image stringlengths 20 66 | question stringclasses 16
values | answer stringlengths 3 10.7k |
|---|---|---|
PMC1780055_F1_8884.jpg | What is the principal component of this image? | A, C Pre-Operative MRI: contrast-enhancing lesion in the left and right frontal lobe. B MRI follow-up after 6 month: no recurrence of the tumor after resection and irradiation (left frontal). D MRI follow-up after 6 month: no progression of the tumor after irradiation only (right frontal). |
PMC1780055_F2_8880.jpg | What's the most prominent thing you notice in this picture? | Whole-body MRI (T2WI) identified structure of increased signal intensity in close relation to the sciatic nerve (arrow). |
PMC1780056_F1_8905.jpg | What is shown in this image? | Pre operative CT scan. Representative pre-operative CT scan of a patient showing a thalamic haemorrhage with associated hydrocephalus and blood in the third and both lateral ventricles. |
PMC1780056_F1_8901.jpg | What key item or scene is captured in this photo? | Pre operative CT scan. Representative pre-operative CT scan of a patient showing a thalamic haemorrhage with associated hydrocephalus and blood in the third and both lateral ventricles. |
PMC1780056_F1_8904.jpg | What key item or scene is captured in this photo? | Pre operative CT scan. Representative pre-operative CT scan of a patient showing a thalamic haemorrhage with associated hydrocephalus and blood in the third and both lateral ventricles. |
PMC1780056_F1_8903.jpg | What is the focal point of this photograph? | Pre operative CT scan. Representative pre-operative CT scan of a patient showing a thalamic haemorrhage with associated hydrocephalus and blood in the third and both lateral ventricles. |
PMC1780056_F1_8902.jpg | What key item or scene is captured in this photo? | Pre operative CT scan. Representative pre-operative CT scan of a patient showing a thalamic haemorrhage with associated hydrocephalus and blood in the third and both lateral ventricles. |
PMC1780056_F2_8891.jpg | What is the main focus of this visual representation? | Pre operative CT scan. Representative pre-operative CT scan of a patient showing a posterior fossa haemorrhage with associated hydrocephalus and blood in the ventricles. |
PMC1780056_F2_8890.jpg | What is shown in this image? | Pre operative CT scan. Representative pre-operative CT scan of a patient showing a posterior fossa haemorrhage with associated hydrocephalus and blood in the ventricles. |
PMC1780056_F2_8893.jpg | What is the main focus of this visual representation? | Pre operative CT scan. Representative pre-operative CT scan of a patient showing a posterior fossa haemorrhage with associated hydrocephalus and blood in the ventricles. |
PMC1780056_F3_8899.jpg | What is the dominant medical problem in this image? | Post operative CT scan. Post operative CT scan of the patient depicted in figure 1. Scan done seven days after surgery showing resolving hydrocephalus and the absence of intraventricular blood. |
PMC1780056_F3_8896.jpg | What can you see in this picture? | Post operative CT scan. Post operative CT scan of the patient depicted in figure 1. Scan done seven days after surgery showing resolving hydrocephalus and the absence of intraventricular blood. |
PMC1780056_F3_8894.jpg | What does this image primarily show? | Post operative CT scan. Post operative CT scan of the patient depicted in figure 1. Scan done seven days after surgery showing resolving hydrocephalus and the absence of intraventricular blood. |
PMC1780056_F3_8897.jpg | What is shown in this image? | Post operative CT scan. Post operative CT scan of the patient depicted in figure 1. Scan done seven days after surgery showing resolving hydrocephalus and the absence of intraventricular blood. |
PMC1780056_F3_8895.jpg | What key item or scene is captured in this photo? | Post operative CT scan. Post operative CT scan of the patient depicted in figure 1. Scan done seven days after surgery showing resolving hydrocephalus and the absence of intraventricular blood. |
PMC1780056_F3_8898.jpg | Can you identify the primary element in this image? | Post operative CT scan. Post operative CT scan of the patient depicted in figure 1. Scan done seven days after surgery showing resolving hydrocephalus and the absence of intraventricular blood. |
PMC1780056_F4_8889.jpg | Describe the main subject of this image. | Post operative CT scan. Post operative CT scan of the patient depicted in figure 2. Scan done five days after surgery showing resolving hydrocephalus. |
PMC1780056_F4_8886.jpg | Can you identify the primary element in this image? | Post operative CT scan. Post operative CT scan of the patient depicted in figure 2. Scan done five days after surgery showing resolving hydrocephalus. |
PMC1780056_F4_8887.jpg | What can you see in this picture? | Post operative CT scan. Post operative CT scan of the patient depicted in figure 2. Scan done five days after surgery showing resolving hydrocephalus. |
PMC1780056_F4_8888.jpg | Can you identify the primary element in this image? | Post operative CT scan. Post operative CT scan of the patient depicted in figure 2. Scan done five days after surgery showing resolving hydrocephalus. |
PMC1781429_F1_8907.jpg | What is the dominant medical problem in this image? | Patient at age 12 showing dsymorphic features including microcephaly (head circumference 43 cm), hypertelorism, broad nasal bridge, broadened tip of the nose, and thin upper lip. A photograph of this patient and the description of her mutations have previously been presented in figure 2 of the report by O'Driscoll et al. [4]. It should be noted that there is a labeling error in the legend of figure 2 in reference [4]: The text corresponding to the photograph of our patient is marked with (B) but should read (C). |
PMC1781431_F4_8912.jpg | What is the core subject represented in this visual? | Sections of early 4-cell stage zebrafish and medaka embryos. Semi-thin section of zebrafish (A) and medaka (B) embryos visualized in a light microscope. Arrows indicate the areas shown in C-F representing the cleavage positions. The insets represent the orientation of the sections. Low magnification at the electron microscope showing the region of the germ plasm of zebrafish (C), and the corresponding position in medaka (D). At a higher magnification, the germ plasm of zebrafish is visible as distinct amorphous inclusions with a regular spherical shape and a filamentous fine structure lacking a surrounding membrane (E). At this magnification germ plasm resembling structure composed of irregularly shaped amorphous inclusions with a granular fine structure can be observed in medaka embryos. As described for zebrafish [28], the putative germ plasm of medaka can be followed in serial sections. |
PMC1781431_F4_8913.jpg | Can you identify the primary element in this image? | Sections of early 4-cell stage zebrafish and medaka embryos. Semi-thin section of zebrafish (A) and medaka (B) embryos visualized in a light microscope. Arrows indicate the areas shown in C-F representing the cleavage positions. The insets represent the orientation of the sections. Low magnification at the electron microscope showing the region of the germ plasm of zebrafish (C), and the corresponding position in medaka (D). At a higher magnification, the germ plasm of zebrafish is visible as distinct amorphous inclusions with a regular spherical shape and a filamentous fine structure lacking a surrounding membrane (E). At this magnification germ plasm resembling structure composed of irregularly shaped amorphous inclusions with a granular fine structure can be observed in medaka embryos. As described for zebrafish [28], the putative germ plasm of medaka can be followed in serial sections. |
PMC1781431_F4_8909.jpg | What is the core subject represented in this visual? | Sections of early 4-cell stage zebrafish and medaka embryos. Semi-thin section of zebrafish (A) and medaka (B) embryos visualized in a light microscope. Arrows indicate the areas shown in C-F representing the cleavage positions. The insets represent the orientation of the sections. Low magnification at the electron microscope showing the region of the germ plasm of zebrafish (C), and the corresponding position in medaka (D). At a higher magnification, the germ plasm of zebrafish is visible as distinct amorphous inclusions with a regular spherical shape and a filamentous fine structure lacking a surrounding membrane (E). At this magnification germ plasm resembling structure composed of irregularly shaped amorphous inclusions with a granular fine structure can be observed in medaka embryos. As described for zebrafish [28], the putative germ plasm of medaka can be followed in serial sections. |
PMC1781437_F1_8915.jpg | What is the dominant medical problem in this image? | Transgene construction and βgal staining of lung lobes. A. Transgene fragment for microinjection. The Cre cDNA and a Neo polyadenylylation signal were placed under the control of the mouse α-SMA promoter (-1070 to +2582, including the first exon and part of the first intron). B. Comparison of βgal staining in the bronchi of R26R and α-SMA-Cre/R26R mice. Positive βgal staining (blue color) is observed in the bronchi of α-SMA-Cre/R26R mice (a, 20× magnification), but not in R26R mice (b, 20× magnification). |
PMC1781437_F2_8926.jpg | What key item or scene is captured in this photo? | βgal and immunofluorescent staining in lung tissues of α-SMA-Cre/R26R mice. In βgal stained sections (a, b, c, d, g), intrapulmonary veins were homogeneously stained (a, b) and pulmonary arteries were heterogeneously stained (a). In the main bronchus of pulmonary hilum, unstained ciliated epithelia were surrounded by a βgal stained muscular layer (a, arrowhead), βgal staining was not detected in terminal bronchioles, although small veins were positively stained (c). The thin layer of βgal staining was observed in the sub-epithelial areas of small and medium bronchi, respectively (arrowheads in b, d, g). The βgal stained areas of bronchus (d, g) paralleled the staining pattern for α-SMA (TRITC-labeled, arrowheads in e, h) and SM-MHC (FITC-labeled, arrowheads in f, i) (a-c, 100×, d-i, 400× magnification). |
PMC1781437_F2_8925.jpg | What stands out most in this visual? | βgal and immunofluorescent staining in lung tissues of α-SMA-Cre/R26R mice. In βgal stained sections (a, b, c, d, g), intrapulmonary veins were homogeneously stained (a, b) and pulmonary arteries were heterogeneously stained (a). In the main bronchus of pulmonary hilum, unstained ciliated epithelia were surrounded by a βgal stained muscular layer (a, arrowhead), βgal staining was not detected in terminal bronchioles, although small veins were positively stained (c). The thin layer of βgal staining was observed in the sub-epithelial areas of small and medium bronchi, respectively (arrowheads in b, d, g). The βgal stained areas of bronchus (d, g) paralleled the staining pattern for α-SMA (TRITC-labeled, arrowheads in e, h) and SM-MHC (FITC-labeled, arrowheads in f, i) (a-c, 100×, d-i, 400× magnification). |
PMC1781437_F2_8921.jpg | What key item or scene is captured in this photo? | βgal and immunofluorescent staining in lung tissues of α-SMA-Cre/R26R mice. In βgal stained sections (a, b, c, d, g), intrapulmonary veins were homogeneously stained (a, b) and pulmonary arteries were heterogeneously stained (a). In the main bronchus of pulmonary hilum, unstained ciliated epithelia were surrounded by a βgal stained muscular layer (a, arrowhead), βgal staining was not detected in terminal bronchioles, although small veins were positively stained (c). The thin layer of βgal staining was observed in the sub-epithelial areas of small and medium bronchi, respectively (arrowheads in b, d, g). The βgal stained areas of bronchus (d, g) paralleled the staining pattern for α-SMA (TRITC-labeled, arrowheads in e, h) and SM-MHC (FITC-labeled, arrowheads in f, i) (a-c, 100×, d-i, 400× magnification). |
PMC1781437_F2_8923.jpg | What is shown in this image? | βgal and immunofluorescent staining in lung tissues of α-SMA-Cre/R26R mice. In βgal stained sections (a, b, c, d, g), intrapulmonary veins were homogeneously stained (a, b) and pulmonary arteries were heterogeneously stained (a). In the main bronchus of pulmonary hilum, unstained ciliated epithelia were surrounded by a βgal stained muscular layer (a, arrowhead), βgal staining was not detected in terminal bronchioles, although small veins were positively stained (c). The thin layer of βgal staining was observed in the sub-epithelial areas of small and medium bronchi, respectively (arrowheads in b, d, g). The βgal stained areas of bronchus (d, g) paralleled the staining pattern for α-SMA (TRITC-labeled, arrowheads in e, h) and SM-MHC (FITC-labeled, arrowheads in f, i) (a-c, 100×, d-i, 400× magnification). |
