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PMC1852118_F3_10408.jpg | What is the principal component of this image? | Colitis development following DSS administration. Representative sections and histological assessment of colonic samples from A) WT and B) VDR KO mice receiving water; C) WT and D) VDR KO mice 5 days after receiving 3.5% DSS; E) WT and F) VDR KO mice 5 days after 2.5% DSS; G) WT and H) VDR KO mice 10 days after 2.5% DSS. Edema (asterisk), cellular inflammation in all layers (arrows). |
PMC1852118_F3_10410.jpg | What can you see in this picture? | Colitis development following DSS administration. Representative sections and histological assessment of colonic samples from A) WT and B) VDR KO mice receiving water; C) WT and D) VDR KO mice 5 days after receiving 3.5% DSS; E) WT and F) VDR KO mice 5 days after 2.5% DSS; G) WT and H) VDR KO mice 10 days after 2.5% DSS. Edema (asterisk), cellular inflammation in all layers (arrows). |
PMC1852118_F3_10409.jpg | What is shown in this image? | Colitis development following DSS administration. Representative sections and histological assessment of colonic samples from A) WT and B) VDR KO mice receiving water; C) WT and D) VDR KO mice 5 days after receiving 3.5% DSS; E) WT and F) VDR KO mice 5 days after 2.5% DSS; G) WT and H) VDR KO mice 10 days after 2.5% DSS. Edema (asterisk), cellular inflammation in all layers (arrows). |
PMC1852118_F3_10413.jpg | What is the central feature of this picture? | Colitis development following DSS administration. Representative sections and histological assessment of colonic samples from A) WT and B) VDR KO mice receiving water; C) WT and D) VDR KO mice 5 days after receiving 3.5% DSS; E) WT and F) VDR KO mice 5 days after 2.5% DSS; G) WT and H) VDR KO mice 10 days after 2.5% DSS. Edema (asterisk), cellular inflammation in all layers (arrows). |
PMC1852118_F3_10411.jpg | Describe the main subject of this image. | Colitis development following DSS administration. Representative sections and histological assessment of colonic samples from A) WT and B) VDR KO mice receiving water; C) WT and D) VDR KO mice 5 days after receiving 3.5% DSS; E) WT and F) VDR KO mice 5 days after 2.5% DSS; G) WT and H) VDR KO mice 10 days after 2.5% DSS. Edema (asterisk), cellular inflammation in all layers (arrows). |
PMC1852119_F4_10418.jpg | Can you identify the primary element in this image? | Immunofluorescence (IF) Analysis of DEK expression. AGN2a (column 2) or AGN2a/DEK (columns 1 and 3) were plated on glass chamber slides, fixed with 4% paraformaldehyde and visualized using a Nuance multispectral imaging system (Nuance 1P46, Cambridge Research and Instrumentation, Inc. Woburn, MA) mounted on a Zeiss Axio Imager Z1 microscope. Image files (200×) were captured and merged using the Axiovision 4.5 package (open program). For all cells, nuclei were stained blue with DAPI. Cells were stained with anti-human DEK antibody (1:100, columns 1 and 2) or similarly diluted isotype control antibody (column 3). Bound antibody was detected with goat anti-mouse IgG (H+L) conjugated to Alexa Fluor 555. Row (A) shows the merged DAPI and Alexa Fluor 555 image, and row (B) shows the staining of the Alexa Fluor 555 image alone. Data is representative of more than three separate experiments. |
PMC1852119_F4_10416.jpg | What stands out most in this visual? | Immunofluorescence (IF) Analysis of DEK expression. AGN2a (column 2) or AGN2a/DEK (columns 1 and 3) were plated on glass chamber slides, fixed with 4% paraformaldehyde and visualized using a Nuance multispectral imaging system (Nuance 1P46, Cambridge Research and Instrumentation, Inc. Woburn, MA) mounted on a Zeiss Axio Imager Z1 microscope. Image files (200×) were captured and merged using the Axiovision 4.5 package (open program). For all cells, nuclei were stained blue with DAPI. Cells were stained with anti-human DEK antibody (1:100, columns 1 and 2) or similarly diluted isotype control antibody (column 3). Bound antibody was detected with goat anti-mouse IgG (H+L) conjugated to Alexa Fluor 555. Row (A) shows the merged DAPI and Alexa Fluor 555 image, and row (B) shows the staining of the Alexa Fluor 555 image alone. Data is representative of more than three separate experiments. |
PMC1852119_F4_10417.jpg | Describe the main subject of this image. | Immunofluorescence (IF) Analysis of DEK expression. AGN2a (column 2) or AGN2a/DEK (columns 1 and 3) were plated on glass chamber slides, fixed with 4% paraformaldehyde and visualized using a Nuance multispectral imaging system (Nuance 1P46, Cambridge Research and Instrumentation, Inc. Woburn, MA) mounted on a Zeiss Axio Imager Z1 microscope. Image files (200×) were captured and merged using the Axiovision 4.5 package (open program). For all cells, nuclei were stained blue with DAPI. Cells were stained with anti-human DEK antibody (1:100, columns 1 and 2) or similarly diluted isotype control antibody (column 3). Bound antibody was detected with goat anti-mouse IgG (H+L) conjugated to Alexa Fluor 555. Row (A) shows the merged DAPI and Alexa Fluor 555 image, and row (B) shows the staining of the Alexa Fluor 555 image alone. Data is representative of more than three separate experiments. |
PMC1852119_F4_10419.jpg | What does this image primarily show? | Immunofluorescence (IF) Analysis of DEK expression. AGN2a (column 2) or AGN2a/DEK (columns 1 and 3) were plated on glass chamber slides, fixed with 4% paraformaldehyde and visualized using a Nuance multispectral imaging system (Nuance 1P46, Cambridge Research and Instrumentation, Inc. Woburn, MA) mounted on a Zeiss Axio Imager Z1 microscope. Image files (200×) were captured and merged using the Axiovision 4.5 package (open program). For all cells, nuclei were stained blue with DAPI. Cells were stained with anti-human DEK antibody (1:100, columns 1 and 2) or similarly diluted isotype control antibody (column 3). Bound antibody was detected with goat anti-mouse IgG (H+L) conjugated to Alexa Fluor 555. Row (A) shows the merged DAPI and Alexa Fluor 555 image, and row (B) shows the staining of the Alexa Fluor 555 image alone. Data is representative of more than three separate experiments. |
