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PMC1781526_F8_9033.jpg | What stands out most in this visual? | Distinguishing between an artifact and the subnucleolar heterogeneity of 15N-uridine incorporation. (a,b) Parallel quantitative mass images of (a) 12C14N- and (b) 12C15N- images of a fibroblast cultured in the presence of 15N-uridine. Ncl, nucleoli; NM, nuclear membrane. Field: 40 × 40 μm (image has been cropped); acquisition time 20 min. (c-e) High-resolution parallel mass images at 12C-, 12C14N- and 12C15N- of the large nucleolus seen in (a,b). Field: 8 × 8 μm; acquisition time 30 min. (c) 12C- image, arising from both tissue and embedding medium; the dark spot (red arrow) was caused by accidental exposure to a stationary high-intensity primary Cs+ ion beam. (d) 12C14N- image. (e) 12C15N- image, showing subnucleolar areas of low local 15N incorporation (white arrows). (f) Ratio of the (d) 12C14N- and (e) 12C15N- images; here, the 'dark spot' (red circle) is barely visible because the value of the 12C15N-/12C15N- ratio is close to that of the surrounding area. (g) HSI image of the 12C15N-/12C14N- ratio (the numerator has been multiplied by 10,000). The 'dark spot' isotope ratio is close to that of the surrounding area. Subnucleolar regions of low incorporation of 15N-uridine stand out in both the (f) ratio and the (g) HSI images. (h) Calibration with 15N-uridine. The graph shows the intranucleolar accumulation of 15N-uridine (measured as 12C15N-/12C14N- (experimental – control)/control) as a function of the concentration of 15N-uridine in the culture medium. |
PMC1781526_F8_9032.jpg | What is the main focus of this visual representation? | Distinguishing between an artifact and the subnucleolar heterogeneity of 15N-uridine incorporation. (a,b) Parallel quantitative mass images of (a) 12C14N- and (b) 12C15N- images of a fibroblast cultured in the presence of 15N-uridine. Ncl, nucleoli; NM, nuclear membrane. Field: 40 × 40 μm (image has been cropped); acquisition time 20 min. (c-e) High-resolution parallel mass images at 12C-, 12C14N- and 12C15N- of the large nucleolus seen in (a,b). Field: 8 × 8 μm; acquisition time 30 min. (c) 12C- image, arising from both tissue and embedding medium; the dark spot (red arrow) was caused by accidental exposure to a stationary high-intensity primary Cs+ ion beam. (d) 12C14N- image. (e) 12C15N- image, showing subnucleolar areas of low local 15N incorporation (white arrows). (f) Ratio of the (d) 12C14N- and (e) 12C15N- images; here, the 'dark spot' (red circle) is barely visible because the value of the 12C15N-/12C15N- ratio is close to that of the surrounding area. (g) HSI image of the 12C15N-/12C14N- ratio (the numerator has been multiplied by 10,000). The 'dark spot' isotope ratio is close to that of the surrounding area. Subnucleolar regions of low incorporation of 15N-uridine stand out in both the (f) ratio and the (g) HSI images. (h) Calibration with 15N-uridine. The graph shows the intranucleolar accumulation of 15N-uridine (measured as 12C15N-/12C14N- (experimental – control)/control) as a function of the concentration of 15N-uridine in the culture medium. |
PMC1781526_F8_9031.jpg | What is the core subject represented in this visual? | Distinguishing between an artifact and the subnucleolar heterogeneity of 15N-uridine incorporation. (a,b) Parallel quantitative mass images of (a) 12C14N- and (b) 12C15N- images of a fibroblast cultured in the presence of 15N-uridine. Ncl, nucleoli; NM, nuclear membrane. Field: 40 × 40 μm (image has been cropped); acquisition time 20 min. (c-e) High-resolution parallel mass images at 12C-, 12C14N- and 12C15N- of the large nucleolus seen in (a,b). Field: 8 × 8 μm; acquisition time 30 min. (c) 12C- image, arising from both tissue and embedding medium; the dark spot (red arrow) was caused by accidental exposure to a stationary high-intensity primary Cs+ ion beam. (d) 12C14N- image. (e) 12C15N- image, showing subnucleolar areas of low local 15N incorporation (white arrows). (f) Ratio of the (d) 12C14N- and (e) 12C15N- images; here, the 'dark spot' (red circle) is barely visible because the value of the 12C15N-/12C15N- ratio is close to that of the surrounding area. (g) HSI image of the 12C15N-/12C14N- ratio (the numerator has been multiplied by 10,000). The 'dark spot' isotope ratio is close to that of the surrounding area. Subnucleolar regions of low incorporation of 15N-uridine stand out in both the (f) ratio and the (g) HSI images. (h) Calibration with 15N-uridine. The graph shows the intranucleolar accumulation of 15N-uridine (measured as 12C15N-/12C14N- (experimental – control)/control) as a function of the concentration of 15N-uridine in the culture medium. |
PMC1781526_F8_9030.jpg | What's the most prominent thing you notice in this picture? | Distinguishing between an artifact and the subnucleolar heterogeneity of 15N-uridine incorporation. (a,b) Parallel quantitative mass images of (a) 12C14N- and (b) 12C15N- images of a fibroblast cultured in the presence of 15N-uridine. Ncl, nucleoli; NM, nuclear membrane. Field: 40 × 40 μm (image has been cropped); acquisition time 20 min. (c-e) High-resolution parallel mass images at 12C-, 12C14N- and 12C15N- of the large nucleolus seen in (a,b). Field: 8 × 8 μm; acquisition time 30 min. (c) 12C- image, arising from both tissue and embedding medium; the dark spot (red arrow) was caused by accidental exposure to a stationary high-intensity primary Cs+ ion beam. (d) 12C14N- image. (e) 12C15N- image, showing subnucleolar areas of low local 15N incorporation (white arrows). (f) Ratio of the (d) 12C14N- and (e) 12C15N- images; here, the 'dark spot' (red circle) is barely visible because the value of the 12C15N-/12C15N- ratio is close to that of the surrounding area. (g) HSI image of the 12C15N-/12C14N- ratio (the numerator has been multiplied by 10,000). The 'dark spot' isotope ratio is close to that of the surrounding area. Subnucleolar regions of low incorporation of 15N-uridine stand out in both the (f) ratio and the (g) HSI images. (h) Calibration with 15N-uridine. The graph shows the intranucleolar accumulation of 15N-uridine (measured as 12C15N-/12C14N- (experimental – control)/control) as a function of the concentration of 15N-uridine in the culture medium. |
PMC1781526_F8_9036.jpg | What is being portrayed in this visual content? | Distinguishing between an artifact and the subnucleolar heterogeneity of 15N-uridine incorporation. (a,b) Parallel quantitative mass images of (a) 12C14N- and (b) 12C15N- images of a fibroblast cultured in the presence of 15N-uridine. Ncl, nucleoli; NM, nuclear membrane. Field: 40 × 40 μm (image has been cropped); acquisition time 20 min. (c-e) High-resolution parallel mass images at 12C-, 12C14N- and 12C15N- of the large nucleolus seen in (a,b). Field: 8 × 8 μm; acquisition time 30 min. (c) 12C- image, arising from both tissue and embedding medium; the dark spot (red arrow) was caused by accidental exposure to a stationary high-intensity primary Cs+ ion beam. (d) 12C14N- image. (e) 12C15N- image, showing subnucleolar areas of low local 15N incorporation (white arrows). (f) Ratio of the (d) 12C14N- and (e) 12C15N- images; here, the 'dark spot' (red circle) is barely visible because the value of the 12C15N-/12C15N- ratio is close to that of the surrounding area. (g) HSI image of the 12C15N-/12C14N- ratio (the numerator has been multiplied by 10,000). The 'dark spot' isotope ratio is close to that of the surrounding area. Subnucleolar regions of low incorporation of 15N-uridine stand out in both the (f) ratio and the (g) HSI images. (h) Calibration with 15N-uridine. The graph shows the intranucleolar accumulation of 15N-uridine (measured as 12C15N-/12C14N- (experimental – control)/control) as a function of the concentration of 15N-uridine in the culture medium. |
PMC1781526_F8_9035.jpg | Can you identify the primary element in this image? | Distinguishing between an artifact and the subnucleolar heterogeneity of 15N-uridine incorporation. (a,b) Parallel quantitative mass images of (a) 12C14N- and (b) 12C15N- images of a fibroblast cultured in the presence of 15N-uridine. Ncl, nucleoli; NM, nuclear membrane. Field: 40 × 40 μm (image has been cropped); acquisition time 20 min. (c-e) High-resolution parallel mass images at 12C-, 12C14N- and 12C15N- of the large nucleolus seen in (a,b). Field: 8 × 8 μm; acquisition time 30 min. (c) 12C- image, arising from both tissue and embedding medium; the dark spot (red arrow) was caused by accidental exposure to a stationary high-intensity primary Cs+ ion beam. (d) 12C14N- image. (e) 12C15N- image, showing subnucleolar areas of low local 15N incorporation (white arrows). (f) Ratio of the (d) 12C14N- and (e) 12C15N- images; here, the 'dark spot' (red circle) is barely visible because the value of the 12C15N-/12C15N- ratio is close to that of the surrounding area. (g) HSI image of the 12C15N-/12C14N- ratio (the numerator has been multiplied by 10,000). The 'dark spot' isotope ratio is close to that of the surrounding area. Subnucleolar regions of low incorporation of 15N-uridine stand out in both the (f) ratio and the (g) HSI images. (h) Calibration with 15N-uridine. The graph shows the intranucleolar accumulation of 15N-uridine (measured as 12C15N-/12C14N- (experimental – control)/control) as a function of the concentration of 15N-uridine in the culture medium. |
PMC1781526_F11_9025.jpg | What is the central feature of this picture? | Rat embryo fibroblasts labeled with 14C-thymidine. Fibroblasts were cultured on silicon chips, deprived of serum for 24 h and pulsed with serum and 19 nmol 14C-thymidine/ml (1 mCi/ml). (a,b,c) Simultaneous quantitative mass images of a fibroblast at (a) 12C15N- (grayscale); (b) 14C- (pseudo-color); (c) overlay of the 14C- and 12C15N- images. Field: 50 × 26 μm; acquisition time 14 h. (d,e) Simultaneous quantitative mass images of a control rat embryo fibroblast at (a) 12C15N-; (b) 14C-. Field: 50 × 41 μm; acquisition time 2 h. |
PMC1781526_F11_9028.jpg | What is the principal component of this image? | Rat embryo fibroblasts labeled with 14C-thymidine. Fibroblasts were cultured on silicon chips, deprived of serum for 24 h and pulsed with serum and 19 nmol 14C-thymidine/ml (1 mCi/ml). (a,b,c) Simultaneous quantitative mass images of a fibroblast at (a) 12C15N- (grayscale); (b) 14C- (pseudo-color); (c) overlay of the 14C- and 12C15N- images. Field: 50 × 26 μm; acquisition time 14 h. (d,e) Simultaneous quantitative mass images of a control rat embryo fibroblast at (a) 12C15N-; (b) 14C-. Field: 50 × 41 μm; acquisition time 2 h. |
