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PMC549593_pmed-0020045-g001_1348.jpg | What's the most prominent thing you notice in this picture? | 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_1350.jpg | Describe the main subject of this image. | 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_1345.jpg | What key item or scene is captured in this photo? | 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_1351.jpg | What can you see in this picture? | 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. |
PMC549606_pmed-0020073-g001_1357.jpg | What is the focal point of this photograph? | Re-Biopsy Studies(A.) Patient 1. CT-guided biopsy of progressing lung lesions after 10 mo on gefitinib (left panel). Two months later, fluid from a right-sided pleural effusion (right panel) was collected for molecular analysis.(B) Patient 2. CT-guided biopsy of a progressing thoracic spine lesion (left panel) and fluoroscopic-guided biopsy of a progressing lung lesion (right panel). The biopsy needles are indicated by white arrows. |
PMC549606_pmed-0020073-g001_1358.jpg | What is the main focus of this visual representation? | Re-Biopsy Studies(A.) Patient 1. CT-guided biopsy of progressing lung lesions after 10 mo on gefitinib (left panel). Two months later, fluid from a right-sided pleural effusion (right panel) was collected for molecular analysis.(B) Patient 2. CT-guided biopsy of a progressing thoracic spine lesion (left panel) and fluoroscopic-guided biopsy of a progressing lung lesion (right panel). The biopsy needles are indicated by white arrows. |
PMC549606_pmed-0020073-g001_1355.jpg | Describe the main subject of this image. | Re-Biopsy Studies(A.) Patient 1. CT-guided biopsy of progressing lung lesions after 10 mo on gefitinib (left panel). Two months later, fluid from a right-sided pleural effusion (right panel) was collected for molecular analysis.(B) Patient 2. CT-guided biopsy of a progressing thoracic spine lesion (left panel) and fluoroscopic-guided biopsy of a progressing lung lesion (right panel). The biopsy needles are indicated by white arrows. |
PMC549606_pmed-0020073-g001_1356.jpg | Can you identify the primary element in this image? | Re-Biopsy Studies(A.) Patient 1. CT-guided biopsy of progressing lung lesions after 10 mo on gefitinib (left panel). Two months later, fluid from a right-sided pleural effusion (right panel) was collected for molecular analysis.(B) Patient 2. CT-guided biopsy of a progressing thoracic spine lesion (left panel) and fluoroscopic-guided biopsy of a progressing lung lesion (right panel). The biopsy needles are indicated by white arrows. |
PMC549712_F5_1362.jpg | Describe the main subject of this image. | Histological analysis of eye development in severely affected eyeless Ptdsr -/- embryos. (a) In anophthalmic Ptdsr -/- embryos, unilateral or bilateral absence of the eyes could be detected. (b-d) Serial H&E-stained sagittal sections of homozygous mutant embryos at (b) E17.5 and (c,d) E18.5 show complex malformation of the optic cup and lack of any lens structure. Careful examination of adjacent sections (b-d) reveals an ectopic misplacement of retinal-pigmented epithelium in the maxillary sinus. Not only is the deposition of pigment clearly visible (higher magnification insets) but also the induction of proliferation of underlying tissues and the change in morphology of the maxillary sinus (d). Scale bar, 100 μm in (b-d). |
PMC549712_F5_1359.jpg | What stands out most in this visual? | Histological analysis of eye development in severely affected eyeless Ptdsr -/- embryos. (a) In anophthalmic Ptdsr -/- embryos, unilateral or bilateral absence of the eyes could be detected. (b-d) Serial H&E-stained sagittal sections of homozygous mutant embryos at (b) E17.5 and (c,d) E18.5 show complex malformation of the optic cup and lack of any lens structure. Careful examination of adjacent sections (b-d) reveals an ectopic misplacement of retinal-pigmented epithelium in the maxillary sinus. Not only is the deposition of pigment clearly visible (higher magnification insets) but also the induction of proliferation of underlying tissues and the change in morphology of the maxillary sinus (d). Scale bar, 100 μm in (b-d). |
PMC549712_F5_1360.jpg | What is the principal component of this image? | Histological analysis of eye development in severely affected eyeless Ptdsr -/- embryos. (a) In anophthalmic Ptdsr -/- embryos, unilateral or bilateral absence of the eyes could be detected. (b-d) Serial H&E-stained sagittal sections of homozygous mutant embryos at (b) E17.5 and (c,d) E18.5 show complex malformation of the optic cup and lack of any lens structure. Careful examination of adjacent sections (b-d) reveals an ectopic misplacement of retinal-pigmented epithelium in the maxillary sinus. Not only is the deposition of pigment clearly visible (higher magnification insets) but also the induction of proliferation of underlying tissues and the change in morphology of the maxillary sinus (d). Scale bar, 100 μm in (b-d). |
PMC550649_F2_1363.jpg | What is the principal component of this image? | Characterization of fibre type specificity of dihydropyridine receptor Two subsequent sections of mouse musculus gastrocnemius were assayed for DHPR localization by fluorescence staining (A) and for fibre type analysis by staining for mATPase (B). After preincubation in pH 4.6, type IIA displays a relatively low acid stability and is stained most lightly (*). The corresponding fibre in (A) is also recognized by fluorophore conjugated DHP blocker. The fibre on the right of the asterisked fibre shows also fluorescence. The intensity is, however, somewhat lower than in the fibre next to it and originates probably from the special fibre type (hybrid, type IIDA). (C) A control sample preincubated with nifedipine. Bar 20 μm. |
PMC550649_F2_1364.jpg | What is the core subject represented in this visual? | Characterization of fibre type specificity of dihydropyridine receptor Two subsequent sections of mouse musculus gastrocnemius were assayed for DHPR localization by fluorescence staining (A) and for fibre type analysis by staining for mATPase (B). After preincubation in pH 4.6, type IIA displays a relatively low acid stability and is stained most lightly (*). The corresponding fibre in (A) is also recognized by fluorophore conjugated DHP blocker. The fibre on the right of the asterisked fibre shows also fluorescence. The intensity is, however, somewhat lower than in the fibre next to it and originates probably from the special fibre type (hybrid, type IIDA). (C) A control sample preincubated with nifedipine. Bar 20 μm. |
PMC550652_F3_1372.jpg | Describe the main subject of this image. | Mannose receptor and MHC class II colocalise in confocal microscope images of secretory organ APC. The subcellular distribution of MR and MHC class II in secretory organ APC was examined by confocal microscopy as indicated. A nuclear counterstain in blue is included in merged images. Single optical planes showing a high degree of colocalisation of MR and MHC class II were selected from z-series in which colocalisation was also observed in adjacent optical sections. Boxed regions of each image are shown at three-fold higher magnification in insets. The scale bar is indicated in the first panel only and is 5 μm. |
PMC550652_F3_1368.jpg | What key item or scene is captured in this photo? | Mannose receptor and MHC class II colocalise in confocal microscope images of secretory organ APC. The subcellular distribution of MR and MHC class II in secretory organ APC was examined by confocal microscopy as indicated. A nuclear counterstain in blue is included in merged images. Single optical planes showing a high degree of colocalisation of MR and MHC class II were selected from z-series in which colocalisation was also observed in adjacent optical sections. Boxed regions of each image are shown at three-fold higher magnification in insets. The scale bar is indicated in the first panel only and is 5 μm. |
PMC550661_F4_1376.jpg | What is the central feature of this picture? | Negative-stain and cryoEM images of isolated sea urchin vaults. (A) Negative-stain electron micrograph. (B) Cryoelectron micrograph. The black arrow indicates a vault that is opening at the midsection, and the white arrow indicates the dark molecular contents within another particle. The scale bar represents 1,000 Å. Note that the magnification of the cryoEM image (B) is slightly higher than that of the negative-stain EM image (A). |
PMC550661_F4_1375.jpg | What is shown in this image? | Negative-stain and cryoEM images of isolated sea urchin vaults. (A) Negative-stain electron micrograph. (B) Cryoelectron micrograph. The black arrow indicates a vault that is opening at the midsection, and the white arrow indicates the dark molecular contents within another particle. The scale bar represents 1,000 Å. Note that the magnification of the cryoEM image (B) is slightly higher than that of the negative-stain EM image (A). |
PMC550667_F1_1384.jpg | What key item or scene is captured in this photo? | Assessment of atrial and ventricular mechanical function. The upper panel shows the systolic and diastolic velocities (a) and the A-V place displacement (b) measured at the basal level of the inter ventricular septum. The lower panel shows the atrial velocity (c), atrial displacement (d), atrial strain rate (e) and atrial strain (f) measured at the inter atrial septum below the mitral ring. |
PMC550667_F1_1381.jpg | What is the core subject represented in this visual? | Assessment of atrial and ventricular mechanical function. The upper panel shows the systolic and diastolic velocities (a) and the A-V place displacement (b) measured at the basal level of the inter ventricular septum. The lower panel shows the atrial velocity (c), atrial displacement (d), atrial strain rate (e) and atrial strain (f) measured at the inter atrial septum below the mitral ring. |
PMC550667_F1_1382.jpg | What is being portrayed in this visual content? | Assessment of atrial and ventricular mechanical function. The upper panel shows the systolic and diastolic velocities (a) and the A-V place displacement (b) measured at the basal level of the inter ventricular septum. The lower panel shows the atrial velocity (c), atrial displacement (d), atrial strain rate (e) and atrial strain (f) measured at the inter atrial septum below the mitral ring. |
PMC550667_F2_1378.jpg | What key item or scene is captured in this photo? | Assessment of some time intervals and Aa' wave velocity at the low level of the inter atrial septum |
PMC550667_F2_1377.jpg | What is the focal point of this photograph? | Assessment of some time intervals and Aa' wave velocity at the low level of the inter atrial septum |
PMC552326_F2_1385.jpg | What does this image primarily show? | Computed tomography depicted a solid tumor with heterogeneous contrast enhancement (arrowheads) in the adipose tissue. |
PMC552326_F3_1386.jpg | What object or scene is depicted here? | The tumor comprised spindle-shaped cells with high cellularity in parts (hematoxylin-and-eosin; original magnification, × 100). |