PMC1781437_F2_8919.jpg | What is the focal point of this photograph? | βgal and immunofluorescent staining in lung tissues of α-SMA-Cre/R26R mice. In βgal stained sections (a, b, c, d, g), intrapulmonary veins were homogeneously stained (a, b) and pulmonary arteries were heterogeneously stained (a). In the main bronchus of pulmonary hilum, unstained ciliated epithelia were surrounded by a βgal stained muscular layer (a, arrowhead), βgal staining was not detected in terminal bronchioles, although small veins were positively stained (c). The thin layer of βgal staining was observed in the sub-epithelial areas of small and medium bronchi, respectively (arrowheads in b, d, g). The βgal stained areas of bronchus (d, g) paralleled the staining pattern for α-SMA (TRITC-labeled, arrowheads in e, h) and SM-MHC (FITC-labeled, arrowheads in f, i) (a-c, 100×, d-i, 400× magnification). |
PMC1781437_F2_8922.jpg | Can you identify the primary element in this image? | βgal and immunofluorescent staining in lung tissues of α-SMA-Cre/R26R mice. In βgal stained sections (a, b, c, d, g), intrapulmonary veins were homogeneously stained (a, b) and pulmonary arteries were heterogeneously stained (a). In the main bronchus of pulmonary hilum, unstained ciliated epithelia were surrounded by a βgal stained muscular layer (a, arrowhead), βgal staining was not detected in terminal bronchioles, although small veins were positively stained (c). The thin layer of βgal staining was observed in the sub-epithelial areas of small and medium bronchi, respectively (arrowheads in b, d, g). The βgal stained areas of bronchus (d, g) paralleled the staining pattern for α-SMA (TRITC-labeled, arrowheads in e, h) and SM-MHC (FITC-labeled, arrowheads in f, i) (a-c, 100×, d-i, 400× magnification). |
PMC1781437_F2_8918.jpg | What object or scene is depicted here? | βgal and immunofluorescent staining in lung tissues of α-SMA-Cre/R26R mice. In βgal stained sections (a, b, c, d, g), intrapulmonary veins were homogeneously stained (a, b) and pulmonary arteries were heterogeneously stained (a). In the main bronchus of pulmonary hilum, unstained ciliated epithelia were surrounded by a βgal stained muscular layer (a, arrowhead), βgal staining was not detected in terminal bronchioles, although small veins were positively stained (c). The thin layer of βgal staining was observed in the sub-epithelial areas of small and medium bronchi, respectively (arrowheads in b, d, g). The βgal stained areas of bronchus (d, g) paralleled the staining pattern for α-SMA (TRITC-labeled, arrowheads in e, h) and SM-MHC (FITC-labeled, arrowheads in f, i) (a-c, 100×, d-i, 400× magnification). |
PMC1781437_F3_8928.jpg | What key item or scene is captured in this photo? | Effects of BLM on lung α-SMA protein levels, ECM deposition and βgal staining. Panel A: βgal and Masson's trichrome-staining in sections of lung tissue shows βgal staining to wholemount left lung lobes of the PBS-treated (a) and the BLM-treated mice (b) (a, b 10× magnification). In moderate bronchi, thickened bronchial wall with homogeneous βgal stained fusiform cells was observed in the BLM-treated lungs (d), and not in the PBS-treated mouse (c), Arrowheads indicate that a few cells in alveolar wall were positively stained (d). In pulmonary bronchioles and vessels, BLM treated lung demonstrated enhanced βgal expression (f, h), compared with that of PBS treated lung (e, g). βgal stained venous wall was thickened (arrowhead in f) and the positively stained cells infiltrated outwards (arrowhead in h). In the Masson's trichrome-stained lung sections (i, j), extensive collagen staining (Blue color) was seen in BLM treated lung (arrowheads in j), but not in the control with PBS (i). (c-j 400× magnification). Panel B: Western blot analysis of protein extracts from lower right lobes of the BLM treated mice (2) and control mice (1). |
PMC1781437_F3_8936.jpg | What's the most prominent thing you notice in this picture? | Effects of BLM on lung α-SMA protein levels, ECM deposition and βgal staining. Panel A: βgal and Masson's trichrome-staining in sections of lung tissue shows βgal staining to wholemount left lung lobes of the PBS-treated (a) and the BLM-treated mice (b) (a, b 10× magnification). In moderate bronchi, thickened bronchial wall with homogeneous βgal stained fusiform cells was observed in the BLM-treated lungs (d), and not in the PBS-treated mouse (c), Arrowheads indicate that a few cells in alveolar wall were positively stained (d). In pulmonary bronchioles and vessels, BLM treated lung demonstrated enhanced βgal expression (f, h), compared with that of PBS treated lung (e, g). βgal stained venous wall was thickened (arrowhead in f) and the positively stained cells infiltrated outwards (arrowhead in h). In the Masson's trichrome-stained lung sections (i, j), extensive collagen staining (Blue color) was seen in BLM treated lung (arrowheads in j), but not in the control with PBS (i). (c-j 400× magnification). Panel B: Western blot analysis of protein extracts from lower right lobes of the BLM treated mice (2) and control mice (1). |
PMC1781437_F3_8930.jpg | What is the core subject represented in this visual? | Effects of BLM on lung α-SMA protein levels, ECM deposition and βgal staining. Panel A: βgal and Masson's trichrome-staining in sections of lung tissue shows βgal staining to wholemount left lung lobes of the PBS-treated (a) and the BLM-treated mice (b) (a, b 10× magnification). In moderate bronchi, thickened bronchial wall with homogeneous βgal stained fusiform cells was observed in the BLM-treated lungs (d), and not in the PBS-treated mouse (c), Arrowheads indicate that a few cells in alveolar wall were positively stained (d). In pulmonary bronchioles and vessels, BLM treated lung demonstrated enhanced βgal expression (f, h), compared with that of PBS treated lung (e, g). βgal stained venous wall was thickened (arrowhead in f) and the positively stained cells infiltrated outwards (arrowhead in h). In the Masson's trichrome-stained lung sections (i, j), extensive collagen staining (Blue color) was seen in BLM treated lung (arrowheads in j), but not in the control with PBS (i). (c-j 400× magnification). Panel B: Western blot analysis of protein extracts from lower right lobes of the BLM treated mice (2) and control mice (1). |
PMC1781437_F3_8929.jpg | What key item or scene is captured in this photo? | Effects of BLM on lung α-SMA protein levels, ECM deposition and βgal staining. Panel A: βgal and Masson's trichrome-staining in sections of lung tissue shows βgal staining to wholemount left lung lobes of the PBS-treated (a) and the BLM-treated mice (b) (a, b 10× magnification). In moderate bronchi, thickened bronchial wall with homogeneous βgal stained fusiform cells was observed in the BLM-treated lungs (d), and not in the PBS-treated mouse (c), Arrowheads indicate that a few cells in alveolar wall were positively stained (d). In pulmonary bronchioles and vessels, BLM treated lung demonstrated enhanced βgal expression (f, h), compared with that of PBS treated lung (e, g). βgal stained venous wall was thickened (arrowhead in f) and the positively stained cells infiltrated outwards (arrowhead in h). In the Masson's trichrome-stained lung sections (i, j), extensive collagen staining (Blue color) was seen in BLM treated lung (arrowheads in j), but not in the control with PBS (i). (c-j 400× magnification). Panel B: Western blot analysis of protein extracts from lower right lobes of the BLM treated mice (2) and control mice (1). |
PMC1781437_F3_8927.jpg | What is the principal component of this image? | Effects of BLM on lung α-SMA protein levels, ECM deposition and βgal staining. Panel A: βgal and Masson's trichrome-staining in sections of lung tissue shows βgal staining to wholemount left lung lobes of the PBS-treated (a) and the BLM-treated mice (b) (a, b 10× magnification). In moderate bronchi, thickened bronchial wall with homogeneous βgal stained fusiform cells was observed in the BLM-treated lungs (d), and not in the PBS-treated mouse (c), Arrowheads indicate that a few cells in alveolar wall were positively stained (d). In pulmonary bronchioles and vessels, BLM treated lung demonstrated enhanced βgal expression (f, h), compared with that of PBS treated lung (e, g). βgal stained venous wall was thickened (arrowhead in f) and the positively stained cells infiltrated outwards (arrowhead in h). In the Masson's trichrome-stained lung sections (i, j), extensive collagen staining (Blue color) was seen in BLM treated lung (arrowheads in j), but not in the control with PBS (i). (c-j 400× magnification). Panel B: Western blot analysis of protein extracts from lower right lobes of the BLM treated mice (2) and control mice (1). |
PMC1781437_F3_8934.jpg | What is the main focus of this visual representation? | Effects of BLM on lung α-SMA protein levels, ECM deposition and βgal staining. Panel A: βgal and Masson's trichrome-staining in sections of lung tissue shows βgal staining to wholemount left lung lobes of the PBS-treated (a) and the BLM-treated mice (b) (a, b 10× magnification). In moderate bronchi, thickened bronchial wall with homogeneous βgal stained fusiform cells was observed in the BLM-treated lungs (d), and not in the PBS-treated mouse (c), Arrowheads indicate that a few cells in alveolar wall were positively stained (d). In pulmonary bronchioles and vessels, BLM treated lung demonstrated enhanced βgal expression (f, h), compared with that of PBS treated lung (e, g). βgal stained venous wall was thickened (arrowhead in f) and the positively stained cells infiltrated outwards (arrowhead in h). In the Masson's trichrome-stained lung sections (i, j), extensive collagen staining (Blue color) was seen in BLM treated lung (arrowheads in j), but not in the control with PBS (i). (c-j 400× magnification). Panel B: Western blot analysis of protein extracts from lower right lobes of the BLM treated mice (2) and control mice (1). |
PMC1781437_F4_8942.jpg | What is the dominant medical problem in this image? | βgal and αSMA positively stained bronchial epithelial cells in the α-SMA-Cre R26R mice treated with BLM. βgal stained lung sections of α-SMA-Cre/R26R mice without and with BLM treatment (a-c). The section from BLM treated mice showed a few βgal stained bronchial epithelial cells (arrowheads in b and c), but not from PBS treated mice (a). Double immunofluorescent staining for α-SMA and E-Cadherin was performed on the sections from PBS (d-f) or BLM (g-i) treated mice. d, g: FITC-labeled E-cadherin; e, h: TRITC labeled α-SMA. Positive double immunofluorescent staining (g, h, i) was observed in the bronchial epithelial cells lining the bronchioles of the BLM-treated lung where βgal staining was detected as above, but not in the control (d, e, f). The images of (d) and (e), or (g) and (h) were merged into (f) and (i). The red fluorescence (h arrowhead) indicated the positive α-SMA staining and yellow fluorescent staining (i arrowhead) indicated that the epithelial cells positively co-stained with α-SMA and E-Cadherin. (all images are 400× magnification). |
PMC1781437_F4_8939.jpg | What is the central feature of this picture? | βgal and αSMA positively stained bronchial epithelial cells in the α-SMA-Cre R26R mice treated with BLM. βgal stained lung sections of α-SMA-Cre/R26R mice without and with BLM treatment (a-c). The section from BLM treated mice showed a few βgal stained bronchial epithelial cells (arrowheads in b and c), but not from PBS treated mice (a). Double immunofluorescent staining for α-SMA and E-Cadherin was performed on the sections from PBS (d-f) or BLM (g-i) treated mice. d, g: FITC-labeled E-cadherin; e, h: TRITC labeled α-SMA. Positive double immunofluorescent staining (g, h, i) was observed in the bronchial epithelial cells lining the bronchioles of the BLM-treated lung where βgal staining was detected as above, but not in the control (d, e, f). The images of (d) and (e), or (g) and (h) were merged into (f) and (i). The red fluorescence (h arrowhead) indicated the positive α-SMA staining and yellow fluorescent staining (i arrowhead) indicated that the epithelial cells positively co-stained with α-SMA and E-Cadherin. (all images are 400× magnification). |
PMC1781437_F4_8944.jpg | What is the core subject represented in this visual? | βgal and αSMA positively stained bronchial epithelial cells in the α-SMA-Cre R26R mice treated with BLM. βgal stained lung sections of α-SMA-Cre/R26R mice without and with BLM treatment (a-c). The section from BLM treated mice showed a few βgal stained bronchial epithelial cells (arrowheads in b and c), but not from PBS treated mice (a). Double immunofluorescent staining for α-SMA and E-Cadherin was performed on the sections from PBS (d-f) or BLM (g-i) treated mice. d, g: FITC-labeled E-cadherin; e, h: TRITC labeled α-SMA. Positive double immunofluorescent staining (g, h, i) was observed in the bronchial epithelial cells lining the bronchioles of the BLM-treated lung where βgal staining was detected as above, but not in the control (d, e, f). The images of (d) and (e), or (g) and (h) were merged into (f) and (i). The red fluorescence (h arrowhead) indicated the positive α-SMA staining and yellow fluorescent staining (i arrowhead) indicated that the epithelial cells positively co-stained with α-SMA and E-Cadherin. (all images are 400× magnification). |