PMC1852146_pbio-0050103-g001_10423.jpg | What stands out most in this visual? | Regions Associated with Normal and Atypical Social Behaviour(A) Medial and lateral view of the PFC.(B) View of the ventral surface of the PFC and temporal poles.(C) Coronal slice illustrating the amygdalar and insular cortex.See also Table 1.ACC, anterior cingulate cortex; dlPFC, dorsolateral PFC; MFd, medial PFC; oMFC, orbitomedial PFC; TP, temporal pole; vlPFC, ventrolateral PFC; vmPFC, ventromedial PFC. |
PMC1852146_pbio-0050103-g001_10422.jpg | What's the most prominent thing you notice in this picture? | Regions Associated with Normal and Atypical Social Behaviour(A) Medial and lateral view of the PFC.(B) View of the ventral surface of the PFC and temporal poles.(C) Coronal slice illustrating the amygdalar and insular cortex.See also Table 1.ACC, anterior cingulate cortex; dlPFC, dorsolateral PFC; MFd, medial PFC; oMFC, orbitomedial PFC; TP, temporal pole; vlPFC, ventrolateral PFC; vmPFC, ventromedial PFC. |
PMC1852146_pbio-0050103-g001_10421.jpg | What is the central feature of this picture? | Regions Associated with Normal and Atypical Social Behaviour(A) Medial and lateral view of the PFC.(B) View of the ventral surface of the PFC and temporal poles.(C) Coronal slice illustrating the amygdalar and insular cortex.See also Table 1.ACC, anterior cingulate cortex; dlPFC, dorsolateral PFC; MFd, medial PFC; oMFC, orbitomedial PFC; TP, temporal pole; vlPFC, ventrolateral PFC; vmPFC, ventromedial PFC. |
PMC1852146_pbio-0050103-g002_10434.jpg | What is the focal point of this photograph? | Cases Where Brain Anomalies Have, or Have Not, Been Linked to Anti-Social Behaviour(A) Brain scan of patient J. S., who exhibited sociopathic behaviour [5]. The image shows a lesion in the orbital frontal cortex.(B) fMRI sagittal slice of the brain of patient J. Z., showing a lesion that was caused by the resection of pituitary tumour [4]. This lesion led to anti-social conduct, which was not exhibited before the surgery.(C) Orbitofrontal damage associated with symptoms of paedophilia and sexual misconduct in the case of a 40-year-old male patient.(D) Photograph of a patient after head injury (right) and fMRI scan 60 years later showing PFC damage (left) [53]. This patient showed personality changes, but no signs of anti-social conduct.(E) Cranial X-ray of a man who attempted suicide with a crossbow. Although the individual exhibited premorbid APD, the PFC damage caused by the crossbow arrow resulted in reversal of anti-social conduct [54]. |
PMC1852146_pbio-0050103-g002_10428.jpg | What can you see in this picture? | Cases Where Brain Anomalies Have, or Have Not, Been Linked to Anti-Social Behaviour(A) Brain scan of patient J. S., who exhibited sociopathic behaviour [5]. The image shows a lesion in the orbital frontal cortex.(B) fMRI sagittal slice of the brain of patient J. Z., showing a lesion that was caused by the resection of pituitary tumour [4]. This lesion led to anti-social conduct, which was not exhibited before the surgery.(C) Orbitofrontal damage associated with symptoms of paedophilia and sexual misconduct in the case of a 40-year-old male patient.(D) Photograph of a patient after head injury (right) and fMRI scan 60 years later showing PFC damage (left) [53]. This patient showed personality changes, but no signs of anti-social conduct.(E) Cranial X-ray of a man who attempted suicide with a crossbow. Although the individual exhibited premorbid APD, the PFC damage caused by the crossbow arrow resulted in reversal of anti-social conduct [54]. |
PMC1852295_F3_10424.jpg | What is the dominant medical problem in this image? | HepG2 cells were treated with 3.45 μg/ml zerumbone for 24 (B), 48 (C) and 72 (D) hours. DMSO treated HepG2 cells served as negative control (A) and thus gave TUNEL-negative results indicating less apoptotic signal. Arrows indicated cells with fragmented DNA due to apoptosis which occurred actively at the beginning of the treatment and the presence of apoptotic bodies after 72 hours at the end of treatment. Magnification: 1000×. |
PMC1852305_F1_10439.jpg | What stands out most in this visual? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10444.jpg | What is the focal point of this photograph? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10453.jpg | What is the core subject represented in this visual? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10438.jpg | What is the core subject represented in this visual? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10446.jpg | Can you identify the primary element in this image? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10443.jpg | What stands out most in this visual? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10445.jpg | What key item or scene is captured in this photo? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10436.jpg | What key item or scene is captured in this photo? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10451.jpg | What does this image primarily show? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10441.jpg | What key item or scene is captured in this photo? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10452.jpg | Describe the main subject of this image. | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10449.jpg | Describe the main subject of this image. | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10440.jpg | What object or scene is depicted here? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10437.jpg | What does this image primarily show? