mutants S396A and S396D with the expected molecular mass. Weak bands at 190 kDa representing endogenous Dnmt1L are indicated. C) and D) localisation of GFP-Dnmt1S phosphorylation mutants in mouse somatic cells and preimplantation embryos, respectively. Both mutant proteins localise to the nucleus of somatic cells and to the cytoplasm of preimplantation embryos like wild type GFP-Dnmt1S (Fig. 1B and C). In D embryos were fixed and immunostained with an anti-GFP antibody detected with a red fluorescent secondary antibody. The upper row shows GFP fluorescence and the lower row shows the immunofluorescent signal (IF). The IF gradient from the periphery to the centre of some embryos is an optical artefact depending on signal intensity [15]. |
PMC1208875_F3_3097.jpg | What is being portrayed in this visual content? | Immunohistochemistry of lesional skin biopsies during psoriatic flare of patient 1 and 2, showing similar features (magnification × 10). Haematoxylin and eosin (H&E) stain showing epidermal hyperplasia, elongation of rete ridges, dilatation of dermal papilla blood vessels, and mononuclear and neutrophil leukocyte infiltration. Some CD3 (BD) T cells infiltrate the dermis and epidermis, and these are mostly CD8+ (BD Pharmingen), although there are less T cells than during untreated psoriasis. Most of the epidermal T cells are CD103+ (Biodesign, Kennebunnk, ME). CD11c+ (BD Pharmingen) and iNOS+ (R&D Systems) cells are dramatically increased compared to non-lesional skin, and stain in a dendritic pattern. |
PMC1208875_F3_3102.jpg | What is shown in this image? | Immunohistochemistry of lesional skin biopsies during psoriatic flare of patient 1 and 2, showing similar features (magnification × 10). Haematoxylin and eosin (H&E) stain showing epidermal hyperplasia, elongation of rete ridges, dilatation of dermal papilla blood vessels, and mononuclear and neutrophil leukocyte infiltration. Some CD3 (BD) T cells infiltrate the dermis and epidermis, and these are mostly CD8+ (BD Pharmingen), although there are less T cells than during untreated psoriasis. Most of the epidermal T cells are CD103+ (Biodesign, Kennebunnk, ME). CD11c+ (BD Pharmingen) and iNOS+ (R&D Systems) cells are dramatically increased compared to non-lesional skin, and stain in a dendritic pattern. |
PMC1208875_F3_3101.jpg | What is the dominant medical problem in this image? | Immunohistochemistry of lesional skin biopsies during psoriatic flare of patient 1 and 2, showing similar features (magnification × 10). Haematoxylin and eosin (H&E) stain showing epidermal hyperplasia, elongation of rete ridges, dilatation of dermal papilla blood vessels, and mononuclear and neutrophil leukocyte infiltration. Some CD3 (BD) T cells infiltrate the dermis and epidermis, and these are mostly CD8+ (BD Pharmingen), although there are less T cells than during untreated psoriasis. Most of the epidermal T cells are CD103+ (Biodesign, Kennebunnk, ME). CD11c+ (BD Pharmingen) and iNOS+ (R&D Systems) cells are dramatically increased compared to non-lesional skin, and stain in a dendritic pattern. |
PMC1208875_F3_3100.jpg | What is the focal point of this photograph? | Immunohistochemistry of lesional skin biopsies during psoriatic flare of patient 1 and 2, showing similar features (magnification × 10). Haematoxylin and eosin (H&E) stain showing epidermal hyperplasia, elongation of rete ridges, dilatation of dermal papilla blood vessels, and mononuclear and neutrophil leukocyte infiltration. Some CD3 (BD) T cells infiltrate the dermis and epidermis, and these are mostly CD8+ (BD Pharmingen), although there are less T cells than during untreated psoriasis. Most of the epidermal T cells are CD103+ (Biodesign, Kennebunnk, ME). CD11c+ (BD Pharmingen) and iNOS+ (R&D Systems) cells are dramatically increased compared to non-lesional skin, and stain in a dendritic pattern. |