PMC1781437_F4_8945.jpg | What can you see in this picture? | βgal and αSMA positively stained bronchial epithelial cells in the α-SMA-Cre R26R mice treated with BLM. βgal stained lung sections of α-SMA-Cre/R26R mice without and with BLM treatment (a-c). The section from BLM treated mice showed a few βgal stained bronchial epithelial cells (arrowheads in b and c), but not from PBS treated mice (a). Double immunofluorescent staining for α-SMA and E-Cadherin was performed on the sections from PBS (d-f) or BLM (g-i) treated mice. d, g: FITC-labeled E-cadherin; e, h: TRITC labeled α-SMA. Positive double immunofluorescent staining (g, h, i) was observed in the bronchial epithelial cells lining the bronchioles of the BLM-treated lung where βgal staining was detected as above, but not in the control (d, e, f). The images of (d) and (e), or (g) and (h) were merged into (f) and (i). The red fluorescence (h arrowhead) indicated the positive α-SMA staining and yellow fluorescent staining (i arrowhead) indicated that the epithelial cells positively co-stained with α-SMA and E-Cadherin. (all images are 400× magnification). |
PMC1781437_F4_8943.jpg | What is shown in this image? | βgal and αSMA positively stained bronchial epithelial cells in the α-SMA-Cre R26R mice treated with BLM. βgal stained lung sections of α-SMA-Cre/R26R mice without and with BLM treatment (a-c). The section from BLM treated mice showed a few βgal stained bronchial epithelial cells (arrowheads in b and c), but not from PBS treated mice (a). Double immunofluorescent staining for α-SMA and E-Cadherin was performed on the sections from PBS (d-f) or BLM (g-i) treated mice. d, g: FITC-labeled E-cadherin; e, h: TRITC labeled α-SMA. Positive double immunofluorescent staining (g, h, i) was observed in the bronchial epithelial cells lining the bronchioles of the BLM-treated lung where βgal staining was detected as above, but not in the control (d, e, f). The images of (d) and (e), or (g) and (h) were merged into (f) and (i). The red fluorescence (h arrowhead) indicated the positive α-SMA staining and yellow fluorescent staining (i arrowhead) indicated that the epithelial cells positively co-stained with α-SMA and E-Cadherin. (all images are 400× magnification). |
PMC1781437_F4_8937.jpg | What is the central feature of this picture? | βgal and αSMA positively stained bronchial epithelial cells in the α-SMA-Cre R26R mice treated with BLM. βgal stained lung sections of α-SMA-Cre/R26R mice without and with BLM treatment (a-c). The section from BLM treated mice showed a few βgal stained bronchial epithelial cells (arrowheads in b and c), but not from PBS treated mice (a). Double immunofluorescent staining for α-SMA and E-Cadherin was performed on the sections from PBS (d-f) or BLM (g-i) treated mice. d, g: FITC-labeled E-cadherin; e, h: TRITC labeled α-SMA. Positive double immunofluorescent staining (g, h, i) was observed in the bronchial epithelial cells lining the bronchioles of the BLM-treated lung where βgal staining was detected as above, but not in the control (d, e, f). The images of (d) and (e), or (g) and (h) were merged into (f) and (i). The red fluorescence (h arrowhead) indicated the positive α-SMA staining and yellow fluorescent staining (i arrowhead) indicated that the epithelial cells positively co-stained with α-SMA and E-Cadherin. (all images are 400× magnification). |
PMC1781437_F4_8940.jpg | What can you see in this picture? | βgal and αSMA positively stained bronchial epithelial cells in the α-SMA-Cre R26R mice treated with BLM. βgal stained lung sections of α-SMA-Cre/R26R mice without and with BLM treatment (a-c). The section from BLM treated mice showed a few βgal stained bronchial epithelial cells (arrowheads in b and c), but not from PBS treated mice (a). Double immunofluorescent staining for α-SMA and E-Cadherin was performed on the sections from PBS (d-f) or BLM (g-i) treated mice. d, g: FITC-labeled E-cadherin; e, h: TRITC labeled α-SMA. Positive double immunofluorescent staining (g, h, i) was observed in the bronchial epithelial cells lining the bronchioles of the BLM-treated lung where βgal staining was detected as above, but not in the control (d, e, f). The images of (d) and (e), or (g) and (h) were merged into (f) and (i). The red fluorescence (h arrowhead) indicated the positive α-SMA staining and yellow fluorescent staining (i arrowhead) indicated that the epithelial cells positively co-stained with α-SMA and E-Cadherin. (all images are 400× magnification). |
PMC1781437_F4_8941.jpg | What is the focal point of this photograph? | βgal and αSMA positively stained bronchial epithelial cells in the α-SMA-Cre R26R mice treated with BLM. βgal stained lung sections of α-SMA-Cre/R26R mice without and with BLM treatment (a-c). The section from BLM treated mice showed a few βgal stained bronchial epithelial cells (arrowheads in b and c), but not from PBS treated mice (a). Double immunofluorescent staining for α-SMA and E-Cadherin was performed on the sections from PBS (d-f) or BLM (g-i) treated mice. d, g: FITC-labeled E-cadherin; e, h: TRITC labeled α-SMA. Positive double immunofluorescent staining (g, h, i) was observed in the bronchial epithelial cells lining the bronchioles of the BLM-treated lung where βgal staining was detected as above, but not in the control (d, e, f). The images of (d) and (e), or (g) and (h) were merged into (f) and (i). The red fluorescence (h arrowhead) indicated the positive α-SMA staining and yellow fluorescent staining (i arrowhead) indicated that the epithelial cells positively co-stained with α-SMA and E-Cadherin. (all images are 400× magnification). |
PMC1781437_F4_8938.jpg | What is the core subject represented in this visual? | βgal and αSMA positively stained bronchial epithelial cells in the α-SMA-Cre R26R mice treated with BLM. βgal stained lung sections of α-SMA-Cre/R26R mice without and with BLM treatment (a-c). The section from BLM treated mice showed a few βgal stained bronchial epithelial cells (arrowheads in b and c), but not from PBS treated mice (a). Double immunofluorescent staining for α-SMA and E-Cadherin was performed on the sections from PBS (d-f) or BLM (g-i) treated mice. d, g: FITC-labeled E-cadherin; e, h: TRITC labeled α-SMA. Positive double immunofluorescent staining (g, h, i) was observed in the bronchial epithelial cells lining the bronchioles of the BLM-treated lung where βgal staining was detected as above, but not in the control (d, e, f). The images of (d) and (e), or (g) and (h) were merged into (f) and (i). The red fluorescence (h arrowhead) indicated the positive α-SMA staining and yellow fluorescent staining (i arrowhead) indicated that the epithelial cells positively co-stained with α-SMA and E-Cadherin. (all images are 400× magnification). |
PMC1781437_F5_8949.jpg | What is the main focus of this visual representation? | Phenotypic analysis of the human bronchial epithelial cell line (16HBE) following exposure to TGF-β1. Immunofluorescent staining for E-cadherin (a, b) showed that exposure to TGF-β1 (b) resulted in an apparent reduction and redistribution of E-cadherin from intercellular junction areas into cytoplasm, compared to control (a). Mesenchymal marker F-actin, was faintly stained at the cell margin in the control (c), whereas the staining was substantially enhanced and abundantly located throughout cytoplasm after TGF-β1 stimulation (d). Immunofluorescent staining for (-SMA was not detected in the cells under basal conditions (e), but was observable in a few cells after TGF-β1 exposure (f). |
PMC1781437_F5_8951.jpg | What is the principal component of this image? | Phenotypic analysis of the human bronchial epithelial cell line (16HBE) following exposure to TGF-β1. Immunofluorescent staining for E-cadherin (a, b) showed that exposure to TGF-β1 (b) resulted in an apparent reduction and redistribution of E-cadherin from intercellular junction areas into cytoplasm, compared to control (a). Mesenchymal marker F-actin, was faintly stained at the cell margin in the control (c), whereas the staining was substantially enhanced and abundantly located throughout cytoplasm after TGF-β1 stimulation (d). Immunofluorescent staining for (-SMA was not detected in the cells under basal conditions (e), but was observable in a few cells after TGF-β1 exposure (f). |
PMC1781437_F5_8948.jpg | What is the dominant medical problem in this image? | Phenotypic analysis of the human bronchial epithelial cell line (16HBE) following exposure to TGF-β1. Immunofluorescent staining for E-cadherin (a, b) showed that exposure to TGF-β1 (b) resulted in an apparent reduction and redistribution of E-cadherin from intercellular junction areas into cytoplasm, compared to control (a). Mesenchymal marker F-actin, was faintly stained at the cell margin in the control (c), whereas the staining was substantially enhanced and abundantly located throughout cytoplasm after TGF-β1 stimulation (d). Immunofluorescent staining for (-SMA was not detected in the cells under basal conditions (e), but was observable in a few cells after TGF-β1 exposure (f). |
PMC1781437_F5_8946.jpg | What stands out most in this visual? | Phenotypic analysis of the human bronchial epithelial cell line (16HBE) following exposure to TGF-β1. Immunofluorescent staining for E-cadherin (a, b) showed that exposure to TGF-β1 (b) resulted in an apparent reduction and redistribution of E-cadherin from intercellular junction areas into cytoplasm, compared to control (a). Mesenchymal marker F-actin, was faintly stained at the cell margin in the control (c), whereas the staining was substantially enhanced and abundantly located throughout cytoplasm after TGF-β1 stimulation (d). Immunofluorescent staining for (-SMA was not detected in the cells under basal conditions (e), but was observable in a few cells after TGF-β1 exposure (f). |
PMC1781437_F5_8950.jpg | What is the dominant medical problem in this image? | Phenotypic analysis of the human bronchial epithelial cell line (16HBE) following exposure to TGF-β1. Immunofluorescent staining for E-cadherin (a, b) showed that exposure to TGF-β1 (b) resulted in an apparent reduction and redistribution of E-cadherin from intercellular junction areas into cytoplasm, compared to control (a). Mesenchymal marker F-actin, was faintly stained at the cell margin in the control (c), whereas the staining was substantially enhanced and abundantly located throughout cytoplasm after TGF-β1 stimulation (d). Immunofluorescent staining for (-SMA was not detected in the cells under basal conditions (e), but was observable in a few cells after TGF-β1 exposure (f). |
PMC1781446_F1_8953.jpg | Can you identify the primary element in this image? | Radiological examination for bone showing absence of epiphysis at the lower end of femur and upper end of tibia in Twin A. |
PMC1781446_F1_8952.jpg | What is the central feature of this picture? | Radiological examination for bone showing absence of epiphysis at the lower end of femur and upper end of tibia in Twin A. |
PMC1781446_F2_8954.jpg | Describe the main subject of this image. | Radiological examination for bone showing epiphysis at the lower end of femur and upper end of tibia in Twin B. |
PMC1781452_F1_8959.jpg | What is the dominant medical problem in this image? | Micrographs of AVIs in the epidermal cells of fully open lisianthus petals. A. Bright field microscopy image of an unstained transverse section of the inner petal region, showing the distinct morphology of AVIs between the adaxial and abaxial epidermal cells. Irregular AVIs in the adaxial epidermal cells (upper) and vesicle-like AVIs in the abaxial epidermal cells (lower). B. Transverse section of adaxial epidermal cells in Fig. A at higher magnification, showing the central vacuoles (V) and the irregular AVIs (arrowhead). C. Adaxial epidermal peel of the inner petal region under bright field, showing the irregular form of the red-colored AVIs (arrowhead). D. Transverse section of abaxial epidermis of the same inner petal region, showing vesicle-like AVIs (arrow) and central vacuoles (V). E. Abaxial epidermal peel of the inner petal region observed under bright light, showing vesicle-like AVIs (arrow) and central vacuoles. |