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852305_F1_10442.jpg | What object or scene is depicted here? | Transfection of the hypoblast. A-E: pCAB-Luc monitored by luciferase detection at time points following hypoblast tranfection: 2 hours (A), 5 hours (B), 7 hours (C), 10 hours (D), 14 hours (E). Coloured pixels represent light intensity with blue being least intense and red most intense. F-M: GFP expression in whole embryo- (F,G) and epiblast-transfected (H,I) tissues (fluorescence images, F, H and overlaid with brightfield images, G, I). Arrowheads indicate cells expressing GFP in H. J-M: dsRed and GFP expression in the hypoblast 8 hours (J,K) and 14 hours (L,M) after transfection. An overlay of fluorescence and brightfield images are shown in K and M. N-Q: longer culture periods reveal the transfected hypoblast (shown here with GFP only) in stage HH5 (N), HH7 (O), HH8- (P) and HH9 (Q) embryos. Arrows indicate labelled cells in the yolk sac. R-S: VEcis-Otx2 driving GFP is detected in transfected hypoblasts after 7–8 hours (R) and is seen in the crescent-shaped hypoblast at stage 4+/5 (S). T-U: Co-electroporation of VEcis-Otx2-GFP and CMV-dsRed shows GFP localised in the embryo in the rostral to the hindbrain (T) and also occasionally in the hindbrain (U) (arrows). dsRed is expressed in the entire electroporated region and is seen more caudally in the embryo and in the area opaca (arrowhead). |
PMC1852307_F3_10461.jpg | What does this image primarily show? | The labeling index is normal at the beginning of cortical neurogenesis, but decreases at late stages in the perlecan-null neocortex. (A-D) Immunofluorescence for BrdU (green) in the cortical primordium after a 30 min (A, B) and a 24 hours (C, D) survival to a BrdU pulse in wild-type (A, C) and perlecan-null (B, D) E16.5 embryos. In both cases, less BrdU+ cells are seen in the perlecan mutants. (E-F) Double immunofluorescence for BrdU (green) and Ki67 (red) in the pallium of E16.5 wild-type and perlecan-null embryos after a 24 h survival to a BrdU pulse at E15.5. Note the panels are high magnification views of the boxed areas in C, D. Observe abundant double-labeled cells (yellow) in the VZ and a thick layer containing BrdU+ cells (and no Ki67+ cells) in the SVZ of wild-type embryos, corresponding to the newly generated neurons (arrow in C and E). Observe the reduced BrdU incorporation in the perlecan-null dorsal cortex, affecting both the VZ and the SVZ. (G) Labeling index (the percentage of BrdU+ cells among Ki67+ progenitors) in cortical sections after 30 min, 4 hours and 24 hours survival to a BrdU pulse at E12.5, E13.5 or E16.5. Means ± SEM values are shown. n = 2 embryos for E12.5; n = 4 for E13.5 BrdU 4 h; n = 5 for E13.5 BrdU 24 h; n = 2 for E16.5 BrdU 30 min; and n = 2 for E16.5 BrdU 24 h. ** p < 0.001. No significant changes of labeling index are evident in the perlecan-deficient embryos at E12.5 and E13.5, but at E16.5 the index is significantly reduced. Scale bars: 100 μm (A-D), 40 μm (E, F). |
PMC1852307_F7_10471.jpg | What key item or scene is captured in this photo? | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852307_F7_10472.jpg | What key item or scene is captured in this photo? | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852307_F7_10467.jpg | What can you see in this picture? | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852307_F7_10474.jpg | What is shown in this image? | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852307_F7_10465.jpg | What is the principal component of this image? | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852307_F7_10466.jpg | Describe the main subject of this image. | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852307_F7_10473.jpg | What is the core subject represented in this visual? | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852307_F7_10469.jpg | What key item or scene is captured in this photo? | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852307_F7_10470.jpg | What is the core subject represented in this visual? | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852307_F7_10468.jpg | What object or scene is depicted here? | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852307_F7_10463.jpg | What can you see in this picture? | Distribution of Sonic Hedgehog protein in the telencephalon of perlecan-null embryos. (A-H) SHH immunostaining in the forebrain of wild-type (A, E) and perlecan-null (B, F) embryos at E10.5 (A-D) and E12.5 (E-H). C, D, G and H are higher magnifications of the boxed areas in A, B, E and F. In the absence of perlecan, the diffusion of SHH into the brain is still present, but there is a significant decrease in the signal intensity in the ventral telencephalon, especially in the medial ganglionic eminences. Note that the floor plate basal lamina shows a strong SHH immunostaining in the wild-type brain (arrows in C and G) whereas no signal is detectable in the perlecan-null embryos (D and H). (I-K) Laminin immunostaining shows basal lamina continuity in the E12.5 wild-type (I) and perlecan-null (J) floor plate. The deposition of perlecan immunostaining in wild-type embryo coincides with that of laminin (K). The region shown in I-K is the same shown between arrows in (G). (L-O) Immunostaining for Patched 1 (Ptch1), the receptor of SHH, in wild-type (L, N) and perlecan-null (M, O) brains at E12.5. Ptch1 distributes in the mantle of the ganglionic eminences and is absent in the midline, the site of strongest SHH signal. In the mutant there is normal distribution of Ptch1. Scale bars: 100 μm (A, B, E, F, L-O), 50 μm (C, D, G, H), 40 μm (I-K). |
PMC1852309_F1_10454.jpg | What object or scene is depicted here? | Pleomorphic Adenoma of the left parotid gland: Ultrasound image axial and Ultrasound image transversal |
PMC1852309_F2_10475.jpg | What object or scene is depicted here? | Pleomorphic Adenoma of the left parotid gland: MRI axial T1-weighted image, MRI contrast enhanced axial T1-weighted image and MRI axial T2-weighted image |