PMC1208875_F3_3094.jpg | What key item or scene is captured in this photo? | Immunohistochemistry of lesional skin biopsies during psoriatic flare of patient 1 and 2, showing similar features (magnification × 10). Haematoxylin and eosin (H&E) stain showing epidermal hyperplasia, elongation of rete ridges, dilatation of dermal papilla blood vessels, and mononuclear and neutrophil leukocyte infiltration. Some CD3 (BD) T cells infiltrate the dermis and epidermis, and these are mostly CD8+ (BD Pharmingen), although there are less T cells than during untreated psoriasis. Most of the epidermal T cells are CD103+ (Biodesign, Kennebunnk, ME). CD11c+ (BD Pharmingen) and iNOS+ (R&D Systems) cells are dramatically increased compared to non-lesional skin, and stain in a dendritic pattern. |
PMC1208875_F3_3096.jpg | What is the core subject represented in this visual? | Immunohistochemistry of lesional skin biopsies during psoriatic flare of patient 1 and 2, showing similar features (magnification × 10). Haematoxylin and eosin (H&E) stain showing epidermal hyperplasia, elongation of rete ridges, dilatation of dermal papilla blood vessels, and mononuclear and neutrophil leukocyte infiltration. Some CD3 (BD) T cells infiltrate the dermis and epidermis, and these are mostly CD8+ (BD Pharmingen), although there are less T cells than during untreated psoriasis. Most of the epidermal T cells are CD103+ (Biodesign, Kennebunnk, ME). CD11c+ (BD Pharmingen) and iNOS+ (R&D Systems) cells are dramatically increased compared to non-lesional skin, and stain in a dendritic pattern. |
PMC1208875_F3_3095.jpg | What is the focal point of this photograph? | Immunohistochemistry of lesional skin biopsies during psoriatic flare of patient 1 and 2, showing similar features (magnification × 10). Haematoxylin and eosin (H&E) stain showing epidermal hyperplasia, elongation of rete ridges, dilatation of dermal papilla blood vessels, and mononuclear and neutrophil leukocyte infiltration. Some CD3 (BD) T cells infiltrate the dermis and epidermis, and these are mostly CD8+ (BD Pharmingen), although there are less T cells than during untreated psoriasis. Most of the epidermal T cells are CD103+ (Biodesign, Kennebunnk, ME). CD11c+ (BD Pharmingen) and iNOS+ (R&D Systems) cells are dramatically increased compared to non-lesional skin, and stain in a dendritic pattern. |
PMC1208875_F3_3098.jpg | What is shown in this image? | Immunohistochemistry of lesional skin biopsies during psoriatic flare of patient 1 and 2, showing similar features (magnification × 10). Haematoxylin and eosin (H&E) stain showing epidermal hyperplasia, elongation of rete ridges, dilatation of dermal papilla blood vessels, and mononuclear and neutrophil leukocyte infiltration. Some CD3 (BD) T cells infiltrate the dermis and epidermis, and these are mostly CD8+ (BD Pharmingen), although there are less T cells than during untreated psoriasis. Most of the epidermal T cells are CD103+ (Biodesign, Kennebunnk, ME). CD11c+ (BD Pharmingen) and iNOS+ (R&D Systems) cells are dramatically increased compared to non-lesional skin, and stain in a dendritic pattern. |
PMC1208875_F3_3093.jpg | What can you see in this picture? | Immunohistochemistry of lesional skin biopsies during psoriatic flare of patient 1 and 2, showing similar features (magnification × 10). Haematoxylin and eosin (H&E) stain showing epidermal hyperplasia, elongation of rete ridges, dilatation of dermal papilla blood vessels, and mononuclear and neutrophil leukocyte infiltration. Some CD3 (BD) T cells infiltrate the dermis and epidermis, and these are mostly CD8+ (BD Pharmingen), although there are less T cells than during untreated psoriasis. Most of the epidermal T cells are CD103+ (Biodesign, Kennebunnk, ME). CD11c+ (BD Pharmingen) and iNOS+ (R&D Systems) cells are dramatically increased compared to non-lesional skin, and stain in a dendritic pattern. |
PMC1208887_F3_3104.jpg | What can you see in this picture? | Confocal microscopy of DENV-Ag expression after in vitro infection of monocyte-rich cultures. Adherent human PBMLs were incubated for three days either with cell culture medium (Figure 3A, 189.5 μm/field), or with infectious DENV (Figure 3B, 125 μm/field). Cells were labelled with antibody to DENV-Ag and anti-mouse IgG-FITC. |
PMC1208887_F3_3103.jpg | What is the main focus of this visual representation? | Confocal microscopy of DENV-Ag expression after in vitro infection of monocyte-rich cultures. Adherent human PBMLs were incubated for three days either with cell culture medium (Figure 3A, 189.5 μm/field), or with infectious DENV (Figure 3B, 125 μm/field). Cells were labelled with antibody to DENV-Ag and anti-mouse IgG-FITC. |
