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PMC1298314_F3_4003.jpg | What object or scene is depicted here? | Overexpression of aurora B kinase does not phosphorylate histone H3 in interphase NRK cells. NRK cells overexpressing aurora B-GFP was stained with antibodies that specifically recognised histone H3 phosphorylated at Ser10 and then examined the expression of aurora B-GFP (a) and phosphorylation of histone H3 (c) by confocal laser microscopy. Corresponding phase and merged images (green; aurora B-GFP, red; phosphorylated histone H3) are shown in panels b and d, respectively. Although a fraction of aurora B-GFP is accumulated in the nucleus in a late telophase cell overexpressing aurora B-GFP, (arrows), phosphorylated histone H3 was not detected in the cell (c, d). Phosphorylated histone H3 was observed in a neighbouring prophase cell (arrowheads). Bar, 10 μm. |
PMC1298314_F3_4004.jpg | Describe the main subject of this image. | Overexpression of aurora B kinase does not phosphorylate histone H3 in interphase NRK cells. NRK cells overexpressing aurora B-GFP was stained with antibodies that specifically recognised histone H3 phosphorylated at Ser10 and then examined the expression of aurora B-GFP (a) and phosphorylation of histone H3 (c) by confocal laser microscopy. Corresponding phase and merged images (green; aurora B-GFP, red; phosphorylated histone H3) are shown in panels b and d, respectively. Although a fraction of aurora B-GFP is accumulated in the nucleus in a late telophase cell overexpressing aurora B-GFP, (arrows), phosphorylated histone H3 was not detected in the cell (c, d). Phosphorylated histone H3 was observed in a neighbouring prophase cell (arrowheads). Bar, 10 μm. |
PMC1298314_F4_4013.jpg | What key item or scene is captured in this photo? | Overexpressed aurora B is colocalized with cortical actin filaments but not stress fibers in interphase NRK cells. An NRK cell overexpressing aurora B-GFP was stained with rhodamine-labelled phalloidin and then examined the subcelluar localization of aurora B-GFP (a) and actin filaments (c) by confocal laser microscopy. Corresponding phase and merged images (green; aurora B-GFP, red; actin filaments) are shown in panels b and d, respectively. Cortical aurora B-GFP is well colocalized with the short fragments of actin filaments around the cortex (a and d, arrows). However, overexpressed aurora B-GFP appeared not to colocalize with the thick stress actin filaments in the peripheral region of the cortical area (c and d, arrowheads). Bar, 10 μm. |
PMC1298314_F4_4012.jpg | What key item or scene is captured in this photo? | Overexpressed aurora B is colocalized with cortical actin filaments but not stress fibers in interphase NRK cells. An NRK cell overexpressing aurora B-GFP was stained with rhodamine-labelled phalloidin and then examined the subcelluar localization of aurora B-GFP (a) and actin filaments (c) by confocal laser microscopy. Corresponding phase and merged images (green; aurora B-GFP, red; actin filaments) are shown in panels b and d, respectively. Cortical aurora B-GFP is well colocalized with the short fragments of actin filaments around the cortex (a and d, arrows). However, overexpressed aurora B-GFP appeared not to colocalize with the thick stress actin filaments in the peripheral region of the cortical area (c and d, arrowheads). Bar, 10 μm. |
PMC1298314_F4_4010.jpg | What stands out most in this visual? | Overexpressed aurora B is colocalized with cortical actin filaments but not stress fibers in interphase NRK cells. An NRK cell overexpressing aurora B-GFP was stained with rhodamine-labelled phalloidin and then examined the subcelluar localization of aurora B-GFP (a) and actin filaments (c) by confocal laser microscopy. Corresponding phase and merged images (green; aurora B-GFP, red; actin filaments) are shown in panels b and d, respectively. Cortical aurora B-GFP is well colocalized with the short fragments of actin filaments around the cortex (a and d, arrows). However, overexpressed aurora B-GFP appeared not to colocalize with the thick stress actin filaments in the peripheral region of the cortical area (c and d, arrowheads). Bar, 10 μm. |
PMC1298314_F5_4006.jpg | What is the central feature of this picture? | Overexpressed aurora B is not colocalized with phosphorylated myosin II regulatory light chain in interphase NRK cells. An NRK cell overexpressing aurora B-GFP was stained with antibodies that specifically recognised myosin II regulatory light chain phosphorylated at Ser19 and then examined the subcelluar localization of aurora B-GFP (a) and phopshorylated myosin II regulatory light chain (c) by confocal laser microscopy. Corresponding phase and merged images (green; aurora B-GFP, red; phosphorylated myosin II regulatory light chain) are shown in panels b and d, respectively. Overexpressed aurora B is associated with the cortex (a and d, arrows), while phosphorylated myosin II regulatory light chain is enriched in the cell periphery (c, and d, arrowheads). Bar, 10 μm. |
PMC1298314_F5_4008.jpg | Describe the main subject of this image. | Overexpressed aurora B is not colocalized with phosphorylated myosin II regulatory light chain in interphase NRK cells. An NRK cell overexpressing aurora B-GFP was stained with antibodies that specifically recognised myosin II regulatory light chain phosphorylated at Ser19 and then examined the subcelluar localization of aurora B-GFP (a) and phopshorylated myosin II regulatory light chain (c) by confocal laser microscopy. Corresponding phase and merged images (green; aurora B-GFP, red; phosphorylated myosin II regulatory light chain) are shown in panels b and d, respectively. Overexpressed aurora B is associated with the cortex (a and d, arrows), while phosphorylated myosin II regulatory light chain is enriched in the cell periphery (c, and d, arrowheads). Bar, 10 μm. |
PMC1298314_F5_4007.jpg | What stands out most in this visual? | Overexpressed aurora B is not colocalized with phosphorylated myosin II regulatory light chain in interphase NRK cells. An NRK cell overexpressing aurora B-GFP was stained with antibodies that specifically recognised myosin II regulatory light chain phosphorylated at Ser19 and then examined the subcelluar localization of aurora B-GFP (a) and phopshorylated myosin II regulatory light chain (c) by confocal laser microscopy. Corresponding phase and merged images (green; aurora B-GFP, red; phosphorylated myosin II regulatory light chain) are shown in panels b and d, respectively. Overexpressed aurora B is associated with the cortex (a and d, arrows), while phosphorylated myosin II regulatory light chain is enriched in the cell periphery (c, and d, arrowheads). Bar, 10 μm. |
PMC1298324_F1_4014.jpg | What object or scene is depicted here? | Fibrillar indirect immunofluorescence stain with obtained with sera of Q fever patients using monkey cardiac muscle sections. Magnification × 400. |
PMC1298335_F2_4016.jpg | What can you see in this picture? | Immunohistochemical study of hBD-4 expression in the human lung. For each pair of images, the upper panels (A1, B1, and C1) are the results of the immunohistochemical study of the lung tissue obtained from a 38-year-old female with pulmonary mucormycosis, and the lower panels (A2, B2, and C2) are those obtained from a 70-year-old male with bullae. Immunoreactive cells are present around the bronchial surface (A1, A2) and bronchiolar surface (B1, B2). hBD-4 immunoreactivity is not detected in alveolar epithelial cells (C1 and C2). No immunoreactivity is detected in tissues following preadsorption of antiserum with 1 μg/ml hBD-4 peptide (D). The bar represents a length of 50 μm in all panels. |
PMC1298335_F2_4015.jpg | What is being portrayed in this visual content? | Immunohistochemical study of hBD-4 expression in the human lung. For each pair of images, the upper panels (A1, B1, and C1) are the results of the immunohistochemical study of the lung tissue obtained from a 38-year-old female with pulmonary mucormycosis, and the lower panels (A2, B2, and C2) are those obtained from a 70-year-old male with bullae. Immunoreactive cells are present around the bronchial surface (A1, A2) and bronchiolar surface (B1, B2). hBD-4 immunoreactivity is not detected in alveolar epithelial cells (C1 and C2). No immunoreactivity is detected in tissues following preadsorption of antiserum with 1 μg/ml hBD-4 peptide (D). The bar represents a length of 50 μm in all panels. |
PMC1298335_F2_4017.jpg | Describe the main subject of this image. | Immunohistochemical study of hBD-4 expression in the human lung. For each pair of images, the upper panels (A1, B1, and C1) are the results of the immunohistochemical study of the lung tissue obtained from a 38-year-old female with pulmonary mucormycosis, and the lower panels (A2, B2, and C2) are those obtained from a 70-year-old male with bullae. Immunoreactive cells are present around the bronchial surface (A1, A2) and bronchiolar surface (B1, B2). hBD-4 immunoreactivity is not detected in alveolar epithelial cells (C1 and C2). No immunoreactivity is detected in tissues following preadsorption of antiserum with 1 μg/ml hBD-4 peptide (D). The bar represents a length of 50 μm in all panels. |