PMC1852309_F2_10477.jpg | What is the central feature of this picture? | Pleomorphic Adenoma of the left parotid gland: MRI axial T1-weighted image, MRI contrast enhanced axial T1-weighted image and MRI axial T2-weighted image |
PMC1852309_F2_10476.jpg | What is the main focus of this visual representation? | Pleomorphic Adenoma of the left parotid gland: MRI axial T1-weighted image, MRI contrast enhanced axial T1-weighted image and MRI axial T2-weighted image |
PMC1852412_F2_10478.jpg | What is the core subject represented in this visual? | Brain gene expression levels of Penk (encoding preproenkephalin) and Foxp1 (encoding forkhead box P1). The signal intensities of two genes, Penk and Foxp1, were imported into the NeuroZoom software tool to visualize the three-dimensional gene expression patterns of these genes in the context of brain anatomy. A ratio of the signal intensities of (a) Penk and (b) Foxp1 between 129S6/SvEvTac (129) and A/J (A) strains is shown in hippocampus (Hi), hypothalamus (Hyp), periaqueductal gray (PAG), and bed nucleus of the stria terminalis (BNST). The expression fold change values are shown in the upper right corner of each panel for each brain region separately, together with color coding that matches the color of each brain region in the three-dimensional mouse brain atlas, shown from four different angles. Note that the gene expression level of Penk in Hi and Hyp is higher in the 129 strain than in the A strain, but in Pag and Bnst it is higher in the A strain than in the 129 strain. Similarly, the expression level of Foxp1 in Hi is higher in the 129 strain than in the A strain, whereas in Hyp, Bnst, and Pag the expression level is higher in the A strain than in the 129 strain. |
PMC1852412_F2_10479.jpg | What does this image primarily show? | Brain gene expression levels of Penk (encoding preproenkephalin) and Foxp1 (encoding forkhead box P1). The signal intensities of two genes, Penk and Foxp1, were imported into the NeuroZoom software tool to visualize the three-dimensional gene expression patterns of these genes in the context of brain anatomy. A ratio of the signal intensities of (a) Penk and (b) Foxp1 between 129S6/SvEvTac (129) and A/J (A) strains is shown in hippocampus (Hi), hypothalamus (Hyp), periaqueductal gray (PAG), and bed nucleus of the stria terminalis (BNST). The expression fold change values are shown in the upper right corner of each panel for each brain region separately, together with color coding that matches the color of each brain region in the three-dimensional mouse brain atlas, shown from four different angles. Note that the gene expression level of Penk in Hi and Hyp is higher in the 129 strain than in the A strain, but in Pag and Bnst it is higher in the A strain than in the 129 strain. Similarly, the expression level of Foxp1 in Hi is higher in the 129 strain than in the A strain, whereas in Hyp, Bnst, and Pag the expression level is higher in the A strain than in the 129 strain. |
PMC1852545_F3_10481.jpg | What's the most prominent thing you notice in this picture? | Coronary angiography. Selective right coronary artery angiography (A) and left coronary artery angiography (B) demonstrating no angiographically detectable coronary artery disease. |
PMC1852545_F3_10480.jpg | Can you identify the primary element in this image? | Coronary angiography. Selective right coronary artery angiography (A) and left coronary artery angiography (B) demonstrating no angiographically detectable coronary artery disease. |
PMC1852545_F4_10482.jpg | What's the most prominent thing you notice in this picture? | Left ventriculograms. Diastolic (A) and systolic (B) morphology of the left ventricle with the typical appearance of apical ballooning in systole. |
PMC1852545_F4_10483.jpg | What does this image primarily show? | Left ventriculograms. Diastolic (A) and systolic (B) morphology of the left ventricle with the typical appearance of apical ballooning in systole. |
PMC1852547_F2_10488.jpg | What is the central feature of this picture? | Mesodermal differentiation potency of culture-expanded hMSC. Characterization of culture-expanded hMSC upon exposure to specific (A) chondrogenic, (B) osteogenic and (C) adipogenic agents, respectively. Chondrogenic, adipogenic and osteogenic differentiation potential were confirmed by means of (A) immunohistochemical staining of collagen type II fibers, (B) Von Kossa and (C) Oil Red O staining, respectively. 64 × 10 original magnification. Stainings shown are representative for at least 5 separate experiments. |
PMC1852547_F2_10489.jpg | What does this image primarily show? | Mesodermal differentiation potency of culture-expanded hMSC. Characterization of culture-expanded hMSC upon exposure to specific (A) chondrogenic, (B) osteogenic and (C) adipogenic agents, respectively. Chondrogenic, adipogenic and osteogenic differentiation potential were confirmed by means of (A) immunohistochemical staining of collagen type II fibers, (B) Von Kossa and (C) Oil Red O staining, respectively. 64 × 10 original magnification. Stainings shown are representative for at least 5 separate experiments. |
PMC1852547_F3_10494.jpg | What is the focal point of this photograph? | Differentiation potential of hMSC upon sequential exposure to hepatogenic agents. Upregulated (A) glycogen storage and (B) CK18 expression was shown by means of PAS-staining and immunofluorescence, respectively. A: 10 × 10 original magnification; B: 32 × 10 original magnification. Stainings shown are representative for at least 5 separate experiments. |
PMC1852547_F3_10495.jpg | What's the most prominent thing you notice in this picture? | Differentiation potential of hMSC upon sequential exposure to hepatogenic agents. Upregulated (A) glycogen storage and (B) CK18 expression was shown by means of PAS-staining and immunofluorescence, respectively. A: 10 × 10 original magnification; B: 32 × 10 original magnification. Stainings shown are representative for at least 5 separate experiments. |