PMC1781452_F1_8961.jpg | What key item or scene is captured in this photo? | Micrographs of AVIs in the epidermal cells of fully open lisianthus petals. A. Bright field microscopy image of an unstained transverse section of the inner petal region, showing the distinct morphology of AVIs between the adaxial and abaxial epidermal cells. Irregular AVIs in the adaxial epidermal cells (upper) and vesicle-like AVIs in the abaxial epidermal cells (lower). B. Transverse section of adaxial epidermal cells in Fig. A at higher magnification, showing the central vacuoles (V) and the irregular AVIs (arrowhead). C. Adaxial epidermal peel of the inner petal region under bright field, showing the irregular form of the red-colored AVIs (arrowhead). D. Transverse section of abaxial epidermis of the same inner petal region, showing vesicle-like AVIs (arrow) and central vacuoles (V). E. Abaxial epidermal peel of the inner petal region observed under bright light, showing vesicle-like AVIs (arrow) and central vacuoles. |
PMC1781452_F1_8962.jpg | What can you see in this picture? | Micrographs of AVIs in the epidermal cells of fully open lisianthus petals. A. Bright field microscopy image of an unstained transverse section of the inner petal region, showing the distinct morphology of AVIs between the adaxial and abaxial epidermal cells. Irregular AVIs in the adaxial epidermal cells (upper) and vesicle-like AVIs in the abaxial epidermal cells (lower). B. Transverse section of adaxial epidermal cells in Fig. A at higher magnification, showing the central vacuoles (V) and the irregular AVIs (arrowhead). C. Adaxial epidermal peel of the inner petal region under bright field, showing the irregular form of the red-colored AVIs (arrowhead). D. Transverse section of abaxial epidermis of the same inner petal region, showing vesicle-like AVIs (arrow) and central vacuoles (V). E. Abaxial epidermal peel of the inner petal region observed under bright light, showing vesicle-like AVIs (arrow) and central vacuoles. |
PMC1781452_F4_8956.jpg | What stands out most in this visual? | Micrographs of in planta and in vitro isolated AVIs of the adaxial cells of the inner petal region of lisianthus flowers. A. Light microscopy section of an isolated AVI stained with Toluidine Blue, showing the uneven distribution of the internal structure. B. TEM image of an isolated AVI, showing the thread-like structure. C. TEM image of an AVI-containing cell, showing dense inner (white arrowhead) and loose outer thread structures of the AVI in the central vacuole (V). CW, cell wall; PM, plasmodesmata. D. Higher magnification image of the transition part between dense and loose AVI thread structure of an AVI. |
PMC1781452_F4_8958.jpg | What can you see in this picture? | Micrographs of in planta and in vitro isolated AVIs of the adaxial cells of the inner petal region of lisianthus flowers. A. Light microscopy section of an isolated AVI stained with Toluidine Blue, showing the uneven distribution of the internal structure. B. TEM image of an isolated AVI, showing the thread-like structure. C. TEM image of an AVI-containing cell, showing dense inner (white arrowhead) and loose outer thread structures of the AVI in the central vacuole (V). CW, cell wall; PM, plasmodesmata. D. Higher magnification image of the transition part between dense and loose AVI thread structure of an AVI. |
PMC1781452_F4_8957.jpg | What is the dominant medical problem in this image? | Micrographs of in planta and in vitro isolated AVIs of the adaxial cells of the inner petal region of lisianthus flowers. A. Light microscopy section of an isolated AVI stained with Toluidine Blue, showing the uneven distribution of the internal structure. B. TEM image of an isolated AVI, showing the thread-like structure. C. TEM image of an AVI-containing cell, showing dense inner (white arrowhead) and loose outer thread structures of the AVI in the central vacuole (V). CW, cell wall; PM, plasmodesmata. D. Higher magnification image of the transition part between dense and loose AVI thread structure of an AVI. |
PMC1781458_F2_8971.jpg | What is the core subject represented in this visual? | MPLSM/SHG imaging reveals native collagen structure in living mammary gland. A: (a) MPE/SHG image at the "top" of the mammary duct, showing both wavy and taut (straight) collagen structures as well as endogenous fluorescence from FAD in stromal cells (most likely fibroblasts and immune cells). (b) MPE/SHG image of a mammary duct demonstrating collagen wrapped around the duct as well as radiating out from the duct (as can be seen predominantly at the top of the micrograph near the end of the duct). (c) Enlarged section from (a) showing some aspects of collagen fibril structure that resemble the standard banding pattern seen in collagen fibrils from connective tissue. (d) SEM of mouse tendon mouse tendon demonstrating the ~67 nm banding pattern characteristic of collagen fibrils. (e) Correlative SEM image of collagen surrounding ductal epithelial cells showing both wavy (upper arrow) and taut (lower arrow) fibers that match the collagen structures obtained with MPE/SHG imaging. (f) MPE/SHG image of the region near the nipple in tissue demonstrating straightened collagen fibers radiating from the central ductal structure. (g) MPE/SHG image "above" the mammary duct showing both wavy and taut fiber structures. Note: all mammary tissues in A are from the B6/129 strain, which serves as the background strain for col1a1 mice. B: (a) Whole mount analysis from wild type control (top) and Wnt-1 mice (bottom), which display hyperplasia compared to wild type glands. (b,c) Histology of mammary glands from wild type control animals (b; H&E) and hyperplastic abnormal ducts from Wnt-1 mice (c; Masson's Trichrome). (d,e) MPLSM/SHG imaging of wild type control mammary duct demonstrating a ductal end (d) and branching (e). (f) MPLSM/SHG imaging of a mammary duct from a Wnt-1 mouse showing hyperplasia of the ductal structure and increased deposition of disorganized collagen. Note: All MPE/SHG images are from live intact tissues that are not fixed, sectioned, or stained; scale bar for MPE/SHG images equals 25 μm; scale bar for histology images equals 50 μm. |
PMC1781458_F2_8978.jpg | What is the central feature of this picture? | MPLSM/SHG imaging reveals native collagen structure in living mammary gland. A: (a) MPE/SHG image at the "top" of the mammary duct, showing both wavy and taut (straight) collagen structures as well as endogenous fluorescence from FAD in stromal cells (most likely fibroblasts and immune cells). (b) MPE/SHG image of a mammary duct demonstrating collagen wrapped around the duct as well as radiating out from the duct (as can be seen predominantly at the top of the micrograph near the end of the duct). (c) Enlarged section from (a) showing some aspects of collagen fibril structure that resemble the standard banding pattern seen in collagen fibrils from connective tissue. (d) SEM of mouse tendon mouse tendon demonstrating the ~67 nm banding pattern characteristic of collagen fibrils. (e) Correlative SEM image of collagen surrounding ductal epithelial cells showing both wavy (upper arrow) and taut (lower arrow) fibers that match the collagen structures obtained with MPE/SHG imaging. (f) MPE/SHG image of the region near the nipple in tissue demonstrating straightened collagen fibers radiating from the central ductal structure. (g) MPE/SHG image "above" the mammary duct showing both wavy and taut fiber structures. Note: all mammary tissues in A are from the B6/129 strain, which serves as the background strain for col1a1 mice. B: (a) Whole mount analysis from wild type control (top) and Wnt-1 mice (bottom), which display hyperplasia compared to wild type glands. (b,c) Histology of mammary glands from wild type control animals (b; H&E) and hyperplastic abnormal ducts from Wnt-1 mice (c; Masson's Trichrome). (d,e) MPLSM/SHG imaging of wild type control mammary duct demonstrating a ductal end (d) and branching (e). (f) MPLSM/SHG imaging of a mammary duct from a Wnt-1 mouse showing hyperplasia of the ductal structure and increased deposition of disorganized collagen. Note: All MPE/SHG images are from live intact tissues that are not fixed, sectioned, or stained; scale bar for MPE/SHG images equals 25 μm; scale bar for histology images equals 50 μm. |
PMC1781458_F2_8979.jpg | What can you see in this picture? | MPLSM/SHG imaging reveals native collagen structure in living mammary gland. A: (a) MPE/SHG image at the "top" of the mammary duct, showing both wavy and taut (straight) collagen structures as well as endogenous fluorescence from FAD in stromal cells (most likely fibroblasts and immune cells). (b) MPE/SHG image of a mammary duct demonstrating collagen wrapped around the duct as well as radiating out from the duct (as can be seen predominantly at the top of the micrograph near the end of the duct). (c) Enlarged section from (a) showing some aspects of collagen fibril structure that resemble the standard banding pattern seen in collagen fibrils from connective tissue. (d) SEM of mouse tendon mouse tendon demonstrating the ~67 nm banding pattern characteristic of collagen fibrils. (e) Correlative SEM image of collagen surrounding ductal epithelial cells showing both wavy (upper arrow) and taut (lower arrow) fibers that match the collagen structures obtained with MPE/SHG imaging. (f) MPE/SHG image of the region near the nipple in tissue demonstrating straightened collagen fibers radiating from the central ductal structure. (g) MPE/SHG image "above" the mammary duct showing both wavy and taut fiber structures. Note: all mammary tissues in A are from the B6/129 strain, which serves as the background strain for col1a1 mice. B: (a) Whole mount analysis from wild type control (top) and Wnt-1 mice (bottom), which display hyperplasia compared to wild type glands. (b,c) Histology of mammary glands from wild type control animals (b; H&E) and hyperplastic abnormal ducts from Wnt-1 mice (c; Masson's Trichrome). (d,e) MPLSM/SHG imaging of wild type control mammary duct demonstrating a ductal end (d) and branching (e). (f) MPLSM/SHG imaging of a mammary duct from a Wnt-1 mouse showing hyperplasia of the ductal structure and increased deposition of disorganized collagen. Note: All MPE/SHG images are from live intact tissues that are not fixed, sectioned, or stained; scale bar for MPE/SHG images equals 25 μm; scale bar for histology images equals 50 μm. |
PMC1781458_F2_8976.jpg | What's the most prominent thing you notice in this picture? | MPLSM/SHG imaging reveals native collagen structure in living mammary gland. A: (a) MPE/SHG image at the "top" of the mammary duct, showing both wavy and taut (straight) collagen structures as well as endogenous fluorescence from FAD in stromal cells (most likely fibroblasts and immune cells). (b) MPE/SHG image of a mammary duct demonstrating collagen wrapped around the duct as well as radiating out from the duct (as can be seen predominantly at the top of the micrograph near the end of the duct). (c) Enlarged section from (a) showing some aspects of collagen fibril structure that resemble the standard banding pattern seen in collagen fibrils from connective tissue. (d) SEM of mouse tendon mouse tendon demonstrating the ~67 nm banding pattern characteristic of collagen fibrils. (e) Correlative SEM image of collagen surrounding ductal epithelial cells showing both wavy (upper arrow) and taut (lower arrow) fibers that match the collagen structures obtained with MPE/SHG imaging. (f) MPE/SHG image of the region near the nipple in tissue demonstrating straightened collagen fibers radiating from the central ductal structure. (g) MPE/SHG image "above" the mammary duct showing both wavy and taut fiber structures. Note: all mammary tissues in A are from the B6/129 strain, which serves as the background strain for col1a1 mice. B: (a) Whole mount analysis from wild type control (top) and Wnt-1 mice (bottom), which display hyperplasia compared to wild type glands. (b,c) Histology of mammary glands from wild type control animals (b; H&E) and hyperplastic abnormal ducts from Wnt-1 mice (c; Masson's Trichrome). (d,e) MPLSM/SHG imaging of wild type control mammary duct demonstrating a ductal end (d) and branching (e). (f) MPLSM/SHG imaging of a mammary duct from a Wnt-1 mouse showing hyperplasia of the ductal structure and increased deposition of disorganized collagen. Note: All MPE/SHG images are from live intact tissues that are not fixed, sectioned, or stained; scale bar for MPE/SHG images equals 25 μm; scale bar for histology images equals 50 μm. |