PMC1208889_F7_3106.jpg | What is the core subject represented in this visual? | Results of PET/CT study on the cylindrical Nema phantom. The CT image reconstructed using FBP (upper left) and corresponding ACF (upper right) followed by 1D vertical and horizontal profiles of the ACF (down). |
PMC1208889_F8_3111.jpg | Describe the main subject of this image. | Results of PET/CT study on the cylindrical Nema phantom. The PET image reconstructed using FBP with applied 4-mm Hanning filter (upper left) and corresponding ACF (upper right) followed by 1D vertical and horizontal profiles of the ACF (down). |
PMC1208889_F8_3112.jpg | What is being portrayed in this visual content? | Results of PET/CT study on the cylindrical Nema phantom. The PET image reconstructed using FBP with applied 4-mm Hanning filter (upper left) and corresponding ACF (upper right) followed by 1D vertical and horizontal profiles of the ACF (down). |
PMC1208889_F9_3109.jpg | What's the most prominent thing you notice in this picture? | Results of PET/CT study on the elliptical Torso phantom. The CT image reconstructed using FBP (upper left) and corresponding ACF (upper right) followed by 1D vertical and horizontal profiles of the ACF (down). |
PMC1208889_F12_3118.jpg | What is the central feature of this picture? | PET results of PET/CT study on cylindrical NEMA phantom. Variance images reconstructed using FBP (upper left) and OSEM (upper right). 1D horizontal profile through the variance image reconstructed using FBP (lower left) and reconstructed using OSEM (lower right). |
PMC1208889_F12_3117.jpg | What is the central feature of this picture? | PET results of PET/CT study on cylindrical NEMA phantom. Variance images reconstructed using FBP (upper left) and OSEM (upper right). 1D horizontal profile through the variance image reconstructed using FBP (lower left) and reconstructed using OSEM (lower right). |
PMC1208889_F13_3122.jpg | What stands out most in this visual? | Results of PET/CT study on elliptical Torso phantom. PET variance images reconstructed using FBP (upper left) and OSEM (upper right). 1D horizontal profile through the variance image reconstructed using FBP (lower left) and reconstructed using OSEM (lower right). |
PMC1208889_F13_3121.jpg | Describe the main subject of this image. | Results of PET/CT study on elliptical Torso phantom. PET variance images reconstructed using FBP (upper left) and OSEM (upper right). 1D horizontal profile through the variance image reconstructed using FBP (lower left) and reconstructed using OSEM (lower right). |
PMC1208889_F17_3125.jpg | Describe the main subject of this image. | Results of the PET/CT study on cylindrical NEMA phantom. Variance images of CT (transmission scan) of Nema (upper left) and Torso phantom (upper right). Corresponding 1D horizontal profile through the variance images of Nema (lower left) and Torso phantom (lower right). |
PMC1208889_F17_3126.jpg | What stands out most in this visual? | Results of the PET/CT study on cylindrical NEMA phantom. Variance images of CT (transmission scan) of Nema (upper left) and Torso phantom (upper right). Corresponding 1D horizontal profile through the variance images of Nema (lower left) and Torso phantom (lower right). |
PMC1208912_F3_3129.jpg | What is the central feature of this picture? | Confocal immunofluorescence for aquaporins and solute transporters in WIF-B cells. WIF-B cells were fixed, permeabilized, and labeled with anti-AQPs, AE2, Mrp2 or Bsep. Fluorescence localization was viewed by laser scanning confocal microscopy (see "Materials and Methods" for details). *, bile canaliculi structures. |
PMC1208912_F3_3133.jpg | What key item or scene is captured in this photo? | Confocal immunofluorescence for aquaporins and solute transporters in WIF-B cells. WIF-B cells were fixed, permeabilized, and labeled with anti-AQPs, AE2, Mrp2 or Bsep. Fluorescence localization was viewed by laser scanning confocal microscopy (see "Materials and Methods" for details). *, bile canaliculi structures. |