PMC1298335_F2_4019.jpg | Describe the main subject of this image. | Immunohistochemical study of hBD-4 expression in the human lung. For each pair of images, the upper panels (A1, B1, and C1) are the results of the immunohistochemical study of the lung tissue obtained from a 38-year-old female with pulmonary mucormycosis, and the lower panels (A2, B2, and C2) are those obtained from a 70-year-old male with bullae. Immunoreactive cells are present around the bronchial surface (A1, A2) and bronchiolar surface (B1, B2). hBD-4 immunoreactivity is not detected in alveolar epithelial cells (C1 and C2). No immunoreactivity is detected in tissues following preadsorption of antiserum with 1 μg/ml hBD-4 peptide (D). The bar represents a length of 50 μm in all panels. |
PMC1298335_F2_4020.jpg | What is the main focus of this visual representation? | Immunohistochemical study of hBD-4 expression in the human lung. For each pair of images, the upper panels (A1, B1, and C1) are the results of the immunohistochemical study of the lung tissue obtained from a 38-year-old female with pulmonary mucormycosis, and the lower panels (A2, B2, and C2) are those obtained from a 70-year-old male with bullae. Immunoreactive cells are present around the bronchial surface (A1, A2) and bronchiolar surface (B1, B2). hBD-4 immunoreactivity is not detected in alveolar epithelial cells (C1 and C2). No immunoreactivity is detected in tissues following preadsorption of antiserum with 1 μg/ml hBD-4 peptide (D). The bar represents a length of 50 μm in all panels. |
PMC1298335_F4_4021.jpg | What's the most prominent thing you notice in this picture? | Immunohistochemical study of hBD-4 expression in patients with chronic lower respiratory tract infection. hBD-4 immunoreactivity presented in bronchial epithelial cells (A), neutrophils and suppurative exudates within bronchial lumen (B). The bar represent a length of 50 μm in (A, B). |
PMC1298335_F4_4022.jpg | What key item or scene is captured in this photo? | Immunohistochemical study of hBD-4 expression in patients with chronic lower respiratory tract infection. hBD-4 immunoreactivity presented in bronchial epithelial cells (A), neutrophils and suppurative exudates within bronchial lumen (B). The bar represent a length of 50 μm in (A, B). |
PMC1298337_F3_4023.jpg | What is the dominant medical problem in this image? | Immunohistochemical localization of PPARγ in biopsies of the nasal mucosa from control subjects (A) and patients with allergic rhinitis (B), and in polyps before (C) and after treatment with steroids (D). Magnification: ×200. |
PMC1298337_F3_4026.jpg | What is being portrayed in this visual content? | Immunohistochemical localization of PPARγ in biopsies of the nasal mucosa from control subjects (A) and patients with allergic rhinitis (B), and in polyps before (C) and after treatment with steroids (D). Magnification: ×200. |
PMC1298337_F3_4025.jpg | What key item or scene is captured in this photo? | Immunohistochemical localization of PPARγ in biopsies of the nasal mucosa from control subjects (A) and patients with allergic rhinitis (B), and in polyps before (C) and after treatment with steroids (D). Magnification: ×200. |
PMC1298342_F1_4027.jpg | What is shown in this image? | Computed tomography scan showing a mass in the right iliac fossa region. |
PMC1298941_pmed-0030006-g006_4034.jpg | What is the principal component of this image? | In Vivo Selectivity of the Approach(A) Pathological analysis of the brains. Intracranial tumors were established and treated as described in Methods. After 24 h, animals were sacrificed and ultrathin slices of the brains were prepared. Slices were stained with H & E and analyzed by light microscopy (20× magnification) for development of pathological signs and immune cell infiltration (yellow arrow). Bottom panel shows the example of slices from the brains treated with (poly IC)PEI-PEG-EGF+PEI-Mel in the experiment described in Figure 5A (7 d post-treatment).(B) Poly IC induces apoptosis in intracranial xenografts. Intracranial tumors were established and treated as described in Methods. Apoptotic death was detected using Cell Death Detection kit-TMR Red (Methods). White dashed lines represent borders of the tumors. |
PMC1298941_pmed-0030006-g006_4033.jpg | What is the main focus of this visual representation? | In Vivo Selectivity of the Approach(A) Pathological analysis of the brains. Intracranial tumors were established and treated as described in Methods. After 24 h, animals were sacrificed and ultrathin slices of the brains were prepared. Slices were stained with H & E and analyzed by light microscopy (20× magnification) for development of pathological signs and immune cell infiltration (yellow arrow). Bottom panel shows the example of slices from the brains treated with (poly IC)PEI-PEG-EGF+PEI-Mel in the experiment described in Figure 5A (7 d post-treatment).(B) Poly IC induces apoptosis in intracranial xenografts. Intracranial tumors were established and treated as described in Methods. Apoptotic death was detected using Cell Death Detection kit-TMR Red (Methods). White dashed lines represent borders of the tumors. |
PMC1298941_pmed-0030006-g006_4029.jpg | What is the main focus of this visual representation? | In Vivo Selectivity of the Approach(A) Pathological analysis of the brains. Intracranial tumors were established and treated as described in Methods. After 24 h, animals were sacrificed and ultrathin slices of the brains were prepared. Slices were stained with H & E and analyzed by light microscopy (20× magnification) for development of pathological signs and immune cell infiltration (yellow arrow). Bottom panel shows the example of slices from the brains treated with (poly IC)PEI-PEG-EGF+PEI-Mel in the experiment described in Figure 5A (7 d post-treatment).(B) Poly IC induces apoptosis in intracranial xenografts. Intracranial tumors were established and treated as described in Methods. Apoptotic death was detected using Cell Death Detection kit-TMR Red (Methods). White dashed lines represent borders of the tumors. |
PMC1298941_pmed-0030006-g006_4031.jpg | What is shown in this image? | In Vivo Selectivity of the Approach(A) Pathological analysis of the brains. Intracranial tumors were established and treated as described in Methods. After 24 h, animals were sacrificed and ultrathin slices of the brains were prepared. Slices were stained with H & E and analyzed by light microscopy (20× magnification) for development of pathological signs and immune cell infiltration (yellow arrow). Bottom panel shows the example of slices from the brains treated with (poly IC)PEI-PEG-EGF+PEI-Mel in the experiment described in Figure 5A (7 d post-treatment).(B) Poly IC induces apoptosis in intracranial xenografts. Intracranial tumors were established and treated as described in Methods. Apoptotic death was detected using Cell Death Detection kit-TMR Red (Methods). White dashed lines represent borders of the tumors. |
PMC1298941_pmed-0030006-g006_4032.jpg | What's the most prominent thing you notice in this picture? | In Vivo Selectivity of the Approach(A) Pathological analysis of the brains. Intracranial tumors were established and treated as described in Methods. After 24 h, animals were sacrificed and ultrathin slices of the brains were prepared. Slices were stained with H & E and analyzed by light microscopy (20× magnification) for development of pathological signs and immune cell infiltration (yellow arrow). Bottom panel shows the example of slices from the brains treated with (poly IC)PEI-PEG-EGF+PEI-Mel in the experiment described in Figure 5A (7 d post-treatment).(B) Poly IC induces apoptosis in intracranial xenografts. Intracranial tumors were established and treated as described in Methods. Apoptotic death was detected using Cell Death Detection kit-TMR Red (Methods). White dashed lines represent borders of the tumors. |
PMC1298941_pmed-0030006-g006_4028.jpg | What is the principal component of this image? | In Vivo Selectivity of the Approach(A) Pathological analysis of the brains. Intracranial tumors were established and treated as described in Methods. After 24 h, animals were sacrificed and ultrathin slices of the brains were prepared. Slices were stained with H & E and analyzed by light microscopy (20× magnification) for development of pathological signs and immune cell infiltration (yellow arrow). Bottom panel shows the example of slices from the brains treated with (poly IC)PEI-PEG-EGF+PEI-Mel in the experiment described in Figure 5A (7 d post-treatment).(B) Poly IC induces apoptosis in intracranial xenografts. Intracranial tumors were established and treated as described in Methods. Apoptotic death was detected using Cell Death Detection kit-TMR Red (Methods). White dashed lines represent borders of the tumors. |
PMC1299324_F2_4037.jpg | What is being portrayed in this visual content? | Strong and diffuse immunohistochemical positivity of the inclusions for fibrinogen, ×40. İnset: Same area with higher magnification. (×200). |
PMC1299324_F2_4035.jpg | What object or scene is depicted here? | Strong and diffuse immunohistochemical positivity of the inclusions for fibrinogen, ×40. İnset: Same area with higher magnification. (×200). |