PMC1852547_F3_10493.jpg | What is being portrayed in this visual content? | Differentiation potential of hMSC upon sequential exposure to hepatogenic agents. Upregulated (A) glycogen storage and (B) CK18 expression was shown by means of PAS-staining and immunofluorescence, respectively. A: 10 × 10 original magnification; B: 32 × 10 original magnification. Stainings shown are representative for at least 5 separate experiments. |
PMC1852547_F4_10484.jpg | What is the principal component of this image? | Cell morphology. Light-microscopic analysis of 17-day old sequentially (+/-1 μM TSA) and cocktail (+/-1 μM TSA)-exposed hMSC; 20 × 10 original magnification, phase contrast. |
PMC1852547_F4_10487.jpg | Can you identify the primary element in this image? | Cell morphology. Light-microscopic analysis of 17-day old sequentially (+/-1 μM TSA) and cocktail (+/-1 μM TSA)-exposed hMSC; 20 × 10 original magnification, phase contrast. |
PMC1852547_F4_10486.jpg | What is the core subject represented in this visual? | Cell morphology. Light-microscopic analysis of 17-day old sequentially (+/-1 μM TSA) and cocktail (+/-1 μM TSA)-exposed hMSC; 20 × 10 original magnification, phase contrast. |
PMC1852547_F4_10485.jpg | What does this image primarily show? | Cell morphology. Light-microscopic analysis of 17-day old sequentially (+/-1 μM TSA) and cocktail (+/-1 μM TSA)-exposed hMSC; 20 × 10 original magnification, phase contrast. |
PMC1852583_pone-0000400-g002_10496.jpg | What key item or scene is captured in this photo? | Full-length Abp1 and its SH3 domain alone both stimulate actin polymerization in vitro.GST-fusion proteins attached to glutathione sepharose 4B beads were incubated with high speed supernatants of brain extracts supplemented with an energy regenerating mix and Alexa Fluor® 568 G-actin. Actin polymerization is detected on the surface of beads coated with N-WASP PWA (A), full-length Abp1 (B, C) and the Abp1 SH3 domain (D). No polymerization was observed when the beads were coated with a mutated version of the Abp1 SH3 domain (E). Left panels (A–E), actin fluorescence of Alexa Fluor® 568 G-actin; right panels (A′–E′), phase contrast. Bars (A and D) = 10 µm; bars (B, C and E) = 25 µm. |
PMC1852583_pone-0000400-g002_10497.jpg | What can you see in this picture? | Full-length Abp1 and its SH3 domain alone both stimulate actin polymerization in vitro.GST-fusion proteins attached to glutathione sepharose 4B beads were incubated with high speed supernatants of brain extracts supplemented with an energy regenerating mix and Alexa Fluor® 568 G-actin. Actin polymerization is detected on the surface of beads coated with N-WASP PWA (A), full-length Abp1 (B, C) and the Abp1 SH3 domain (D). No polymerization was observed when the beads were coated with a mutated version of the Abp1 SH3 domain (E). Left panels (A–E), actin fluorescence of Alexa Fluor® 568 G-actin; right panels (A′–E′), phase contrast. Bars (A and D) = 10 µm; bars (B, C and E) = 25 µm. |
PMC1852583_pone-0000400-g002_10501.jpg | What is being portrayed in this visual content? | Full-length Abp1 and its SH3 domain alone both stimulate actin polymerization in vitro.GST-fusion proteins attached to glutathione sepharose 4B beads were incubated with high speed supernatants of brain extracts supplemented with an energy regenerating mix and Alexa Fluor® 568 G-actin. Actin polymerization is detected on the surface of beads coated with N-WASP PWA (A), full-length Abp1 (B, C) and the Abp1 SH3 domain (D). No polymerization was observed when the beads were coated with a mutated version of the Abp1 SH3 domain (E). Left panels (A–E), actin fluorescence of Alexa Fluor® 568 G-actin; right panels (A′–E′), phase contrast. Bars (A and D) = 10 µm; bars (B, C and E) = 25 µm. |
PMC1852583_pone-0000400-g002_10503.jpg | What is the core subject represented in this visual? | Full-length Abp1 and its SH3 domain alone both stimulate actin polymerization in vitro.GST-fusion proteins attached to glutathione sepharose 4B beads were incubated with high speed supernatants of brain extracts supplemented with an energy regenerating mix and Alexa Fluor® 568 G-actin. Actin polymerization is detected on the surface of beads coated with N-WASP PWA (A), full-length Abp1 (B, C) and the Abp1 SH3 domain (D). No polymerization was observed when the beads were coated with a mutated version of the Abp1 SH3 domain (E). Left panels (A–E), actin fluorescence of Alexa Fluor® 568 G-actin; right panels (A′–E′), phase contrast. Bars (A and D) = 10 µm; bars (B, C and E) = 25 µm. |
PMC1852583_pone-0000400-g002_10500.jpg | What object or scene is depicted here? | Full-length Abp1 and its SH3 domain alone both stimulate actin polymerization in vitro.GST-fusion proteins attached to glutathione sepharose 4B beads were incubated with high speed supernatants of brain extracts supplemented with an energy regenerating mix and Alexa Fluor® 568 G-actin. Actin polymerization is detected on the surface of beads coated with N-WASP PWA (A), full-length Abp1 (B, C) and the Abp1 SH3 domain (D). No polymerization was observed when the beads were coated with a mutated version of the Abp1 SH3 domain (E). Left panels (A–E), actin fluorescence of Alexa Fluor® 568 G-actin; right panels (A′–E′), phase contrast. Bars (A and D) = 10 µm; bars (B, C and E) = 25 µm. |
PMC1852583_pone-0000400-g002_10498.jpg | What is being portrayed in this visual content? | Full-length Abp1 and its SH3 domain alone both stimulate actin polymerization in vitro.GST-fusion proteins attached to glutathione sepharose 4B beads were incubated with high speed supernatants of brain extracts supplemented with an energy regenerating mix and Alexa Fluor® 568 G-actin. Actin polymerization is detected on the surface of beads coated with N-WASP PWA (A), full-length Abp1 (B, C) and the Abp1 SH3 domain (D). No polymerization was observed when the beads were coated with a mutated version of the Abp1 SH3 domain (E). Left panels (A–E), actin fluorescence of Alexa Fluor® 568 G-actin; right panels (A′–E′), phase contrast. Bars (A and D) = 10 µm; bars (B, C and E) = 25 µm. |