PMC1208912_F3_3131.jpg | Can you identify the primary element in this image? | Confocal immunofluorescence for aquaporins and solute transporters in WIF-B cells. WIF-B cells were fixed, permeabilized, and labeled with anti-AQPs, AE2, Mrp2 or Bsep. Fluorescence localization was viewed by laser scanning confocal microscopy (see "Materials and Methods" for details). *, bile canaliculi structures. |
PMC1208912_F3_3132.jpg | What stands out most in this visual? | Confocal immunofluorescence for aquaporins and solute transporters in WIF-B cells. WIF-B cells were fixed, permeabilized, and labeled with anti-AQPs, AE2, Mrp2 or Bsep. Fluorescence localization was viewed by laser scanning confocal microscopy (see "Materials and Methods" for details). *, bile canaliculi structures. |
PMC1208912_F4_3135.jpg | Describe the main subject of this image. | Co-immunostaining of AQP8 and AE2 by confocal immunofluorescence. WIF-B cells were fixed, permeabilized, and labelled simultaneously with rabbit anti-AE2 and goat anti-AQP8. Fluorescence localization was viewed by laser scanning confocal microscopy (see "Materials and Methods" for details). *, bile canaliculi structures. |
PMC1208912_F4_3137.jpg | What does this image primarily show? | Co-immunostaining of AQP8 and AE2 by confocal immunofluorescence. WIF-B cells were fixed, permeabilized, and labelled simultaneously with rabbit anti-AE2 and goat anti-AQP8. Fluorescence localization was viewed by laser scanning confocal microscopy (see "Materials and Methods" for details). *, bile canaliculi structures. |
PMC1208912_F4_3136.jpg | Describe the main subject of this image. | Co-immunostaining of AQP8 and AE2 by confocal immunofluorescence. WIF-B cells were fixed, permeabilized, and labelled simultaneously with rabbit anti-AE2 and goat anti-AQP8. Fluorescence localization was viewed by laser scanning confocal microscopy (see "Materials and Methods" for details). *, bile canaliculi structures. |
PMC1208923_F3_3138.jpg | Can you identify the primary element in this image? | MRI cine turbo-flash images acquired on a 1.5 T scanner(Magnetom Vision-Siemens) in four-chamber (3A) and transverse plane, short-axis view (Fig. 4). These images didn't show congenital heart disease. |
PMC1208923_F4_3139.jpg | Describe the main subject of this image. | MRI cine turbo-flash images acquired on a 1.5 T scanner(Magnetom Vision-Siemens) in four-chamber (3A) and transverse plane, short-axis view. These images did n't show congenital heart disease. |
PMC1208925_F1_3140.jpg | What's the most prominent thing you notice in this picture? | Right ventricular hypertrophy and dilatation at initial investigation with transthoracic echocardiography. |
PMC1208925_F2_3141.jpg | What is the focal point of this photograph? | Tricuspid insufficiency grade II–III with a morphological normal valve at initial investigation with transthoracic echocardiography. |
PMC1208937_F1_3147.jpg | What is the focal point of this photograph? | Two-dimensional vs three-dimensional transvaginal color Doppler sonography. (a) Diagram (left) and two-dimensional TV-CDS (right) showing arcuate, radial, and spiral vessels in follicular phase. (b) Diagram (left) are two-dimensional TV-CDS (right) showing changes in endometrial vascularity throughout the menstral cycle. During the luteal phase, several spiral vessels are detected. (c) Diagram (top) and multiplanar images (left) and magnified 3D TV-CDS (right) of corpus luteum. The multiplanar image shows the vascular "wreath" surrounding the functioning corpus luteum in the longitudinal (top left), short (axial) (top right) and coronal (bottom right) planes. The combined gray scale and 3D TV-CDS image (both left) which is also magnified and shown as the right depicts the numerous vessels surrounding this corpus luteum. |