PMC1299324_F2_4036.jpg | Can you identify the primary element in this image? | Strong and diffuse immunohistochemical positivity of the inclusions for fibrinogen, ×40. İnset: Same area with higher magnification. (×200). |
PMC1299324_F4_4038.jpg | What can you see in this picture? | In the second biopsy, inclusions and chronic hepatitic changes are dramatically reduced, (H&E, ×200). |
PMC1307534_pmed-0030031-g001_4044.jpg | What is the dominant medical problem in this image? | Representative Clinical, Pathological, and Molecular Genetic Features of Glioblastoma MultiformeThe top panel shows an illustrative set of neuroimages from a patient with glioblastoma multiforme. On the left and in the center are gadolinium-enhanced T1-weighted axial magnetic resonance images from the day before and the day after resection of a large left frontal GBM. The patient was treated with postoperative radiation and chemotherapy. He presented again, 11 months after the first surgery, with stupor and a contrast-enhanced computed tomographic scan (right), which showed a massive and fatal recurrence.The middle panel shows histopathological examples of this patient's tumor. In the left image, there is evidence of hypercellularity, pseudopalisading necrosis (small arrow), and vascular proliferation with hemorrhage (large arrow). In the center image, there is hypercellularity with intermittent mitotic figures (small arrows), while in the image to the right, there are several areas with florid endothelial proliferation (small arrows). See also Table 1. All figures are 200× magnification.The bottom panel shows a schematic of current models of astrocytoma development and progression. The de novo pathway is located on top, and the secondary pathway is located on bottom. The principal genetic changes are noted for each pathway. Neuronal tumors and oligodendrogliomas (left top and bottom, respectively) appear to arise independently. Average survivals are noted for each astrocytoma type. While basic genetic features have been elaborated, they have been inconsistently found in GBMs, and as yet appear not to be consistently effective for targeted therapy. There remains a great deal unknown about the process by which these tumors progress to the most malignant state, whether the tumor is a de novo GBM or arises secondarily. Unknown steps from potential progenitor or pluripotent tumor cell(s) are indicated by small arrows. |
PMC1307534_pmed-0030031-g001_4043.jpg | Can you identify the primary element in this image? | Representative Clinical, Pathological, and Molecular Genetic Features of Glioblastoma MultiformeThe top panel shows an illustrative set of neuroimages from a patient with glioblastoma multiforme. On the left and in the center are gadolinium-enhanced T1-weighted axial magnetic resonance images from the day before and the day after resection of a large left frontal GBM. The patient was treated with postoperative radiation and chemotherapy. He presented again, 11 months after the first surgery, with stupor and a contrast-enhanced computed tomographic scan (right), which showed a massive and fatal recurrence.The middle panel shows histopathological examples of this patient's tumor. In the left image, there is evidence of hypercellularity, pseudopalisading necrosis (small arrow), and vascular proliferation with hemorrhage (large arrow). In the center image, there is hypercellularity with intermittent mitotic figures (small arrows), while in the image to the right, there are several areas with florid endothelial proliferation (small arrows). See also Table 1. All figures are 200× magnification.The bottom panel shows a schematic of current models of astrocytoma development and progression. The de novo pathway is located on top, and the secondary pathway is located on bottom. The principal genetic changes are noted for each pathway. Neuronal tumors and oligodendrogliomas (left top and bottom, respectively) appear to arise independently. Average survivals are noted for each astrocytoma type. While basic genetic features have been elaborated, they have been inconsistently found in GBMs, and as yet appear not to be consistently effective for targeted therapy. There remains a great deal unknown about the process by which these tumors progress to the most malignant state, whether the tumor is a de novo GBM or arises secondarily. Unknown steps from potential progenitor or pluripotent tumor cell(s) are indicated by small arrows. |
PMC1307534_pmed-0030031-g001_4040.jpg | What is the main focus of this visual representation? | Representative Clinical, Pathological, and Molecular Genetic Features of Glioblastoma MultiformeThe top panel shows an illustrative set of neuroimages from a patient with glioblastoma multiforme. On the left and in the center are gadolinium-enhanced T1-weighted axial magnetic resonance images from the day before and the day after resection of a large left frontal GBM. The patient was treated with postoperative radiation and chemotherapy. He presented again, 11 months after the first surgery, with stupor and a contrast-enhanced computed tomographic scan (right), which showed a massive and fatal recurrence.The middle panel shows histopathological examples of this patient's tumor. In the left image, there is evidence of hypercellularity, pseudopalisading necrosis (small arrow), and vascular proliferation with hemorrhage (large arrow). In the center image, there is hypercellularity with intermittent mitotic figures (small arrows), while in the image to the right, there are several areas with florid endothelial proliferation (small arrows). See also Table 1. All figures are 200× magnification.The bottom panel shows a schematic of current models of astrocytoma development and progression. The de novo pathway is located on top, and the secondary pathway is located on bottom. The principal genetic changes are noted for each pathway. Neuronal tumors and oligodendrogliomas (left top and bottom, respectively) appear to arise independently. Average survivals are noted for each astrocytoma type. While basic genetic features have been elaborated, they have been inconsistently found in GBMs, and as yet appear not to be consistently effective for targeted therapy. There remains a great deal unknown about the process by which these tumors progress to the most malignant state, whether the tumor is a de novo GBM or arises secondarily. Unknown steps from potential progenitor or pluripotent tumor cell(s) are indicated by small arrows. |
PMC1307534_pmed-0030031-g001_4045.jpg | What is the principal component of this image? | Representative Clinical, Pathological, and Molecular Genetic Features of Glioblastoma MultiformeThe top panel shows an illustrative set of neuroimages from a patient with glioblastoma multiforme. On the left and in the center are gadolinium-enhanced T1-weighted axial magnetic resonance images from the day before and the day after resection of a large left frontal GBM. The patient was treated with postoperative radiation and chemotherapy. He presented again, 11 months after the first surgery, with stupor and a contrast-enhanced computed tomographic scan (right), which showed a massive and fatal recurrence.The middle panel shows histopathological examples of this patient's tumor. In the left image, there is evidence of hypercellularity, pseudopalisading necrosis (small arrow), and vascular proliferation with hemorrhage (large arrow). In the center image, there is hypercellularity with intermittent mitotic figures (small arrows), while in the image to the right, there are several areas with florid endothelial proliferation (small arrows). See also Table 1. All figures are 200× magnification.The bottom panel shows a schematic of current models of astrocytoma development and progression. The de novo pathway is located on top, and the secondary pathway is located on bottom. The principal genetic changes are noted for each pathway. Neuronal tumors and oligodendrogliomas (left top and bottom, respectively) appear to arise independently. Average survivals are noted for each astrocytoma type. While basic genetic features have been elaborated, they have been inconsistently found in GBMs, and as yet appear not to be consistently effective for targeted therapy. There remains a great deal unknown about the process by which these tumors progress to the most malignant state, whether the tumor is a de novo GBM or arises secondarily. Unknown steps from potential progenitor or pluripotent tumor cell(s) are indicated by small arrows. |
PMC1308848_F1_4046.jpg | What is the central feature of this picture? | Skin and fat necrosis of the right breast secondary to injection of methylene blue dye for SLNB. |