PMC1781458_F2_8975.jpg | What's the most prominent thing you notice in this picture? | MPLSM/SHG imaging reveals native collagen structure in living mammary gland. A: (a) MPE/SHG image at the "top" of the mammary duct, showing both wavy and taut (straight) collagen structures as well as endogenous fluorescence from FAD in stromal cells (most likely fibroblasts and immune cells). (b) MPE/SHG image of a mammary duct demonstrating collagen wrapped around the duct as well as radiating out from the duct (as can be seen predominantly at the top of the micrograph near the end of the duct). (c) Enlarged section from (a) showing some aspects of collagen fibril structure that resemble the standard banding pattern seen in collagen fibrils from connective tissue. (d) SEM of mouse tendon mouse tendon demonstrating the ~67 nm banding pattern characteristic of collagen fibrils. (e) Correlative SEM image of collagen surrounding ductal epithelial cells showing both wavy (upper arrow) and taut (lower arrow) fibers that match the collagen structures obtained with MPE/SHG imaging. (f) MPE/SHG image of the region near the nipple in tissue demonstrating straightened collagen fibers radiating from the central ductal structure. (g) MPE/SHG image "above" the mammary duct showing both wavy and taut fiber structures. Note: all mammary tissues in A are from the B6/129 strain, which serves as the background strain for col1a1 mice. B: (a) Whole mount analysis from wild type control (top) and Wnt-1 mice (bottom), which display hyperplasia compared to wild type glands. (b,c) Histology of mammary glands from wild type control animals (b; H&E) and hyperplastic abnormal ducts from Wnt-1 mice (c; Masson's Trichrome). (d,e) MPLSM/SHG imaging of wild type control mammary duct demonstrating a ductal end (d) and branching (e). (f) MPLSM/SHG imaging of a mammary duct from a Wnt-1 mouse showing hyperplasia of the ductal structure and increased deposition of disorganized collagen. Note: All MPE/SHG images are from live intact tissues that are not fixed, sectioned, or stained; scale bar for MPE/SHG images equals 25 μm; scale bar for histology images equals 50 μm. |
PMC1781458_F2_8974.jpg | What is the dominant medical problem in this image? | MPLSM/SHG imaging reveals native collagen structure in living mammary gland. A: (a) MPE/SHG image at the "top" of the mammary duct, showing both wavy and taut (straight) collagen structures as well as endogenous fluorescence from FAD in stromal cells (most likely fibroblasts and immune cells). (b) MPE/SHG image of a mammary duct demonstrating collagen wrapped around the duct as well as radiating out from the duct (as can be seen predominantly at the top of the micrograph near the end of the duct). (c) Enlarged section from (a) showing some aspects of collagen fibril structure that resemble the standard banding pattern seen in collagen fibrils from connective tissue. (d) SEM of mouse tendon mouse tendon demonstrating the ~67 nm banding pattern characteristic of collagen fibrils. (e) Correlative SEM image of collagen surrounding ductal epithelial cells showing both wavy (upper arrow) and taut (lower arrow) fibers that match the collagen structures obtained with MPE/SHG imaging. (f) MPE/SHG image of the region near the nipple in tissue demonstrating straightened collagen fibers radiating from the central ductal structure. (g) MPE/SHG image "above" the mammary duct showing both wavy and taut fiber structures. Note: all mammary tissues in A are from the B6/129 strain, which serves as the background strain for col1a1 mice. B: (a) Whole mount analysis from wild type control (top) and Wnt-1 mice (bottom), which display hyperplasia compared to wild type glands. (b,c) Histology of mammary glands from wild type control animals (b; H&E) and hyperplastic abnormal ducts from Wnt-1 mice (c; Masson's Trichrome). (d,e) MPLSM/SHG imaging of wild type control mammary duct demonstrating a ductal end (d) and branching (e). (f) MPLSM/SHG imaging of a mammary duct from a Wnt-1 mouse showing hyperplasia of the ductal structure and increased deposition of disorganized collagen. Note: All MPE/SHG images are from live intact tissues that are not fixed, sectioned, or stained; scale bar for MPE/SHG images equals 25 μm; scale bar for histology images equals 50 μm. |
PMC1781458_F2_8972.jpg | What is shown in this image? | MPLSM/SHG imaging reveals native collagen structure in living mammary gland. A: (a) MPE/SHG image at the "top" of the mammary duct, showing both wavy and taut (straight) collagen structures as well as endogenous fluorescence from FAD in stromal cells (most likely fibroblasts and immune cells). (b) MPE/SHG image of a mammary duct demonstrating collagen wrapped around the duct as well as radiating out from the duct (as can be seen predominantly at the top of the micrograph near the end of the duct). (c) Enlarged section from (a) showing some aspects of collagen fibril structure that resemble the standard banding pattern seen in collagen fibrils from connective tissue. (d) SEM of mouse tendon mouse tendon demonstrating the ~67 nm banding pattern characteristic of collagen fibrils. (e) Correlative SEM image of collagen surrounding ductal epithelial cells showing both wavy (upper arrow) and taut (lower arrow) fibers that match the collagen structures obtained with MPE/SHG imaging. (f) MPE/SHG image of the region near the nipple in tissue demonstrating straightened collagen fibers radiating from the central ductal structure. (g) MPE/SHG image "above" the mammary duct showing both wavy and taut fiber structures. Note: all mammary tissues in A are from the B6/129 strain, which serves as the background strain for col1a1 mice. B: (a) Whole mount analysis from wild type control (top) and Wnt-1 mice (bottom), which display hyperplasia compared to wild type glands. (b,c) Histology of mammary glands from wild type control animals (b; H&E) and hyperplastic abnormal ducts from Wnt-1 mice (c; Masson's Trichrome). (d,e) MPLSM/SHG imaging of wild type control mammary duct demonstrating a ductal end (d) and branching (e). (f) MPLSM/SHG imaging of a mammary duct from a Wnt-1 mouse showing hyperplasia of the ductal structure and increased deposition of disorganized collagen. Note: All MPE/SHG images are from live intact tissues that are not fixed, sectioned, or stained; scale bar for MPE/SHG images equals 25 μm; scale bar for histology images equals 50 μm. |
PMC1781458_F2_8970.jpg | What is the focal point of this photograph? | MPLSM/SHG imaging reveals native collagen structure in living mammary gland. A: (a) MPE/SHG image at the "top" of the mammary duct, showing both wavy and taut (straight) collagen structures as well as endogenous fluorescence from FAD in stromal cells (most likely fibroblasts and immune cells). (b) MPE/SHG image of a mammary duct demonstrating collagen wrapped around the duct as well as radiating out from the duct (as can be seen predominantly at the top of the micrograph near the end of the duct). (c) Enlarged section from (a) showing some aspects of collagen fibril structure that resemble the standard banding pattern seen in collagen fibrils from connective tissue. (d) SEM of mouse tendon mouse tendon demonstrating the ~67 nm banding pattern characteristic of collagen fibrils. (e) Correlative SEM image of collagen surrounding ductal epithelial cells showing both wavy (upper arrow) and taut (lower arrow) fibers that match the collagen structures obtained with MPE/SHG imaging. (f) MPE/SHG image of the region near the nipple in tissue demonstrating straightened collagen fibers radiating from the central ductal structure. (g) MPE/SHG image "above" the mammary duct showing both wavy and taut fiber structures. Note: all mammary tissues in A are from the B6/129 strain, which serves as the background strain for col1a1 mice. B: (a) Whole mount analysis from wild type control (top) and Wnt-1 mice (bottom), which display hyperplasia compared to wild type glands. (b,c) Histology of mammary glands from wild type control animals (b; H&E) and hyperplastic abnormal ducts from Wnt-1 mice (c; Masson's Trichrome). (d,e) MPLSM/SHG imaging of wild type control mammary duct demonstrating a ductal end (d) and branching (e). (f) MPLSM/SHG imaging of a mammary duct from a Wnt-1 mouse showing hyperplasia of the ductal structure and increased deposition of disorganized collagen. Note: All MPE/SHG images are from live intact tissues that are not fixed, sectioned, or stained; scale bar for MPE/SHG images equals 25 μm; scale bar for histology images equals 50 μm. |
PMC1781458_F6_8985.jpg | What is being portrayed in this visual content? | TACS-3 – radially aligned collagen fibers associated with invasion. Combined MPE/SHG imaging of live intact PyVT mammary tumors indicates that (A) non-invading regions (*) possess taut collagen (TACS-2; white arrowhead) wrapped around the tumor, while regions of invasion (x) are linked to aligned collagen, with cells invading along radially aligned collagen fibers (TACS-3; black arrowheads). Examination of invasion at the tumor-stromal interface at higher magnification (B and C) clearly reveals the collagen alignment at specific regions of invasion (B) with tumor cells (*) in between, and in association with, aligned collagen fibers (C). (D) Example of an individual tumor cell attached to a collagen fiber leading away from the primary tumor. Additionally, tumor cells that have invaded across the tumor-stromal boundary can be visualized by separating the MPE and SHG signals or imaging with FLIM. (E) Combined MPE/SHG image of a TACS-3 region facilitating local invasion. The tumor-stromal boundary is not well preserved at this stage, but is roughly outlined in red. Examples of regions of cells that have invaded past the boundary are marked with an asterisk (t = the primary tumor). The red arrowhead indicates cells near the tumor boundary that are migrating along aligned collagen fibers away from the primary tumor. (F) MPE and SHG signal separation of the image shown in E. MPE signal is represented in red pseudo-color while SHG is shown in green pseudo-color. Note the interdigitation of aligned collagen fibers (green) into the tumor, with individual, or lines of, cells (* in E) migrating away from the tumor on collagen fibers. (G) FLIM micrograph of invading cells at the TACS-3 region shown in E and F. Collagen (blue; no fluorescence lifetime) can be distinguished from cells (green to yellow), confirming the presence of invading cells at the tumor-stromal boundary and cells that have migrated past the boundary in association with collagen. The color bar in G ranges represents the weighted mean ranging from 100 ps (blue) to 1 ns (red). Scale bars equal 25 μm in A, E, F, and G; 10 μm in B, C, and D. |
PMC1781458_F6_8984.jpg | Can you identify the primary element in this image? | TACS-3 – radially aligned collagen fibers associated with invasion. Combined MPE/SHG imaging of live intact PyVT mammary tumors indicates that (A) non-invading regions (*) possess taut collagen (TACS-2; white arrowhead) wrapped around the tumor, while regions of invasion (x) are linked to aligned collagen, with cells invading along radially aligned collagen fibers (TACS-3; black arrowheads). Examination of invasion at the tumor-stromal interface at higher magnification (B and C) clearly reveals the collagen alignment at specific regions of invasion (B) with tumor cells (*) in between, and in association with, aligned collagen fibers (C). (D) Example of an individual tumor cell attached to a collagen fiber leading away from the primary tumor. Additionally, tumor cells that have invaded across the tumor-stromal boundary can be visualized by separating the MPE and SHG signals or imaging with FLIM. (E) Combined MPE/SHG image of a TACS-3 region facilitating local invasion. The tumor-stromal boundary is not well preserved at this stage, but is roughly outlined in red. Examples of regions of cells that have invaded past the boundary are marked with an asterisk (t = the primary tumor). The red arrowhead indicates cells near the tumor boundary that are migrating along aligned collagen fibers away from the primary tumor. (F) MPE and SHG signal separation of the image shown in E. MPE signal is represented in red pseudo-color while SHG is shown in green pseudo-color. Note the interdigitation of aligned collagen fibers (green) into the tumor, with individual, or lines of, cells (* in E) migrating away from the tumor on collagen fibers. (G) FLIM micrograph of invading cells at the TACS-3 region shown in E and F. Collagen (blue; no fluorescence lifetime) can be distinguished from cells (green to yellow), confirming the presence of invading cells at the tumor-stromal boundary and cells that have migrated past the boundary in association with collagen. The color bar in G ranges represents the weighted mean ranging from 100 ps (blue) to 1 ns (red). Scale bars equal 25 μm in A, E, F, and G; 10 μm in B, C, and D. |