PMC1208937_F1_3144.jpg | What is the main focus of this visual representation? | Two-dimensional vs three-dimensional transvaginal color Doppler sonography. (a) Diagram (left) and two-dimensional TV-CDS (right) showing arcuate, radial, and spiral vessels in follicular phase. (b) Diagram (left) are two-dimensional TV-CDS (right) showing changes in endometrial vascularity throughout the menstral cycle. During the luteal phase, several spiral vessels are detected. (c) Diagram (top) and multiplanar images (left) and magnified 3D TV-CDS (right) of corpus luteum. The multiplanar image shows the vascular "wreath" surrounding the functioning corpus luteum in the longitudinal (top left), short (axial) (top right) and coronal (bottom right) planes. The combined gray scale and 3D TV-CDS image (both left) which is also magnified and shown as the right depicts the numerous vessels surrounding this corpus luteum. |
PMC1208937_F1_3142.jpg | What is the main focus of this visual representation? | Two-dimensional vs three-dimensional transvaginal color Doppler sonography. (a) Diagram (left) and two-dimensional TV-CDS (right) showing arcuate, radial, and spiral vessels in follicular phase. (b) Diagram (left) are two-dimensional TV-CDS (right) showing changes in endometrial vascularity throughout the menstral cycle. During the luteal phase, several spiral vessels are detected. (c) Diagram (top) and multiplanar images (left) and magnified 3D TV-CDS (right) of corpus luteum. The multiplanar image shows the vascular "wreath" surrounding the functioning corpus luteum in the longitudinal (top left), short (axial) (top right) and coronal (bottom right) planes. The combined gray scale and 3D TV-CDS image (both left) which is also magnified and shown as the right depicts the numerous vessels surrounding this corpus luteum. |
PMC1208937_F1_3143.jpg | What is the focal point of this photograph? | Two-dimensional vs three-dimensional transvaginal color Doppler sonography. (a) Diagram (left) and two-dimensional TV-CDS (right) showing arcuate, radial, and spiral vessels in follicular phase. (b) Diagram (left) are two-dimensional TV-CDS (right) showing changes in endometrial vascularity throughout the menstral cycle. During the luteal phase, several spiral vessels are detected. (c) Diagram (top) and multiplanar images (left) and magnified 3D TV-CDS (right) of corpus luteum. The multiplanar image shows the vascular "wreath" surrounding the functioning corpus luteum in the longitudinal (top left), short (axial) (top right) and coronal (bottom right) planes. The combined gray scale and 3D TV-CDS image (both left) which is also magnified and shown as the right depicts the numerous vessels surrounding this corpus luteum. |
PMC1208937_F1_3148.jpg | What is the principal component of this image? | Two-dimensional vs three-dimensional transvaginal color Doppler sonography. (a) Diagram (left) and two-dimensional TV-CDS (right) showing arcuate, radial, and spiral vessels in follicular phase. (b) Diagram (left) are two-dimensional TV-CDS (right) showing changes in endometrial vascularity throughout the menstral cycle. During the luteal phase, several spiral vessels are detected. (c) Diagram (top) and multiplanar images (left) and magnified 3D TV-CDS (right) of corpus luteum. The multiplanar image shows the vascular "wreath" surrounding the functioning corpus luteum in the longitudinal (top left), short (axial) (top right) and coronal (bottom right) planes. The combined gray scale and 3D TV-CDS image (both left) which is also magnified and shown as the right depicts the numerous vessels surrounding this corpus luteum. |
PMC1208937_F2_3164.jpg | What object or scene is depicted here? | The techniques of volume calculation. Both figures show the typical multiplanar display of a three-dimensional sonographic dataset of the uterus with the three mutually related orthogonal planes at 90-degrees to one another. The upper left image in both displays represents the longitudinal plane (the A plane), the upper right image the transverse plane (the B plane) and the lower left image the coronal plane (the C plane). Volume calculation can be conducted in either the B or C plane. (a) shows the conventional technique of volume calculation in which a series of 'slices' are taken through the volume of interest whilst the contour is outlined in another plane (the transverse plane in this case). The distance between consecutive slices can be varied according to the degree of change in the surface contour and increased for more complex structures. (b) shows the rotational technique of volume calculation in which the dataset is rotated through 180° about a central axis defined by the application of two callipers. The number of planes available for volume calculation are determined by the rotation step shown in the lower left of the image. Here the 30-degree rotation step has been used and the contour outlined in the coronal or C plane using the manual mode. The resultant three-dimensional model is shown in the lower right of the image. |