PMC1308863_F6_4051.jpg | Can you identify the primary element in this image? | Subcellular localization of wild-type M-PMV Gag, ΔKKPKR Gag, and RSV Gag-GFP under steady state growth conditions or after treatment with LMB. HeLa cells were transfected with either pSARM-4, ΔKKPKR, or RSV Gag-GFP and left untreated or treated with LMB. The cells were fixed in methanol and the subcellular localizations of Gag were viewed by confocal microscopy using rabbit anti-Pr78 antibodies and Cy2 conjugated secondary antibodies. RSV Gag-GFP was directly visualized by fluorescence of the Gag-GFP fusion protein. Drug treatments: Wild-type M-PMV (untreated, panel 6A), wild-type MPMV (LMB treated, panel 6B) ΔKKPKR (untreated, panel 6C, ΔKKPKR (LMB treated, panel 6D), RSV Gag-GFP (untreated, panel 6E), and RSV Gag-GFP (LMB treated, panel 6F). Colocalization of wild-type M-PMV Gag, ΔKKPKR, and nuclear pores. Transfected HeLa cells were fixed with 4% paraformaldyhyde, and permiablized with 0.2% TX-100. Wild-type Gag (panels G-J), ΔKKPKR Gag (panels k-N), and nuclear pore localization were visualized by confocal microscopy using affinity purified anti-Pr78 and MAb414 antibodies, respectively, and counter stained with Cy2 anti-rabbit and Cy5 anti-mouse antibodies. 0.3 um Z-sections were stacked and orthogonal views through the cell were generated using Flowview imaging analysis software. |
PMC1308863_F6_4047.jpg | What stands out most in this visual? | Subcellular localization of wild-type M-PMV Gag, ΔKKPKR Gag, and RSV Gag-GFP under steady state growth conditions or after treatment with LMB. HeLa cells were transfected with either pSARM-4, ΔKKPKR, or RSV Gag-GFP and left untreated or treated with LMB. The cells were fixed in methanol and the subcellular localizations of Gag were viewed by confocal microscopy using rabbit anti-Pr78 antibodies and Cy2 conjugated secondary antibodies. RSV Gag-GFP was directly visualized by fluorescence of the Gag-GFP fusion protein. Drug treatments: Wild-type M-PMV (untreated, panel 6A), wild-type MPMV (LMB treated, panel 6B) ΔKKPKR (untreated, panel 6C, ΔKKPKR (LMB treated, panel 6D), RSV Gag-GFP (untreated, panel 6E), and RSV Gag-GFP (LMB treated, panel 6F). Colocalization of wild-type M-PMV Gag, ΔKKPKR, and nuclear pores. Transfected HeLa cells were fixed with 4% paraformaldyhyde, and permiablized with 0.2% TX-100. Wild-type Gag (panels G-J), ΔKKPKR Gag (panels k-N), and nuclear pore localization were visualized by confocal microscopy using affinity purified anti-Pr78 and MAb414 antibodies, respectively, and counter stained with Cy2 anti-rabbit and Cy5 anti-mouse antibodies. 0.3 um Z-sections were stacked and orthogonal views through the cell were generated using Flowview imaging analysis software. |
PMC1308863_F6_4059.jpg | Describe the main subject of this image. | Subcellular localization of wild-type M-PMV Gag, ΔKKPKR Gag, and RSV Gag-GFP under steady state growth conditions or after treatment with LMB. HeLa cells were transfected with either pSARM-4, ΔKKPKR, or RSV Gag-GFP and left untreated or treated with LMB. The cells were fixed in methanol and the subcellular localizations of Gag were viewed by confocal microscopy using rabbit anti-Pr78 antibodies and Cy2 conjugated secondary antibodies. RSV Gag-GFP was directly visualized by fluorescence of the Gag-GFP fusion protein. Drug treatments: Wild-type M-PMV (untreated, panel 6A), wild-type MPMV (LMB treated, panel 6B) ΔKKPKR (untreated, panel 6C, ΔKKPKR (LMB treated, panel 6D), RSV Gag-GFP (untreated, panel 6E), and RSV Gag-GFP (LMB treated, panel 6F). Colocalization of wild-type M-PMV Gag, ΔKKPKR, and nuclear pores. Transfected HeLa cells were fixed with 4% paraformaldyhyde, and permiablized with 0.2% TX-100. Wild-type Gag (panels G-J), ΔKKPKR Gag (panels k-N), and nuclear pore localization were visualized by confocal microscopy using affinity purified anti-Pr78 and MAb414 antibodies, respectively, and counter stained with Cy2 anti-rabbit and Cy5 anti-mouse antibodies. 0.3 um Z-sections were stacked and orthogonal views through the cell were generated using Flowview imaging analysis software. |
PMC1308863_F6_4055.jpg | What can you see in this picture? | Subcellular localization of wild-type M-PMV Gag, ΔKKPKR Gag, and RSV Gag-GFP under steady state growth conditions or after treatment with LMB. HeLa cells were transfected with either pSARM-4, ΔKKPKR, or RSV Gag-GFP and left untreated or treated with LMB. The cells were fixed in methanol and the subcellular localizations of Gag were viewed by confocal microscopy using rabbit anti-Pr78 antibodies and Cy2 conjugated secondary antibodies. RSV Gag-GFP was directly visualized by fluorescence of the Gag-GFP fusion protein. Drug treatments: Wild-type M-PMV (untreated, panel 6A), wild-type MPMV (LMB treated, panel 6B) ΔKKPKR (untreated, panel 6C, ΔKKPKR (LMB treated, panel 6D), RSV Gag-GFP (untreated, panel 6E), and RSV Gag-GFP (LMB treated, panel 6F). Colocalization of wild-type M-PMV Gag, ΔKKPKR, and nuclear pores. Transfected HeLa cells were fixed with 4% paraformaldyhyde, and permiablized with 0.2% TX-100. Wild-type Gag (panels G-J), ΔKKPKR Gag (panels k-N), and nuclear pore localization were visualized by confocal microscopy using affinity purified anti-Pr78 and MAb414 antibodies, respectively, and counter stained with Cy2 anti-rabbit and Cy5 anti-mouse antibodies. 0.3 um Z-sections were stacked and orthogonal views through the cell were generated using Flowview imaging analysis software. |
PMC1308863_F6_4056.jpg | What is the central feature of this picture? | Subcellular localization of wild-type M-PMV Gag, ΔKKPKR Gag, and RSV Gag-GFP under steady state growth conditions or after treatment with LMB. HeLa cells were transfected with either pSARM-4, ΔKKPKR, or RSV Gag-GFP and left untreated or treated with LMB. The cells were fixed in methanol and the subcellular localizations of Gag were viewed by confocal microscopy using rabbit anti-Pr78 antibodies and Cy2 conjugated secondary antibodies. RSV Gag-GFP was directly visualized by fluorescence of the Gag-GFP fusion protein. Drug treatments: Wild-type M-PMV (untreated, panel 6A), wild-type MPMV (LMB treated, panel 6B) ΔKKPKR (untreated, panel 6C, ΔKKPKR (LMB treated, panel 6D), RSV Gag-GFP (untreated, panel 6E), and RSV Gag-GFP (LMB treated, panel 6F). Colocalization of wild-type M-PMV Gag, ΔKKPKR, and nuclear pores. Transfected HeLa cells were fixed with 4% paraformaldyhyde, and permiablized with 0.2% TX-100. Wild-type Gag (panels G-J), ΔKKPKR Gag (panels k-N), and nuclear pore localization were visualized by confocal microscopy using affinity purified anti-Pr78 and MAb414 antibodies, respectively, and counter stained with Cy2 anti-rabbit and Cy5 anti-mouse antibodies. 0.3 um Z-sections were stacked and orthogonal views through the cell were generated using Flowview imaging analysis software. |
PMC1308863_F6_4054.jpg | Can you identify the primary element in this image? | Subcellular localization of wild-type M-PMV Gag, ΔKKPKR Gag, and RSV Gag-GFP under steady state growth conditions or after treatment with LMB. HeLa cells were transfected with either pSARM-4, ΔKKPKR, or RSV Gag-GFP and left untreated or treated with LMB. The cells were fixed in methanol and the subcellular localizations of Gag were viewed by confocal microscopy using rabbit anti-Pr78 antibodies and Cy2 conjugated secondary antibodies. RSV Gag-GFP was directly visualized by fluorescence of the Gag-GFP fusion protein. Drug treatments: Wild-type M-PMV (untreated, panel 6A), wild-type MPMV (LMB treated, panel 6B) ΔKKPKR (untreated, panel 6C, ΔKKPKR (LMB treated, panel 6D), RSV Gag-GFP (untreated, panel 6E), and RSV Gag-GFP (LMB treated, panel 6F). Colocalization of wild-type M-PMV Gag, ΔKKPKR, and nuclear pores. Transfected HeLa cells were fixed with 4% paraformaldyhyde, and permiablized with 0.2% TX-100. Wild-type Gag (panels G-J), ΔKKPKR Gag (panels k-N), and nuclear pore localization were visualized by confocal microscopy using affinity purified anti-Pr78 and MAb414 antibodies, respectively, and counter stained with Cy2 anti-rabbit and Cy5 anti-mouse antibodies. 0.3 um Z-sections were stacked and orthogonal views through the cell were generated using Flowview imaging analysis software. |
PMC1308863_F6_4050.jpg | What is the main focus of this visual representation? | Subcellular localization of wild-type M-PMV Gag, ΔKKPKR Gag, and RSV Gag-GFP under steady state growth conditions or after treatment with LMB. HeLa cells were transfected with either pSARM-4, ΔKKPKR, or RSV Gag-GFP and left untreated or treated with LMB. The cells were fixed in methanol and the subcellular localizations of Gag were viewed by confocal microscopy using rabbit anti-Pr78 antibodies and Cy2 conjugated secondary antibodies. RSV Gag-GFP was directly visualized by fluorescence of the Gag-GFP fusion protein. Drug treatments: Wild-type M-PMV (untreated, panel 6A), wild-type MPMV (LMB treated, panel 6B) ΔKKPKR (untreated, panel 6C, ΔKKPKR (LMB treated, panel 6D), RSV Gag-GFP (untreated, panel 6E), and RSV Gag-GFP (LMB treated, panel 6F). Colocalization of wild-type M-PMV Gag, ΔKKPKR, and nuclear pores. Transfected HeLa cells were fixed with 4% paraformaldyhyde, and permiablized with 0.2% TX-100. Wild-type Gag (panels G-J), ΔKKPKR Gag (panels k-N), and nuclear pore localization were visualized by confocal microscopy using affinity purified anti-Pr78 and MAb414 antibodies, respectively, and counter stained with Cy2 anti-rabbit and Cy5 anti-mouse antibodies. 0.3 um Z-sections were stacked and orthogonal views through the cell were generated using Flowview imaging analysis software. |