PMC553966_F6_1396.jpg | What stands out most in this visual? | A Strong focal expression of mouse S100A7/psoriasin RNA in mammary gland tumors compared to little expression in matched normal mammary gland tissue using in situ hybridization Sections from formalin fixed paraffin-embedded mammary tissue samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression: A, C, D, F show hybridization with mouse S100A7/psoriasin 35S-labeled antisense cRNA; B, E show hybridization with mouse S100A7/psoriasin 35S-labeled sense cRNA. A = high magnification (400X) section of normal mammary gland, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = high magnification (400X) adjacent section to A hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C = low magnification (100X) of section from the matched DMBA mammary tumor from same animal shown in A hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. D = higher magnification (400X) of C. E = high magnification (400X) of adjacent section from the same mammary tumor shown in D, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. F = low magnification (100X) of a single tissue section (tissue from a different mouse to that shown in A-E)) hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, where strong focal expression of mouse S100A7/psoriasin RNA is observed in the mammary gland tumor (black arrow) with little or no expression in the surrounding normal mammary gland tissue. B Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in DMBA-induced mammary gland tumors Sections from formalin fixed paraffin-embedded DMBA-induced mammary tumor samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A = low magnification (100X) of tumor section hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = higher magnification of A (200X), C = high magnification of B. D = adjacent section to that seen in A, B, C, and at same magnification as B but hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. E and F are haematoxylin and eosin stains of adjacent sections to that shown in A, B, C, and D. E is the same magnification as in B, and F is the same magnification as that shown in C. Squamous differentiation in the haematoxylin and eosin stained adjacent sections is visualized as a characteristic "pearling" pattern where epithelial tumor cells (purple) differentiate into keratinocytes (pink) before denucleating and sloughing off into the inner lumen (white). Thus cells on the outer margin of the pearled area are undergoing squamous differentiation, and those correspond to cells expressing mouse S100A7/psoriasin RNA, in A, B, and C. |
PMC553966_F6_1398.jpg | Describe the main subject of this image. | A Strong focal expression of mouse S100A7/psoriasin RNA in mammary gland tumors compared to little expression in matched normal mammary gland tissue using in situ hybridization Sections from formalin fixed paraffin-embedded mammary tissue samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression: A, C, D, F show hybridization with mouse S100A7/psoriasin 35S-labeled antisense cRNA; B, E show hybridization with mouse S100A7/psoriasin 35S-labeled sense cRNA. A = high magnification (400X) section of normal mammary gland, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = high magnification (400X) adjacent section to A hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C = low magnification (100X) of section from the matched DMBA mammary tumor from same animal shown in A hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. D = higher magnification (400X) of C. E = high magnification (400X) of adjacent section from the same mammary tumor shown in D, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. F = low magnification (100X) of a single tissue section (tissue from a different mouse to that shown in A-E)) hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, where strong focal expression of mouse S100A7/psoriasin RNA is observed in the mammary gland tumor (black arrow) with little or no expression in the surrounding normal mammary gland tissue. B Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in DMBA-induced mammary gland tumors Sections from formalin fixed paraffin-embedded DMBA-induced mammary tumor samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A = low magnification (100X) of tumor section hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = higher magnification of A (200X), C = high magnification of B. D = adjacent section to that seen in A, B, C, and at same magnification as B but hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. E and F are haematoxylin and eosin stains of adjacent sections to that shown in A, B, C, and D. E is the same magnification as in B, and F is the same magnification as that shown in C. Squamous differentiation in the haematoxylin and eosin stained adjacent sections is visualized as a characteristic "pearling" pattern where epithelial tumor cells (purple) differentiate into keratinocytes (pink) before denucleating and sloughing off into the inner lumen (white). Thus cells on the outer margin of the pearled area are undergoing squamous differentiation, and those correspond to cells expressing mouse S100A7/psoriasin RNA, in A, B, and C. |
PMC553966_F6_1399.jpg | What does this image primarily show? | A Strong focal expression of mouse S100A7/psoriasin RNA in mammary gland tumors compared to little expression in matched normal mammary gland tissue using in situ hybridization Sections from formalin fixed paraffin-embedded mammary tissue samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression: A, C, D, F show hybridization with mouse S100A7/psoriasin 35S-labeled antisense cRNA; B, E show hybridization with mouse S100A7/psoriasin 35S-labeled sense cRNA. A = high magnification (400X) section of normal mammary gland, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = high magnification (400X) adjacent section to A hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C = low magnification (100X) of section from the matched DMBA mammary tumor from same animal shown in A hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. D = higher magnification (400X) of C. E = high magnification (400X) of adjacent section from the same mammary tumor shown in D, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. F = low magnification (100X) of a single tissue section (tissue from a different mouse to that shown in A-E)) hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, where strong focal expression of mouse S100A7/psoriasin RNA is observed in the mammary gland tumor (black arrow) with little or no expression in the surrounding normal mammary gland tissue. B Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in DMBA-induced mammary gland tumors Sections from formalin fixed paraffin-embedded DMBA-induced mammary tumor samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A = low magnification (100X) of tumor section hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = higher magnification of A (200X), C = high magnification of B. D = adjacent section to that seen in A, B, C, and at same magnification as B but hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. E and F are haematoxylin and eosin stains of adjacent sections to that shown in A, B, C, and D. E is the same magnification as in B, and F is the same magnification as that shown in C. Squamous differentiation in the haematoxylin and eosin stained adjacent sections is visualized as a characteristic "pearling" pattern where epithelial tumor cells (purple) differentiate into keratinocytes (pink) before denucleating and sloughing off into the inner lumen (white). Thus cells on the outer margin of the pearled area are undergoing squamous differentiation, and those correspond to cells expressing mouse S100A7/psoriasin RNA, in A, B, and C. |
PMC553966_F6_1403.jpg | What's the most prominent thing you notice in this picture? | A Strong focal expression of mouse S100A7/psoriasin RNA in mammary gland tumors compared to little expression in matched normal mammary gland tissue using in situ hybridization Sections from formalin fixed paraffin-embedded mammary tissue samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression: A, C, D, F show hybridization with mouse S100A7/psoriasin 35S-labeled antisense cRNA; B, E show hybridization with mouse S100A7/psoriasin 35S-labeled sense cRNA. A = high magnification (400X) section of normal mammary gland, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = high magnification (400X) adjacent section to A hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C = low magnification (100X) of section from the matched DMBA mammary tumor from same animal shown in A hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. D = higher magnification (400X) of C. E = high magnification (400X) of adjacent section from the same mammary tumor shown in D, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. F = low magnification (100X) of a single tissue section (tissue from a different mouse to that shown in A-E)) hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, where strong focal expression of mouse S100A7/psoriasin RNA is observed in the mammary gland tumor (black arrow) with little or no expression in the surrounding normal mammary gland tissue. B Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in DMBA-induced mammary gland tumors Sections from formalin fixed paraffin-embedded DMBA-induced mammary tumor samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A = low magnification (100X) of tumor section hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = higher magnification of A (200X), C = high magnification of B. D = adjacent section to that seen in A, B, C, and at same magnification as B but hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. E and F are haematoxylin and eosin stains of adjacent sections to that shown in A, B, C, and D. E is the same magnification as in B, and F is the same magnification as that shown in C. Squamous differentiation in the haematoxylin and eosin stained adjacent sections is visualized as a characteristic "pearling" pattern where epithelial tumor cells (purple) differentiate into keratinocytes (pink) before denucleating and sloughing off into the inner lumen (white). Thus cells on the outer margin of the pearled area are undergoing squamous differentiation, and those correspond to cells expressing mouse S100A7/psoriasin RNA, in A, B, and C. |