PMC1781526_F11_9026.jpg | What is the principal component of this image? | Rat embryo fibroblasts labeled with 14C-thymidine. Fibroblasts were cultured on silicon chips, deprived of serum for 24 h and pulsed with serum and 19 nmol 14C-thymidine/ml (1 mCi/ml). (a,b,c) Simultaneous quantitative mass images of a fibroblast at (a) 12C15N- (grayscale); (b) 14C- (pseudo-color); (c) overlay of the 14C- and 12C15N- images. Field: 50 × 26 μm; acquisition time 14 h. (d,e) Simultaneous quantitative mass images of a control rat embryo fibroblast at (a) 12C15N-; (b) 14C-. Field: 50 × 41 μm; acquisition time 2 h. |
PMC1781933_F3_9039.jpg | What can you see in this picture? | EM examination of particle assembly of L1 mutant proteins. A) The purified proteins from four different L1 constructs. Lane 1: full-length HPV16 L1; lane 2: D1-L1 deletion mutant of HPV16 L1; lane 3: D2-L1 deletion mutant of HPV16 L1; lane 4: D2-L1 deletion mutant of HPV18 L1. B-E) EM images of the purified proteins treated under assembly condition. The proteins were in incubated in the assembly buffer at 25°C for 30 minutes. Uranyl acetate was then used to treat the protein samples on a carbon grid for EM examination. The scale of the images is indicated by the bar above panel B. The images shown are: (B) full-length HPV16 L1; (C): D1-L1 mutant of HPV16 L1; (D): D2-L1 mutant of HPV16 L1; (E): D2-L1 mutant of HPV18 L1. |
PMC1781933_F3_9037.jpg | What is the main focus of this visual representation? | EM examination of particle assembly of L1 mutant proteins. A) The purified proteins from four different L1 constructs. Lane 1: full-length HPV16 L1; lane 2: D1-L1 deletion mutant of HPV16 L1; lane 3: D2-L1 deletion mutant of HPV16 L1; lane 4: D2-L1 deletion mutant of HPV18 L1. B-E) EM images of the purified proteins treated under assembly condition. The proteins were in incubated in the assembly buffer at 25°C for 30 minutes. Uranyl acetate was then used to treat the protein samples on a carbon grid for EM examination. The scale of the images is indicated by the bar above panel B. The images shown are: (B) full-length HPV16 L1; (C): D1-L1 mutant of HPV16 L1; (D): D2-L1 mutant of HPV16 L1; (E): D2-L1 mutant of HPV18 L1. |
PMC1781933_F3_9040.jpg | What is the focal point of this photograph? | EM examination of particle assembly of L1 mutant proteins. A) The purified proteins from four different L1 constructs. Lane 1: full-length HPV16 L1; lane 2: D1-L1 deletion mutant of HPV16 L1; lane 3: D2-L1 deletion mutant of HPV16 L1; lane 4: D2-L1 deletion mutant of HPV18 L1. B-E) EM images of the purified proteins treated under assembly condition. The proteins were in incubated in the assembly buffer at 25°C for 30 minutes. Uranyl acetate was then used to treat the protein samples on a carbon grid for EM examination. The scale of the images is indicated by the bar above panel B. The images shown are: (B) full-length HPV16 L1; (C): D1-L1 mutant of HPV16 L1; (D): D2-L1 mutant of HPV16 L1; (E): D2-L1 mutant of HPV18 L1. |
PMC1781933_F3_9038.jpg | What's the most prominent thing you notice in this picture? | EM examination of particle assembly of L1 mutant proteins. A) The purified proteins from four different L1 constructs. Lane 1: full-length HPV16 L1; lane 2: D1-L1 deletion mutant of HPV16 L1; lane 3: D2-L1 deletion mutant of HPV16 L1; lane 4: D2-L1 deletion mutant of HPV18 L1. B-E) EM images of the purified proteins treated under assembly condition. The proteins were in incubated in the assembly buffer at 25°C for 30 minutes. Uranyl acetate was then used to treat the protein samples on a carbon grid for EM examination. The scale of the images is indicated by the bar above panel B. The images shown are: (B) full-length HPV16 L1; (C): D1-L1 mutant of HPV16 L1; (D): D2-L1 mutant of HPV16 L1; (E): D2-L1 mutant of HPV18 L1. |
PMC1781937_F3_9045.jpg | What is shown in this image? | IL-10 reduces NFATc1 immunostaining intensity and nuclear translocation. NFATc1 staining was noted in the cytoplasm and nuclei of RANKL treated RAW264.7 cells (B and C), whereas only weak cytoplasmic staining was observed in RANKL + IL-10 treated cells (D.) No staining was noted in control cultures (A). Photographs taken at a magnification of × 400 A, B, D and ×1000 C. |
PMC1781937_F3_9042.jpg | What is the dominant medical problem in this image? | IL-10 reduces NFATc1 immunostaining intensity and nuclear translocation. NFATc1 staining was noted in the cytoplasm and nuclei of RANKL treated RAW264.7 cells (B and C), whereas only weak cytoplasmic staining was observed in RANKL + IL-10 treated cells (D.) No staining was noted in control cultures (A). Photographs taken at a magnification of × 400 A, B, D and ×1000 C. |
PMC1783647_F2_9046.jpg | What stands out most in this visual? | panoramic radiograph showing left mandibular lesion in patient n°1. |
PMC1783647_F7_9047.jpg | What is the principal component of this image? | panoramic radiograph of patient n°1, six months after surgery. |
PMC1783647_F8_9048.jpg | What is being portrayed in this visual content? | panoramic radiograph of patient n°1, six months after surgery, and after the plate removal and implants insertion. |
PMC1783647_F11_9049.jpg | What is being portrayed in this visual content? | panoramic radiograph of patient n°2. Note the erosion of the bone on the left side of the mandible. |
PMC1783647_F18_9050.jpg | What object or scene is depicted here? | panoramic radiograph of patient n°2, 1 year after surgery. |
PMC1783654_F1_9051.jpg | What is the main focus of this visual representation? | Computer tomography (CT) scan of pelvis. a). showing normal uterus and a pelvic mass located in the area of the left adnexa. b). showing cystic mass with solid areas. |
PMC1783654_F1_9052.jpg | What's the most prominent thing you notice in this picture? | Computer tomography (CT) scan of pelvis. a). showing normal uterus and a pelvic mass located in the area of the left adnexa. b). showing cystic mass with solid areas. |
PMC1783657_F3_9056.jpg | What can you see in this picture? | D1- and D2 modulation of individual varicosities on the same axonal segment. A. The MSN imaged is shown in a 3D reconstruction of a confocal z series of Alexa594 images. The cell body and multiple spiny dendrites are shown in blue and the single non-spine bearing axon is shown in red. The area imaged is outlined (black rectangle) and shown in panel B. B. In the OG1 fluorescence image, the stretch of axon that contained five hot spots (numbered). The spline used for the time scan is shown as a red line superimposed on the axonal segment. C. The spline scan images show no change in the Alexa594 fluorescence and a stimulus-dependent increase in OG1 fluorescence. D. Ca2+ imaging was carried out at 10 min intervals. The total duration of the experiment was 40 min. Asterisks identify Ca2+ responses that were significantly modulated by DA (> 5% of control). Note that the majority of varicosities showed modulation with both D1 and D2 agonists. The relative magnitude of modulation was strikingly heterogeneous. |
PMC1783657_F3_9057.jpg | Can you identify the primary element in this image? | D1- and D2 modulation of individual varicosities on the same axonal segment. A. The MSN imaged is shown in a 3D reconstruction of a confocal z series of Alexa594 images. The cell body and multiple spiny dendrites are shown in blue and the single non-spine bearing axon is shown in red. The area imaged is outlined (black rectangle) and shown in panel B. B. In the OG1 fluorescence image, the stretch of axon that contained five hot spots (numbered). The spline used for the time scan is shown as a red line superimposed on the axonal segment. C. The spline scan images show no change in the Alexa594 fluorescence and a stimulus-dependent increase in OG1 fluorescence. D. Ca2+ imaging was carried out at 10 min intervals. The total duration of the experiment was 40 min. Asterisks identify Ca2+ responses that were significantly modulated by DA (> 5% of control). Note that the majority of varicosities showed modulation with both D1 and D2 agonists. The relative magnitude of modulation was strikingly heterogeneous. |
PMC1783657_F3_9054.jpg | What is the focal point of this photograph? | D1- and D2 modulation of individual varicosities on the same axonal segment. A. The MSN imaged is shown in a 3D reconstruction of a confocal z series of Alexa594 images. The cell body and multiple spiny dendrites are shown in blue and the single non-spine bearing axon is shown in red. The area imaged is outlined (black rectangle) and shown in panel B. B. In the OG1 fluorescence image, the stretch of axon that contained five hot spots (numbered). The spline used for the time scan is shown as a red line superimposed on the axonal segment. C. The spline scan images show no change in the Alexa594 fluorescence and a stimulus-dependent increase in OG1 fluorescence. D. Ca2+ imaging was carried out at 10 min intervals. The total duration of the experiment was 40 min. Asterisks identify Ca2+ responses that were significantly modulated by DA (> 5% of control). Note that the majority of varicosities showed modulation with both D1 and D2 agonists. The relative magnitude of modulation was strikingly heterogeneous. |
PMC1783657_F3_9055.jpg | What is the principal component of this image? | D1- and D2 modulation of individual varicosities on the same axonal segment. A. The MSN imaged is shown in a 3D reconstruction of a confocal z series of Alexa594 images. The cell body and multiple spiny dendrites are shown in blue and the single non-spine bearing axon is shown in red. The area imaged is outlined (black rectangle) and shown in panel B. B. In the OG1 fluorescence image, the stretch of axon that contained five hot spots (numbered). The spline used for the time scan is shown as a red line superimposed on the axonal segment. C. The spline scan images show no change in the Alexa594 fluorescence and a stimulus-dependent increase in OG1 fluorescence. D. Ca2+ imaging was carried out at 10 min intervals. The total duration of the experiment was 40 min. Asterisks identify Ca2+ responses that were significantly modulated by DA (> 5% of control). Note that the majority of varicosities showed modulation with both D1 and D2 agonists. The relative magnitude of modulation was strikingly heterogeneous. |