PMC1208937_F2_3162.jpg | What object or scene is depicted here? | The techniques of volume calculation. Both figures show the typical multiplanar display of a three-dimensional sonographic dataset of the uterus with the three mutually related orthogonal planes at 90-degrees to one another. The upper left image in both displays represents the longitudinal plane (the A plane), the upper right image the transverse plane (the B plane) and the lower left image the coronal plane (the C plane). Volume calculation can be conducted in either the B or C plane. (a) shows the conventional technique of volume calculation in which a series of 'slices' are taken through the volume of interest whilst the contour is outlined in another plane (the transverse plane in this case). The distance between consecutive slices can be varied according to the degree of change in the surface contour and increased for more complex structures. (b) shows the rotational technique of volume calculation in which the dataset is rotated through 180° about a central axis defined by the application of two callipers. The number of planes available for volume calculation are determined by the rotation step shown in the lower left of the image. Here the 30-degree rotation step has been used and the contour outlined in the coronal or C plane using the manual mode. The resultant three-dimensional model is shown in the lower right of the image. |
PMC1208937_F2_3159.jpg | What is the focal point of this photograph? | The techniques of volume calculation. Both figures show the typical multiplanar display of a three-dimensional sonographic dataset of the uterus with the three mutually related orthogonal planes at 90-degrees to one another. The upper left image in both displays represents the longitudinal plane (the A plane), the upper right image the transverse plane (the B plane) and the lower left image the coronal plane (the C plane). Volume calculation can be conducted in either the B or C plane. (a) shows the conventional technique of volume calculation in which a series of 'slices' are taken through the volume of interest whilst the contour is outlined in another plane (the transverse plane in this case). The distance between consecutive slices can be varied according to the degree of change in the surface contour and increased for more complex structures. (b) shows the rotational technique of volume calculation in which the dataset is rotated through 180° about a central axis defined by the application of two callipers. The number of planes available for volume calculation are determined by the rotation step shown in the lower left of the image. Here the 30-degree rotation step has been used and the contour outlined in the coronal or C plane using the manual mode. The resultant three-dimensional model is shown in the lower right of the image. |
PMC1208937_F2_3161.jpg | What can you see in this picture? | The techniques of volume calculation. Both figures show the typical multiplanar display of a three-dimensional sonographic dataset of the uterus with the three mutually related orthogonal planes at 90-degrees to one another. The upper left image in both displays represents the longitudinal plane (the A plane), the upper right image the transverse plane (the B plane) and the lower left image the coronal plane (the C plane). Volume calculation can be conducted in either the B or C plane. (a) shows the conventional technique of volume calculation in which a series of 'slices' are taken through the volume of interest whilst the contour is outlined in another plane (the transverse plane in this case). The distance between consecutive slices can be varied according to the degree of change in the surface contour and increased for more complex structures. (b) shows the rotational technique of volume calculation in which the dataset is rotated through 180° about a central axis defined by the application of two callipers. The number of planes available for volume calculation are determined by the rotation step shown in the lower left of the image. Here the 30-degree rotation step has been used and the contour outlined in the coronal or C plane using the manual mode. The resultant three-dimensional model is shown in the lower right of the image. |