PMC553966_F6_1402.jpg | What is the central feature of this picture? | A Strong focal expression of mouse S100A7/psoriasin RNA in mammary gland tumors compared to little expression in matched normal mammary gland tissue using in situ hybridization Sections from formalin fixed paraffin-embedded mammary tissue samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression: A, C, D, F show hybridization with mouse S100A7/psoriasin 35S-labeled antisense cRNA; B, E show hybridization with mouse S100A7/psoriasin 35S-labeled sense cRNA. A = high magnification (400X) section of normal mammary gland, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = high magnification (400X) adjacent section to A hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C = low magnification (100X) of section from the matched DMBA mammary tumor from same animal shown in A hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. D = higher magnification (400X) of C. E = high magnification (400X) of adjacent section from the same mammary tumor shown in D, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. F = low magnification (100X) of a single tissue section (tissue from a different mouse to that shown in A-E)) hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, where strong focal expression of mouse S100A7/psoriasin RNA is observed in the mammary gland tumor (black arrow) with little or no expression in the surrounding normal mammary gland tissue. B Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in DMBA-induced mammary gland tumors Sections from formalin fixed paraffin-embedded DMBA-induced mammary tumor samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A = low magnification (100X) of tumor section hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = higher magnification of A (200X), C = high magnification of B. D = adjacent section to that seen in A, B, C, and at same magnification as B but hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. E and F are haematoxylin and eosin stains of adjacent sections to that shown in A, B, C, and D. E is the same magnification as in B, and F is the same magnification as that shown in C. Squamous differentiation in the haematoxylin and eosin stained adjacent sections is visualized as a characteristic "pearling" pattern where epithelial tumor cells (purple) differentiate into keratinocytes (pink) before denucleating and sloughing off into the inner lumen (white). Thus cells on the outer margin of the pearled area are undergoing squamous differentiation, and those correspond to cells expressing mouse S100A7/psoriasin RNA, in A, B, and C. |
PMC553966_F6_1395.jpg | What key item or scene is captured in this photo? | A Strong focal expression of mouse S100A7/psoriasin RNA in mammary gland tumors compared to little expression in matched normal mammary gland tissue using in situ hybridization Sections from formalin fixed paraffin-embedded mammary tissue samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression: A, C, D, F show hybridization with mouse S100A7/psoriasin 35S-labeled antisense cRNA; B, E show hybridization with mouse S100A7/psoriasin 35S-labeled sense cRNA. A = high magnification (400X) section of normal mammary gland, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = high magnification (400X) adjacent section to A hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C = low magnification (100X) of section from the matched DMBA mammary tumor from same animal shown in A hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. D = higher magnification (400X) of C. E = high magnification (400X) of adjacent section from the same mammary tumor shown in D, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. F = low magnification (100X) of a single tissue section (tissue from a different mouse to that shown in A-E)) hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, where strong focal expression of mouse S100A7/psoriasin RNA is observed in the mammary gland tumor (black arrow) with little or no expression in the surrounding normal mammary gland tissue. B Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in DMBA-induced mammary gland tumors Sections from formalin fixed paraffin-embedded DMBA-induced mammary tumor samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A = low magnification (100X) of tumor section hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = higher magnification of A (200X), C = high magnification of B. D = adjacent section to that seen in A, B, C, and at same magnification as B but hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. E and F are haematoxylin and eosin stains of adjacent sections to that shown in A, B, C, and D. E is the same magnification as in B, and F is the same magnification as that shown in C. Squamous differentiation in the haematoxylin and eosin stained adjacent sections is visualized as a characteristic "pearling" pattern where epithelial tumor cells (purple) differentiate into keratinocytes (pink) before denucleating and sloughing off into the inner lumen (white). Thus cells on the outer margin of the pearled area are undergoing squamous differentiation, and those correspond to cells expressing mouse S100A7/psoriasin RNA, in A, B, and C. |
PMC553966_F6_1397.jpg | What object or scene is depicted here? | A Strong focal expression of mouse S100A7/psoriasin RNA in mammary gland tumors compared to little expression in matched normal mammary gland tissue using in situ hybridization Sections from formalin fixed paraffin-embedded mammary tissue samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression: A, C, D, F show hybridization with mouse S100A7/psoriasin 35S-labeled antisense cRNA; B, E show hybridization with mouse S100A7/psoriasin 35S-labeled sense cRNA. A = high magnification (400X) section of normal mammary gland, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = high magnification (400X) adjacent section to A hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C = low magnification (100X) of section from the matched DMBA mammary tumor from same animal shown in A hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. D = higher magnification (400X) of C. E = high magnification (400X) of adjacent section from the same mammary tumor shown in D, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. F = low magnification (100X) of a single tissue section (tissue from a different mouse to that shown in A-E)) hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, where strong focal expression of mouse S100A7/psoriasin RNA is observed in the mammary gland tumor (black arrow) with little or no expression in the surrounding normal mammary gland tissue. B Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in DMBA-induced mammary gland tumors Sections from formalin fixed paraffin-embedded DMBA-induced mammary tumor samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A = low magnification (100X) of tumor section hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = higher magnification of A (200X), C = high magnification of B. D = adjacent section to that seen in A, B, C, and at same magnification as B but hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. E and F are haematoxylin and eosin stains of adjacent sections to that shown in A, B, C, and D. E is the same magnification as in B, and F is the same magnification as that shown in C. Squamous differentiation in the haematoxylin and eosin stained adjacent sections is visualized as a characteristic "pearling" pattern where epithelial tumor cells (purple) differentiate into keratinocytes (pink) before denucleating and sloughing off into the inner lumen (white). Thus cells on the outer margin of the pearled area are undergoing squamous differentiation, and those correspond to cells expressing mouse S100A7/psoriasin RNA, in A, B, and C. |
PMC553966_F6_1394.jpg | What stands out most in this visual? | A Strong focal expression of mouse S100A7/psoriasin RNA in mammary gland tumors compared to little expression in matched normal mammary gland tissue using in situ hybridization Sections from formalin fixed paraffin-embedded mammary tissue samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression: A, C, D, F show hybridization with mouse S100A7/psoriasin 35S-labeled antisense cRNA; B, E show hybridization with mouse S100A7/psoriasin 35S-labeled sense cRNA. A = high magnification (400X) section of normal mammary gland, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = high magnification (400X) adjacent section to A hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C = low magnification (100X) of section from the matched DMBA mammary tumor from same animal shown in A hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. D = higher magnification (400X) of C. E = high magnification (400X) of adjacent section from the same mammary tumor shown in D, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. F = low magnification (100X) of a single tissue section (tissue from a different mouse to that shown in A-E)) hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, where strong focal expression of mouse S100A7/psoriasin RNA is observed in the mammary gland tumor (black arrow) with little or no expression in the surrounding normal mammary gland tissue. B Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in DMBA-induced mammary gland tumors Sections from formalin fixed paraffin-embedded DMBA-induced mammary tumor samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A = low magnification (100X) of tumor section hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = higher magnification of A (200X), C = high magnification of B. D = adjacent section to that seen in A, B, C, and at same magnification as B but hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. E and F are haematoxylin and eosin stains of adjacent sections to that shown in A, B, C, and D. E is the same magnification as in B, and F is the same magnification as that shown in C. Squamous differentiation in the haematoxylin and eosin stained adjacent sections is visualized as a characteristic "pearling" pattern where epithelial tumor cells (purple) differentiate into keratinocytes (pink) before denucleating and sloughing off into the inner lumen (white). Thus cells on the outer margin of the pearled area are undergoing squamous differentiation, and those correspond to cells expressing mouse S100A7/psoriasin RNA, in A, B, and C. |
PMC553966_F6_1400.jpg | What is the dominant medical problem in this image? | A Strong focal expression of mouse S100A7/psoriasin RNA in mammary gland tumors compared to little expression in matched normal mammary gland tissue using in situ hybridization Sections from formalin fixed paraffin-embedded mammary tissue samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression: A, C, D, F show hybridization with mouse S100A7/psoriasin 35S-labeled antisense cRNA; B, E show hybridization with mouse S100A7/psoriasin 35S-labeled sense cRNA. A = high magnification (400X) section of normal mammary gland, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = high magnification (400X) adjacent section to A hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C = low magnification (100X) of section from the matched DMBA mammary tumor from same animal shown in A hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. D = higher magnification (400X) of C. E = high magnification (400X) of adjacent section from the same mammary tumor shown in D, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. F = low magnification (100X) of a single tissue section (tissue from a different mouse to that shown in A-E)) hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, where strong focal expression of mouse S100A7/psoriasin RNA is observed in the mammary gland tumor (black arrow) with little or no expression in the surrounding normal mammary gland tissue. B Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in DMBA-induced mammary gland tumors Sections from formalin fixed paraffin-embedded DMBA-induced mammary tumor samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A = low magnification (100X) of tumor section hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = higher magnification of A (200X), C = high magnification of B. D = adjacent section to that seen in A, B, C, and at same magnification as B but hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. E and F are haematoxylin and eosin stains of adjacent sections to that shown in A, B, C, and D. E is the same magnification as in B, and F is the same magnification as that shown in C. Squamous differentiation in the haematoxylin and eosin stained adjacent sections is visualized as a characteristic "pearling" pattern where epithelial tumor cells (purple) differentiate into keratinocytes (pink) before denucleating and sloughing off into the inner lumen (white). Thus cells on the outer margin of the pearled area are undergoing squamous differentiation, and those correspond to cells expressing mouse S100A7/psoriasin RNA, in A, B, and C. |