PMC1852583_pone-0000400-g002_10505.jpg | What is the dominant medical problem in this image? | Full-length Abp1 and its SH3 domain alone both stimulate actin polymerization in vitro.GST-fusion proteins attached to glutathione sepharose 4B beads were incubated with high speed supernatants of brain extracts supplemented with an energy regenerating mix and Alexa Fluor® 568 G-actin. Actin polymerization is detected on the surface of beads coated with N-WASP PWA (A), full-length Abp1 (B, C) and the Abp1 SH3 domain (D). No polymerization was observed when the beads were coated with a mutated version of the Abp1 SH3 domain (E). Left panels (A–E), actin fluorescence of Alexa Fluor® 568 G-actin; right panels (A′–E′), phase contrast. Bars (A and D) = 10 µm; bars (B, C and E) = 25 µm. |
PMC1852649_f5-ehp0115-000541_10515.jpg | What is being portrayed in this visual content? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852649_f5-ehp0115-000541_10514.jpg | What key item or scene is captured in this photo? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852649_f5-ehp0115-000541_10516.jpg | What is the principal component of this image? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852649_f5-ehp0115-000541_10509.jpg | What does this image primarily show? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852649_f5-ehp0115-000541_10510.jpg | What is the central feature of this picture? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852649_f5-ehp0115-000541_10517.jpg | What is being portrayed in this visual content? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852649_f5-ehp0115-000541_10506.jpg | What is the core subject represented in this visual? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852649_f5-ehp0115-000541_10508.jpg | What's the most prominent thing you notice in this picture? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852649_f5-ehp0115-000541_10511.jpg | What is the main focus of this visual representation? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852649_f5-ehp0115-000541_10507.jpg | Can you identify the primary element in this image? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852649_f5-ehp0115-000541_10519.jpg | Can you identify the primary element in this image? | Mammary gland whole mounts from female offspring prenatally exposed to AMM or ATR (mg/kg bw/day). Images (at 16 × magnification) represent the mean scores for each treatment and age as indicated in Table 4, and illustrate significant changes with increased AMM exposure, such as fewer and smaller ductal buds and lateral branching (PND4); undifferentiated end buds and glands not grown together (PND33); and TEBs, large lobuloaveolar units, and immature branching (PND60). Large dark structures present in a few segments are stained lymph nodes. Bars = 2 mm. |
PMC1852692_f1-ehp0115-000519_10520.jpg | What is being portrayed in this visual content? | Example MRI and magnetic resonance spectroscopy spectra from participants in the low (A) and high (B) bone lead groups. The left panels show the region of interest outlined by a thick white box overlying the right hippocampal region on the MRIs. The right panels show the accompanying spectra with peaks for mI, Cho, Cr, and NAA indicated. |
PMC1852692_f1-ehp0115-000519_10521.jpg | Can you identify the primary element in this image? | Example MRI and magnetic resonance spectroscopy spectra from participants in the low (A) and high (B) bone lead groups. The left panels show the region of interest outlined by a thick white box overlying the right hippocampal region on the MRIs. The right panels show the accompanying spectra with peaks for mI, Cho, Cr, and NAA indicated. |
PMC1853075_F7_10525.jpg | What is the core subject represented in this visual? | Chromatin interphase. Transcription occurs at the interface of chromatin. (A) Electron micrograph showing transcription by RNA pol II (gold particles) at the border of condensed chromatin masses. Figure reproduced from reference 52, with permission from Springer. Activation of transcription proceeds with nuclear volume change. The amount of chromatin (blue) is stable and only the dynamic phase (red) can be changed. As a result by increasing the amount of proteins/RNA, the nuclear volume changes and also the interface between DNA and proteins/RNA, where transcription occurs. (B) Cell with low level of activity (small interface). (C) Very active cell (Large interface). |
PMC1853103_F1_10527.jpg | What key item or scene is captured in this photo? | ABCG2+ cells in the prostate epithelium. Serial sections of normal human prostate were stained for ABCG2 (A – C) or CD138 (D – F). A subpopulation of cells in the basal epithelium is ABCG2+. Endothelial cells of capillaries (black arrow) are also ABCG2+ but are CD138- (red arrow). All basal cells of a particular small gland were ABCG2+/CD138+ (B). Original magnification is 100×, magnification for C and F is 200×. |
PMC1853103_F1_10528.jpg | What is the principal component of this image? | ABCG2+ cells in the prostate epithelium. Serial sections of normal human prostate were stained for ABCG2 (A – C) or CD138 (D – F). A subpopulation of cells in the basal epithelium is ABCG2+. Endothelial cells of capillaries (black arrow) are also ABCG2+ but are CD138- (red arrow). All basal cells of a particular small gland were ABCG2+/CD138+ (B). Original magnification is 100×, magnification for C and F is 200×. |
PMC1853103_F1_10530.jpg | What is being portrayed in this visual content? | ABCG2+ cells in the prostate epithelium. Serial sections of normal human prostate were stained for ABCG2 (A – C) or CD138 (D – F). A subpopulation of cells in the basal epithelium is ABCG2+. Endothelial cells of capillaries (black arrow) are also ABCG2+ but are CD138- (red arrow). All basal cells of a particular small gland were ABCG2+/CD138+ (B). Original magnification is 100×, magnification for C and F is 200×. |