PMC1308863_F6_4058.jpg | What can you see in this picture? | Subcellular localization of wild-type M-PMV Gag, ΔKKPKR Gag, and RSV Gag-GFP under steady state growth conditions or after treatment with LMB. HeLa cells were transfected with either pSARM-4, ΔKKPKR, or RSV Gag-GFP and left untreated or treated with LMB. The cells were fixed in methanol and the subcellular localizations of Gag were viewed by confocal microscopy using rabbit anti-Pr78 antibodies and Cy2 conjugated secondary antibodies. RSV Gag-GFP was directly visualized by fluorescence of the Gag-GFP fusion protein. Drug treatments: Wild-type M-PMV (untreated, panel 6A), wild-type MPMV (LMB treated, panel 6B) ΔKKPKR (untreated, panel 6C, ΔKKPKR (LMB treated, panel 6D), RSV Gag-GFP (untreated, panel 6E), and RSV Gag-GFP (LMB treated, panel 6F). Colocalization of wild-type M-PMV Gag, ΔKKPKR, and nuclear pores. Transfected HeLa cells were fixed with 4% paraformaldyhyde, and permiablized with 0.2% TX-100. Wild-type Gag (panels G-J), ΔKKPKR Gag (panels k-N), and nuclear pore localization were visualized by confocal microscopy using affinity purified anti-Pr78 and MAb414 antibodies, respectively, and counter stained with Cy2 anti-rabbit and Cy5 anti-mouse antibodies. 0.3 um Z-sections were stacked and orthogonal views through the cell were generated using Flowview imaging analysis software. |
PMC1308863_F6_4052.jpg | What is the main focus of this visual representation? | Subcellular localization of wild-type M-PMV Gag, ΔKKPKR Gag, and RSV Gag-GFP under steady state growth conditions or after treatment with LMB. HeLa cells were transfected with either pSARM-4, ΔKKPKR, or RSV Gag-GFP and left untreated or treated with LMB. The cells were fixed in methanol and the subcellular localizations of Gag were viewed by confocal microscopy using rabbit anti-Pr78 antibodies and Cy2 conjugated secondary antibodies. RSV Gag-GFP was directly visualized by fluorescence of the Gag-GFP fusion protein. Drug treatments: Wild-type M-PMV (untreated, panel 6A), wild-type MPMV (LMB treated, panel 6B) ΔKKPKR (untreated, panel 6C, ΔKKPKR (LMB treated, panel 6D), RSV Gag-GFP (untreated, panel 6E), and RSV Gag-GFP (LMB treated, panel 6F). Colocalization of wild-type M-PMV Gag, ΔKKPKR, and nuclear pores. Transfected HeLa cells were fixed with 4% paraformaldyhyde, and permiablized with 0.2% TX-100. Wild-type Gag (panels G-J), ΔKKPKR Gag (panels k-N), and nuclear pore localization were visualized by confocal microscopy using affinity purified anti-Pr78 and MAb414 antibodies, respectively, and counter stained with Cy2 anti-rabbit and Cy5 anti-mouse antibodies. 0.3 um Z-sections were stacked and orthogonal views through the cell were generated using Flowview imaging analysis software. |
PMC1308863_F6_4053.jpg | What is the central feature of this picture? | Subcellular localization of wild-type M-PMV Gag, ΔKKPKR Gag, and RSV Gag-GFP under steady state growth conditions or after treatment with LMB. HeLa cells were transfected with either pSARM-4, ΔKKPKR, or RSV Gag-GFP and left untreated or treated with LMB. The cells were fixed in methanol and the subcellular localizations of Gag were viewed by confocal microscopy using rabbit anti-Pr78 antibodies and Cy2 conjugated secondary antibodies. RSV Gag-GFP was directly visualized by fluorescence of the Gag-GFP fusion protein. Drug treatments: Wild-type M-PMV (untreated, panel 6A), wild-type MPMV (LMB treated, panel 6B) ΔKKPKR (untreated, panel 6C, ΔKKPKR (LMB treated, panel 6D), RSV Gag-GFP (untreated, panel 6E), and RSV Gag-GFP (LMB treated, panel 6F). Colocalization of wild-type M-PMV Gag, ΔKKPKR, and nuclear pores. Transfected HeLa cells were fixed with 4% paraformaldyhyde, and permiablized with 0.2% TX-100. Wild-type Gag (panels G-J), ΔKKPKR Gag (panels k-N), and nuclear pore localization were visualized by confocal microscopy using affinity purified anti-Pr78 and MAb414 antibodies, respectively, and counter stained with Cy2 anti-rabbit and Cy5 anti-mouse antibodies. 0.3 um Z-sections were stacked and orthogonal views through the cell were generated using Flowview imaging analysis software. |
PMC1308872_F2_4063.jpg | What is the main focus of this visual representation? | E-cadherin reactivity in metastatic "lobular" carcinoma (case 2). A: Well-differentiated invasive ductal carcinoma (Hematoxylin and eosin, left) exhibiting weak cell membrane positivity for E-cadherin (Immunoperoxidase stain for E-cadherin, right). B: Nodal metastasis demonstrating strong cell membrane immunoreactivity for E-cadherin; higher magnification of tumor cells (inset) (Immunoperoxidase stain for E-cadherin). |
PMC1308872_F2_4062.jpg | What object or scene is depicted here? | E-cadherin reactivity in metastatic "lobular" carcinoma (case 2). A: Well-differentiated invasive ductal carcinoma (Hematoxylin and eosin, left) exhibiting weak cell membrane positivity for E-cadherin (Immunoperoxidase stain for E-cadherin, right). B: Nodal metastasis demonstrating strong cell membrane immunoreactivity for E-cadherin; higher magnification of tumor cells (inset) (Immunoperoxidase stain for E-cadherin). |
PMC1308872_F5_4069.jpg | What is the core subject represented in this visual? | Invasive lobular carcinoma with glandular "ductal" differentiation (case 5). A: Moderately differentiated invasive "ductal" carcinoma and carcinoma in situ on core biopsy (Hematoxylin and eosin, right) showing complete absence of E-cadherin immunoreactivity. (Immunoperoxidase stain for E-cadherin, left). B: No immunoreactivity for E-cadherin (Immunoperoxidase stain for E-cadherin, left) confirms invasive lobular carcinoma with glandular differentiation in the excision biopsy (Hematoxylin and eosin, right). C: Invasive lobular carcinoma with gland formation (Hematoxylin and eosin, right and immunoperoxidase stain for E-cadherin, left). |
PMC1308872_F5_4071.jpg | What is the dominant medical problem in this image? | Invasive lobular carcinoma with glandular "ductal" differentiation (case 5). A: Moderately differentiated invasive "ductal" carcinoma and carcinoma in situ on core biopsy (Hematoxylin and eosin, right) showing complete absence of E-cadherin immunoreactivity. (Immunoperoxidase stain for E-cadherin, left). B: No immunoreactivity for E-cadherin (Immunoperoxidase stain for E-cadherin, left) confirms invasive lobular carcinoma with glandular differentiation in the excision biopsy (Hematoxylin and eosin, right). C: Invasive lobular carcinoma with gland formation (Hematoxylin and eosin, right and immunoperoxidase stain for E-cadherin, left). |
PMC1308872_F5_4068.jpg | What is the focal point of this photograph? | Invasive lobular carcinoma with glandular "ductal" differentiation (case 5). A: Moderately differentiated invasive "ductal" carcinoma and carcinoma in situ on core biopsy (Hematoxylin and eosin, right) showing complete absence of E-cadherin immunoreactivity. (Immunoperoxidase stain for E-cadherin, left). B: No immunoreactivity for E-cadherin (Immunoperoxidase stain for E-cadherin, left) confirms invasive lobular carcinoma with glandular differentiation in the excision biopsy (Hematoxylin and eosin, right). C: Invasive lobular carcinoma with gland formation (Hematoxylin and eosin, right and immunoperoxidase stain for E-cadherin, left). |
PMC1308872_F5_4072.jpg | What is the focal point of this photograph? | Invasive lobular carcinoma with glandular "ductal" differentiation (case 5). A: Moderately differentiated invasive "ductal" carcinoma and carcinoma in situ on core biopsy (Hematoxylin and eosin, right) showing complete absence of E-cadherin immunoreactivity. (Immunoperoxidase stain for E-cadherin, left). B: No immunoreactivity for E-cadherin (Immunoperoxidase stain for E-cadherin, left) confirms invasive lobular carcinoma with glandular differentiation in the excision biopsy (Hematoxylin and eosin, right). C: Invasive lobular carcinoma with gland formation (Hematoxylin and eosin, right and immunoperoxidase stain for E-cadherin, left). |
PMC1308872_F5_4070.jpg | What key item or scene is captured in this photo? | Invasive lobular carcinoma with glandular "ductal" differentiation (case 5). A: Moderately differentiated invasive "ductal" carcinoma and carcinoma in situ on core biopsy (Hematoxylin and eosin, right) showing complete absence of E-cadherin immunoreactivity. (Immunoperoxidase stain for E-cadherin, left). B: No immunoreactivity for E-cadherin (Immunoperoxidase stain for E-cadherin, left) confirms invasive lobular carcinoma with glandular differentiation in the excision biopsy (Hematoxylin and eosin, right). C: Invasive lobular carcinoma with gland formation (Hematoxylin and eosin, right and immunoperoxidase stain for E-cadherin, left). |
PMC1308873_F1_4061.jpg | What can you see in this picture? | Preoperative chest X-ray showing total atelectasis of the left lung and deviation of the cardiac silhouette to the right. |
PMC1308873_F1_4060.jpg | Can you identify the primary element in this image? | Preoperative chest X-ray showing total atelectasis of the left lung and deviation of the cardiac silhouette to the right. |
PMC1308873_F3_4067.jpg | What can you see in this picture? | Preoperative MRI showing the teratoma, its anatomic relations to the mediastinum, and its expansion to the left hemithorax. |
PMC1308873_F3_4066.jpg | What is shown in this image? | Preoperative MRI showing the teratoma, its anatomic relations to the mediastinum, and its expansion to the left hemithorax. |