PMC1783662_F1_9059.jpg | What object or scene is depicted here? | Imaging of scrotal ancient schwannoma. a) Ultrasound image and b) CT image showing an intra-scrotal and extra-testicular mass in the mid-scrotal region [Capital red T – tumour, red t – testes]. |
PMC1783662_F1_9058.jpg | What is being portrayed in this visual content? | Imaging of scrotal ancient schwannoma. a) Ultrasound image and b) CT image showing an intra-scrotal and extra-testicular mass in the mid-scrotal region [Capital red T – tumour, red t – testes]. |
PMC1783662_F3_9061.jpg | Can you identify the primary element in this image? | Microscopic appearance of ancient schwannoma. a) spindle cells in an Antoni type A area; a red arrow indicates a large bizarre hyperchromatic nucleus b) Antoni B areas consisting of spindle cells within a loose myxoid matrix, c) occasional pleomorphic nuclei within Antoni A areas, and d) positive S100 immunohistochemical staining. |
PMC1783662_F3_9060.jpg | What can you see in this picture? | Microscopic appearance of ancient schwannoma. a) spindle cells in an Antoni type A area; a red arrow indicates a large bizarre hyperchromatic nucleus b) Antoni B areas consisting of spindle cells within a loose myxoid matrix, c) occasional pleomorphic nuclei within Antoni A areas, and d) positive S100 immunohistochemical staining. |
PMC1783845_F2_9079.jpg | What is the main focus of this visual representation? | β-catenin KO pancreata display extensive loss of exocrine tissue. Hematoxylin and eosin stained paraffin sections were used to compare the histology of wildtype versus β-catenin KO pancreata at one day, one month and two months of age. Compared to one day old wildtype pancreas [A], the absence of acini is readily apparent at low power [D]. At two months of age, compared to wildtype [B, C] the β-catenin KO pancreas is hypoplastic with increased areas of interlobular fibrosis [E]. Under 20× magnification, increased formation of tubular duct-like structures are present suggesting acinar to duct metaplasia (arrows) and inflammatory infiltrate (circled) are evident [F and H]. By two months, low power views demonstrate extensive fibrosis and near complete absence of exocrine pancreatic tissue, likely accounting for the shortened lifespan seen in these animals [E and G]. In several mice aged beyond three months, areas of pancreatic parenchyma histologically resemble liver. Immunostaining for albumin is absent in wildtype pancreas [J], but abundant in normal liver [I] and in β-catenin KO pancreata [K]. |
PMC1783845_F2_9077.jpg | What is being portrayed in this visual content? | β-catenin KO pancreata display extensive loss of exocrine tissue. Hematoxylin and eosin stained paraffin sections were used to compare the histology of wildtype versus β-catenin KO pancreata at one day, one month and two months of age. Compared to one day old wildtype pancreas [A], the absence of acini is readily apparent at low power [D]. At two months of age, compared to wildtype [B, C] the β-catenin KO pancreas is hypoplastic with increased areas of interlobular fibrosis [E]. Under 20× magnification, increased formation of tubular duct-like structures are present suggesting acinar to duct metaplasia (arrows) and inflammatory infiltrate (circled) are evident [F and H]. By two months, low power views demonstrate extensive fibrosis and near complete absence of exocrine pancreatic tissue, likely accounting for the shortened lifespan seen in these animals [E and G]. In several mice aged beyond three months, areas of pancreatic parenchyma histologically resemble liver. Immunostaining for albumin is absent in wildtype pancreas [J], but abundant in normal liver [I] and in β-catenin KO pancreata [K]. |
PMC1783845_F2_9073.jpg | What is the principal component of this image? | β-catenin KO pancreata display extensive loss of exocrine tissue. Hematoxylin and eosin stained paraffin sections were used to compare the histology of wildtype versus β-catenin KO pancreata at one day, one month and two months of age. Compared to one day old wildtype pancreas [A], the absence of acini is readily apparent at low power [D]. At two months of age, compared to wildtype [B, C] the β-catenin KO pancreas is hypoplastic with increased areas of interlobular fibrosis [E]. Under 20× magnification, increased formation of tubular duct-like structures are present suggesting acinar to duct metaplasia (arrows) and inflammatory infiltrate (circled) are evident [F and H]. By two months, low power views demonstrate extensive fibrosis and near complete absence of exocrine pancreatic tissue, likely accounting for the shortened lifespan seen in these animals [E and G]. In several mice aged beyond three months, areas of pancreatic parenchyma histologically resemble liver. Immunostaining for albumin is absent in wildtype pancreas [J], but abundant in normal liver [I] and in β-catenin KO pancreata [K]. |
PMC1783845_F2_9074.jpg | Describe the main subject of this image. | β-catenin KO pancreata display extensive loss of exocrine tissue. Hematoxylin and eosin stained paraffin sections were used to compare the histology of wildtype versus β-catenin KO pancreata at one day, one month and two months of age. Compared to one day old wildtype pancreas [A], the absence of acini is readily apparent at low power [D]. At two months of age, compared to wildtype [B, C] the β-catenin KO pancreas is hypoplastic with increased areas of interlobular fibrosis [E]. Under 20× magnification, increased formation of tubular duct-like structures are present suggesting acinar to duct metaplasia (arrows) and inflammatory infiltrate (circled) are evident [F and H]. By two months, low power views demonstrate extensive fibrosis and near complete absence of exocrine pancreatic tissue, likely accounting for the shortened lifespan seen in these animals [E and G]. In several mice aged beyond three months, areas of pancreatic parenchyma histologically resemble liver. Immunostaining for albumin is absent in wildtype pancreas [J], but abundant in normal liver [I] and in β-catenin KO pancreata [K]. |
PMC1783845_F2_9075.jpg | What key item or scene is captured in this photo? | β-catenin KO pancreata display extensive loss of exocrine tissue. Hematoxylin and eosin stained paraffin sections were used to compare the histology of wildtype versus β-catenin KO pancreata at one day, one month and two months of age. Compared to one day old wildtype pancreas [A], the absence of acini is readily apparent at low power [D]. At two months of age, compared to wildtype [B, C] the β-catenin KO pancreas is hypoplastic with increased areas of interlobular fibrosis [E]. Under 20× magnification, increased formation of tubular duct-like structures are present suggesting acinar to duct metaplasia (arrows) and inflammatory infiltrate (circled) are evident [F and H]. By two months, low power views demonstrate extensive fibrosis and near complete absence of exocrine pancreatic tissue, likely accounting for the shortened lifespan seen in these animals [E and G]. In several mice aged beyond three months, areas of pancreatic parenchyma histologically resemble liver. Immunostaining for albumin is absent in wildtype pancreas [J], but abundant in normal liver [I] and in β-catenin KO pancreata [K]. |
PMC1783845_F2_9080.jpg | What is the main focus of this visual representation? | β-catenin KO pancreata display extensive loss of exocrine tissue. Hematoxylin and eosin stained paraffin sections were used to compare the histology of wildtype versus β-catenin KO pancreata at one day, one month and two months of age. Compared to one day old wildtype pancreas [A], the absence of acini is readily apparent at low power [D]. At two months of age, compared to wildtype [B, C] the β-catenin KO pancreas is hypoplastic with increased areas of interlobular fibrosis [E]. Under 20× magnification, increased formation of tubular duct-like structures are present suggesting acinar to duct metaplasia (arrows) and inflammatory infiltrate (circled) are evident [F and H]. By two months, low power views demonstrate extensive fibrosis and near complete absence of exocrine pancreatic tissue, likely accounting for the shortened lifespan seen in these animals [E and G]. In several mice aged beyond three months, areas of pancreatic parenchyma histologically resemble liver. Immunostaining for albumin is absent in wildtype pancreas [J], but abundant in normal liver [I] and in β-catenin KO pancreata [K]. |
PMC1783845_F2_9082.jpg | What key item or scene is captured in this photo? | β-catenin KO pancreata display extensive loss of exocrine tissue. Hematoxylin and eosin stained paraffin sections were used to compare the histology of wildtype versus β-catenin KO pancreata at one day, one month and two months of age. Compared to one day old wildtype pancreas [A], the absence of acini is readily apparent at low power [D]. At two months of age, compared to wildtype [B, C] the β-catenin KO pancreas is hypoplastic with increased areas of interlobular fibrosis [E]. Under 20× magnification, increased formation of tubular duct-like structures are present suggesting acinar to duct metaplasia (arrows) and inflammatory infiltrate (circled) are evident [F and H]. By two months, low power views demonstrate extensive fibrosis and near complete absence of exocrine pancreatic tissue, likely accounting for the shortened lifespan seen in these animals [E and G]. In several mice aged beyond three months, areas of pancreatic parenchyma histologically resemble liver. Immunostaining for albumin is absent in wildtype pancreas [J], but abundant in normal liver [I] and in β-catenin KO pancreata [K]. |