PMC553966_F6_1401.jpg | Describe the main subject of this image. | A Strong focal expression of mouse S100A7/psoriasin RNA in mammary gland tumors compared to little expression in matched normal mammary gland tissue using in situ hybridization Sections from formalin fixed paraffin-embedded mammary tissue samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression: A, C, D, F show hybridization with mouse S100A7/psoriasin 35S-labeled antisense cRNA; B, E show hybridization with mouse S100A7/psoriasin 35S-labeled sense cRNA. A = high magnification (400X) section of normal mammary gland, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = high magnification (400X) adjacent section to A hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C = low magnification (100X) of section from the matched DMBA mammary tumor from same animal shown in A hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. D = higher magnification (400X) of C. E = high magnification (400X) of adjacent section from the same mammary tumor shown in D, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. F = low magnification (100X) of a single tissue section (tissue from a different mouse to that shown in A-E)) hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, where strong focal expression of mouse S100A7/psoriasin RNA is observed in the mammary gland tumor (black arrow) with little or no expression in the surrounding normal mammary gland tissue. B Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in DMBA-induced mammary gland tumors Sections from formalin fixed paraffin-embedded DMBA-induced mammary tumor samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A = low magnification (100X) of tumor section hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. B = higher magnification of A (200X), C = high magnification of B. D = adjacent section to that seen in A, B, C, and at same magnification as B but hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. E and F are haematoxylin and eosin stains of adjacent sections to that shown in A, B, C, and D. E is the same magnification as in B, and F is the same magnification as that shown in C. Squamous differentiation in the haematoxylin and eosin stained adjacent sections is visualized as a characteristic "pearling" pattern where epithelial tumor cells (purple) differentiate into keratinocytes (pink) before denucleating and sloughing off into the inner lumen (white). Thus cells on the outer margin of the pearled area are undergoing squamous differentiation, and those correspond to cells expressing mouse S100A7/psoriasin RNA, in A, B, and C. |
PMC553966_F7_1393.jpg | What can you see in this picture? | A Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in skin Sections from formalin fixed paraffin-embedded normal mouse skin samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A, B, C increasing magnifications (original is 200X) of sections hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, showing strong focal expression of mouse S100A7/psoriasin RNA in a particular subset of cells surrounding the hair shafts, which are associated with squamous differentiation. D, adjacent section hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. B Upregulation of mouse S100A7/psoriasin expression in a model of skin inflammation Sections from formalin fixed paraffin-embedded mouse skin tissue at 0 mins and 24 hours after croton application to the tail skin as described in Materials and Methods. A and D, haematoxylin and eosin stained sections, from 0 and 24 hr treated skin, respectively. B and E adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C and F, adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. |
PMC553966_F7_1392.jpg | What key item or scene is captured in this photo? | A Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in skin Sections from formalin fixed paraffin-embedded normal mouse skin samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A, B, C increasing magnifications (original is 200X) of sections hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, showing strong focal expression of mouse S100A7/psoriasin RNA in a particular subset of cells surrounding the hair shafts, which are associated with squamous differentiation. D, adjacent section hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. B Upregulation of mouse S100A7/psoriasin expression in a model of skin inflammation Sections from formalin fixed paraffin-embedded mouse skin tissue at 0 mins and 24 hours after croton application to the tail skin as described in Materials and Methods. A and D, haematoxylin and eosin stained sections, from 0 and 24 hr treated skin, respectively. B and E adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C and F, adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. |
PMC553966_F7_1389.jpg | What is the central feature of this picture? | A Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in skin Sections from formalin fixed paraffin-embedded normal mouse skin samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A, B, C increasing magnifications (original is 200X) of sections hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, showing strong focal expression of mouse S100A7/psoriasin RNA in a particular subset of cells surrounding the hair shafts, which are associated with squamous differentiation. D, adjacent section hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. B Upregulation of mouse S100A7/psoriasin expression in a model of skin inflammation Sections from formalin fixed paraffin-embedded mouse skin tissue at 0 mins and 24 hours after croton application to the tail skin as described in Materials and Methods. A and D, haematoxylin and eosin stained sections, from 0 and 24 hr treated skin, respectively. B and E adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C and F, adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. |
PMC553966_F7_1388.jpg | What can you see in this picture? | A Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in skin Sections from formalin fixed paraffin-embedded normal mouse skin samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A, B, C increasing magnifications (original is 200X) of sections hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, showing strong focal expression of mouse S100A7/psoriasin RNA in a particular subset of cells surrounding the hair shafts, which are associated with squamous differentiation. D, adjacent section hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. B Upregulation of mouse S100A7/psoriasin expression in a model of skin inflammation Sections from formalin fixed paraffin-embedded mouse skin tissue at 0 mins and 24 hours after croton application to the tail skin as described in Materials and Methods. A and D, haematoxylin and eosin stained sections, from 0 and 24 hr treated skin, respectively. B and E adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C and F, adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. |
PMC553966_F7_1391.jpg | What's the most prominent thing you notice in this picture? | A Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in skin Sections from formalin fixed paraffin-embedded normal mouse skin samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A, B, C increasing magnifications (original is 200X) of sections hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, showing strong focal expression of mouse S100A7/psoriasin RNA in a particular subset of cells surrounding the hair shafts, which are associated with squamous differentiation. D, adjacent section hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. B Upregulation of mouse S100A7/psoriasin expression in a model of skin inflammation Sections from formalin fixed paraffin-embedded mouse skin tissue at 0 mins and 24 hours after croton application to the tail skin as described in Materials and Methods. A and D, haematoxylin and eosin stained sections, from 0 and 24 hr treated skin, respectively. B and E adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C and F, adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. |
PMC553966_F7_1387.jpg | What is the dominant medical problem in this image? | A Localization of mouse S100A7/psoriasin expression to areas of squamous differentiation in skin Sections from formalin fixed paraffin-embedded normal mouse skin samples matched to the frozen tissue from which RNA was previously isolated for RT-PCR analysis were used for in situ hybridization analysis of mouse S100A7/psoriasin expression. A, B, C increasing magnifications (original is 200X) of sections hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA, showing strong focal expression of mouse S100A7/psoriasin RNA in a particular subset of cells surrounding the hair shafts, which are associated with squamous differentiation. D, adjacent section hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. B Upregulation of mouse S100A7/psoriasin expression in a model of skin inflammation Sections from formalin fixed paraffin-embedded mouse skin tissue at 0 mins and 24 hours after croton application to the tail skin as described in Materials and Methods. A and D, haematoxylin and eosin stained sections, from 0 and 24 hr treated skin, respectively. B and E adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled sense cRNA. C and F, adjacent sections from 0 and 24 hr croton oil treated skin, respectively, hybridized with mouse S100A7/psoriasin 35S-labeled antisense cRNA. |
PMC554094_F4_1421.jpg | What key item or scene is captured in this photo? | Different aspects of collateral compensation in presence of the same occlusive pattern of LAD. A, relatively few very enlarged collaterals and (B) numerous relatively small collaterals. This divergency may be due to progressive atherosclerotic obstruction of other main vessels or lost of the intramural vasculature, including collaterals, following an infarct. Chart C shows all the possibilities of flow redistribution. The histology of the enlarged anastomoses corresponds to a capillar-like wall, even in the rare extramural collaterals with rudimentary focal tunica media (C). D), enlarged collaterals in a case of anomalous origin of LAD from the pulmonary artery and (E,G) different aspects of giant capillaries (or plexus) in various stages of an acute/old infarction. The absence of new vessel formation is well documented in recent infarcts associated with endocardial thrombus (G). In the latter numerous new vessels form in the granulation tissue repair of the thrombus in contrast to their absence in infarct (arrow; postmortem coronary injection for vessels identification). |