PMC1853103_F1_10529.jpg | What does this image primarily show? | ABCG2+ cells in the prostate epithelium. Serial sections of normal human prostate were stained for ABCG2 (A – C) or CD138 (D – F). A subpopulation of cells in the basal epithelium is ABCG2+. Endothelial cells of capillaries (black arrow) are also ABCG2+ but are CD138- (red arrow). All basal cells of a particular small gland were ABCG2+/CD138+ (B). Original magnification is 100×, magnification for C and F is 200×. |
PMC1853103_F1_10531.jpg | Describe the main subject of this image. | ABCG2+ cells in the prostate epithelium. Serial sections of normal human prostate were stained for ABCG2 (A – C) or CD138 (D – F). A subpopulation of cells in the basal epithelium is ABCG2+. Endothelial cells of capillaries (black arrow) are also ABCG2+ but are CD138- (red arrow). All basal cells of a particular small gland were ABCG2+/CD138+ (B). Original magnification is 100×, magnification for C and F is 200×. |
PMC1853103_F1_10532.jpg | What is the dominant medical problem in this image? | ABCG2+ cells in the prostate epithelium. Serial sections of normal human prostate were stained for ABCG2 (A – C) or CD138 (D – F). A subpopulation of cells in the basal epithelium is ABCG2+. Endothelial cells of capillaries (black arrow) are also ABCG2+ but are CD138- (red arrow). All basal cells of a particular small gland were ABCG2+/CD138+ (B). Original magnification is 100×, magnification for C and F is 200×. |
PMC1853108_F3_10533.jpg | What is the central feature of this picture? | PAR4-AP induces bladder inflammation. Anesthetized female C57BL6 mice were catheterized, the bladder was emptied, and a volume of 200 μl of a solution of PAR4-AP (10 μM) was instilled into the urinary bladder. Twenty four hours later, bladders were removed, processed for histology, and stained with H&E. At low magnification, photomicrograph illustrates the distribution of inflammatory cells extending from the submucosa to deep regions in the detrusor smooth muscle (green arrows). Magnifications = ×100 |
PMC1853108_F4_10535.jpg | What object or scene is depicted here? | A-D. PAR4-AP induces bladder inflammation. Anesthetized female C57BL6 mice were catheterized, the bladder was emptied, and a volume of 200 μl of a solution of PAR4-AP (10 μM) was instilled into the urinary bladder. Twenty four hours later, bladders were removed, processed for histology, and stained with H&E. A characteristic photomicrograph represents sub-urothelium inflammatory infiltrate around a blood vessel (A) and dilation of blood vessels (white arrow). At higher magnification (B), it was possible to visualize that the majority of inflammatory cells in response to PAR4-AP presented a characteristic "doughnut" shape indicative of mouse PMNs (green arrowhead). The submucosal edema is illustrated in C. Figure 4D illustrates inflammatory cells surrounding a structure resembling a nerve element (black arrow). Magnifications A = ×200, B = ×400, C = ×200, and D = ×400. |
PMC1853108_F4_10537.jpg | What is the principal component of this image? | A-D. PAR4-AP induces bladder inflammation. Anesthetized female C57BL6 mice were catheterized, the bladder was emptied, and a volume of 200 μl of a solution of PAR4-AP (10 μM) was instilled into the urinary bladder. Twenty four hours later, bladders were removed, processed for histology, and stained with H&E. A characteristic photomicrograph represents sub-urothelium inflammatory infiltrate around a blood vessel (A) and dilation of blood vessels (white arrow). At higher magnification (B), it was possible to visualize that the majority of inflammatory cells in response to PAR4-AP presented a characteristic "doughnut" shape indicative of mouse PMNs (green arrowhead). The submucosal edema is illustrated in C. Figure 4D illustrates inflammatory cells surrounding a structure resembling a nerve element (black arrow). Magnifications A = ×200, B = ×400, C = ×200, and D = ×400. |
PMC1853108_F4_10534.jpg | What's the most prominent thing you notice in this picture? | A-D. PAR4-AP induces bladder inflammation. Anesthetized female C57BL6 mice were catheterized, the bladder was emptied, and a volume of 200 μl of a solution of PAR4-AP (10 μM) was instilled into the urinary bladder. Twenty four hours later, bladders were removed, processed for histology, and stained with H&E. A characteristic photomicrograph represents sub-urothelium inflammatory infiltrate around a blood vessel (A) and dilation of blood vessels (white arrow). At higher magnification (B), it was possible to visualize that the majority of inflammatory cells in response to PAR4-AP presented a characteristic "doughnut" shape indicative of mouse PMNs (green arrowhead). The submucosal edema is illustrated in C. Figure 4D illustrates inflammatory cells surrounding a structure resembling a nerve element (black arrow). Magnifications A = ×200, B = ×400, C = ×200, and D = ×400. |
PMC1853117_ppat-0030057-g001_10542.jpg | What is the main focus of this visual representation? |
S. epidermidis Kills C. elegans and Causes Intestinal Distension(A) C. elegans killing assays on lawns of live S. epidermidis 9142 (squares), heat-killed S. epidermidis 9142 (triangles), or B. subtilis strain RL2244 (diamonds).(B) Survival of C. elegans exposed to live S. epidermidis 9142 (squares), admixtures of live S. epidermidis 9142 and heat-killed E. coli OP50 at a ratio of 1:1 (circles) or 1:5 (diamonds), or heat-killed E. coli OP50 alone (triangles).(C) N2 C. elegans were exposed to B. subtilis RL2244 or S. epidermidis 9142 for 24 h and then visualized by Nomarski differential contrast microscopy. Arrows demarcate the intestinal tract lumen. Magnification, ×40. |