PMC1310517_F4_4074.jpg | What object or scene is depicted here? | Macrophages. (A-C) The areas marked with asterisk (*) are shown with a higher magnification (×420). Black arrows indicate macrophages. (A) At day 3 macrophages are present in the epineurium (EP) of distal 1 area (×210). A few ED-1 positive cells are also seen in the endoneurium (EN). (B) In distal 1 area at day 14 there are numerous macrophages in the endoneurium (×210). (C) Some macrophages are still present in both epi- and endoneurium in the proximal 2 area at 35 days (× 210). (D-F) Longitudinal sections studied by confocal microscope. Macrophages are visualized with red color, endoneurial vessels with green, and yellow color indicates macrophages inside blood vessels. White arrows indicate the epineurial area. The pictures are focused to the endoneurial level in the middle. (D) At day 14 several macrophages can be observed in the epineurial and endoneurial area of proximal 2 area (× 120). (E) At day 35 several macrophages are still present in the epineurium of proximal 2 area, but start to decrease in the endoneurium (× 120). (F) Control from sciatic nerve (non-operated control animal) (× 120). |
PMC1310517_F4_4075.jpg | What stands out most in this visual? | Macrophages. (A-C) The areas marked with asterisk (*) are shown with a higher magnification (×420). Black arrows indicate macrophages. (A) At day 3 macrophages are present in the epineurium (EP) of distal 1 area (×210). A few ED-1 positive cells are also seen in the endoneurium (EN). (B) In distal 1 area at day 14 there are numerous macrophages in the endoneurium (×210). (C) Some macrophages are still present in both epi- and endoneurium in the proximal 2 area at 35 days (× 210). (D-F) Longitudinal sections studied by confocal microscope. Macrophages are visualized with red color, endoneurial vessels with green, and yellow color indicates macrophages inside blood vessels. White arrows indicate the epineurial area. The pictures are focused to the endoneurial level in the middle. (D) At day 14 several macrophages can be observed in the epineurial and endoneurial area of proximal 2 area (× 120). (E) At day 35 several macrophages are still present in the epineurium of proximal 2 area, but start to decrease in the endoneurium (× 120). (F) Control from sciatic nerve (non-operated control animal) (× 120). |
PMC1310517_F4_4078.jpg | What is the focal point of this photograph? | Macrophages. (A-C) The areas marked with asterisk (*) are shown with a higher magnification (×420). Black arrows indicate macrophages. (A) At day 3 macrophages are present in the epineurium (EP) of distal 1 area (×210). A few ED-1 positive cells are also seen in the endoneurium (EN). (B) In distal 1 area at day 14 there are numerous macrophages in the endoneurium (×210). (C) Some macrophages are still present in both epi- and endoneurium in the proximal 2 area at 35 days (× 210). (D-F) Longitudinal sections studied by confocal microscope. Macrophages are visualized with red color, endoneurial vessels with green, and yellow color indicates macrophages inside blood vessels. White arrows indicate the epineurial area. The pictures are focused to the endoneurial level in the middle. (D) At day 14 several macrophages can be observed in the epineurial and endoneurial area of proximal 2 area (× 120). (E) At day 35 several macrophages are still present in the epineurium of proximal 2 area, but start to decrease in the endoneurium (× 120). (F) Control from sciatic nerve (non-operated control animal) (× 120). |
PMC1310517_F4_4077.jpg | What object or scene is depicted here? | Macrophages. (A-C) The areas marked with asterisk (*) are shown with a higher magnification (×420). Black arrows indicate macrophages. (A) At day 3 macrophages are present in the epineurium (EP) of distal 1 area (×210). A few ED-1 positive cells are also seen in the endoneurium (EN). (B) In distal 1 area at day 14 there are numerous macrophages in the endoneurium (×210). (C) Some macrophages are still present in both epi- and endoneurium in the proximal 2 area at 35 days (× 210). (D-F) Longitudinal sections studied by confocal microscope. Macrophages are visualized with red color, endoneurial vessels with green, and yellow color indicates macrophages inside blood vessels. White arrows indicate the epineurial area. The pictures are focused to the endoneurial level in the middle. (D) At day 14 several macrophages can be observed in the epineurial and endoneurial area of proximal 2 area (× 120). (E) At day 35 several macrophages are still present in the epineurium of proximal 2 area, but start to decrease in the endoneurium (× 120). (F) Control from sciatic nerve (non-operated control animal) (× 120). |
PMC1310521_F1_4079.jpg | Describe the main subject of this image. | Left fifth digit with marked swelling. Photo taken after biopsy. |
PMC1310521_F2_4082.jpg | What is being portrayed in this visual content? | Plain radiograph of left hand demonstrated soft tissue swelling of the fifth digit, joint space narrowing with mottled lucency of the proximal phalanx, and cystic degenerative changes. |
PMC1310524_F1_4084.jpg | What is the principal component of this image? | Bladder washing, cytospin preparation, Papanicolaou stain, ×400. Mixed small undifferentiated carcinoma and large urothelial carcinoma cells. The small cells are seen singly and in clusters with scanty cytoplasm, moderate cellular pleomorphism, nuclear molding, dark chromatin, irregular nuclear contour, and background of blood and necrosis consistent with a small cell carcinoma. In addition, there are a few atypical cells with a moderate amount of cytoplasm, small nucleoli, and irregular nuclear contours consistent with high-grade urothelial carcinoma. Figure 2 inset: comparison of two small cell carcinoma cells and one large urothelial carcinoma cell. |
PMC1310524_F2_4085.jpg | Can you identify the primary element in this image? | Bladder washing, cytospin preparation, Papanicolaou stain, ×400. Mixed small undifferentiated carcinoma and large urothelial carcinoma cells. The small cells are seen singly and in clusters with scanty cytoplasm, moderate cellular pleomorphism, nuclear molding, dark chromatin, irregular nuclear contour, and background of blood and necrosis consistent with a small cell carcinoma. In addition, there are a few atypical cells with a moderate amount of cytoplasm, small nucleoli, and irregular nuclear contours consistent with high-grade urothelial carcinoma. Figure 2 inset: comparison of two small cell carcinoma cells and one large urothelial carcinoma cell. |
PMC1310524_F2_4087.jpg | What is the core subject represented in this visual? | Bladder washing, cytospin preparation, Papanicolaou stain, ×400. Mixed small undifferentiated carcinoma and large urothelial carcinoma cells. The small cells are seen singly and in clusters with scanty cytoplasm, moderate cellular pleomorphism, nuclear molding, dark chromatin, irregular nuclear contour, and background of blood and necrosis consistent with a small cell carcinoma. In addition, there are a few atypical cells with a moderate amount of cytoplasm, small nucleoli, and irregular nuclear contours consistent with high-grade urothelial carcinoma. Figure 2 inset: comparison of two small cell carcinoma cells and one large urothelial carcinoma cell. |
PMC1310524_F2_4086.jpg | What is the focal point of this photograph? | Bladder washing, cytospin preparation, Papanicolaou stain, ×400. Mixed small undifferentiated carcinoma and large urothelial carcinoma cells. The small cells are seen singly and in clusters with scanty cytoplasm, moderate cellular pleomorphism, nuclear molding, dark chromatin, irregular nuclear contour, and background of blood and necrosis consistent with a small cell carcinoma. In addition, there are a few atypical cells with a moderate amount of cytoplasm, small nucleoli, and irregular nuclear contours consistent with high-grade urothelial carcinoma. Figure 2 inset: comparison of two small cell carcinoma cells and one large urothelial carcinoma cell. |
PMC1310524_F7_4088.jpg | What is the focal point of this photograph? | Tissue biopsy of the bladder tumor, H&E, ×200. Figure 7; Small cell carcinoma. Figure 8; Urothelial carcinoma with active mitosis evident. |
PMC1310524_F8_4089.jpg | What is the focal point of this photograph? | Tissue biopsy of the bladder tumor, H&E, ×200. Figure 7; Small cell carcinoma. Figure 8; Urothelial carcinoma with active mitosis evident. |
PMC1310524_F9_4090.jpg | What is being portrayed in this visual content? | Tissue biopsy of the bladder tumor, synaptophysin immunostain. The bottom half of the section is the small cell carcinoma component of the bladder tumor which demonstrated synaptophysin positivity. The top half of the section is urothelial carcinoma that is negative for synaptophysin. |
PMC1310526_F10_4094.jpg | What is being portrayed in this visual content? | Immunoblotting of human granulocyte extracts with various HP1 antibodies. Samples: F, normal female; M, normal male; H, HeLa. Panels: a, monoclonal anti-HP1 α (Upstate); b, monoclonal anti-HP1 β (Chemicon); c, rabbit anti-HP1 β (Upstate); d, monoclonal anti-HP1 γ (Chemicon). Note the trace reaction of anti-HP1 γ with the granulocyte extract (panel d). |