PMC554094_F4_1418.jpg | What is the principal component of this image? | Different aspects of collateral compensation in presence of the same occlusive pattern of LAD. A, relatively few very enlarged collaterals and (B) numerous relatively small collaterals. This divergency may be due to progressive atherosclerotic obstruction of other main vessels or lost of the intramural vasculature, including collaterals, following an infarct. Chart C shows all the possibilities of flow redistribution. The histology of the enlarged anastomoses corresponds to a capillar-like wall, even in the rare extramural collaterals with rudimentary focal tunica media (C). D), enlarged collaterals in a case of anomalous origin of LAD from the pulmonary artery and (E,G) different aspects of giant capillaries (or plexus) in various stages of an acute/old infarction. The absence of new vessel formation is well documented in recent infarcts associated with endocardial thrombus (G). In the latter numerous new vessels form in the granulation tissue repair of the thrombus in contrast to their absence in infarct (arrow; postmortem coronary injection for vessels identification). |
PMC554094_F4_1424.jpg | What object or scene is depicted here? | Different aspects of collateral compensation in presence of the same occlusive pattern of LAD. A, relatively few very enlarged collaterals and (B) numerous relatively small collaterals. This divergency may be due to progressive atherosclerotic obstruction of other main vessels or lost of the intramural vasculature, including collaterals, following an infarct. Chart C shows all the possibilities of flow redistribution. The histology of the enlarged anastomoses corresponds to a capillar-like wall, even in the rare extramural collaterals with rudimentary focal tunica media (C). D), enlarged collaterals in a case of anomalous origin of LAD from the pulmonary artery and (E,G) different aspects of giant capillaries (or plexus) in various stages of an acute/old infarction. The absence of new vessel formation is well documented in recent infarcts associated with endocardial thrombus (G). In the latter numerous new vessels form in the granulation tissue repair of the thrombus in contrast to their absence in infarct (arrow; postmortem coronary injection for vessels identification). |
PMC554094_F4_1419.jpg | What stands out most in this visual? | Different aspects of collateral compensation in presence of the same occlusive pattern of LAD. A, relatively few very enlarged collaterals and (B) numerous relatively small collaterals. This divergency may be due to progressive atherosclerotic obstruction of other main vessels or lost of the intramural vasculature, including collaterals, following an infarct. Chart C shows all the possibilities of flow redistribution. The histology of the enlarged anastomoses corresponds to a capillar-like wall, even in the rare extramural collaterals with rudimentary focal tunica media (C). D), enlarged collaterals in a case of anomalous origin of LAD from the pulmonary artery and (E,G) different aspects of giant capillaries (or plexus) in various stages of an acute/old infarction. The absence of new vessel formation is well documented in recent infarcts associated with endocardial thrombus (G). In the latter numerous new vessels form in the granulation tissue repair of the thrombus in contrast to their absence in infarct (arrow; postmortem coronary injection for vessels identification). |
PMC554094_F4_1417.jpg | What key item or scene is captured in this photo? | Different aspects of collateral compensation in presence of the same occlusive pattern of LAD. A, relatively few very enlarged collaterals and (B) numerous relatively small collaterals. This divergency may be due to progressive atherosclerotic obstruction of other main vessels or lost of the intramural vasculature, including collaterals, following an infarct. Chart C shows all the possibilities of flow redistribution. The histology of the enlarged anastomoses corresponds to a capillar-like wall, even in the rare extramural collaterals with rudimentary focal tunica media (C). D), enlarged collaterals in a case of anomalous origin of LAD from the pulmonary artery and (E,G) different aspects of giant capillaries (or plexus) in various stages of an acute/old infarction. The absence of new vessel formation is well documented in recent infarcts associated with endocardial thrombus (G). In the latter numerous new vessels form in the granulation tissue repair of the thrombus in contrast to their absence in infarct (arrow; postmortem coronary injection for vessels identification). |
PMC554094_F4_1422.jpg | What does this image primarily show? | Different aspects of collateral compensation in presence of the same occlusive pattern of LAD. A, relatively few very enlarged collaterals and (B) numerous relatively small collaterals. This divergency may be due to progressive atherosclerotic obstruction of other main vessels or lost of the intramural vasculature, including collaterals, following an infarct. Chart C shows all the possibilities of flow redistribution. The histology of the enlarged anastomoses corresponds to a capillar-like wall, even in the rare extramural collaterals with rudimentary focal tunica media (C). D), enlarged collaterals in a case of anomalous origin of LAD from the pulmonary artery and (E,G) different aspects of giant capillaries (or plexus) in various stages of an acute/old infarction. The absence of new vessel formation is well documented in recent infarcts associated with endocardial thrombus (G). In the latter numerous new vessels form in the granulation tissue repair of the thrombus in contrast to their absence in infarct (arrow; postmortem coronary injection for vessels identification). |
PMC554094_F4_1423.jpg | What key item or scene is captured in this photo? | Different aspects of collateral compensation in presence of the same occlusive pattern of LAD. A, relatively few very enlarged collaterals and (B) numerous relatively small collaterals. This divergency may be due to progressive atherosclerotic obstruction of other main vessels or lost of the intramural vasculature, including collaterals, following an infarct. Chart C shows all the possibilities of flow redistribution. The histology of the enlarged anastomoses corresponds to a capillar-like wall, even in the rare extramural collaterals with rudimentary focal tunica media (C). D), enlarged collaterals in a case of anomalous origin of LAD from the pulmonary artery and (E,G) different aspects of giant capillaries (or plexus) in various stages of an acute/old infarction. The absence of new vessel formation is well documented in recent infarcts associated with endocardial thrombus (G). In the latter numerous new vessels form in the granulation tissue repair of the thrombus in contrast to their absence in infarct (arrow; postmortem coronary injection for vessels identification). |
PMC554094_F5_1414.jpg | What is the focal point of this photograph? | Avascular area of an infarct. By plastic cast (A anterior, B posterior view) or postmortem angiogram (C) the infarcted zone (arrow) lacks of intramural vessel injection ("avascular area"). Stretching of the necrotic myocardium and secondary vascular damage with wall degeneration and thrombosis (D), explain this vascular "sequestration" which occurs in early phase. This may indicate a blockage without possibility of therapeutical intervention via blood flow within the infarcted myocardium. Note that the avascular area in this AMI case documented histologically, depended from LAD without evidence of occlusion or severe stenosis. The occluded vessel (arrow) was (B) the RCA, the distal part of which was filled by numerous anastomoses. No myocardial damage was seen in its territory. By dissection even an expert pathologist, the diagnosis could be of myocardial infarction following occlusion of the RCA. E) obliterative intimal hyperplasia in arterioles around a seven days old infarct with early repair process. |
PMC554094_F5_1416.jpg | What stands out most in this visual? | Avascular area of an infarct. By plastic cast (A anterior, B posterior view) or postmortem angiogram (C) the infarcted zone (arrow) lacks of intramural vessel injection ("avascular area"). Stretching of the necrotic myocardium and secondary vascular damage with wall degeneration and thrombosis (D), explain this vascular "sequestration" which occurs in early phase. This may indicate a blockage without possibility of therapeutical intervention via blood flow within the infarcted myocardium. Note that the avascular area in this AMI case documented histologically, depended from LAD without evidence of occlusion or severe stenosis. The occluded vessel (arrow) was (B) the RCA, the distal part of which was filled by numerous anastomoses. No myocardial damage was seen in its territory. By dissection even an expert pathologist, the diagnosis could be of myocardial infarction following occlusion of the RCA. E) obliterative intimal hyperplasia in arterioles around a seven days old infarct with early repair process. |
PMC554094_F5_1412.jpg | What stands out most in this visual? | Avascular area of an infarct. By plastic cast (A anterior, B posterior view) or postmortem angiogram (C) the infarcted zone (arrow) lacks of intramural vessel injection ("avascular area"). Stretching of the necrotic myocardium and secondary vascular damage with wall degeneration and thrombosis (D), explain this vascular "sequestration" which occurs in early phase. This may indicate a blockage without possibility of therapeutical intervention via blood flow within the infarcted myocardium. Note that the avascular area in this AMI case documented histologically, depended from LAD without evidence of occlusion or severe stenosis. The occluded vessel (arrow) was (B) the RCA, the distal part of which was filled by numerous anastomoses. No myocardial damage was seen in its territory. By dissection even an expert pathologist, the diagnosis could be of myocardial infarction following occlusion of the RCA. E) obliterative intimal hyperplasia in arterioles around a seven days old infarct with early repair process. |
PMC554094_F5_1415.jpg | What is the dominant medical problem in this image? | Avascular area of an infarct. By plastic cast (A anterior, B posterior view) or postmortem angiogram (C) the infarcted zone (arrow) lacks of intramural vessel injection ("avascular area"). Stretching of the necrotic myocardium and secondary vascular damage with wall degeneration and thrombosis (D), explain this vascular "sequestration" which occurs in early phase. This may indicate a blockage without possibility of therapeutical intervention via blood flow within the infarcted myocardium. Note that the avascular area in this AMI case documented histologically, depended from LAD without evidence of occlusion or severe stenosis. The occluded vessel (arrow) was (B) the RCA, the distal part of which was filled by numerous anastomoses. No myocardial damage was seen in its territory. By dissection even an expert pathologist, the diagnosis could be of myocardial infarction following occlusion of the RCA. E) obliterative intimal hyperplasia in arterioles around a seven days old infarct with early repair process. |