PMC1783845_F2_9078.jpg | What is being portrayed in this visual content? | β-catenin KO pancreata display extensive loss of exocrine tissue. Hematoxylin and eosin stained paraffin sections were used to compare the histology of wildtype versus β-catenin KO pancreata at one day, one month and two months of age. Compared to one day old wildtype pancreas [A], the absence of acini is readily apparent at low power [D]. At two months of age, compared to wildtype [B, C] the β-catenin KO pancreas is hypoplastic with increased areas of interlobular fibrosis [E]. Under 20× magnification, increased formation of tubular duct-like structures are present suggesting acinar to duct metaplasia (arrows) and inflammatory infiltrate (circled) are evident [F and H]. By two months, low power views demonstrate extensive fibrosis and near complete absence of exocrine pancreatic tissue, likely accounting for the shortened lifespan seen in these animals [E and G]. In several mice aged beyond three months, areas of pancreatic parenchyma histologically resemble liver. Immunostaining for albumin is absent in wildtype pancreas [J], but abundant in normal liver [I] and in β-catenin KO pancreata [K]. |
PMC1783845_F2_9081.jpg | What is the central feature of this picture? | β-catenin KO pancreata display extensive loss of exocrine tissue. Hematoxylin and eosin stained paraffin sections were used to compare the histology of wildtype versus β-catenin KO pancreata at one day, one month and two months of age. Compared to one day old wildtype pancreas [A], the absence of acini is readily apparent at low power [D]. At two months of age, compared to wildtype [B, C] the β-catenin KO pancreas is hypoplastic with increased areas of interlobular fibrosis [E]. Under 20× magnification, increased formation of tubular duct-like structures are present suggesting acinar to duct metaplasia (arrows) and inflammatory infiltrate (circled) are evident [F and H]. By two months, low power views demonstrate extensive fibrosis and near complete absence of exocrine pancreatic tissue, likely accounting for the shortened lifespan seen in these animals [E and G]. In several mice aged beyond three months, areas of pancreatic parenchyma histologically resemble liver. Immunostaining for albumin is absent in wildtype pancreas [J], but abundant in normal liver [I] and in β-catenin KO pancreata [K]. |
PMC1783845_F2_9072.jpg | What is the principal component of this image? | β-catenin KO pancreata display extensive loss of exocrine tissue. Hematoxylin and eosin stained paraffin sections were used to compare the histology of wildtype versus β-catenin KO pancreata at one day, one month and two months of age. Compared to one day old wildtype pancreas [A], the absence of acini is readily apparent at low power [D]. At two months of age, compared to wildtype [B, C] the β-catenin KO pancreas is hypoplastic with increased areas of interlobular fibrosis [E]. Under 20× magnification, increased formation of tubular duct-like structures are present suggesting acinar to duct metaplasia (arrows) and inflammatory infiltrate (circled) are evident [F and H]. By two months, low power views demonstrate extensive fibrosis and near complete absence of exocrine pancreatic tissue, likely accounting for the shortened lifespan seen in these animals [E and G]. In several mice aged beyond three months, areas of pancreatic parenchyma histologically resemble liver. Immunostaining for albumin is absent in wildtype pancreas [J], but abundant in normal liver [I] and in β-catenin KO pancreata [K]. |
PMC1783845_F4_9069.jpg | What is the dominant medical problem in this image? | β-catenin KO pancreas is hypoplastic by E16.5. Panels A and B depict hematoxylin and eosin staining of E 16.5 wildtype and β-catenin KO pancreas, respectively, each at 25× magnification. Hypoplasia of the developing pancreas is already apparent and was consistently present by this stage. Panels C, D, and E demonstrate wild-type pancreata at E 12.5, 14.5 and 16.5, respectively, stained with an antibody specific for the transcriptionally active, dephosphorylated form of β-catenin. Note that staining is abundant at ED12.5, but is undetectable following the secondary transition at E16.5. |
PMC1783845_F4_9070.jpg | What can you see in this picture? | β-catenin KO pancreas is hypoplastic by E16.5. Panels A and B depict hematoxylin and eosin staining of E 16.5 wildtype and β-catenin KO pancreas, respectively, each at 25× magnification. Hypoplasia of the developing pancreas is already apparent and was consistently present by this stage. Panels C, D, and E demonstrate wild-type pancreata at E 12.5, 14.5 and 16.5, respectively, stained with an antibody specific for the transcriptionally active, dephosphorylated form of β-catenin. Note that staining is abundant at ED12.5, but is undetectable following the secondary transition at E16.5. |
PMC1783845_F4_9071.jpg | What is the principal component of this image? | β-catenin KO pancreas is hypoplastic by E16.5. Panels A and B depict hematoxylin and eosin staining of E 16.5 wildtype and β-catenin KO pancreas, respectively, each at 25× magnification. Hypoplasia of the developing pancreas is already apparent and was consistently present by this stage. Panels C, D, and E demonstrate wild-type pancreata at E 12.5, 14.5 and 16.5, respectively, stained with an antibody specific for the transcriptionally active, dephosphorylated form of β-catenin. Note that staining is abundant at ED12.5, but is undetectable following the secondary transition at E16.5. |
PMC1783845_F7_9064.jpg | What stands out most in this visual? | Cell proliferation is decreased in β-catenin KO pancreas. Panel A and B depict hematoxylin and eosin staining [25× magnification] of E 14.5 pancreata from wildtype and β-catenin KO mice. Panels C and D demonstrate costaining for β-catenin and DAPI. Insets reveal characteristic fields immunostained for phosphohistone H3, demonstrating significantly fewer proliferating cells in the β-catenin KO pancreas. |
PMC1783845_F7_9063.jpg | What does this image primarily show? | Cell proliferation is decreased in β-catenin KO pancreas. Panel A and B depict hematoxylin and eosin staining [25× magnification] of E 14.5 pancreata from wildtype and β-catenin KO mice. Panels C and D demonstrate costaining for β-catenin and DAPI. Insets reveal characteristic fields immunostained for phosphohistone H3, demonstrating significantly fewer proliferating cells in the β-catenin KO pancreas. |
PMC1783845_F7_9065.jpg | What stands out most in this visual? | Cell proliferation is decreased in β-catenin KO pancreas. Panel A and B depict hematoxylin and eosin staining [25× magnification] of E 14.5 pancreata from wildtype and β-catenin KO mice. Panels C and D demonstrate costaining for β-catenin and DAPI. Insets reveal characteristic fields immunostained for phosphohistone H3, demonstrating significantly fewer proliferating cells in the β-catenin KO pancreas. |
PMC1783845_F7_9066.jpg | What object or scene is depicted here? | Cell proliferation is decreased in β-catenin KO pancreas. Panel A and B depict hematoxylin and eosin staining [25× magnification] of E 14.5 pancreata from wildtype and β-catenin KO mice. Panels C and D demonstrate costaining for β-catenin and DAPI. Insets reveal characteristic fields immunostained for phosphohistone H3, demonstrating significantly fewer proliferating cells in the β-catenin KO pancreas. |
PMC1783847_F2_9087.jpg | What is the principal component of this image? | Distribution of VP2 within infected and transfected Vero cells by fluorescence microscopy. A) Cells infected with BTV-10, B-E) transfected cells expressing B) VP2, C) VP2-GFP, D) GFP-VP2 and E) GFP only. VP2 in A and B were detected with anti VP2 monoclonal antibody (rabbit) and either FITC (A) or TRITC (B) conjugated secondary antibody. C-E were visualised based on GFP fluorescence. Expression of full-length, tagged VP2 variants was confirmed by western blot using an anti-GFP antibody (F). |
PMC1783847_F2_9084.jpg | What is the dominant medical problem in this image? | Distribution of VP2 within infected and transfected Vero cells by fluorescence microscopy. A) Cells infected with BTV-10, B-E) transfected cells expressing B) VP2, C) VP2-GFP, D) GFP-VP2 and E) GFP only. VP2 in A and B were detected with anti VP2 monoclonal antibody (rabbit) and either FITC (A) or TRITC (B) conjugated secondary antibody. C-E were visualised based on GFP fluorescence. Expression of full-length, tagged VP2 variants was confirmed by western blot using an anti-GFP antibody (F). |
PMC1783851_F5_9089.jpg | What does this image primarily show? | Representation of Z-distribution. The empirical distribution of the absolute value of the log-ratio of logarithms of intensities (Z) of all the signals recorded from the analyzed arrays is represented. On the x-axis the value of the variable Z is plotted; on the y-axis the value of the density function of the variable Z probability is reported. The Z-distribution appears as a bimodal density with two peaks, and it can be decomposed into two normal distributions: one with positive mean (see the peak on the right), representing the distribution of those SNPs with very different intensity values for the two alleles (homozygous genotypes), and the other with mean zero (see the peak on the left), representing the distribution of those SNPs with similar intensity values for both the alleles (heterozygous genotypes). The bold line (with filled triangles) represents the best fitting to a mixture of normal distributions obtained through an E-M algorithm, while the dashed line (with open squares) represents the real data. |
PMC1783858_F3_9095.jpg | What is shown in this image? | Histology of KCI-18 kidney tumors and lung metastases. Following implantation of KCI-18/IK cells in the kidney of nude mice; tumors were resected at different time points and processed for histology. Kidney tumor and lung sections were stained with H&E. Panel A: Development of high-grade carcinoma (arrowheads) with sinusoidal vascular pattern in the kidney (×10). Panel B: Kidney tumor morphology distinct from normal kidney tissue tubular morphology (×25). Panel C: Kidney tumor consisting of cells with large pleomorphic nuclei, prominent nucleoli and abundant eosinophilic cytoplasm (×100). Panel D: Metastatic nodules in lung (×25). Panels E, F: Kidney tumor sections immunostained for cytokeratin (E) and vimentin (F) showing positive cytoplasmic staining for both markers (×50). Magnifications (×-fold) are shown for each picture. |