PMC1310526_F10_4091.jpg | What is the central feature of this picture? | Immunoblotting of human granulocyte extracts with various HP1 antibodies. Samples: F, normal female; M, normal male; H, HeLa. Panels: a, monoclonal anti-HP1 α (Upstate); b, monoclonal anti-HP1 β (Chemicon); c, rabbit anti-HP1 β (Upstate); d, monoclonal anti-HP1 γ (Chemicon). Note the trace reaction of anti-HP1 γ with the granulocyte extract (panel d). |
PMC1310526_F10_4092.jpg | What is the focal point of this photograph? | Immunoblotting of human granulocyte extracts with various HP1 antibodies. Samples: F, normal female; M, normal male; H, HeLa. Panels: a, monoclonal anti-HP1 α (Upstate); b, monoclonal anti-HP1 β (Chemicon); c, rabbit anti-HP1 β (Upstate); d, monoclonal anti-HP1 γ (Chemicon). Note the trace reaction of anti-HP1 γ with the granulocyte extract (panel d). |
PMC1310616_F4_4097.jpg | Describe the main subject of this image. | Immunohistochemistry for PC1 in normal and unaffected liver compared to colorectal (CRC) liver metastases. A. Light microscopy immunohistochemistry of normal liver (N), using 100 × magnification. Arrowheads indicate the scarcely positively stained hepatic cells. B. Light microscopy PC1 immunohistochemistry of liver metastasis (T) and adjacent unaffected parenchyma (U), using 20 × magnification. Arrowheads indicate positively stained tumor cells. C. Light microscopy PC1 immunohistochemistry of liver metastasis (T) using 400 × magnification. Arrowheads indicate positively stained tumor cells. |
PMC1310616_F4_4095.jpg | What can you see in this picture? | Immunohistochemistry for PC1 in normal and unaffected liver compared to colorectal (CRC) liver metastases. A. Light microscopy immunohistochemistry of normal liver (N), using 100 × magnification. Arrowheads indicate the scarcely positively stained hepatic cells. B. Light microscopy PC1 immunohistochemistry of liver metastasis (T) and adjacent unaffected parenchyma (U), using 20 × magnification. Arrowheads indicate positively stained tumor cells. C. Light microscopy PC1 immunohistochemistry of liver metastasis (T) using 400 × magnification. Arrowheads indicate positively stained tumor cells. |
PMC1310616_F4_4096.jpg | What can you see in this picture? | Immunohistochemistry for PC1 in normal and unaffected liver compared to colorectal (CRC) liver metastases. A. Light microscopy immunohistochemistry of normal liver (N), using 100 × magnification. Arrowheads indicate the scarcely positively stained hepatic cells. B. Light microscopy PC1 immunohistochemistry of liver metastasis (T) and adjacent unaffected parenchyma (U), using 20 × magnification. Arrowheads indicate positively stained tumor cells. C. Light microscopy PC1 immunohistochemistry of liver metastasis (T) using 400 × magnification. Arrowheads indicate positively stained tumor cells. |
PMC1310616_F5_4100.jpg | What is being portrayed in this visual content? | Immunohistochemistry for PC2 in normal and unaffected liver compared to colorectal (CRC) liver metastases. A. Light microscopy PC2 immunohistochemistry of normal liver (N), using 400 × magnification. Arrowheads indicate positively stained hepatic cells. B. Light microscopy PC2 immunohistochemistry of liver metastasis (T) and adjacent unaffected parenchyma (U), using 25 × magnification. Arrowheads indicate positively stained cells mainly in the unaffected liver. C. Light microscopy PC2 immunohistochemistry of liver metastasis (T) using 200 × magnification. Arrowheads indicate positively stained tumor cells. |
PMC1310616_F5_4099.jpg | What is being portrayed in this visual content? | Immunohistochemistry for PC2 in normal and unaffected liver compared to colorectal (CRC) liver metastases. A. Light microscopy PC2 immunohistochemistry of normal liver (N), using 400 × magnification. Arrowheads indicate positively stained hepatic cells. B. Light microscopy PC2 immunohistochemistry of liver metastasis (T) and adjacent unaffected parenchyma (U), using 25 × magnification. Arrowheads indicate positively stained cells mainly in the unaffected liver. C. Light microscopy PC2 immunohistochemistry of liver metastasis (T) using 200 × magnification. Arrowheads indicate positively stained tumor cells. |
PMC1310616_F5_4098.jpg | What stands out most in this visual? | Immunohistochemistry for PC2 in normal and unaffected liver compared to colorectal (CRC) liver metastases. A. Light microscopy PC2 immunohistochemistry of normal liver (N), using 400 × magnification. Arrowheads indicate positively stained hepatic cells. B. Light microscopy PC2 immunohistochemistry of liver metastasis (T) and adjacent unaffected parenchyma (U), using 25 × magnification. Arrowheads indicate positively stained cells mainly in the unaffected liver. C. Light microscopy PC2 immunohistochemistry of liver metastasis (T) using 200 × magnification. Arrowheads indicate positively stained tumor cells. |
PMC1310616_F6_4101.jpg | What is being portrayed in this visual content? | Immunohistochemistry for 7B2 in normal and unaffected liver compared to colorectal (CRC) liver metastases. A. Light microscopy 7B2 immunohistochemistry of normal liver (N), using 400 × magnification. No positive cells were identified. B. Light microscopy 7B2 immunohistochemistry of liver metastasis (T) and adjacent unaffected parenchyma (U), using 100 × magnification. Arrowheads indicate positively stained cells uniquely in the metastasis. C. Light microscopy 7B2 immunohistochemistry of liver metastasis (T) using 400 × magnification. Arrowheads indicate dense positively stained tumor cells. |
PMC1310616_F6_4102.jpg | What is the central feature of this picture? | Immunohistochemistry for 7B2 in normal and unaffected liver compared to colorectal (CRC) liver metastases. A. Light microscopy 7B2 immunohistochemistry of normal liver (N), using 400 × magnification. No positive cells were identified. B. Light microscopy 7B2 immunohistochemistry of liver metastasis (T) and adjacent unaffected parenchyma (U), using 100 × magnification. Arrowheads indicate positively stained cells uniquely in the metastasis. C. Light microscopy 7B2 immunohistochemistry of liver metastasis (T) using 400 × magnification. Arrowheads indicate dense positively stained tumor cells. |
PMC1310653_pbio-0040010-g006_4111.jpg | Can you identify the primary element in this image? | etsrp RNA Overexpression Induces Ectopic Expression of Vascular Endothelial MarkersDorsal view, anterior to the left in all panels except for (E,F) which are lateral views. (A, C, E, and G) Control uninjected embryo; (B, D, F, and H) 100 pg of etsrp RNA-injected embryo. (A,B) scl expression at the eight-somite stage; (C,D) flk1 expression at the nine-somite stage. Note the strong ectopic induction of scl and fli1 upon overexpression of etsrp RNA. (E,F) Live flk1-GFP embryo at the 14-somite stage; fluorescent and transmitted light images were overlayed. Note the very strong ectopic induction of GFP expression in different tissues including neuroectoderm (arrow, F) upon etsrp RNA overexpression. Fluorescence in the control uninjected flk1-GFP embryo in (E) is not detectable under the same exposure. (G,H) gata1 expression at the 16-somite stage. Note that gata1 expression is not affected upon etsrp overexpression. (I–L) etsrp RNA induces flk1 expression in clo mutant embryos as analyzed using flk1 probe at the ten- to 12-somite stages. (I) wt (or clo+/−) embryo, (J) wt (or clo+/−) embryo injected with 100 pg of etsrp RNA, (K) clo−/− embryo, (L) clo−/−embryo injected with 100 pg of etsrp RNA. Note that in a clo+/− (or wt) embryo etsrp RNA induces ectopic flk1 (arrow, J) in addition to the endogenous flk1 expression (arrowheads, J) while clo-/− etsrp RNA-injected embryo shows only ectopic flk1 (arrows, L). |
PMC1310653_pbio-0040010-g006_4108.jpg | What is being portrayed in this visual content? | etsrp RNA Overexpression Induces Ectopic Expression of Vascular Endothelial MarkersDorsal view, anterior to the left in all panels except for (E,F) which are lateral views. (A, C, E, and G) Control uninjected embryo; (B, D, F, and H) 100 pg of etsrp RNA-injected embryo. (A,B) scl expression at the eight-somite stage; (C,D) flk1 expression at the nine-somite stage. Note the strong ectopic induction of scl and fli1 upon overexpression of etsrp RNA. (E,F) Live flk1-GFP embryo at the 14-somite stage; fluorescent and transmitted light images were overlayed. Note the very strong ectopic induction of GFP expression in different tissues including neuroectoderm (arrow, F) upon etsrp RNA overexpression. Fluorescence in the control uninjected flk1-GFP embryo in (E) is not detectable under the same exposure. (G,H) gata1 expression at the 16-somite stage. Note that gata1 expression is not affected upon etsrp overexpression. (I–L) etsrp RNA induces flk1 expression in clo mutant embryos as analyzed using flk1 probe at the ten- to 12-somite stages. (I) wt (or clo+/−) embryo, (J) wt (or clo+/−) embryo injected with 100 pg of etsrp RNA, (K) clo−/− embryo, (L) clo−/−embryo injected with 100 pg of etsrp RNA. Note that in a clo+/− (or wt) embryo etsrp RNA induces ectopic flk1 (arrow, J) in addition to the endogenous flk1 expression (arrowheads, J) while clo-/− etsrp RNA-injected embryo shows only ectopic flk1 (arrows, L). |