PMC1208937_F4_3150.jpg | What is shown in this image? | Three-dimensional power Doppler angiography of the uterine blood supply. A three-dimensional dataset containing power Doppler information has been acquired from the uterus. VOCAL has then been used to define the myometrial-endometrial border and to apply a shell 5 mm outside of that contour to define the sub-endometrium, which can be clearly seen to be more vascular than the endometrium itself. |
PMC1208937_F4_3153.jpg | What is the focal point of this photograph? | Three-dimensional power Doppler angiography of the uterine blood supply. A three-dimensional dataset containing power Doppler information has been acquired from the uterus. VOCAL has then been used to define the myometrial-endometrial border and to apply a shell 5 mm outside of that contour to define the sub-endometrium, which can be clearly seen to be more vascular than the endometrium itself. |
PMC1208937_F4_3154.jpg | What does this image primarily show? | Three-dimensional power Doppler angiography of the uterine blood supply. A three-dimensional dataset containing power Doppler information has been acquired from the uterus. VOCAL has then been used to define the myometrial-endometrial border and to apply a shell 5 mm outside of that contour to define the sub-endometrium, which can be clearly seen to be more vascular than the endometrium itself. |
PMC1208937_F4_3152.jpg | Describe the main subject of this image. | Three-dimensional power Doppler angiography of the uterine blood supply. A three-dimensional dataset containing power Doppler information has been acquired from the uterus. VOCAL has then been used to define the myometrial-endometrial border and to apply a shell 5 mm outside of that contour to define the sub-endometrium, which can be clearly seen to be more vascular than the endometrium itself. |
PMC1208937_F5_3156.jpg | What is the focal point of this photograph? | The 'Histogram'. The three indices of vascularity have been calculated for the endometrial model together with the mean grey value. The Vascularisation Index (VI) reflects the degree of power Doppler information within the model and is considered as a percentage therefore whilst the Flow Index (FI) and Vascularisation Flow Index (VFI) include information on the mean power Doppler signal intensity referenced against a scale from zero to one hundred to indicate the minimal and maximum range accordingly. |
PMC1208937_F6_3158.jpg | What is the principal component of this image? | Intra-subject variation in endometrial blood flow. The degree of power Doppler information seen within Figure 6a is clearly superior to that seen in Figure 6b and this difference is quantifiable through the 'histogram' facility. These images also serve to demonstrate how vascularity is independent of morphometry and varies throughout different phases of the menstrual cycle as the less vascular homogenous endometrium characteristic of the luteal phase in Figure 6b is of greater volume than that in Figure 6a, which is the same endometrium at the end of follicular phase. |
PMC1208937_F6_3157.jpg | What stands out most in this visual? | Intra-subject variation in endometrial blood flow. The degree of power Doppler information seen within Figure 6a is clearly superior to that seen in Figure 6b and this difference is quantifiable through the 'histogram' facility. These images also serve to demonstrate how vascularity is independent of morphometry and varies throughout different phases of the menstrual cycle as the less vascular homogenous endometrium characteristic of the luteal phase in Figure 6b is of greater volume than that in Figure 6a, which is the same endometrium at the end of follicular phase. |