PMC1781458_F6_8986.jpg | What stands out most in this visual? | TACS-3 – radially aligned collagen fibers associated with invasion. Combined MPE/SHG imaging of live intact PyVT mammary tumors indicates that (A) non-invading regions (*) possess taut collagen (TACS-2; white arrowhead) wrapped around the tumor, while regions of invasion (x) are linked to aligned collagen, with cells invading along radially aligned collagen fibers (TACS-3; black arrowheads). Examination of invasion at the tumor-stromal interface at higher magnification (B and C) clearly reveals the collagen alignment at specific regions of invasion (B) with tumor cells (*) in between, and in association with, aligned collagen fibers (C). (D) Example of an individual tumor cell attached to a collagen fiber leading away from the primary tumor. Additionally, tumor cells that have invaded across the tumor-stromal boundary can be visualized by separating the MPE and SHG signals or imaging with FLIM. (E) Combined MPE/SHG image of a TACS-3 region facilitating local invasion. The tumor-stromal boundary is not well preserved at this stage, but is roughly outlined in red. Examples of regions of cells that have invaded past the boundary are marked with an asterisk (t = the primary tumor). The red arrowhead indicates cells near the tumor boundary that are migrating along aligned collagen fibers away from the primary tumor. (F) MPE and SHG signal separation of the image shown in E. MPE signal is represented in red pseudo-color while SHG is shown in green pseudo-color. Note the interdigitation of aligned collagen fibers (green) into the tumor, with individual, or lines of, cells (* in E) migrating away from the tumor on collagen fibers. (G) FLIM micrograph of invading cells at the TACS-3 region shown in E and F. Collagen (blue; no fluorescence lifetime) can be distinguished from cells (green to yellow), confirming the presence of invading cells at the tumor-stromal boundary and cells that have migrated past the boundary in association with collagen. The color bar in G ranges represents the weighted mean ranging from 100 ps (blue) to 1 ns (red). Scale bars equal 25 μm in A, E, F, and G; 10 μm in B, C, and D. |
PMC1781458_F6_8983.jpg | What key item or scene is captured in this photo? | TACS-3 – radially aligned collagen fibers associated with invasion. Combined MPE/SHG imaging of live intact PyVT mammary tumors indicates that (A) non-invading regions (*) possess taut collagen (TACS-2; white arrowhead) wrapped around the tumor, while regions of invasion (x) are linked to aligned collagen, with cells invading along radially aligned collagen fibers (TACS-3; black arrowheads). Examination of invasion at the tumor-stromal interface at higher magnification (B and C) clearly reveals the collagen alignment at specific regions of invasion (B) with tumor cells (*) in between, and in association with, aligned collagen fibers (C). (D) Example of an individual tumor cell attached to a collagen fiber leading away from the primary tumor. Additionally, tumor cells that have invaded across the tumor-stromal boundary can be visualized by separating the MPE and SHG signals or imaging with FLIM. (E) Combined MPE/SHG image of a TACS-3 region facilitating local invasion. The tumor-stromal boundary is not well preserved at this stage, but is roughly outlined in red. Examples of regions of cells that have invaded past the boundary are marked with an asterisk (t = the primary tumor). The red arrowhead indicates cells near the tumor boundary that are migrating along aligned collagen fibers away from the primary tumor. (F) MPE and SHG signal separation of the image shown in E. MPE signal is represented in red pseudo-color while SHG is shown in green pseudo-color. Note the interdigitation of aligned collagen fibers (green) into the tumor, with individual, or lines of, cells (* in E) migrating away from the tumor on collagen fibers. (G) FLIM micrograph of invading cells at the TACS-3 region shown in E and F. Collagen (blue; no fluorescence lifetime) can be distinguished from cells (green to yellow), confirming the presence of invading cells at the tumor-stromal boundary and cells that have migrated past the boundary in association with collagen. The color bar in G ranges represents the weighted mean ranging from 100 ps (blue) to 1 ns (red). Scale bars equal 25 μm in A, E, F, and G; 10 μm in B, C, and D. |
PMC1781458_F6_8980.jpg | Can you identify the primary element in this image? | TACS-3 – radially aligned collagen fibers associated with invasion. Combined MPE/SHG imaging of live intact PyVT mammary tumors indicates that (A) non-invading regions (*) possess taut collagen (TACS-2; white arrowhead) wrapped around the tumor, while regions of invasion (x) are linked to aligned collagen, with cells invading along radially aligned collagen fibers (TACS-3; black arrowheads). Examination of invasion at the tumor-stromal interface at higher magnification (B and C) clearly reveals the collagen alignment at specific regions of invasion (B) with tumor cells (*) in between, and in association with, aligned collagen fibers (C). (D) Example of an individual tumor cell attached to a collagen fiber leading away from the primary tumor. Additionally, tumor cells that have invaded across the tumor-stromal boundary can be visualized by separating the MPE and SHG signals or imaging with FLIM. (E) Combined MPE/SHG image of a TACS-3 region facilitating local invasion. The tumor-stromal boundary is not well preserved at this stage, but is roughly outlined in red. Examples of regions of cells that have invaded past the boundary are marked with an asterisk (t = the primary tumor). The red arrowhead indicates cells near the tumor boundary that are migrating along aligned collagen fibers away from the primary tumor. (F) MPE and SHG signal separation of the image shown in E. MPE signal is represented in red pseudo-color while SHG is shown in green pseudo-color. Note the interdigitation of aligned collagen fibers (green) into the tumor, with individual, or lines of, cells (* in E) migrating away from the tumor on collagen fibers. (G) FLIM micrograph of invading cells at the TACS-3 region shown in E and F. Collagen (blue; no fluorescence lifetime) can be distinguished from cells (green to yellow), confirming the presence of invading cells at the tumor-stromal boundary and cells that have migrated past the boundary in association with collagen. The color bar in G ranges represents the weighted mean ranging from 100 ps (blue) to 1 ns (red). Scale bars equal 25 μm in A, E, F, and G; 10 μm in B, C, and D. |
PMC1781458_F6_8981.jpg | What key item or scene is captured in this photo? | TACS-3 – radially aligned collagen fibers associated with invasion. Combined MPE/SHG imaging of live intact PyVT mammary tumors indicates that (A) non-invading regions (*) possess taut collagen (TACS-2; white arrowhead) wrapped around the tumor, while regions of invasion (x) are linked to aligned collagen, with cells invading along radially aligned collagen fibers (TACS-3; black arrowheads). Examination of invasion at the tumor-stromal interface at higher magnification (B and C) clearly reveals the collagen alignment at specific regions of invasion (B) with tumor cells (*) in between, and in association with, aligned collagen fibers (C). (D) Example of an individual tumor cell attached to a collagen fiber leading away from the primary tumor. Additionally, tumor cells that have invaded across the tumor-stromal boundary can be visualized by separating the MPE and SHG signals or imaging with FLIM. (E) Combined MPE/SHG image of a TACS-3 region facilitating local invasion. The tumor-stromal boundary is not well preserved at this stage, but is roughly outlined in red. Examples of regions of cells that have invaded past the boundary are marked with an asterisk (t = the primary tumor). The red arrowhead indicates cells near the tumor boundary that are migrating along aligned collagen fibers away from the primary tumor. (F) MPE and SHG signal separation of the image shown in E. MPE signal is represented in red pseudo-color while SHG is shown in green pseudo-color. Note the interdigitation of aligned collagen fibers (green) into the tumor, with individual, or lines of, cells (* in E) migrating away from the tumor on collagen fibers. (G) FLIM micrograph of invading cells at the TACS-3 region shown in E and F. Collagen (blue; no fluorescence lifetime) can be distinguished from cells (green to yellow), confirming the presence of invading cells at the tumor-stromal boundary and cells that have migrated past the boundary in association with collagen. The color bar in G ranges represents the weighted mean ranging from 100 ps (blue) to 1 ns (red). Scale bars equal 25 μm in A, E, F, and G; 10 μm in B, C, and D. |
PMC1781458_F6_8982.jpg | What does this image primarily show? | TACS-3 – radially aligned collagen fibers associated with invasion. Combined MPE/SHG imaging of live intact PyVT mammary tumors indicates that (A) non-invading regions (*) possess taut collagen (TACS-2; white arrowhead) wrapped around the tumor, while regions of invasion (x) are linked to aligned collagen, with cells invading along radially aligned collagen fibers (TACS-3; black arrowheads). Examination of invasion at the tumor-stromal interface at higher magnification (B and C) clearly reveals the collagen alignment at specific regions of invasion (B) with tumor cells (*) in between, and in association with, aligned collagen fibers (C). (D) Example of an individual tumor cell attached to a collagen fiber leading away from the primary tumor. Additionally, tumor cells that have invaded across the tumor-stromal boundary can be visualized by separating the MPE and SHG signals or imaging with FLIM. (E) Combined MPE/SHG image of a TACS-3 region facilitating local invasion. The tumor-stromal boundary is not well preserved at this stage, but is roughly outlined in red. Examples of regions of cells that have invaded past the boundary are marked with an asterisk (t = the primary tumor). The red arrowhead indicates cells near the tumor boundary that are migrating along aligned collagen fibers away from the primary tumor. (F) MPE and SHG signal separation of the image shown in E. MPE signal is represented in red pseudo-color while SHG is shown in green pseudo-color. Note the interdigitation of aligned collagen fibers (green) into the tumor, with individual, or lines of, cells (* in E) migrating away from the tumor on collagen fibers. (G) FLIM micrograph of invading cells at the TACS-3 region shown in E and F. Collagen (blue; no fluorescence lifetime) can be distinguished from cells (green to yellow), confirming the presence of invading cells at the tumor-stromal boundary and cells that have migrated past the boundary in association with collagen. The color bar in G ranges represents the weighted mean ranging from 100 ps (blue) to 1 ns (red). Scale bars equal 25 μm in A, E, F, and G; 10 μm in B, C, and D. |
PMC1781458_F7_8967.jpg | What is the core subject represented in this visual? | Collagen matrix reorganization by tumor cells facilitates local invasion of tumor cells. Combined MPE/SHG imaging of tumor explants cultured within 3D collagen gels for eight hours demonstrates that tumor cells reorganize a previously random matrix to facilitate invasion. (A) Region of 3D collagen gel remote from the tumor demonstrating the random orientation of collagen present within 3D collagen gels in a region that has not been reorganized by a specific outside force. This random organization is specifically altered by cells from tumor explants as the cells contract and reorganize the collagen matrix. Similar to data in live intact tissues, non-invading regions show collagen pulled in near the explant but wrapped around the tumor boundary (B), while at regions of tumor cell invasion into the collagen gel, collagen has been radially aligned by the tumor cells (white arrow heads C) with cells (*) in direct contact with the collagen matrix (white arrowheads; D). Therefore, at regions of tumor cell invasion, collagen has been reorganized to a radial alignment from a random orientation, indicating a structural realignment of collagen fibers facilitates local invasion. Scale bar equals 25 μm. |
PMC1781458_F7_8965.jpg | What is the principal component of this image? | Collagen matrix reorganization by tumor cells facilitates local invasion of tumor cells. Combined MPE/SHG imaging of tumor explants cultured within 3D collagen gels for eight hours demonstrates that tumor cells reorganize a previously random matrix to facilitate invasion. (A) Region of 3D collagen gel remote from the tumor demonstrating the random orientation of collagen present within 3D collagen gels in a region that has not been reorganized by a specific outside force. This random organization is specifically altered by cells from tumor explants as the cells contract and reorganize the collagen matrix. Similar to data in live intact tissues, non-invading regions show collagen pulled in near the explant but wrapped around the tumor boundary (B), while at regions of tumor cell invasion into the collagen gel, collagen has been radially aligned by the tumor cells (white arrow heads C) with cells (*) in direct contact with the collagen matrix (white arrowheads; D). Therefore, at regions of tumor cell invasion, collagen has been reorganized to a radial alignment from a random orientation, indicating a structural realignment of collagen fibers facilitates local invasion. Scale bar equals 25 μm. |