PMC554094_F5_1411.jpg | What stands out most in this visual? | Avascular area of an infarct. By plastic cast (A anterior, B posterior view) or postmortem angiogram (C) the infarcted zone (arrow) lacks of intramural vessel injection ("avascular area"). Stretching of the necrotic myocardium and secondary vascular damage with wall degeneration and thrombosis (D), explain this vascular "sequestration" which occurs in early phase. This may indicate a blockage without possibility of therapeutical intervention via blood flow within the infarcted myocardium. Note that the avascular area in this AMI case documented histologically, depended from LAD without evidence of occlusion or severe stenosis. The occluded vessel (arrow) was (B) the RCA, the distal part of which was filled by numerous anastomoses. No myocardial damage was seen in its territory. By dissection even an expert pathologist, the diagnosis could be of myocardial infarction following occlusion of the RCA. E) obliterative intimal hyperplasia in arterioles around a seven days old infarct with early repair process. |
PMC554094_F7_1407.jpg | What object or scene is depicted here? | Cineangiographic monitoring in a patient with non occlusive LAD stenosis (A) who developed an extensive infarct without angiographic occlusion. The subsequent imaging of occlusion began distally (B) and ascended to the origin (C) of the vessel (arrow) indicating that the angiographic "pseudocclusion" was due to stasis for increased peripheral resistance and not for primitive thrombosis, not shown morphologically (see text). |
PMC554094_F7_1408.jpg | What key item or scene is captured in this photo? | Cineangiographic monitoring in a patient with non occlusive LAD stenosis (A) who developed an extensive infarct without angiographic occlusion. The subsequent imaging of occlusion began distally (B) and ascended to the origin (C) of the vessel (arrow) indicating that the angiographic "pseudocclusion" was due to stasis for increased peripheral resistance and not for primitive thrombosis, not shown morphologically (see text). |
PMC554094_F7_1410.jpg | Describe the main subject of this image. | Cineangiographic monitoring in a patient with non occlusive LAD stenosis (A) who developed an extensive infarct without angiographic occlusion. The subsequent imaging of occlusion began distally (B) and ascended to the origin (C) of the vessel (arrow) indicating that the angiographic "pseudocclusion" was due to stasis for increased peripheral resistance and not for primitive thrombosis, not shown morphologically (see text). |
PMC554097_F3_1429.jpg | What key item or scene is captured in this photo? | Cytokinesis failure does not significantly delay the exit frommitosis. (A) Images from time-lapse series of HDF cells at the indicated times after release from nocodazole-mediated mitotic arrest. "Control" cells were not treated with blebbistatin; "Blebbistatin" cells were treated with blebbistatin beginning at 30 min after release from nocodazole. (B) MPM-2 immunofluorescence as a marker for mitotic exit. Fluorescence image of a mitotic cell with condensed DNA and intense MPM-2 staining (top) and a cytokinetic cell with decondensed DNA and diminished MPM-2 staining (bottom). DNA, blue; MPM-2, green. Scale bar represents 10 μm. (C) Mitotic index of control and blebbistatin-treated cells after mitotic release. "Control" cells were not treated with blebbistatin; "Blebbistatin" cells were treated with blebbistatin beginning at 30 min after release from nocodazole. Mitotic index was determined by MPM-2 staining and DNA morphology, as in (B). For each point n = 100 cells. |
PMC554097_F3_1426.jpg | What is the dominant medical problem in this image? | Cytokinesis failure does not significantly delay the exit frommitosis. (A) Images from time-lapse series of HDF cells at the indicated times after release from nocodazole-mediated mitotic arrest. "Control" cells were not treated with blebbistatin; "Blebbistatin" cells were treated with blebbistatin beginning at 30 min after release from nocodazole. (B) MPM-2 immunofluorescence as a marker for mitotic exit. Fluorescence image of a mitotic cell with condensed DNA and intense MPM-2 staining (top) and a cytokinetic cell with decondensed DNA and diminished MPM-2 staining (bottom). DNA, blue; MPM-2, green. Scale bar represents 10 μm. (C) Mitotic index of control and blebbistatin-treated cells after mitotic release. "Control" cells were not treated with blebbistatin; "Blebbistatin" cells were treated with blebbistatin beginning at 30 min after release from nocodazole. Mitotic index was determined by MPM-2 staining and DNA morphology, as in (B). For each point n = 100 cells. |
PMC554097_F3_1427.jpg | What is the main focus of this visual representation? | Cytokinesis failure does not significantly delay the exit frommitosis. (A) Images from time-lapse series of HDF cells at the indicated times after release from nocodazole-mediated mitotic arrest. "Control" cells were not treated with blebbistatin; "Blebbistatin" cells were treated with blebbistatin beginning at 30 min after release from nocodazole. (B) MPM-2 immunofluorescence as a marker for mitotic exit. Fluorescence image of a mitotic cell with condensed DNA and intense MPM-2 staining (top) and a cytokinetic cell with decondensed DNA and diminished MPM-2 staining (bottom). DNA, blue; MPM-2, green. Scale bar represents 10 μm. (C) Mitotic index of control and blebbistatin-treated cells after mitotic release. "Control" cells were not treated with blebbistatin; "Blebbistatin" cells were treated with blebbistatin beginning at 30 min after release from nocodazole. Mitotic index was determined by MPM-2 staining and DNA morphology, as in (B). For each point n = 100 cells. |
PMC554097_F3_1425.jpg | Can you identify the primary element in this image? | Cytokinesis failure does not significantly delay the exit frommitosis. (A) Images from time-lapse series of HDF cells at the indicated times after release from nocodazole-mediated mitotic arrest. "Control" cells were not treated with blebbistatin; "Blebbistatin" cells were treated with blebbistatin beginning at 30 min after release from nocodazole. (B) MPM-2 immunofluorescence as a marker for mitotic exit. Fluorescence image of a mitotic cell with condensed DNA and intense MPM-2 staining (top) and a cytokinetic cell with decondensed DNA and diminished MPM-2 staining (bottom). DNA, blue; MPM-2, green. Scale bar represents 10 μm. (C) Mitotic index of control and blebbistatin-treated cells after mitotic release. "Control" cells were not treated with blebbistatin; "Blebbistatin" cells were treated with blebbistatin beginning at 30 min after release from nocodazole. Mitotic index was determined by MPM-2 staining and DNA morphology, as in (B). For each point n = 100 cells. |
PMC554979_F1_1431.jpg | What is being portrayed in this visual content? | Immunohistochemistry for CD8 and CXCR3 in lung biopsy from HP patient. Most lymphocytes positive for CD8 (panel a) and CXCR3 (panel b) were clearly visible in a subpleural focus. Original Magnification × 25. |
PMC554979_F1_1430.jpg | Can you identify the primary element in this image? | Immunohistochemistry for CD8 and CXCR3 in lung biopsy from HP patient. Most lymphocytes positive for CD8 (panel a) and CXCR3 (panel b) were clearly visible in a subpleural focus. Original Magnification × 25. |
PMC554981_F3_1439.jpg | What object or scene is depicted here? | Confocal microscopy analysis of survivin 2α sub-cellular localization. HeLa cells were transfected with GFP-survivin 2α or HcRed survivin, as detailed on the top of the figure. Green pixels correspond to GFP expression, red pixels correspond to HcRed expression and blue pixels represent DNA labeled with Hoechst dye. When co-localization of GFP and HcRed occurs the pixels are yellow. A: Expression of survivin 2α at interphase localizes to nuclear and cytoplasmic structures. B: During M-phase survivin 2α is excluded from the condensed/dividing chromosomes and is localized in the cytoplasm of the dividing cell. C, D, E, F: When co-expressed with survivin, survivin 2α localization does not change at interphase. During M-phase survivin 2α co-localizes with survivin to the centromeres of the dividing chromosomes (D and E), and in the midbody region at cytokinesis (F). Scale bar = 5 μm |
PMC554981_F3_1440.jpg | What is being portrayed in this visual content? | Confocal microscopy analysis of survivin 2α sub-cellular localization. HeLa cells were transfected with GFP-survivin 2α or HcRed survivin, as detailed on the top of the figure. Green pixels correspond to GFP expression, red pixels correspond to HcRed expression and blue pixels represent DNA labeled with Hoechst dye. When co-localization of GFP and HcRed occurs the pixels are yellow. A: Expression of survivin 2α at interphase localizes to nuclear and cytoplasmic structures. B: During M-phase survivin 2α is excluded from the condensed/dividing chromosomes and is localized in the cytoplasm of the dividing cell. C, D, E, F: When co-expressed with survivin, survivin 2α localization does not change at interphase. During M-phase survivin 2α co-localizes with survivin to the centromeres of the dividing chromosomes (D and E), and in the midbody region at cytokinesis (F). Scale bar = 5 μm |
PMC554981_F3_1441.jpg | What key item or scene is captured in this photo? | Confocal microscopy analysis of survivin 2α sub-cellular localization. HeLa cells were transfected with GFP-survivin 2α or HcRed survivin, as detailed on the top of the figure. Green pixels correspond to GFP expression, red pixels correspond to HcRed expression and blue pixels represent DNA labeled with Hoechst dye. When co-localization of GFP and HcRed occurs the pixels are yellow. A: Expression of survivin 2α at interphase localizes to nuclear and cytoplasmic structures. B: During M-phase survivin 2α is excluded from the condensed/dividing chromosomes and is localized in the cytoplasm of the dividing cell. C, D, E, F: When co-expressed with survivin, survivin 2α localization does not change at interphase. During M-phase survivin 2α co-localizes with survivin to the centromeres of the dividing chromosomes (D and E), and in the midbody region at cytokinesis (F). Scale bar = 5 μm |
PMC554981_F3_1434.jpg | What is the core subject represented in this visual? | Confocal microscopy analysis of survivin 2α sub-cellular localization. HeLa cells were transfected with GFP-survivin 2α or HcRed survivin, as detailed on the top of the figure. Green pixels correspond to GFP expression, red pixels correspond to HcRed expression and blue pixels represent DNA labeled with Hoechst dye. When co-localization of GFP and HcRed occurs the pixels are yellow. A: Expression of survivin 2α at interphase localizes to nuclear and cytoplasmic structures. B: During M-phase survivin 2α is excluded from the condensed/dividing chromosomes and is localized in the cytoplasm of the dividing cell. C, D, E, F: When co-expressed with survivin, survivin 2α localization does not change at interphase. During M-phase survivin 2α co-localizes with survivin to the centromeres of the dividing chromosomes (D and E), and in the midbody region at cytokinesis (F). Scale bar = 5 μm |