PMC1783858_F3_9097.jpg | What key item or scene is captured in this photo? | Histology of KCI-18 kidney tumors and lung metastases. Following implantation of KCI-18/IK cells in the kidney of nude mice; tumors were resected at different time points and processed for histology. Kidney tumor and lung sections were stained with H&E. Panel A: Development of high-grade carcinoma (arrowheads) with sinusoidal vascular pattern in the kidney (×10). Panel B: Kidney tumor morphology distinct from normal kidney tissue tubular morphology (×25). Panel C: Kidney tumor consisting of cells with large pleomorphic nuclei, prominent nucleoli and abundant eosinophilic cytoplasm (×100). Panel D: Metastatic nodules in lung (×25). Panels E, F: Kidney tumor sections immunostained for cytokeratin (E) and vimentin (F) showing positive cytoplasmic staining for both markers (×50). Magnifications (×-fold) are shown for each picture. |
PMC1783858_F3_9096.jpg | What is the dominant medical problem in this image? | Histology of KCI-18 kidney tumors and lung metastases. Following implantation of KCI-18/IK cells in the kidney of nude mice; tumors were resected at different time points and processed for histology. Kidney tumor and lung sections were stained with H&E. Panel A: Development of high-grade carcinoma (arrowheads) with sinusoidal vascular pattern in the kidney (×10). Panel B: Kidney tumor morphology distinct from normal kidney tissue tubular morphology (×25). Panel C: Kidney tumor consisting of cells with large pleomorphic nuclei, prominent nucleoli and abundant eosinophilic cytoplasm (×100). Panel D: Metastatic nodules in lung (×25). Panels E, F: Kidney tumor sections immunostained for cytokeratin (E) and vimentin (F) showing positive cytoplasmic staining for both markers (×50). Magnifications (×-fold) are shown for each picture. |
PMC1783858_F3_9094.jpg | What is the core subject represented in this visual? | Histology of KCI-18 kidney tumors and lung metastases. Following implantation of KCI-18/IK cells in the kidney of nude mice; tumors were resected at different time points and processed for histology. Kidney tumor and lung sections were stained with H&E. Panel A: Development of high-grade carcinoma (arrowheads) with sinusoidal vascular pattern in the kidney (×10). Panel B: Kidney tumor morphology distinct from normal kidney tissue tubular morphology (×25). Panel C: Kidney tumor consisting of cells with large pleomorphic nuclei, prominent nucleoli and abundant eosinophilic cytoplasm (×100). Panel D: Metastatic nodules in lung (×25). Panels E, F: Kidney tumor sections immunostained for cytokeratin (E) and vimentin (F) showing positive cytoplasmic staining for both markers (×50). Magnifications (×-fold) are shown for each picture. |
PMC1783858_F3_9093.jpg | Describe the main subject of this image. | Histology of KCI-18 kidney tumors and lung metastases. Following implantation of KCI-18/IK cells in the kidney of nude mice; tumors were resected at different time points and processed for histology. Kidney tumor and lung sections were stained with H&E. Panel A: Development of high-grade carcinoma (arrowheads) with sinusoidal vascular pattern in the kidney (×10). Panel B: Kidney tumor morphology distinct from normal kidney tissue tubular morphology (×25). Panel C: Kidney tumor consisting of cells with large pleomorphic nuclei, prominent nucleoli and abundant eosinophilic cytoplasm (×100). Panel D: Metastatic nodules in lung (×25). Panels E, F: Kidney tumor sections immunostained for cytokeratin (E) and vimentin (F) showing positive cytoplasmic staining for both markers (×50). Magnifications (×-fold) are shown for each picture. |
PMC1783858_F5_9102.jpg | What is the main focus of this visual representation? | Histology of KCI-18 kidney tumors treated with genistein and radiation. Kidney tumors, resected from mice of the experiment described in Figure 4, were processed for histology and tumor sections were stained with H&E. The main findings were labeled on the prints with T for tumor, V for vessel, M for mitosis, H for hemorrhages, DG for degenerative, N for necrosis, A for apoptosis, F for fibrosis, DC for detached cells, R for rhabdoid cells, NKT for normal kidney tissue, IF for inflammatory cells and AM for abnormal mitosis. Panels A, B: Kidney tumor from control mice showing high-grade and very vascularized carcinoma (A, ×50) with frequent mitosis (B, ×100). Panels C, D: Kidney tumor from mice treated with genistein showing extensive hemorrhages (C, ×50), degenerative changes in tumor cells, apoptotic cells and areas of necrosis (D, ×100). Panels E, F: Irradiated kidney tumor, with areas of tumor destruction, showing fibrosis and apoptotic cells (E, ×50), focal areas with atypical detached rhabdoid cells (F, ×100). Panels G, H: Kidney tumor from mice treated with genistein and radiation, showing smaller residual tumor area adjacent to normal kidney tissue (G, ×25). The residual tumor looked hemorrhagic and consisted of large areas of detached rhabdoid cells, atypical giant cells with large nuclei and inflammatory cells (H, ×100). Lower and higher magnifications (×-fold) are presented to both show wider areas of tumor histology and focus on major findings. |
PMC1783858_F5_9104.jpg | What is shown in this image? | Histology of KCI-18 kidney tumors treated with genistein and radiation. Kidney tumors, resected from mice of the experiment described in Figure 4, were processed for histology and tumor sections were stained with H&E. The main findings were labeled on the prints with T for tumor, V for vessel, M for mitosis, H for hemorrhages, DG for degenerative, N for necrosis, A for apoptosis, F for fibrosis, DC for detached cells, R for rhabdoid cells, NKT for normal kidney tissue, IF for inflammatory cells and AM for abnormal mitosis. Panels A, B: Kidney tumor from control mice showing high-grade and very vascularized carcinoma (A, ×50) with frequent mitosis (B, ×100). Panels C, D: Kidney tumor from mice treated with genistein showing extensive hemorrhages (C, ×50), degenerative changes in tumor cells, apoptotic cells and areas of necrosis (D, ×100). Panels E, F: Irradiated kidney tumor, with areas of tumor destruction, showing fibrosis and apoptotic cells (E, ×50), focal areas with atypical detached rhabdoid cells (F, ×100). Panels G, H: Kidney tumor from mice treated with genistein and radiation, showing smaller residual tumor area adjacent to normal kidney tissue (G, ×25). The residual tumor looked hemorrhagic and consisted of large areas of detached rhabdoid cells, atypical giant cells with large nuclei and inflammatory cells (H, ×100). Lower and higher magnifications (×-fold) are presented to both show wider areas of tumor histology and focus on major findings. |
PMC1783858_F5_9105.jpg | Can you identify the primary element in this image? | Histology of KCI-18 kidney tumors treated with genistein and radiation. Kidney tumors, resected from mice of the experiment described in Figure 4, were processed for histology and tumor sections were stained with H&E. The main findings were labeled on the prints with T for tumor, V for vessel, M for mitosis, H for hemorrhages, DG for degenerative, N for necrosis, A for apoptosis, F for fibrosis, DC for detached cells, R for rhabdoid cells, NKT for normal kidney tissue, IF for inflammatory cells and AM for abnormal mitosis. Panels A, B: Kidney tumor from control mice showing high-grade and very vascularized carcinoma (A, ×50) with frequent mitosis (B, ×100). Panels C, D: Kidney tumor from mice treated with genistein showing extensive hemorrhages (C, ×50), degenerative changes in tumor cells, apoptotic cells and areas of necrosis (D, ×100). Panels E, F: Irradiated kidney tumor, with areas of tumor destruction, showing fibrosis and apoptotic cells (E, ×50), focal areas with atypical detached rhabdoid cells (F, ×100). Panels G, H: Kidney tumor from mice treated with genistein and radiation, showing smaller residual tumor area adjacent to normal kidney tissue (G, ×25). The residual tumor looked hemorrhagic and consisted of large areas of detached rhabdoid cells, atypical giant cells with large nuclei and inflammatory cells (H, ×100). Lower and higher magnifications (×-fold) are presented to both show wider areas of tumor histology and focus on major findings. |
PMC1783858_F5_9108.jpg | What stands out most in this visual? | Histology of KCI-18 kidney tumors treated with genistein and radiation. Kidney tumors, resected from mice of the experiment described in Figure 4, were processed for histology and tumor sections were stained with H&E. The main findings were labeled on the prints with T for tumor, V for vessel, M for mitosis, H for hemorrhages, DG for degenerative, N for necrosis, A for apoptosis, F for fibrosis, DC for detached cells, R for rhabdoid cells, NKT for normal kidney tissue, IF for inflammatory cells and AM for abnormal mitosis. Panels A, B: Kidney tumor from control mice showing high-grade and very vascularized carcinoma (A, ×50) with frequent mitosis (B, ×100). Panels C, D: Kidney tumor from mice treated with genistein showing extensive hemorrhages (C, ×50), degenerative changes in tumor cells, apoptotic cells and areas of necrosis (D, ×100). Panels E, F: Irradiated kidney tumor, with areas of tumor destruction, showing fibrosis and apoptotic cells (E, ×50), focal areas with atypical detached rhabdoid cells (F, ×100). Panels G, H: Kidney tumor from mice treated with genistein and radiation, showing smaller residual tumor area adjacent to normal kidney tissue (G, ×25). The residual tumor looked hemorrhagic and consisted of large areas of detached rhabdoid cells, atypical giant cells with large nuclei and inflammatory cells (H, ×100). Lower and higher magnifications (×-fold) are presented to both show wider areas of tumor histology and focus on major findings. |