PMC1781458_F7_8964.jpg | What object or scene is depicted here? | Collagen matrix reorganization by tumor cells facilitates local invasion of tumor cells. Combined MPE/SHG imaging of tumor explants cultured within 3D collagen gels for eight hours demonstrates that tumor cells reorganize a previously random matrix to facilitate invasion. (A) Region of 3D collagen gel remote from the tumor demonstrating the random orientation of collagen present within 3D collagen gels in a region that has not been reorganized by a specific outside force. This random organization is specifically altered by cells from tumor explants as the cells contract and reorganize the collagen matrix. Similar to data in live intact tissues, non-invading regions show collagen pulled in near the explant but wrapped around the tumor boundary (B), while at regions of tumor cell invasion into the collagen gel, collagen has been radially aligned by the tumor cells (white arrow heads C) with cells (*) in direct contact with the collagen matrix (white arrowheads; D). Therefore, at regions of tumor cell invasion, collagen has been reorganized to a radial alignment from a random orientation, indicating a structural realignment of collagen fibers facilitates local invasion. Scale bar equals 25 μm. |
PMC1781462_F1_8992.jpg | What is the main focus of this visual representation? | Immunochemical localizations of P-LAP/IRAP, GLUT4, IR, and IRS-1 in human endometrioid adenocarcinoma tissues (Magnification, × 200). A: P-LAP/IRAP in a grade 2 endometrioid adenocarcinoma. B: GLUT4. C: IR. D: IRS 1. Immunoreactivites of P-LAP/IRAP, GLUT4, IR, and IRS-1 were positive in carcinoma cells. E: Negative control (no primary antibody) in normal endometrial tissue. |
PMC1781462_F1_8989.jpg | What is the principal component of this image? | Immunochemical localizations of P-LAP/IRAP, GLUT4, IR, and IRS-1 in human endometrioid adenocarcinoma tissues (Magnification, × 200). A: P-LAP/IRAP in a grade 2 endometrioid adenocarcinoma. B: GLUT4. C: IR. D: IRS 1. Immunoreactivites of P-LAP/IRAP, GLUT4, IR, and IRS-1 were positive in carcinoma cells. E: Negative control (no primary antibody) in normal endometrial tissue. |
PMC1781462_F1_8988.jpg | Describe the main subject of this image. | Immunochemical localizations of P-LAP/IRAP, GLUT4, IR, and IRS-1 in human endometrioid adenocarcinoma tissues (Magnification, × 200). A: P-LAP/IRAP in a grade 2 endometrioid adenocarcinoma. B: GLUT4. C: IR. D: IRS 1. Immunoreactivites of P-LAP/IRAP, GLUT4, IR, and IRS-1 were positive in carcinoma cells. E: Negative control (no primary antibody) in normal endometrial tissue. |
PMC1781462_F1_8991.jpg | Describe the main subject of this image. | Immunochemical localizations of P-LAP/IRAP, GLUT4, IR, and IRS-1 in human endometrioid adenocarcinoma tissues (Magnification, × 200). A: P-LAP/IRAP in a grade 2 endometrioid adenocarcinoma. B: GLUT4. C: IR. D: IRS 1. Immunoreactivites of P-LAP/IRAP, GLUT4, IR, and IRS-1 were positive in carcinoma cells. E: Negative control (no primary antibody) in normal endometrial tissue. |
PMC1781496_pgen-0030018-g002_9012.jpg | What does this image primarily show? | Dynamic Expression of Notch Components in the IM and Pronephric Duct(A–D) notch1a (A) and notch3 (C) are expressed in the IM at 10 ss. notch1a (B) is expressed in the distal duct region from somite 10 to 14 (see also Figure S3B) at 18 ss, and notch3 (D) is expressed in the whole duct from somite 3 to 20 at 24 hpf as indicated by the arrows.(E–G) jagged2a expression in the IM appears gradually from anterior to posterior from 5 ss (E) (as indicated by the arrow) to 10 ss (F), and reaches the posterior by 15 ss (G).(H–K) jagged2a expression is higher in some cells (arrows point to these cells in [I], which is magnified from [H]) than in neighboring cells in the distal duct at 17 ss (H and I), and transcription is limited to individual cells from 20 ss (J), to 24 hpf (K), to at least 36 hpf (unpublished data) in the demarcated region from somite 8 to 14 (see also Figure S3D and S3F) as indicated by arrows.(L and M) her9 is expressed in the distal pronephric duct at 18 ss (L) from somite 10 to 12 (Figure S3H) and at 21 hpf (M). The arrowhead marks the glomerulus, and arrows demarcate the her9 expression region. Left and right inserts in (M) are the magnified images in the glomerulus and distal duct, respectively.All embryos, anterior to the left. (A), (C), and (E–I) are dorsal views; the rest are lateral views. Bar scale: 200 μm (A, C, and E), 110 μm (B and D), 180 μm (F), 230 μm (G and H), 90 μm (I), 115 μm (J), 190 μm (K), and 100 μm (L and M). |
PMC1781496_pgen-0030018-g002_9009.jpg | What key item or scene is captured in this photo? | Dynamic Expression of Notch Components in the IM and Pronephric Duct(A–D) notch1a (A) and notch3 (C) are expressed in the IM at 10 ss. notch1a (B) is expressed in the distal duct region from somite 10 to 14 (see also Figure S3B) at 18 ss, and notch3 (D) is expressed in the whole duct from somite 3 to 20 at 24 hpf as indicated by the arrows.(E–G) jagged2a expression in the IM appears gradually from anterior to posterior from 5 ss (E) (as indicated by the arrow) to 10 ss (F), and reaches the posterior by 15 ss (G).(H–K) jagged2a expression is higher in some cells (arrows point to these cells in [I], which is magnified from [H]) than in neighboring cells in the distal duct at 17 ss (H and I), and transcription is limited to individual cells from 20 ss (J), to 24 hpf (K), to at least 36 hpf (unpublished data) in the demarcated region from somite 8 to 14 (see also Figure S3D and S3F) as indicated by arrows.(L and M) her9 is expressed in the distal pronephric duct at 18 ss (L) from somite 10 to 12 (Figure S3H) and at 21 hpf (M). The arrowhead marks the glomerulus, and arrows demarcate the her9 expression region. Left and right inserts in (M) are the magnified images in the glomerulus and distal duct, respectively.All embryos, anterior to the left. (A), (C), and (E–I) are dorsal views; the rest are lateral views. Bar scale: 200 μm (A, C, and E), 110 μm (B and D), 180 μm (F), 230 μm (G and H), 90 μm (I), 115 μm (J), 190 μm (K), and 100 μm (L and M). |
PMC1781496_pgen-0030018-g002_9004.jpg | What stands out most in this visual? | Dynamic Expression of Notch Components in the IM and Pronephric Duct(A–D) notch1a (A) and notch3 (C) are expressed in the IM at 10 ss. notch1a (B) is expressed in the distal duct region from somite 10 to 14 (see also Figure S3B) at 18 ss, and notch3 (D) is expressed in the whole duct from somite 3 to 20 at 24 hpf as indicated by the arrows.(E–G) jagged2a expression in the IM appears gradually from anterior to posterior from 5 ss (E) (as indicated by the arrow) to 10 ss (F), and reaches the posterior by 15 ss (G).(H–K) jagged2a expression is higher in some cells (arrows point to these cells in [I], which is magnified from [H]) than in neighboring cells in the distal duct at 17 ss (H and I), and transcription is limited to individual cells from 20 ss (J), to 24 hpf (K), to at least 36 hpf (unpublished data) in the demarcated region from somite 8 to 14 (see also Figure S3D and S3F) as indicated by arrows.(L and M) her9 is expressed in the distal pronephric duct at 18 ss (L) from somite 10 to 12 (Figure S3H) and at 21 hpf (M). The arrowhead marks the glomerulus, and arrows demarcate the her9 expression region. Left and right inserts in (M) are the magnified images in the glomerulus and distal duct, respectively.All embryos, anterior to the left. (A), (C), and (E–I) are dorsal views; the rest are lateral views. Bar scale: 200 μm (A, C, and E), 110 μm (B and D), 180 μm (F), 230 μm (G and H), 90 μm (I), 115 μm (J), 190 μm (K), and 100 μm (L and M). |
PMC1781496_pgen-0030018-g002_9008.jpg | What is shown in this image? | Dynamic Expression of Notch Components in the IM and Pronephric Duct(A–D) notch1a (A) and notch3 (C) are expressed in the IM at 10 ss. notch1a (B) is expressed in the distal duct region from somite 10 to 14 (see also Figure S3B) at 18 ss, and notch3 (D) is expressed in the whole duct from somite 3 to 20 at 24 hpf as indicated by the arrows.(E–G) jagged2a expression in the IM appears gradually from anterior to posterior from 5 ss (E) (as indicated by the arrow) to 10 ss (F), and reaches the posterior by 15 ss (G).(H–K) jagged2a expression is higher in some cells (arrows point to these cells in [I], which is magnified from [H]) than in neighboring cells in the distal duct at 17 ss (H and I), and transcription is limited to individual cells from 20 ss (J), to 24 hpf (K), to at least 36 hpf (unpublished data) in the demarcated region from somite 8 to 14 (see also Figure S3D and S3F) as indicated by arrows.(L and M) her9 is expressed in the distal pronephric duct at 18 ss (L) from somite 10 to 12 (Figure S3H) and at 21 hpf (M). The arrowhead marks the glomerulus, and arrows demarcate the her9 expression region. Left and right inserts in (M) are the magnified images in the glomerulus and distal duct, respectively.All embryos, anterior to the left. (A), (C), and (E–I) are dorsal views; the rest are lateral views. Bar scale: 200 μm (A, C, and E), 110 μm (B and D), 180 μm (F), 230 μm (G and H), 90 μm (I), 115 μm (J), 190 μm (K), and 100 μm (L and M). |
PMC1781496_pgen-0030018-g002_9005.jpg | What is the dominant medical problem in this image? | Dynamic Expression of Notch Components in the IM and Pronephric Duct(A–D) notch1a (A) and notch3 (C) are expressed in the IM at 10 ss. notch1a (B) is expressed in the distal duct region from somite 10 to 14 (see also Figure S3B) at 18 ss, and notch3 (D) is expressed in the whole duct from somite 3 to 20 at 24 hpf as indicated by the arrows.(E–G) jagged2a expression in the IM appears gradually from anterior to posterior from 5 ss (E) (as indicated by the arrow) to 10 ss (F), and reaches the posterior by 15 ss (G).(H–K) jagged2a expression is higher in some cells (arrows point to these cells in [I], which is magnified from [H]) than in neighboring cells in the distal duct at 17 ss (H and I), and transcription is limited to individual cells from 20 ss (J), to 24 hpf (K), to at least 36 hpf (unpublished data) in the demarcated region from somite 8 to 14 (see also Figure S3D and S3F) as indicated by arrows.(L and M) her9 is expressed in the distal pronephric duct at 18 ss (L) from somite 10 to 12 (Figure S3H) and at 21 hpf (M). The arrowhead marks the glomerulus, and arrows demarcate the her9 expression region. Left and right inserts in (M) are the magnified images in the glomerulus and distal duct, respectively.All embryos, anterior to the left. (A), (C), and (E–I) are dorsal views; the rest are lateral views. Bar scale: 200 μm (A, C, and E), 110 μm (B and D), 180 μm (F), 230 μm (G and H), 90 μm (I), 115 μm (J), 190 μm (K), and 100 μm (L and M). |
PMC1781496_pgen-0030018-g005_8997.jpg | What is shown in this image? |
her9 is a Downstream Target Gene of Jagged2a-Notch1a/Notch3 Signaling(A and B) Compared to (A) wt embryos, her9 expression in the pronephric duct region at 18 ss is severely down-regulated in (B) jagged2a-sp morphants.(C–F) Compared to (C) wt embryos, her9 expression in the pronephric duct region at 17 ss is mildly down-regulated in (D) notch1a (desth35b) mutants and (E) notch3-sp morphants, and is severely down-regulated in (F) notch3-sp MO-injected notch1a (desth35b) mutants.(G and H) Compared to (G) wt embryos, her9 expression in the pronephric duct region at 18 ss is severely down-regulated in (H) mibta52b mutants.(I and J) Coinjection of GFP mRNA (50 pg) and notch1aicd mRNA (100 pg) into one blastomere at the two-cell stage leads to (I) somite boundary disruption in the right half of the embryo, while somites on the left side are segmented properly. (J) GFP expression demonstrates that mRNA is localized to the right half of the embryo.(K) Compared to the left side of the embryo, her9 expression in the duct (arrows) and glomerulus (arrowheads) is increased in the right side at 18 ss.(L and M) Compared to (L) wt embryos, the multi-cilia cell number is increased in (M) her9-utr morphants as shown by rfx2 expression at 24 hpf.All embryos, anterior to the left. (A–K) are dorsal views; (L and M) are lateral views. Bar scale: 100 μm (A–J), 130 μm (K), and 50 μm (L and M). |
PMC1781496_pgen-0030018-g005_9001.jpg | What can you see in this picture? |
her9 is a Downstream Target Gene of Jagged2a-Notch1a/Notch3 Signaling(A and B) Compared to (A) wt embryos, her9 expression in the pronephric duct region at 18 ss is severely down-regulated in (B) jagged2a-sp morphants.(C–F) Compared to (C) wt embryos, her9 expression in the pronephric duct region at 17 ss is mildly down-regulated in (D) notch1a (desth35b) mutants and (E) notch3-sp morphants, and is severely down-regulated in (F) notch3-sp MO-injected notch1a (desth35b) mutants.(G and H) Compared to (G) wt embryos, her9 expression in the pronephric duct region at 18 ss is severely down-regulated in (H) mibta52b mutants.(I and J) Coinjection of GFP mRNA (50 pg) and notch1aicd mRNA (100 pg) into one blastomere at the two-cell stage leads to (I) somite boundary disruption in the right half of the embryo, while somites on the left side are segmented properly. (J) GFP expression demonstrates that mRNA is localized to the right half of the embryo.(K) Compared to the left side of the embryo, her9 expression in the duct (arrows) and glomerulus (arrowheads) is increased in the right side at 18 ss.(L and M) Compared to (L) wt embryos, the multi-cilia cell number is increased in (M) her9-utr morphants as shown by rfx2 expression at 24 hpf.All embryos, anterior to the left. (A–K) are dorsal views; (L and M) are lateral views. Bar scale: 100 μm (A–J), 130 μm (K), and 50 μm (L and M). |