PMC1208937_F7_3175.jpg | What object or scene is depicted here? | Uterine anomalies. Three-dimensional sonography has become the 'gold standard' investigation for the diagnosis and exclusion of congenital uterine anomalies. Its extremely high sensitivity and specificity relate to its ability to demonstrate the plane coronal perpendicular to the transducer face and in doing so allow visualisation of the fundal contour and comparison of the myometrium with the endometrium throughout the uterine length. Figure 7a shows normal cornna with straight contours at the upper aspect of the cavity in contrast to the characteristic concave contour seen in arcuate uteri (Fig. 7b) and the deeper contour of various length seen in sub-septate uteri (Figs. 7c, 7d & 7e). Any indentation of the fundal contour may also be appreciated in the coronal plane as seen in the multiplanar display in Figure 7f. This uterus had been considered normal with conventional ultrasound, which only provides the longitudinal and transverse views seen in the upper two images, but laparoscopy had demonstrated a bulky uterus with a possible fundal defect and a follow-up three-dimensional ultrasound confirmed the presence of a significant septum. The size of the septal defect can be measured as shown in Figure 7g but may be less important than the remaining length of the cavity shown as a bold dashed line. |
PMC1208937_F7_3171.jpg | What key item or scene is captured in this photo? | Uterine anomalies. Three-dimensional sonography has become the 'gold standard' investigation for the diagnosis and exclusion of congenital uterine anomalies. Its extremely high sensitivity and specificity relate to its ability to demonstrate the plane coronal perpendicular to the transducer face and in doing so allow visualisation of the fundal contour and comparison of the myometrium with the endometrium throughout the uterine length. Figure 7a shows normal cornna with straight contours at the upper aspect of the cavity in contrast to the characteristic concave contour seen in arcuate uteri (Fig. 7b) and the deeper contour of various length seen in sub-septate uteri (Figs. 7c, 7d & 7e). Any indentation of the fundal contour may also be appreciated in the coronal plane as seen in the multiplanar display in Figure 7f. This uterus had been considered normal with conventional ultrasound, which only provides the longitudinal and transverse views seen in the upper two images, but laparoscopy had demonstrated a bulky uterus with a possible fundal defect and a follow-up three-dimensional ultrasound confirmed the presence of a significant septum. The size of the septal defect can be measured as shown in Figure 7g but may be less important than the remaining length of the cavity shown as a bold dashed line. |
PMC1208937_F7_3174.jpg | What stands out most in this visual? | Uterine anomalies. Three-dimensional sonography has become the 'gold standard' investigation for the diagnosis and exclusion of congenital uterine anomalies. Its extremely high sensitivity and specificity relate to its ability to demonstrate the plane coronal perpendicular to the transducer face and in doing so allow visualisation of the fundal contour and comparison of the myometrium with the endometrium throughout the uterine length. Figure 7a shows normal cornna with straight contours at the upper aspect of the cavity in contrast to the characteristic concave contour seen in arcuate uteri (Fig. 7b) and the deeper contour of various length seen in sub-septate uteri (Figs. 7c, 7d & 7e). Any indentation of the fundal contour may also be appreciated in the coronal plane as seen in the multiplanar display in Figure 7f. This uterus had been considered normal with conventional ultrasound, which only provides the longitudinal and transverse views seen in the upper two images, but laparoscopy had demonstrated a bulky uterus with a possible fundal defect and a follow-up three-dimensional ultrasound confirmed the presence of a significant septum. The size of the septal defect can be measured as shown in Figure 7g but may be less important than the remaining length of the cavity shown as a bold dashed line. |
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