PMC1853117_ppat-0030057-g001_10543.jpg | What is the dominant medical problem in this image? |
S. epidermidis Kills C. elegans and Causes Intestinal Distension(A) C. elegans killing assays on lawns of live S. epidermidis 9142 (squares), heat-killed S. epidermidis 9142 (triangles), or B. subtilis strain RL2244 (diamonds).(B) Survival of C. elegans exposed to live S. epidermidis 9142 (squares), admixtures of live S. epidermidis 9142 and heat-killed E. coli OP50 at a ratio of 1:1 (circles) or 1:5 (diamonds), or heat-killed E. coli OP50 alone (triangles).(C) N2 C. elegans were exposed to B. subtilis RL2244 or S. epidermidis 9142 for 24 h and then visualized by Nomarski differential contrast microscopy. Arrows demarcate the intestinal tract lumen. Magnification, ×40. |
PMC1853117_ppat-0030057-g005_10549.jpg | Describe the main subject of this image. | Production of PIA by S. epidermidis within the C. elegans Intestinal TractConfocal microscopy images of C. elegans feeding on S. epidermidis labeled with FITC-conjugated WGA lectin, which selectively labels the exopolysaccharide of the biofilm matrix.Nematodes feeding on labeled wild-type S. epidermidis 9142 (A–D) or 9142-M10 (E–H).(A and E) Nomarski differential interference contrast image of anterior portion of nematodes.(B and F) Green fluorescence due to FITC-labeled lectin adhering to S. epidermidis exopolysaccharide and C. elegans intestinal autofluorescence.(C and G) Red fluorescence resulting from intestinal autofluorescence.(D and H) Merged fluorescent images in which green demonstrates bound lectin and yellow demonstrates intestinal autofluorescence. |
PMC1853117_ppat-0030057-g005_10547.jpg | What is the focal point of this photograph? | Production of PIA by S. epidermidis within the C. elegans Intestinal TractConfocal microscopy images of C. elegans feeding on S. epidermidis labeled with FITC-conjugated WGA lectin, which selectively labels the exopolysaccharide of the biofilm matrix.Nematodes feeding on labeled wild-type S. epidermidis 9142 (A–D) or 9142-M10 (E–H).(A and E) Nomarski differential interference contrast image of anterior portion of nematodes.(B and F) Green fluorescence due to FITC-labeled lectin adhering to S. epidermidis exopolysaccharide and C. elegans intestinal autofluorescence.(C and G) Red fluorescence resulting from intestinal autofluorescence.(D and H) Merged fluorescent images in which green demonstrates bound lectin and yellow demonstrates intestinal autofluorescence. |
PMC1853117_ppat-0030057-g005_10550.jpg | What is shown in this image? | Production of PIA by S. epidermidis within the C. elegans Intestinal TractConfocal microscopy images of C. elegans feeding on S. epidermidis labeled with FITC-conjugated WGA lectin, which selectively labels the exopolysaccharide of the biofilm matrix.Nematodes feeding on labeled wild-type S. epidermidis 9142 (A–D) or 9142-M10 (E–H).(A and E) Nomarski differential interference contrast image of anterior portion of nematodes.(B and F) Green fluorescence due to FITC-labeled lectin adhering to S. epidermidis exopolysaccharide and C. elegans intestinal autofluorescence.(C and G) Red fluorescence resulting from intestinal autofluorescence.(D and H) Merged fluorescent images in which green demonstrates bound lectin and yellow demonstrates intestinal autofluorescence. |
PMC1853117_ppat-0030057-g005_10551.jpg | What is being portrayed in this visual content? | Production of PIA by S. epidermidis within the C. elegans Intestinal TractConfocal microscopy images of C. elegans feeding on S. epidermidis labeled with FITC-conjugated WGA lectin, which selectively labels the exopolysaccharide of the biofilm matrix.Nematodes feeding on labeled wild-type S. epidermidis 9142 (A–D) or 9142-M10 (E–H).(A and E) Nomarski differential interference contrast image of anterior portion of nematodes.(B and F) Green fluorescence due to FITC-labeled lectin adhering to S. epidermidis exopolysaccharide and C. elegans intestinal autofluorescence.(C and G) Red fluorescence resulting from intestinal autofluorescence.(D and H) Merged fluorescent images in which green demonstrates bound lectin and yellow demonstrates intestinal autofluorescence. |
PMC1853117_ppat-0030057-g005_10546.jpg | What is the core subject represented in this visual? | Production of PIA by S. epidermidis within the C. elegans Intestinal TractConfocal microscopy images of C. elegans feeding on S. epidermidis labeled with FITC-conjugated WGA lectin, which selectively labels the exopolysaccharide of the biofilm matrix.Nematodes feeding on labeled wild-type S. epidermidis 9142 (A–D) or 9142-M10 (E–H).(A and E) Nomarski differential interference contrast image of anterior portion of nematodes.(B and F) Green fluorescence due to FITC-labeled lectin adhering to S. epidermidis exopolysaccharide and C. elegans intestinal autofluorescence.(C and G) Red fluorescence resulting from intestinal autofluorescence.(D and H) Merged fluorescent images in which green demonstrates bound lectin and yellow demonstrates intestinal autofluorescence. |
PMC1853120_pgen-0030062-g001_10560.jpg | What is shown in this image? | Expression of Dmrt7 mRNA and Protein(A) RT-PCR analysis of Dmrt7 mRNA from ten organs of adult mouse. cDNA from each organ was amplified with primers specific for Dmrt7 (top row) and β-actin (bottom row).(B) Dmrt7 mRNA expression during the first round of spermatogenesis. cDNAs obtained from testis at the indicated days after birth were amplified as in (A).(C) DMRT7 protein expression. Immunofluorescence of testis sections from 6-wk-old male stained with antibody to DMRT7 (green) and DAPI (blue).(D) DMRT7 subcellular localization to XY body. Testis sections from 6-wk-old male stained with antibodies to DMRT7 (red) and SUMO-1 (green). SUMO-1 is localized to the XY body. Right-most panel shows merge of other two panels. Inserts show higher magnification of pachytene spermatocytes with XY bodies. |
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