PMC1783858_F5_9107.jpg | What key item or scene is captured in this photo? | Histology of KCI-18 kidney tumors treated with genistein and radiation. Kidney tumors, resected from mice of the experiment described in Figure 4, were processed for histology and tumor sections were stained with H&E. The main findings were labeled on the prints with T for tumor, V for vessel, M for mitosis, H for hemorrhages, DG for degenerative, N for necrosis, A for apoptosis, F for fibrosis, DC for detached cells, R for rhabdoid cells, NKT for normal kidney tissue, IF for inflammatory cells and AM for abnormal mitosis. Panels A, B: Kidney tumor from control mice showing high-grade and very vascularized carcinoma (A, ×50) with frequent mitosis (B, ×100). Panels C, D: Kidney tumor from mice treated with genistein showing extensive hemorrhages (C, ×50), degenerative changes in tumor cells, apoptotic cells and areas of necrosis (D, ×100). Panels E, F: Irradiated kidney tumor, with areas of tumor destruction, showing fibrosis and apoptotic cells (E, ×50), focal areas with atypical detached rhabdoid cells (F, ×100). Panels G, H: Kidney tumor from mice treated with genistein and radiation, showing smaller residual tumor area adjacent to normal kidney tissue (G, ×25). The residual tumor looked hemorrhagic and consisted of large areas of detached rhabdoid cells, atypical giant cells with large nuclei and inflammatory cells (H, ×100). Lower and higher magnifications (×-fold) are presented to both show wider areas of tumor histology and focus on major findings. |
PMC1783858_F5_9101.jpg | What stands out most in this visual? | Histology of KCI-18 kidney tumors treated with genistein and radiation. Kidney tumors, resected from mice of the experiment described in Figure 4, were processed for histology and tumor sections were stained with H&E. The main findings were labeled on the prints with T for tumor, V for vessel, M for mitosis, H for hemorrhages, DG for degenerative, N for necrosis, A for apoptosis, F for fibrosis, DC for detached cells, R for rhabdoid cells, NKT for normal kidney tissue, IF for inflammatory cells and AM for abnormal mitosis. Panels A, B: Kidney tumor from control mice showing high-grade and very vascularized carcinoma (A, ×50) with frequent mitosis (B, ×100). Panels C, D: Kidney tumor from mice treated with genistein showing extensive hemorrhages (C, ×50), degenerative changes in tumor cells, apoptotic cells and areas of necrosis (D, ×100). Panels E, F: Irradiated kidney tumor, with areas of tumor destruction, showing fibrosis and apoptotic cells (E, ×50), focal areas with atypical detached rhabdoid cells (F, ×100). Panels G, H: Kidney tumor from mice treated with genistein and radiation, showing smaller residual tumor area adjacent to normal kidney tissue (G, ×25). The residual tumor looked hemorrhagic and consisted of large areas of detached rhabdoid cells, atypical giant cells with large nuclei and inflammatory cells (H, ×100). Lower and higher magnifications (×-fold) are presented to both show wider areas of tumor histology and focus on major findings. |
PMC1783858_F6_9091.jpg | What is the central feature of this picture? | Histology of mesentery tumor nodules following treatment with genistein. Sections of the mouse bowel were stained with H&E. Panel A: Section of bowel (B) from mice treated with genistein showing tumor nodules (TN) in mesentery adipose tissue (AD). Panel B: Section of bowel (B) from mice treated with genistein and radiation and adipose tissue (AD) showing normal morphology of mesentery lining the bowel. Magnifications, ×25. |
PMC1783858_F6_9090.jpg | What does this image primarily show? | Histology of mesentery tumor nodules following treatment with genistein. Sections of the mouse bowel were stained with H&E. Panel A: Section of bowel (B) from mice treated with genistein showing tumor nodules (TN) in mesentery adipose tissue (AD). Panel B: Section of bowel (B) from mice treated with genistein and radiation and adipose tissue (AD) showing normal morphology of mesentery lining the bowel. Magnifications, ×25. |
PMC1783859_F1_9100.jpg | Describe the main subject of this image. | Cat. Mammary gland. VEGFR-3 (red) and laminin (brown) double immunohistochemical stain in an extratumoral area of a stage 0 carcinoma. Lymphatic vessels are laminin negative (asterisk) whereas blood vessels are laminin positive (circle) 20X. Inset: higher magnification of VEGFR-3 positive endothelial cells in a lymphatic vessel. 63X. |
PMC1783859_F1_9098.jpg | What is the core subject represented in this visual? | Cat. Mammary gland. VEGFR-3 (red) and laminin (brown) double immunohistochemical stain in an extratumoral area of a stage 0 carcinoma. Lymphatic vessels are laminin negative (asterisk) whereas blood vessels are laminin positive (circle) 20X. Inset: higher magnification of VEGFR-3 positive endothelial cells in a lymphatic vessel. 63X. |
PMC1783859_F1_9099.jpg | What is the main focus of this visual representation? | Cat. Mammary gland. VEGFR-3 (red) and laminin (brown) double immunohistochemical stain in an extratumoral area of a stage 0 carcinoma. Lymphatic vessels are laminin negative (asterisk) whereas blood vessels are laminin positive (circle) 20X. Inset: higher magnification of VEGFR-3 positive endothelial cells in a lymphatic vessel. 63X. |
PMC1784065_pone-0000206-g002_9109.jpg | What object or scene is depicted here? | Transmission electron-microscopic views of the lymphocyte-like cells in follicle-associated epithelium of amphioxus gill. (A) Follicle-associated epithelium cells in the gill contained follicle (F) rootlet (R), and cilia (C). Magnification 29000. (B) The lymphocyte-like cells contained large nuclei (N) with heterochromatin forming a peripheral rim adjacent to the nuclear envelope. Magnification 48000. (C) Under the FAE of normal amphioxus gill, lots of lymphocyte-like cells (L) were seen. The cells contained large nuclei (N) with heterochromatin forming a peripheral rim adjacent to the nuclear envelope. Magnification 5800. (D) At the same magnification, after the microbial challenge, the lymphocyte-like cells were bigger than those of normal cells. |
PMC1784065_pone-0000206-g002_9111.jpg | What is the central feature of this picture? | Transmission electron-microscopic views of the lymphocyte-like cells in follicle-associated epithelium of amphioxus gill. (A) Follicle-associated epithelium cells in the gill contained follicle (F) rootlet (R), and cilia (C). Magnification 29000. (B) The lymphocyte-like cells contained large nuclei (N) with heterochromatin forming a peripheral rim adjacent to the nuclear envelope. Magnification 48000. (C) Under the FAE of normal amphioxus gill, lots of lymphocyte-like cells (L) were seen. The cells contained large nuclei (N) with heterochromatin forming a peripheral rim adjacent to the nuclear envelope. Magnification 5800. (D) At the same magnification, after the microbial challenge, the lymphocyte-like cells were bigger than those of normal cells. |
PMC1784065_pone-0000206-g002_9112.jpg | What is the central feature of this picture? | Transmission electron-microscopic views of the lymphocyte-like cells in follicle-associated epithelium of amphioxus gill. (A) Follicle-associated epithelium cells in the gill contained follicle (F) rootlet (R), and cilia (C). Magnification 29000. (B) The lymphocyte-like cells contained large nuclei (N) with heterochromatin forming a peripheral rim adjacent to the nuclear envelope. Magnification 48000. (C) Under the FAE of normal amphioxus gill, lots of lymphocyte-like cells (L) were seen. The cells contained large nuclei (N) with heterochromatin forming a peripheral rim adjacent to the nuclear envelope. Magnification 5800. (D) At the same magnification, after the microbial challenge, the lymphocyte-like cells were bigger than those of normal cells. |
PMC1784065_pone-0000206-g002_9110.jpg | What is shown in this image? | Transmission electron-microscopic views of the lymphocyte-like cells in follicle-associated epithelium of amphioxus gill. (A) Follicle-associated epithelium cells in the gill contained follicle (F) rootlet (R), and cilia (C). Magnification 29000. (B) The lymphocyte-like cells contained large nuclei (N) with heterochromatin forming a peripheral rim adjacent to the nuclear envelope. Magnification 48000. (C) Under the FAE of normal amphioxus gill, lots of lymphocyte-like cells (L) were seen. The cells contained large nuclei (N) with heterochromatin forming a peripheral rim adjacent to the nuclear envelope. Magnification 5800. (D) At the same magnification, after the microbial challenge, the lymphocyte-like cells were bigger than those of normal cells. |
PMC1784069_pone-0000200-g004_9119.jpg | Can you identify the primary element in this image? | Single condition map for each optic flow stimulus at different eye positions in the right hemisphere of M1R. The baseline normalization analysis images from all correct trials in each condition were averaged together providing eight maps (4 optic flow stimuli by 2 eye positions). The average images were multiplied by “−1” to produce images whose brightness indicates expected neuronal activity. The grey scale at the bottom provides the amplitudes. The average of all maps was subtracted from each image. A. Clockwise (CW) during upward fixation. B. CW during downward fixation. C. Counter-clockwise (CCW) during upward fixation. D. CCW during downward fixation. E. Expansion (Exp) during upward fixation. F. Exp during downward fixation. G. Contraction (Contr) during upward fixation. H. Contr during downward fixation. The black lines indicate the putative border between 7a and DP. Horizontal bars: 1 mm. Data set: M1R 12-05-2001. |
PMC1784069_pone-0000200-g004_9114.jpg | What can you see in this picture? | Single condition map for each optic flow stimulus at different eye positions in the right hemisphere of M1R. The baseline normalization analysis images from all correct trials in each condition were averaged together providing eight maps (4 optic flow stimuli by 2 eye positions). The average images were multiplied by “−1” to produce images whose brightness indicates expected neuronal activity. The grey scale at the bottom provides the amplitudes. The average of all maps was subtracted from each image. A. Clockwise (CW) during upward fixation. B. CW during downward fixation. C. Counter-clockwise (CCW) during upward fixation. D. CCW during downward fixation. E. Expansion (Exp) during upward fixation. F. Exp during downward fixation. G. Contraction (Contr) during upward fixation. H. Contr during downward fixation. The black lines indicate the putative border between 7a and DP. Horizontal bars: 1 mm. Data set: M1R 12-05-2001. |