PMC554981_F3_1433.jpg | What is shown in this image? | Confocal microscopy analysis of survivin 2α sub-cellular localization. HeLa cells were transfected with GFP-survivin 2α or HcRed survivin, as detailed on the top of the figure. Green pixels correspond to GFP expression, red pixels correspond to HcRed expression and blue pixels represent DNA labeled with Hoechst dye. When co-localization of GFP and HcRed occurs the pixels are yellow. A: Expression of survivin 2α at interphase localizes to nuclear and cytoplasmic structures. B: During M-phase survivin 2α is excluded from the condensed/dividing chromosomes and is localized in the cytoplasm of the dividing cell. C, D, E, F: When co-expressed with survivin, survivin 2α localization does not change at interphase. During M-phase survivin 2α co-localizes with survivin to the centromeres of the dividing chromosomes (D and E), and in the midbody region at cytokinesis (F). Scale bar = 5 μm |
PMC554981_F3_1437.jpg | What is the core subject represented in this visual? | Confocal microscopy analysis of survivin 2α sub-cellular localization. HeLa cells were transfected with GFP-survivin 2α or HcRed survivin, as detailed on the top of the figure. Green pixels correspond to GFP expression, red pixels correspond to HcRed expression and blue pixels represent DNA labeled with Hoechst dye. When co-localization of GFP and HcRed occurs the pixels are yellow. A: Expression of survivin 2α at interphase localizes to nuclear and cytoplasmic structures. B: During M-phase survivin 2α is excluded from the condensed/dividing chromosomes and is localized in the cytoplasm of the dividing cell. C, D, E, F: When co-expressed with survivin, survivin 2α localization does not change at interphase. During M-phase survivin 2α co-localizes with survivin to the centromeres of the dividing chromosomes (D and E), and in the midbody region at cytokinesis (F). Scale bar = 5 μm |
PMC554981_F3_1436.jpg | What is the focal point of this photograph? | Confocal microscopy analysis of survivin 2α sub-cellular localization. HeLa cells were transfected with GFP-survivin 2α or HcRed survivin, as detailed on the top of the figure. Green pixels correspond to GFP expression, red pixels correspond to HcRed expression and blue pixels represent DNA labeled with Hoechst dye. When co-localization of GFP and HcRed occurs the pixels are yellow. A: Expression of survivin 2α at interphase localizes to nuclear and cytoplasmic structures. B: During M-phase survivin 2α is excluded from the condensed/dividing chromosomes and is localized in the cytoplasm of the dividing cell. C, D, E, F: When co-expressed with survivin, survivin 2α localization does not change at interphase. During M-phase survivin 2α co-localizes with survivin to the centromeres of the dividing chromosomes (D and E), and in the midbody region at cytokinesis (F). Scale bar = 5 μm |
PMC554989_F4_1450.jpg | Describe the main subject of this image. | Examination of width differences between automated and manual identified two outliers with relatively large differences. These are shown as two pairs. Note the uneven heterogeneous cell distribution in these cases, a result that is technical suboptimal and not desired, likely from an error in the excoriation (creation of clear channel). These are a poor sample pairs for technical reasons, and in retrospect domain expert still had no significant difference in preference of manual result over the automatic result. |
PMC554989_F4_1448.jpg | What object or scene is depicted here? | Examination of width differences between automated and manual identified two outliers with relatively large differences. These are shown as two pairs. Note the uneven heterogeneous cell distribution in these cases, a result that is technical suboptimal and not desired, likely from an error in the excoriation (creation of clear channel). These are a poor sample pairs for technical reasons, and in retrospect domain expert still had no significant difference in preference of manual result over the automatic result. |
PMC555542_F2_1452.jpg | What does this image primarily show? | Central microvessel count – VEGF. After scanning at low power (40×), the central area of the tumor was estimated. From this area, six high power (200×) fields were evaluated for each section. The average number of microvessels per high power field was determined and reported as CMC. |
PMC555542_F3_1451.jpg | What is the dominant medical problem in this image? | Highest microvessel count – VEGF. After scanning at low power (40×), three areas with the highest concentration of microvessels (vascular hot spots) were selected. Each area was evaluated with one high power (200×) field in such a way as to include the maximum number of microvessels. The highest value obtained among the three fields was reported as HMC. |
PMC555544_F2_1453.jpg | Describe the main subject of this image. | Computerized tomography showed a hypodense area in right lobe of liver with peripheral enhancement |
PMC555548_F2_1454.jpg | Describe the main subject of this image. | Photograph of HOLA plate, including DNA extraction method and expected results. Abbreviations: SS, homozygous susceptible. RR, homozygous resistant. RS, heterozygous. aLivak [14] extraction method bBallinger-Crabtree [15] extraction method cArtificially created heterozygote |
PMC555567_F1_1457.jpg | What is the core subject represented in this visual? | Preoperative CT scan. Preoperative coronal CT scan which shows a large bony tumor arising from the left ethmoid sinus with orbital and intracranial extension. |
PMC555567_F7_1464.jpg | What is shown in this image? | Postoperative CT. Postoperative CT scan of the patient showing total excision of the tumor and the presence of free temporalis graft in the ethmoid and sphenoid sinus (arrow). |
PMC555568_F1_1458.jpg | What object or scene is depicted here? | Chest radiograph demonstrating no obvious abnormality |
PMC555568_F2_1460.jpg | What is shown in this image? | CT scan of thorax and abdomen demonstrating the abnormal anatomy |
PMC555568_F2_1459.jpg | What is the main focus of this visual representation? | CT scan of thorax and abdomen demonstrating the abnormal anatomy |
PMC555568_F3_1461.jpg | What stands out most in this visual? | CT scan of thorax and abdomen demonstrating the abnormal anatomy |
PMC555568_F3_1462.jpg | What stands out most in this visual? | CT scan of thorax and abdomen demonstrating the abnormal anatomy |
PMC555568_F4_1466.jpg | What is the focal point of this photograph? | Three-dimensional CT reconstruction demonstrating the diaphragmatic defect |
PMC555568_F5_1465.jpg | What can you see in this picture? | Three-dimensional CT reconstruction demonstrating the diaphragmatic defect |
PMC555568_F6_1467.jpg | What is shown in this image? | Abdominal radiograph demonstrating the large colon present in the abdominal cavity |
PMC555739_F1_1469.jpg | What object or scene is depicted here? | Clusters of small round tumor cells showing rosette-like features in smear of fine needle aspiration specimen of DSRCT. |
PMC555745_F3_1473.jpg | What is the main focus of this visual representation? | Activation of mast cell and eosinophil in the colonic mucosa. Representative photomicrographs (10 for each mouse) were taken from colonic mucosa of naïve mice (Fig 3A, 3C) and sensitized mice (Fig 3B, 3D). Bars stand for ratio of degranulation that was calculated with the numbers of degranulated granules divided by the numbers of total granules of mast cells (Fig 3E) and eosinophils (Fig 3F). *, p < 0.05, compared with naïve controls. |
PMC555745_F3_1471.jpg | What is shown in this image? | Activation of mast cell and eosinophil in the colonic mucosa. Representative photomicrographs (10 for each mouse) were taken from colonic mucosa of naïve mice (Fig 3A, 3C) and sensitized mice (Fig 3B, 3D). Bars stand for ratio of degranulation that was calculated with the numbers of degranulated granules divided by the numbers of total granules of mast cells (Fig 3E) and eosinophils (Fig 3F). *, p < 0.05, compared with naïve controls. |
PMC555846_F1_1478.jpg | What is being portrayed in this visual content? | Cytopathic effect of ONYX-015 on GFP and HSP72 transfected glioma cells. Photographs (100× magnification) of RT2-GFP and RT2-HSP72 cells 96 hours after ONYX-015 infection at various dosages are represented. A – RT2-GFP cells mock infected with virus. B – RT2-HSP72 cells mock infected with virus. C – RT2-GFP cells infected at MOI of 100. D – RT2-HSP72 cells infected at MOI of 100. E – RT2-GFP cells infected at MOI of 300. F – RT2-HSP72 cells infected at MOI of 300. |
PMC555846_F1_1476.jpg | What is the dominant medical problem in this image? | Cytopathic effect of ONYX-015 on GFP and HSP72 transfected glioma cells. Photographs (100× magnification) of RT2-GFP and RT2-HSP72 cells 96 hours after ONYX-015 infection at various dosages are represented. A – RT2-GFP cells mock infected with virus. B – RT2-HSP72 cells mock infected with virus. C – RT2-GFP cells infected at MOI of 100. D – RT2-HSP72 cells infected at MOI of 100. E – RT2-GFP cells infected at MOI of 300. F – RT2-HSP72 cells infected at MOI of 300. |
PMC555846_F1_1477.jpg | What is the dominant medical problem in this image? | Cytopathic effect of ONYX-015 on GFP and HSP72 transfected glioma cells. Photographs (100× magnification) of RT2-GFP and RT2-HSP72 cells 96 hours after ONYX-015 infection at various dosages are represented. A – RT2-GFP cells mock infected with virus. B – RT2-HSP72 cells mock infected with virus. C – RT2-GFP cells infected at MOI of 100. D – RT2-HSP72 cells infected at MOI of 100. E – RT2-GFP cells infected at MOI of 300. F – RT2-HSP72 cells infected at MOI of 300. |
PMC555846_F1_1479.jpg | What can you see in this picture? | Cytopathic effect of ONYX-015 on GFP and HSP72 transfected glioma cells. Photographs (100× magnification) of RT2-GFP and RT2-HSP72 cells 96 hours after ONYX-015 infection at various dosages are represented. A – RT2-GFP cells mock infected with virus. B – RT2-HSP72 cells mock infected with virus. C – RT2-GFP cells infected at MOI of 100. D – RT2-HSP72 cells infected at MOI of 100. E – RT2-GFP cells infected at MOI of 300. F – RT2-HSP72 cells infected at MOI of 300. |
PMC555846_F1_1480.jpg | What is the main focus of this visual representation? | Cytopathic effect of ONYX-015 on GFP and HSP72 transfected glioma cells. Photographs (100× magnification) of RT2-GFP and RT2-HSP72 cells 96 hours after ONYX-015 infection at various dosages are represented. A – RT2-GFP cells mock infected with virus. B – RT2-HSP72 cells mock infected with virus. C – RT2-GFP cells infected at MOI of 100. D – RT2-HSP72 cells infected at MOI of 100. E – RT2-GFP cells infected at MOI of 300. F – RT2-HSP72 cells infected at MOI of 300. |