PMC1781496_pgen-0030018-g005_8999.jpg | What is shown in this image? |
her9 is a Downstream Target Gene of Jagged2a-Notch1a/Notch3 Signaling(A and B) Compared to (A) wt embryos, her9 expression in the pronephric duct region at 18 ss is severely down-regulated in (B) jagged2a-sp morphants.(C–F) Compared to (C) wt embryos, her9 expression in the pronephric duct region at 17 ss is mildly down-regulated in (D) notch1a (desth35b) mutants and (E) notch3-sp morphants, and is severely down-regulated in (F) notch3-sp MO-injected notch1a (desth35b) mutants.(G and H) Compared to (G) wt embryos, her9 expression in the pronephric duct region at 18 ss is severely down-regulated in (H) mibta52b mutants.(I and J) Coinjection of GFP mRNA (50 pg) and notch1aicd mRNA (100 pg) into one blastomere at the two-cell stage leads to (I) somite boundary disruption in the right half of the embryo, while somites on the left side are segmented properly. (J) GFP expression demonstrates that mRNA is localized to the right half of the embryo.(K) Compared to the left side of the embryo, her9 expression in the duct (arrows) and glomerulus (arrowheads) is increased in the right side at 18 ss.(L and M) Compared to (L) wt embryos, the multi-cilia cell number is increased in (M) her9-utr morphants as shown by rfx2 expression at 24 hpf.All embryos, anterior to the left. (A–K) are dorsal views; (L and M) are lateral views. Bar scale: 100 μm (A–J), 130 μm (K), and 50 μm (L and M). |
PMC1781496_pgen-0030018-g005_8994.jpg | Describe the main subject of this image. |
her9 is a Downstream Target Gene of Jagged2a-Notch1a/Notch3 Signaling(A and B) Compared to (A) wt embryos, her9 expression in the pronephric duct region at 18 ss is severely down-regulated in (B) jagged2a-sp morphants.(C–F) Compared to (C) wt embryos, her9 expression in the pronephric duct region at 17 ss is mildly down-regulated in (D) notch1a (desth35b) mutants and (E) notch3-sp morphants, and is severely down-regulated in (F) notch3-sp MO-injected notch1a (desth35b) mutants.(G and H) Compared to (G) wt embryos, her9 expression in the pronephric duct region at 18 ss is severely down-regulated in (H) mibta52b mutants.(I and J) Coinjection of GFP mRNA (50 pg) and notch1aicd mRNA (100 pg) into one blastomere at the two-cell stage leads to (I) somite boundary disruption in the right half of the embryo, while somites on the left side are segmented properly. (J) GFP expression demonstrates that mRNA is localized to the right half of the embryo.(K) Compared to the left side of the embryo, her9 expression in the duct (arrows) and glomerulus (arrowheads) is increased in the right side at 18 ss.(L and M) Compared to (L) wt embryos, the multi-cilia cell number is increased in (M) her9-utr morphants as shown by rfx2 expression at 24 hpf.All embryos, anterior to the left. (A–K) are dorsal views; (L and M) are lateral views. Bar scale: 100 μm (A–J), 130 μm (K), and 50 μm (L and M). |
PMC1781496_pgen-0030018-g007_9015.jpg | What is the principal component of this image? | Notch-Dependent Binary Choice between Multi-Cilia cells and Principal Cells in the Pronephric Duct(A–D) double antibody staining of Pax2a (red) and phospho-histone-3 (pH3, green) of 18 ss (A and B) wt embryos and (C and D) mibta52b mutants. In (A) and (C), some pH3-positive nuclei seem to overlap with Pax2a-positive nuclei in the pronephric duct (arrows and arrowheads). Higher magnification of the distal duct domain marked by the white box of the same (B) wt embryo and (D) mibta52b mutant revealed that the pH3-positive nuclei indicated by arrowheads are not found in pronephric duct, while the nuclei indicated by arrows are overlapping with Pax2a-positive nuclei. A 3-D reconstruction of the domain revealed that the nuclei are not overlapping with Pax2a-positive nuclei (Videos S1 and S2). Pax2a staining in the neural tube (asterisk) indicates the neurogenic phenotype in (C) mibta52b mutants compared to that of (A) wt embryos. Three wt embryos and four mibta52b mutants were examined. In addition, three wt embryos and three mibta52b mutants were sectioned, and all sectioned slices were examined. No proliferating cells were found in the duct domain (unpublished data).(E and F) Apoptosis assay with TUNEL method on (E) wt embryos and (F) mibta52b mutants at 21 hpf. TUNEL staining was found in the somite and neural tube (arrowheads), while TUNEL staining was not found in the pronephric duct (arrows). The brown staining in the duct is background staining. Ten wt embryos and five mibta52b mutants were examined.(G and H) Fluorescent double in situ hybridization of rfx2 (red) and Na+, K+ ATPase β1a (green) in 24-hpf embryos demonstrated that multi-cilia cells interpolate principal cells in (G) heat-shocked hsp70:Gal4 control embryos, while in (H) heat-shocked hsp70:Gal4/UAS:myc-notch1a-intra embryos, Na+, K+ ATPase β1a expression is robustly found in the duct cells but rfx2 is not. Arrows point to rfx2-expressing cells.(A–D) are anterior to the right; (E–H) are anterior to the left. Bar scale: 100 μm (A and C), 50 μm (B and D), 100 μm (E and F), and 50 μm (G and H). |
PMC1781496_pgen-0030018-g007_9018.jpg | What is the principal component of this image? | Notch-Dependent Binary Choice between Multi-Cilia cells and Principal Cells in the Pronephric Duct(A–D) double antibody staining of Pax2a (red) and phospho-histone-3 (pH3, green) of 18 ss (A and B) wt embryos and (C and D) mibta52b mutants. In (A) and (C), some pH3-positive nuclei seem to overlap with Pax2a-positive nuclei in the pronephric duct (arrows and arrowheads). Higher magnification of the distal duct domain marked by the white box of the same (B) wt embryo and (D) mibta52b mutant revealed that the pH3-positive nuclei indicated by arrowheads are not found in pronephric duct, while the nuclei indicated by arrows are overlapping with Pax2a-positive nuclei. A 3-D reconstruction of the domain revealed that the nuclei are not overlapping with Pax2a-positive nuclei (Videos S1 and S2). Pax2a staining in the neural tube (asterisk) indicates the neurogenic phenotype in (C) mibta52b mutants compared to that of (A) wt embryos. Three wt embryos and four mibta52b mutants were examined. In addition, three wt embryos and three mibta52b mutants were sectioned, and all sectioned slices were examined. No proliferating cells were found in the duct domain (unpublished data).(E and F) Apoptosis assay with TUNEL method on (E) wt embryos and (F) mibta52b mutants at 21 hpf. TUNEL staining was found in the somite and neural tube (arrowheads), while TUNEL staining was not found in the pronephric duct (arrows). The brown staining in the duct is background staining. Ten wt embryos and five mibta52b mutants were examined.(G and H) Fluorescent double in situ hybridization of rfx2 (red) and Na+, K+ ATPase β1a (green) in 24-hpf embryos demonstrated that multi-cilia cells interpolate principal cells in (G) heat-shocked hsp70:Gal4 control embryos, while in (H) heat-shocked hsp70:Gal4/UAS:myc-notch1a-intra embryos, Na+, K+ ATPase β1a expression is robustly found in the duct cells but rfx2 is not. Arrows point to rfx2-expressing cells.(A–D) are anterior to the right; (E–H) are anterior to the left. Bar scale: 100 μm (A and C), 50 μm (B and D), 100 μm (E and F), and 50 μm (G and H). |
PMC1781496_pgen-0030018-g007_9019.jpg | What is the dominant medical problem in this image? | Notch-Dependent Binary Choice between Multi-Cilia cells and Principal Cells in the Pronephric Duct(A–D) double antibody staining of Pax2a (red) and phospho-histone-3 (pH3, green) of 18 ss (A and B) wt embryos and (C and D) mibta52b mutants. In (A) and (C), some pH3-positive nuclei seem to overlap with Pax2a-positive nuclei in the pronephric duct (arrows and arrowheads). Higher magnification of the distal duct domain marked by the white box of the same (B) wt embryo and (D) mibta52b mutant revealed that the pH3-positive nuclei indicated by arrowheads are not found in pronephric duct, while the nuclei indicated by arrows are overlapping with Pax2a-positive nuclei. A 3-D reconstruction of the domain revealed that the nuclei are not overlapping with Pax2a-positive nuclei (Videos S1 and S2). Pax2a staining in the neural tube (asterisk) indicates the neurogenic phenotype in (C) mibta52b mutants compared to that of (A) wt embryos. Three wt embryos and four mibta52b mutants were examined. In addition, three wt embryos and three mibta52b mutants were sectioned, and all sectioned slices were examined. No proliferating cells were found in the duct domain (unpublished data).(E and F) Apoptosis assay with TUNEL method on (E) wt embryos and (F) mibta52b mutants at 21 hpf. TUNEL staining was found in the somite and neural tube (arrowheads), while TUNEL staining was not found in the pronephric duct (arrows). The brown staining in the duct is background staining. Ten wt embryos and five mibta52b mutants were examined.(G and H) Fluorescent double in situ hybridization of rfx2 (red) and Na+, K+ ATPase β1a (green) in 24-hpf embryos demonstrated that multi-cilia cells interpolate principal cells in (G) heat-shocked hsp70:Gal4 control embryos, while in (H) heat-shocked hsp70:Gal4/UAS:myc-notch1a-intra embryos, Na+, K+ ATPase β1a expression is robustly found in the duct cells but rfx2 is not. Arrows point to rfx2-expressing cells.(A–D) are anterior to the right; (E–H) are anterior to the left. Bar scale: 100 μm (A and C), 50 μm (B and D), 100 μm (E and F), and 50 μm (G and H). |
PMC1781526_F7_9022.jpg | What is the main focus of this visual representation? | Qualitative co-localization of DNA and RNA through simultaneous imaging of RNA and DNA. Rat embryo fibroblasts were pulsed with 15N-uridine and BrdU as markers of newly synthesized RNA and DNA, respectively. (a,b) Parallel mass images at (a) 12C15N- and (b) 81Br-. (c) Overlay of 12C15N- and 81Br- images. 12C15N- is depicted as red (R) and 81Br- as green (G); the overlap between them shows up as yellow. (d) Overlay of 12C14N- and 12C15N- images. 12C14N- is depicted as red (R) and 12C15N- as green (G); the overlap between them shows up as yellow. Conditions of MIMS analysis: beam current 2pA; beam diameter 100 nm; field 20 × 20 μm. |
PMC1781526_F7_9021.jpg | Can you identify the primary element in this image? | Qualitative co-localization of DNA and RNA through simultaneous imaging of RNA and DNA. Rat embryo fibroblasts were pulsed with 15N-uridine and BrdU as markers of newly synthesized RNA and DNA, respectively. (a,b) Parallel mass images at (a) 12C15N- and (b) 81Br-. (c) Overlay of 12C15N- and 81Br- images. 12C15N- is depicted as red (R) and 81Br- as green (G); the overlap between them shows up as yellow. (d) Overlay of 12C14N- and 12C15N- images. 12C14N- is depicted as red (R) and 12C15N- as green (G); the overlap between them shows up as yellow. Conditions of MIMS analysis: beam current 2pA; beam diameter 100 nm; field 20 × 20 μm. |
PMC1781526_F7_9023.jpg | What is the dominant medical problem in this image? | Qualitative co-localization of DNA and RNA through simultaneous imaging of RNA and DNA. Rat embryo fibroblasts were pulsed with 15N-uridine and BrdU as markers of newly synthesized RNA and DNA, respectively. (a,b) Parallel mass images at (a) 12C15N- and (b) 81Br-. (c) Overlay of 12C15N- and 81Br- images. 12C15N- is depicted as red (R) and 81Br- as green (G); the overlap between them shows up as yellow. (d) Overlay of 12C14N- and 12C15N- images. 12C14N- is depicted as red (R) and 12C15N- as green (G); the overlap between them shows up as yellow. Conditions of MIMS analysis: beam current 2pA; beam diameter 100 nm; field 20 × 20 μm. |
PMC1781526_F7_9024.jpg | What is the central feature of this picture? | Qualitative co-localization of DNA and RNA through simultaneous imaging of RNA and DNA. Rat embryo fibroblasts were pulsed with 15N-uridine and BrdU as markers of newly synthesized RNA and DNA, respectively. (a,b) Parallel mass images at (a) 12C15N- and (b) 81Br-. (c) Overlay of 12C15N- and 81Br- images. 12C15N- is depicted as red (R) and 81Br- as green (G); the overlap between them shows up as yellow. (d) Overlay of 12C14N- and 12C15N- images. 12C14N- is depicted as red (R) and 12C15N- as green (G); the overlap between them shows up as yellow. Conditions of MIMS analysis: beam current 2pA; beam diameter 100 nm; field 20 × 20 μm. |
PMC1781526_F8_9034.jpg | What is the dominant medical problem 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. |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.