PMC1784069_pone-0000200-g004_9116.jpg | What is shown in this image? | Single condition map for each optic flow stimulus at different eye positions in the right hemisphere of M1R. The baseline normalization analysis images from all correct trials in each condition were averaged together providing eight maps (4 optic flow stimuli by 2 eye positions). The average images were multiplied by “−1” to produce images whose brightness indicates expected neuronal activity. The grey scale at the bottom provides the amplitudes. The average of all maps was subtracted from each image. A. Clockwise (CW) during upward fixation. B. CW during downward fixation. C. Counter-clockwise (CCW) during upward fixation. D. CCW during downward fixation. E. Expansion (Exp) during upward fixation. F. Exp during downward fixation. G. Contraction (Contr) during upward fixation. H. Contr during downward fixation. The black lines indicate the putative border between 7a and DP. Horizontal bars: 1 mm. Data set: M1R 12-05-2001. |
PMC1784069_pone-0000200-g004_9115.jpg | What stands out most in this visual? | Single condition map for each optic flow stimulus at different eye positions in the right hemisphere of M1R. The baseline normalization analysis images from all correct trials in each condition were averaged together providing eight maps (4 optic flow stimuli by 2 eye positions). The average images were multiplied by “−1” to produce images whose brightness indicates expected neuronal activity. The grey scale at the bottom provides the amplitudes. The average of all maps was subtracted from each image. A. Clockwise (CW) during upward fixation. B. CW during downward fixation. C. Counter-clockwise (CCW) during upward fixation. D. CCW during downward fixation. E. Expansion (Exp) during upward fixation. F. Exp during downward fixation. G. Contraction (Contr) during upward fixation. H. Contr during downward fixation. The black lines indicate the putative border between 7a and DP. Horizontal bars: 1 mm. Data set: M1R 12-05-2001. |
PMC1784069_pone-0000200-g004_9120.jpg | Can you identify the primary element in this image? | Single condition map for each optic flow stimulus at different eye positions in the right hemisphere of M1R. The baseline normalization analysis images from all correct trials in each condition were averaged together providing eight maps (4 optic flow stimuli by 2 eye positions). The average images were multiplied by “−1” to produce images whose brightness indicates expected neuronal activity. The grey scale at the bottom provides the amplitudes. The average of all maps was subtracted from each image. A. Clockwise (CW) during upward fixation. B. CW during downward fixation. C. Counter-clockwise (CCW) during upward fixation. D. CCW during downward fixation. E. Expansion (Exp) during upward fixation. F. Exp during downward fixation. G. Contraction (Contr) during upward fixation. H. Contr during downward fixation. The black lines indicate the putative border between 7a and DP. Horizontal bars: 1 mm. Data set: M1R 12-05-2001. |
PMC1784069_pone-0000200-g004_9113.jpg | What is the core subject represented in this visual? | Single condition map for each optic flow stimulus at different eye positions in the right hemisphere of M1R. The baseline normalization analysis images from all correct trials in each condition were averaged together providing eight maps (4 optic flow stimuli by 2 eye positions). The average images were multiplied by “−1” to produce images whose brightness indicates expected neuronal activity. The grey scale at the bottom provides the amplitudes. The average of all maps was subtracted from each image. A. Clockwise (CW) during upward fixation. B. CW during downward fixation. C. Counter-clockwise (CCW) during upward fixation. D. CCW during downward fixation. E. Expansion (Exp) during upward fixation. F. Exp during downward fixation. G. Contraction (Contr) during upward fixation. H. Contr during downward fixation. The black lines indicate the putative border between 7a and DP. Horizontal bars: 1 mm. Data set: M1R 12-05-2001. |
PMC1784078_F3_9123.jpg | What is the core subject represented in this visual? | (A) An anteroposterior radiograph revealed complete absence of the femorotibial joint space. (B) At revision, the rotating platform was entrapped in the notch of the femoral component with 90° of rotation. (C) Wearing of the rotating platform is shown. |
PMC1784078_F3_9121.jpg | What is the dominant medical problem in this image? | (A) An anteroposterior radiograph revealed complete absence of the femorotibial joint space. (B) At revision, the rotating platform was entrapped in the notch of the femoral component with 90° of rotation. (C) Wearing of the rotating platform is shown. |
PMC1784091_F1_9139.jpg | What is the focal point of this photograph? | clinical synopsis of a 6 years old girl with a history of short stature. Figure 1a shows the patient at the time of suspected growth hormone releasing hormone failure. 2 months after growth hormone therapy started a painful swelling of the cheek was noted (figure 1c) which worsened at the time of presentation 3 months later (figure 1d). Initial magnetic resonance imaging (MRI) was normal (figure 1b: T2-weighted transversal image (slice thickness 5 mm)). Subsequent MRI 5 months later did show a diffuse bone lesion affecting the os zygomaticum and involving surrounding soft tissue (figure 1e: Fat saturated strongly T2-weighted transversal image (slice thickness 5 mm)). Malignancy could not be excluded. Computed tomography revealed hyperostosis in addition to osteolysis (arrows) of the cortical bone (figure 1f). Conventional x-ray of the right hemithorax showed hyperostosis of the anterior 4th rip (figure 1g). Technetium 99m-MDP bone scan showed the involvement of the os zygomaticum and the clinically silent costal lesion (figure 1h). 1 year of non-steroidal anti-inflammatory treatment induced clinical remission (figure 1i). MRI did show a very small signal elevation in the area of the biopsy (figure j: Fat saturated strongly T2-weighted transversal image (slice thickness 5 mm)). |
PMC1784091_F1_9147.jpg | What can you see in this picture? | clinical synopsis of a 6 years old girl with a history of short stature. Figure 1a shows the patient at the time of suspected growth hormone releasing hormone failure. 2 months after growth hormone therapy started a painful swelling of the cheek was noted (figure 1c) which worsened at the time of presentation 3 months later (figure 1d). Initial magnetic resonance imaging (MRI) was normal (figure 1b: T2-weighted transversal image (slice thickness 5 mm)). Subsequent MRI 5 months later did show a diffuse bone lesion affecting the os zygomaticum and involving surrounding soft tissue (figure 1e: Fat saturated strongly T2-weighted transversal image (slice thickness 5 mm)). Malignancy could not be excluded. Computed tomography revealed hyperostosis in addition to osteolysis (arrows) of the cortical bone (figure 1f). Conventional x-ray of the right hemithorax showed hyperostosis of the anterior 4th rip (figure 1g). Technetium 99m-MDP bone scan showed the involvement of the os zygomaticum and the clinically silent costal lesion (figure 1h). 1 year of non-steroidal anti-inflammatory treatment induced clinical remission (figure 1i). MRI did show a very small signal elevation in the area of the biopsy (figure j: Fat saturated strongly T2-weighted transversal image (slice thickness 5 mm)). |
PMC1784091_F1_9141.jpg | What can you see in this picture? | clinical synopsis of a 6 years old girl with a history of short stature. Figure 1a shows the patient at the time of suspected growth hormone releasing hormone failure. 2 months after growth hormone therapy started a painful swelling of the cheek was noted (figure 1c) which worsened at the time of presentation 3 months later (figure 1d). Initial magnetic resonance imaging (MRI) was normal (figure 1b: T2-weighted transversal image (slice thickness 5 mm)). Subsequent MRI 5 months later did show a diffuse bone lesion affecting the os zygomaticum and involving surrounding soft tissue (figure 1e: Fat saturated strongly T2-weighted transversal image (slice thickness 5 mm)). Malignancy could not be excluded. Computed tomography revealed hyperostosis in addition to osteolysis (arrows) of the cortical bone (figure 1f). Conventional x-ray of the right hemithorax showed hyperostosis of the anterior 4th rip (figure 1g). Technetium 99m-MDP bone scan showed the involvement of the os zygomaticum and the clinically silent costal lesion (figure 1h). 1 year of non-steroidal anti-inflammatory treatment induced clinical remission (figure 1i). MRI did show a very small signal elevation in the area of the biopsy (figure j: Fat saturated strongly T2-weighted transversal image (slice thickness 5 mm)). |
PMC1784091_F1_9146.jpg | What is the core subject represented in this visual? | clinical synopsis of a 6 years old girl with a history of short stature. Figure 1a shows the patient at the time of suspected growth hormone releasing hormone failure. 2 months after growth hormone therapy started a painful swelling of the cheek was noted (figure 1c) which worsened at the time of presentation 3 months later (figure 1d). Initial magnetic resonance imaging (MRI) was normal (figure 1b: T2-weighted transversal image (slice thickness 5 mm)). Subsequent MRI 5 months later did show a diffuse bone lesion affecting the os zygomaticum and involving surrounding soft tissue (figure 1e: Fat saturated strongly T2-weighted transversal image (slice thickness 5 mm)). Malignancy could not be excluded. Computed tomography revealed hyperostosis in addition to osteolysis (arrows) of the cortical bone (figure 1f). Conventional x-ray of the right hemithorax showed hyperostosis of the anterior 4th rip (figure 1g). Technetium 99m-MDP bone scan showed the involvement of the os zygomaticum and the clinically silent costal lesion (figure 1h). 1 year of non-steroidal anti-inflammatory treatment induced clinical remission (figure 1i). MRI did show a very small signal elevation in the area of the biopsy (figure j: Fat saturated strongly T2-weighted transversal image (slice thickness 5 mm)). |