PMC555846_F1_1481.jpg | What object or scene is depicted here? | Cytopathic effect of ONYX-015 on GFP and HSP72 transfected glioma cells. Photographs (100× magnification) of RT2-GFP and RT2-HSP72 cells 96 hours after ONYX-015 infection at various dosages are represented. A – RT2-GFP cells mock infected with virus. B – RT2-HSP72 cells mock infected with virus. C – RT2-GFP cells infected at MOI of 100. D – RT2-HSP72 cells infected at MOI of 100. E – RT2-GFP cells infected at MOI of 300. F – RT2-HSP72 cells infected at MOI of 300. |
PMC555956_F1_1482.jpg | What is the central feature of this picture? | CK-positive cells detected after immunomagnetic enrichment of BM from breast cancer patients. One single cell and one 2-cell cluster is shown in a 400× magnification. |
PMC1043860_pbio-0030085-g005_1488.jpg | What is the central feature of this picture? | Target Specificity of miRNA Family Members(A) Diagrams of 3′ UTR conservation in six drosophilid genomes (horizontal black bars) and the location of predicted miRNA target sites. Above is the 3′ UTR of the myogenic transcription factor bagpipe (bap) showing the predicted target site for the Brd box miRNA family, miR-4 and miR-79 (black box below the UTR). Alignment of miR-4 and miR-79 illustrates that they share a similar seed sequence (except that mir-4 has one extra 5′ base) but have little 3′ end similarity. Below are the conserved sequences in the3′ UTRs of the pro-apoptotic genes grim and sickle. Predicted target sites for the K Box miRNAs miR-11, miR-2b, and miR-6 are shown below the UTR. Alignment of miR-11, miR-2b, and miR-6 illustrates that they share the same family motif but have little similarity in their 3′ ends.(B) The bagpipe (bap) 3′ UTR reporter gene is regulated by miR-4 and miR-79. Alignments of the two miRNAs to the predicted target site show good 8mer seed matches (left). Overexpression of miR-4 or miR-79 under ptcGal4 control downregulated the bagpipe 3′ UTR reporter (right).(C) Left: Alignment of K box miRNAs with the single predicted site in the grim 3′ UTR and regulation by overexpression of miR-2 (top), but not by miR-6 (middle) or miR-11 (bottom). Right: Alignment of K box miRNAs with the two predicted sites in the sickle 3′ UTR. Regulation by overexpression of miR-2 was strong (top), regulation by miR-6 was weaker (middle), and miR-11 had little effect (bottom).(D) Effect of clones of cells lacking dicer-1 on expression of UTR reporters for predicted miRNA-regulated genes. Mutant cells were marked by the absence of β-Gal expression (red). EGFP expression is shown in green. Both channels are shown separately below in black and white. Mutant clones are indicated by yellow arrows. Expression of a uniformly transcribed reporter construct lacking miRNA target sites was unaffected in dicer-1 mutant cells (first column). The UTR reporter for the bantam miRNA target hid was upregulated in the mutant cells (second column). The bagpipe (bap) UTR reporter was upregulated in dicer-1 clones (third column). The grim (fourth column) and sickle (fifth column) UTR reporters were upregulated. |
PMC1043860_pbio-0030085-g005_1489.jpg | What key item or scene is captured in this photo? | Target Specificity of miRNA Family Members(A) Diagrams of 3′ UTR conservation in six drosophilid genomes (horizontal black bars) and the location of predicted miRNA target sites. Above is the 3′ UTR of the myogenic transcription factor bagpipe (bap) showing the predicted target site for the Brd box miRNA family, miR-4 and miR-79 (black box below the UTR). Alignment of miR-4 and miR-79 illustrates that they share a similar seed sequence (except that mir-4 has one extra 5′ base) but have little 3′ end similarity. Below are the conserved sequences in the3′ UTRs of the pro-apoptotic genes grim and sickle. Predicted target sites for the K Box miRNAs miR-11, miR-2b, and miR-6 are shown below the UTR. Alignment of miR-11, miR-2b, and miR-6 illustrates that they share the same family motif but have little similarity in their 3′ ends.(B) The bagpipe (bap) 3′ UTR reporter gene is regulated by miR-4 and miR-79. Alignments of the two miRNAs to the predicted target site show good 8mer seed matches (left). Overexpression of miR-4 or miR-79 under ptcGal4 control downregulated the bagpipe 3′ UTR reporter (right).(C) Left: Alignment of K box miRNAs with the single predicted site in the grim 3′ UTR and regulation by overexpression of miR-2 (top), but not by miR-6 (middle) or miR-11 (bottom). Right: Alignment of K box miRNAs with the two predicted sites in the sickle 3′ UTR. Regulation by overexpression of miR-2 was strong (top), regulation by miR-6 was weaker (middle), and miR-11 had little effect (bottom).(D) Effect of clones of cells lacking dicer-1 on expression of UTR reporters for predicted miRNA-regulated genes. Mutant cells were marked by the absence of β-Gal expression (red). EGFP expression is shown in green. Both channels are shown separately below in black and white. Mutant clones are indicated by yellow arrows. Expression of a uniformly transcribed reporter construct lacking miRNA target sites was unaffected in dicer-1 mutant cells (first column). The UTR reporter for the bantam miRNA target hid was upregulated in the mutant cells (second column). The bagpipe (bap) UTR reporter was upregulated in dicer-1 clones (third column). The grim (fourth column) and sickle (fifth column) UTR reporters were upregulated. |
PMC1043860_pbio-0030085-g005_1485.jpg | What stands out most in this visual? | Target Specificity of miRNA Family Members(A) Diagrams of 3′ UTR conservation in six drosophilid genomes (horizontal black bars) and the location of predicted miRNA target sites. Above is the 3′ UTR of the myogenic transcription factor bagpipe (bap) showing the predicted target site for the Brd box miRNA family, miR-4 and miR-79 (black box below the UTR). Alignment of miR-4 and miR-79 illustrates that they share a similar seed sequence (except that mir-4 has one extra 5′ base) but have little 3′ end similarity. Below are the conserved sequences in the3′ UTRs of the pro-apoptotic genes grim and sickle. Predicted target sites for the K Box miRNAs miR-11, miR-2b, and miR-6 are shown below the UTR. Alignment of miR-11, miR-2b, and miR-6 illustrates that they share the same family motif but have little similarity in their 3′ ends.(B) The bagpipe (bap) 3′ UTR reporter gene is regulated by miR-4 and miR-79. Alignments of the two miRNAs to the predicted target site show good 8mer seed matches (left). Overexpression of miR-4 or miR-79 under ptcGal4 control downregulated the bagpipe 3′ UTR reporter (right).(C) Left: Alignment of K box miRNAs with the single predicted site in the grim 3′ UTR and regulation by overexpression of miR-2 (top), but not by miR-6 (middle) or miR-11 (bottom). Right: Alignment of K box miRNAs with the two predicted sites in the sickle 3′ UTR. Regulation by overexpression of miR-2 was strong (top), regulation by miR-6 was weaker (middle), and miR-11 had little effect (bottom).(D) Effect of clones of cells lacking dicer-1 on expression of UTR reporters for predicted miRNA-regulated genes. Mutant cells were marked by the absence of β-Gal expression (red). EGFP expression is shown in green. Both channels are shown separately below in black and white. Mutant clones are indicated by yellow arrows. Expression of a uniformly transcribed reporter construct lacking miRNA target sites was unaffected in dicer-1 mutant cells (first column). The UTR reporter for the bantam miRNA target hid was upregulated in the mutant cells (second column). The bagpipe (bap) UTR reporter was upregulated in dicer-1 clones (third column). The grim (fourth column) and sickle (fifth column) UTR reporters were upregulated. |
PMC1043860_pbio-0030085-g005_1486.jpg | What is the principal component of this image? | Target Specificity of miRNA Family Members(A) Diagrams of 3′ UTR conservation in six drosophilid genomes (horizontal black bars) and the location of predicted miRNA target sites. Above is the 3′ UTR of the myogenic transcription factor bagpipe (bap) showing the predicted target site for the Brd box miRNA family, miR-4 and miR-79 (black box below the UTR). Alignment of miR-4 and miR-79 illustrates that they share a similar seed sequence (except that mir-4 has one extra 5′ base) but have little 3′ end similarity. Below are the conserved sequences in the3′ UTRs of the pro-apoptotic genes grim and sickle. Predicted target sites for the K Box miRNAs miR-11, miR-2b, and miR-6 are shown below the UTR. Alignment of miR-11, miR-2b, and miR-6 illustrates that they share the same family motif but have little similarity in their 3′ ends.(B) The bagpipe (bap) 3′ UTR reporter gene is regulated by miR-4 and miR-79. Alignments of the two miRNAs to the predicted target site show good 8mer seed matches (left). Overexpression of miR-4 or miR-79 under ptcGal4 control downregulated the bagpipe 3′ UTR reporter (right).(C) Left: Alignment of K box miRNAs with the single predicted site in the grim 3′ UTR and regulation by overexpression of miR-2 (top), but not by miR-6 (middle) or miR-11 (bottom). Right: Alignment of K box miRNAs with the two predicted sites in the sickle 3′ UTR. Regulation by overexpression of miR-2 was strong (top), regulation by miR-6 was weaker (middle), and miR-11 had little effect (bottom).(D) Effect of clones of cells lacking dicer-1 on expression of UTR reporters for predicted miRNA-regulated genes. Mutant cells were marked by the absence of β-Gal expression (red). EGFP expression is shown in green. Both channels are shown separately below in black and white. Mutant clones are indicated by yellow arrows. Expression of a uniformly transcribed reporter construct lacking miRNA target sites was unaffected in dicer-1 mutant cells (first column). The UTR reporter for the bantam miRNA target hid was upregulated in the mutant cells (second column). The bagpipe (bap) UTR reporter was upregulated in dicer-1 clones (third column). The grim (fourth column) and sickle (fifth column) UTR reporters were upregulated. |
PMC1044835_pbio-0030079-g005_1493.jpg | What stands out most in this visual? | Significant Signal Changes in Subjects Receiving Explicit Instructions Compared to Subjects Receiving Implicit Instructions in the Three Tasks Versus RestThreshold of Z = 2.3 at voxel level and a cluster level corrected for the whole brain at p < 0.05. The two black arrows indicate two foci of activity in dorsal premotor cortex that are located deep in the sulci and thus not easily visible on the three-dimensional surface rendering. See Tables S3–S5 for coordinates of local maxima. |
PMC1044835_pbio-0030079-g005_1495.jpg | What does this image primarily show? | Significant Signal Changes in Subjects Receiving Explicit Instructions Compared to Subjects Receiving Implicit Instructions in the Three Tasks Versus RestThreshold of Z = 2.3 at voxel level and a cluster level corrected for the whole brain at p < 0.05. The two black arrows indicate two foci of activity in dorsal premotor cortex that are located deep in the sulci and thus not easily visible on the three-dimensional surface rendering. See Tables S3–S5 for coordinates of local maxima. |
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