PMC1784091_F1_9142.jpg | What is the principal component of this image? | clinical synopsis of a 6 years old girl with a history of short stature. Figure 1a shows the patient at the time of suspected growth hormone releasing hormone failure. 2 months after growth hormone therapy started a painful swelling of the cheek was noted (figure 1c) which worsened at the time of presentation 3 months later (figure 1d). Initial magnetic resonance imaging (MRI) was normal (figure 1b: T2-weighted transversal image (slice thickness 5 mm)). Subsequent MRI 5 months later did show a diffuse bone lesion affecting the os zygomaticum and involving surrounding soft tissue (figure 1e: Fat saturated strongly T2-weighted transversal image (slice thickness 5 mm)). Malignancy could not be excluded. Computed tomography revealed hyperostosis in addition to osteolysis (arrows) of the cortical bone (figure 1f). Conventional x-ray of the right hemithorax showed hyperostosis of the anterior 4th rip (figure 1g). Technetium 99m-MDP bone scan showed the involvement of the os zygomaticum and the clinically silent costal lesion (figure 1h). 1 year of non-steroidal anti-inflammatory treatment induced clinical remission (figure 1i). MRI did show a very small signal elevation in the area of the biopsy (figure j: Fat saturated strongly T2-weighted transversal image (slice thickness 5 mm)). |
PMC1784091_F2_9131.jpg | What is the central feature of this picture? | clinical synopsis of a 10 years old girl with a history of back pain. Technetium 99m-MDP bone scan (figure 2a and b) shows the rib and multiple osseous spine lesions at diagnosis. Initial magnetic resonance imaging (MRI) revealed a compression of vertebra #9 and 11 (figure 2c: T1-weighted sagittal image (arrows); figure 2d: T1-weighted sagittal image after i.v. gadolinium enhancement), in addition to oedematous changes predominantly in the 8th vertebra (figure 2e: strongly T2-weighted sagittal image; arrow). Subsequent MRI 12 months later no longer showed oedematous changes, however the vertebral compressions were still present (figure 2f: T1-weighted sagittal image (arrows); figure 2g: T1-weighted sagittal image after i.v. gadolinium enhancement; figure 2h: strongly T2-weighted sagittal image). |
PMC1784091_F2_9137.jpg | What is the main focus of this visual representation? | clinical synopsis of a 10 years old girl with a history of back pain. Technetium 99m-MDP bone scan (figure 2a and b) shows the rib and multiple osseous spine lesions at diagnosis. Initial magnetic resonance imaging (MRI) revealed a compression of vertebra #9 and 11 (figure 2c: T1-weighted sagittal image (arrows); figure 2d: T1-weighted sagittal image after i.v. gadolinium enhancement), in addition to oedematous changes predominantly in the 8th vertebra (figure 2e: strongly T2-weighted sagittal image; arrow). Subsequent MRI 12 months later no longer showed oedematous changes, however the vertebral compressions were still present (figure 2f: T1-weighted sagittal image (arrows); figure 2g: T1-weighted sagittal image after i.v. gadolinium enhancement; figure 2h: strongly T2-weighted sagittal image). |
PMC1784091_F2_9135.jpg | What is being portrayed in this visual content? | clinical synopsis of a 10 years old girl with a history of back pain. Technetium 99m-MDP bone scan (figure 2a and b) shows the rib and multiple osseous spine lesions at diagnosis. Initial magnetic resonance imaging (MRI) revealed a compression of vertebra #9 and 11 (figure 2c: T1-weighted sagittal image (arrows); figure 2d: T1-weighted sagittal image after i.v. gadolinium enhancement), in addition to oedematous changes predominantly in the 8th vertebra (figure 2e: strongly T2-weighted sagittal image; arrow). Subsequent MRI 12 months later no longer showed oedematous changes, however the vertebral compressions were still present (figure 2f: T1-weighted sagittal image (arrows); figure 2g: T1-weighted sagittal image after i.v. gadolinium enhancement; figure 2h: strongly T2-weighted sagittal image). |
PMC1784091_F2_9132.jpg | What can you see in this picture? | clinical synopsis of a 10 years old girl with a history of back pain. Technetium 99m-MDP bone scan (figure 2a and b) shows the rib and multiple osseous spine lesions at diagnosis. Initial magnetic resonance imaging (MRI) revealed a compression of vertebra #9 and 11 (figure 2c: T1-weighted sagittal image (arrows); figure 2d: T1-weighted sagittal image after i.v. gadolinium enhancement), in addition to oedematous changes predominantly in the 8th vertebra (figure 2e: strongly T2-weighted sagittal image; arrow). Subsequent MRI 12 months later no longer showed oedematous changes, however the vertebral compressions were still present (figure 2f: T1-weighted sagittal image (arrows); figure 2g: T1-weighted sagittal image after i.v. gadolinium enhancement; figure 2h: strongly T2-weighted sagittal image). |
PMC1784091_F2_9133.jpg | What's the most prominent thing you notice in this picture? | clinical synopsis of a 10 years old girl with a history of back pain. Technetium 99m-MDP bone scan (figure 2a and b) shows the rib and multiple osseous spine lesions at diagnosis. Initial magnetic resonance imaging (MRI) revealed a compression of vertebra #9 and 11 (figure 2c: T1-weighted sagittal image (arrows); figure 2d: T1-weighted sagittal image after i.v. gadolinium enhancement), in addition to oedematous changes predominantly in the 8th vertebra (figure 2e: strongly T2-weighted sagittal image; arrow). Subsequent MRI 12 months later no longer showed oedematous changes, however the vertebral compressions were still present (figure 2f: T1-weighted sagittal image (arrows); figure 2g: T1-weighted sagittal image after i.v. gadolinium enhancement; figure 2h: strongly T2-weighted sagittal image). |
PMC1784091_F2_9134.jpg | What is the focal point of this photograph? | clinical synopsis of a 10 years old girl with a history of back pain. Technetium 99m-MDP bone scan (figure 2a and b) shows the rib and multiple osseous spine lesions at diagnosis. Initial magnetic resonance imaging (MRI) revealed a compression of vertebra #9 and 11 (figure 2c: T1-weighted sagittal image (arrows); figure 2d: T1-weighted sagittal image after i.v. gadolinium enhancement), in addition to oedematous changes predominantly in the 8th vertebra (figure 2e: strongly T2-weighted sagittal image; arrow). Subsequent MRI 12 months later no longer showed oedematous changes, however the vertebral compressions were still present (figure 2f: T1-weighted sagittal image (arrows); figure 2g: T1-weighted sagittal image after i.v. gadolinium enhancement; figure 2h: strongly T2-weighted sagittal image). |
PMC1784092_F2_9126.jpg | Can you identify the primary element in this image? | Sagittal MRI of the left popliteal fossa showing two involved nodes anterior to the neurovascular bundle. |
PMC1784092_F3_9129.jpg | What is the principal component of this image? | PET whole-body showing systemic uptake of the radiotracer. |
PMC1784092_F4_9125.jpg | What is the focal point of this photograph? | PET whole-body performed after chemotherapy, showing no signs of systemic disease. |
PMC1784092_F5_9127.jpg | What is the main focus of this visual representation? | PET whole-body performed after chemotherapy, showing no evidence of disease in the left popliteal fossa. |
PMC1784092_F5_9128.jpg | What is the central feature of this picture? | PET whole-body performed after chemotherapy, showing no evidence of disease in the left popliteal fossa. |
PMC1784113_F4_9151.jpg | What object or scene is depicted here? | Microscopic appearance of rat thyroid after bone marrow cell transplant. A. Group I H + E. 10 weeks after left intra ventricular transplantation. B. Group II H + E. 10 weeks after direct intra thyroid transplantation. C. Group III H+E. (Positive Controls). D. Group IV H + E. (Negative Controls). |
PMC1784113_F4_9149.jpg | What is the focal point of this photograph? | Microscopic appearance of rat thyroid after bone marrow cell transplant. A. Group I H + E. 10 weeks after left intra ventricular transplantation. B. Group II H + E. 10 weeks after direct intra thyroid transplantation. C. Group III H+E. (Positive Controls). D. Group IV H + E. (Negative Controls). |
PMC1784113_F4_9148.jpg | What is shown in this image? | Microscopic appearance of rat thyroid after bone marrow cell transplant. A. Group I H + E. 10 weeks after left intra ventricular transplantation. B. Group II H + E. 10 weeks after direct intra thyroid transplantation. C. Group III H+E. (Positive Controls). D. Group IV H + E. (Negative Controls). |
PMC1784113_F4_9150.jpg | What is the main focus of this visual representation? | Microscopic appearance of rat thyroid after bone marrow cell transplant. A. Group I H + E. 10 weeks after left intra ventricular transplantation. B. Group II H + E. 10 weeks after direct intra thyroid transplantation. C. Group III H+E. (Positive Controls). D. Group IV H + E. (Negative Controls). |
PMC1785375_F1_9153.jpg | What does this image primarily show? | GFP expression patterns driven by Promoterome reporter gene fusions. The ceh-32 Promoterome insert drives GFP expression in specific nerve cells in the head of a larva (A) and adult (B), and in anterior cells of an early embryo (C), in the C. elegans strain UL2623. An adult's anterior body wall muscle cells express GFP under the direction of the ceh-33 Promoterome insert in UL1265 (E). Additional head body wall muscle cells, as well as tail body wall muscle cells, express GFP driven by the ceh-34 Promoterome insert in larvae and adults of UL1512 (F). The unc-39 Promoterome insert drives GFP expression in specific nerve cells in an adult's head of UL2387 (G). The DIC images D and H correspond to fluorescent micrographs C and G respectively. All images were captured at 200× magnification, apart from C and D, captured at 400×, and F, captured at 100×. |
PMC1785375_F1_9158.jpg | What is the main focus of this visual representation? | GFP expression patterns driven by Promoterome reporter gene fusions. The ceh-32 Promoterome insert drives GFP expression in specific nerve cells in the head of a larva (A) and adult (B), and in anterior cells of an early embryo (C), in the C. elegans strain UL2623. An adult's anterior body wall muscle cells express GFP under the direction of the ceh-33 Promoterome insert in UL1265 (E). Additional head body wall muscle cells, as well as tail body wall muscle cells, express GFP driven by the ceh-34 Promoterome insert in larvae and adults of UL1512 (F). The unc-39 Promoterome insert drives GFP expression in specific nerve cells in an adult's head of UL2387 (G). The DIC images D and H correspond to fluorescent micrographs C and G respectively. All images were captured at 200× magnification, apart from C and D, captured at 400×, and F, captured at 100×. |
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