PMC1310653_pbio-0040010-g006_4114.jpg | Describe the main subject of this image. | etsrp RNA Overexpression Induces Ectopic Expression of Vascular Endothelial MarkersDorsal view, anterior to the left in all panels except for (E,F) which are lateral views. (A, C, E, and G) Control uninjected embryo; (B, D, F, and H) 100 pg of etsrp RNA-injected embryo. (A,B) scl expression at the eight-somite stage; (C,D) flk1 expression at the nine-somite stage. Note the strong ectopic induction of scl and fli1 upon overexpression of etsrp RNA. (E,F) Live flk1-GFP embryo at the 14-somite stage; fluorescent and transmitted light images were overlayed. Note the very strong ectopic induction of GFP expression in different tissues including neuroectoderm (arrow, F) upon etsrp RNA overexpression. Fluorescence in the control uninjected flk1-GFP embryo in (E) is not detectable under the same exposure. (G,H) gata1 expression at the 16-somite stage. Note that gata1 expression is not affected upon etsrp overexpression. (I–L) etsrp RNA induces flk1 expression in clo mutant embryos as analyzed using flk1 probe at the ten- to 12-somite stages. (I) wt (or clo+/−) embryo, (J) wt (or clo+/−) embryo injected with 100 pg of etsrp RNA, (K) clo−/− embryo, (L) clo−/−embryo injected with 100 pg of etsrp RNA. Note that in a clo+/− (or wt) embryo etsrp RNA induces ectopic flk1 (arrow, J) in addition to the endogenous flk1 expression (arrowheads, J) while clo-/− etsrp RNA-injected embryo shows only ectopic flk1 (arrows, L). |
PMC1310653_pbio-0040010-g006_4110.jpg | What is the dominant medical problem in this image? | etsrp RNA Overexpression Induces Ectopic Expression of Vascular Endothelial MarkersDorsal view, anterior to the left in all panels except for (E,F) which are lateral views. (A, C, E, and G) Control uninjected embryo; (B, D, F, and H) 100 pg of etsrp RNA-injected embryo. (A,B) scl expression at the eight-somite stage; (C,D) flk1 expression at the nine-somite stage. Note the strong ectopic induction of scl and fli1 upon overexpression of etsrp RNA. (E,F) Live flk1-GFP embryo at the 14-somite stage; fluorescent and transmitted light images were overlayed. Note the very strong ectopic induction of GFP expression in different tissues including neuroectoderm (arrow, F) upon etsrp RNA overexpression. Fluorescence in the control uninjected flk1-GFP embryo in (E) is not detectable under the same exposure. (G,H) gata1 expression at the 16-somite stage. Note that gata1 expression is not affected upon etsrp overexpression. (I–L) etsrp RNA induces flk1 expression in clo mutant embryos as analyzed using flk1 probe at the ten- to 12-somite stages. (I) wt (or clo+/−) embryo, (J) wt (or clo+/−) embryo injected with 100 pg of etsrp RNA, (K) clo−/− embryo, (L) clo−/−embryo injected with 100 pg of etsrp RNA. Note that in a clo+/− (or wt) embryo etsrp RNA induces ectopic flk1 (arrow, J) in addition to the endogenous flk1 expression (arrowheads, J) while clo-/− etsrp RNA-injected embryo shows only ectopic flk1 (arrows, L). |
PMC1310653_pbio-0040010-g006_4109.jpg | What is the core subject represented in this visual? | etsrp RNA Overexpression Induces Ectopic Expression of Vascular Endothelial MarkersDorsal view, anterior to the left in all panels except for (E,F) which are lateral views. (A, C, E, and G) Control uninjected embryo; (B, D, F, and H) 100 pg of etsrp RNA-injected embryo. (A,B) scl expression at the eight-somite stage; (C,D) flk1 expression at the nine-somite stage. Note the strong ectopic induction of scl and fli1 upon overexpression of etsrp RNA. (E,F) Live flk1-GFP embryo at the 14-somite stage; fluorescent and transmitted light images were overlayed. Note the very strong ectopic induction of GFP expression in different tissues including neuroectoderm (arrow, F) upon etsrp RNA overexpression. Fluorescence in the control uninjected flk1-GFP embryo in (E) is not detectable under the same exposure. (G,H) gata1 expression at the 16-somite stage. Note that gata1 expression is not affected upon etsrp overexpression. (I–L) etsrp RNA induces flk1 expression in clo mutant embryos as analyzed using flk1 probe at the ten- to 12-somite stages. (I) wt (or clo+/−) embryo, (J) wt (or clo+/−) embryo injected with 100 pg of etsrp RNA, (K) clo−/− embryo, (L) clo−/−embryo injected with 100 pg of etsrp RNA. Note that in a clo+/− (or wt) embryo etsrp RNA induces ectopic flk1 (arrow, J) in addition to the endogenous flk1 expression (arrowheads, J) while clo-/− etsrp RNA-injected embryo shows only ectopic flk1 (arrows, L). |
PMC1310653_pbio-0040010-g006_4106.jpg | What key item or scene is captured in this photo? | etsrp RNA Overexpression Induces Ectopic Expression of Vascular Endothelial MarkersDorsal view, anterior to the left in all panels except for (E,F) which are lateral views. (A, C, E, and G) Control uninjected embryo; (B, D, F, and H) 100 pg of etsrp RNA-injected embryo. (A,B) scl expression at the eight-somite stage; (C,D) flk1 expression at the nine-somite stage. Note the strong ectopic induction of scl and fli1 upon overexpression of etsrp RNA. (E,F) Live flk1-GFP embryo at the 14-somite stage; fluorescent and transmitted light images were overlayed. Note the very strong ectopic induction of GFP expression in different tissues including neuroectoderm (arrow, F) upon etsrp RNA overexpression. Fluorescence in the control uninjected flk1-GFP embryo in (E) is not detectable under the same exposure. (G,H) gata1 expression at the 16-somite stage. Note that gata1 expression is not affected upon etsrp overexpression. (I–L) etsrp RNA induces flk1 expression in clo mutant embryos as analyzed using flk1 probe at the ten- to 12-somite stages. (I) wt (or clo+/−) embryo, (J) wt (or clo+/−) embryo injected with 100 pg of etsrp RNA, (K) clo−/− embryo, (L) clo−/−embryo injected with 100 pg of etsrp RNA. Note that in a clo+/− (or wt) embryo etsrp RNA induces ectopic flk1 (arrow, J) in addition to the endogenous flk1 expression (arrowheads, J) while clo-/− etsrp RNA-injected embryo shows only ectopic flk1 (arrows, L). |
PMC1310653_pbio-0040010-g006_4107.jpg | What is being portrayed in this visual content? | etsrp RNA Overexpression Induces Ectopic Expression of Vascular Endothelial MarkersDorsal view, anterior to the left in all panels except for (E,F) which are lateral views. (A, C, E, and G) Control uninjected embryo; (B, D, F, and H) 100 pg of etsrp RNA-injected embryo. (A,B) scl expression at the eight-somite stage; (C,D) flk1 expression at the nine-somite stage. Note the strong ectopic induction of scl and fli1 upon overexpression of etsrp RNA. (E,F) Live flk1-GFP embryo at the 14-somite stage; fluorescent and transmitted light images were overlayed. Note the very strong ectopic induction of GFP expression in different tissues including neuroectoderm (arrow, F) upon etsrp RNA overexpression. Fluorescence in the control uninjected flk1-GFP embryo in (E) is not detectable under the same exposure. (G,H) gata1 expression at the 16-somite stage. Note that gata1 expression is not affected upon etsrp overexpression. (I–L) etsrp RNA induces flk1 expression in clo mutant embryos as analyzed using flk1 probe at the ten- to 12-somite stages. (I) wt (or clo+/−) embryo, (J) wt (or clo+/−) embryo injected with 100 pg of etsrp RNA, (K) clo−/− embryo, (L) clo−/−embryo injected with 100 pg of etsrp RNA. Note that in a clo+/− (or wt) embryo etsrp RNA induces ectopic flk1 (arrow, J) in addition to the endogenous flk1 expression (arrowheads, J) while clo-/− etsrp RNA-injected embryo shows only ectopic flk1 (arrows, L). |
PMC1310653_pbio-0040010-g006_4112.jpg | What is the core subject represented in this visual? | etsrp RNA Overexpression Induces Ectopic Expression of Vascular Endothelial MarkersDorsal view, anterior to the left in all panels except for (E,F) which are lateral views. (A, C, E, and G) Control uninjected embryo; (B, D, F, and H) 100 pg of etsrp RNA-injected embryo. (A,B) scl expression at the eight-somite stage; (C,D) flk1 expression at the nine-somite stage. Note the strong ectopic induction of scl and fli1 upon overexpression of etsrp RNA. (E,F) Live flk1-GFP embryo at the 14-somite stage; fluorescent and transmitted light images were overlayed. Note the very strong ectopic induction of GFP expression in different tissues including neuroectoderm (arrow, F) upon etsrp RNA overexpression. Fluorescence in the control uninjected flk1-GFP embryo in (E) is not detectable under the same exposure. (G,H) gata1 expression at the 16-somite stage. Note that gata1 expression is not affected upon etsrp overexpression. (I–L) etsrp RNA induces flk1 expression in clo mutant embryos as analyzed using flk1 probe at the ten- to 12-somite stages. (I) wt (or clo+/−) embryo, (J) wt (or clo+/−) embryo injected with 100 pg of etsrp RNA, (K) clo−/− embryo, (L) clo−/−embryo injected with 100 pg of etsrp RNA. Note that in a clo+/− (or wt) embryo etsrp RNA induces ectopic flk1 (arrow, J) in addition to the endogenous flk1 expression (arrowheads, J) while clo-/− etsrp RNA-injected embryo shows only ectopic flk1 (arrows, L). |
PMC1310920_f3-ehp0113-001569_4116.jpg | What object or scene is depicted here? | Mild bile duct proliferation accompanied by portal fibrosis (H&E; 20×). Bar = 50 μm. |
PMC1310924_f2-ehp0113-001594_4119.jpg | What does this image primarily show? | CYP1A1 expression in lung and bladder endothelium from beluga whale. CYP1A1 is labeled pink to dark red; arrows indicate cells with labeling and the identical cell type without labeling. (A) CYP1A1 expression in lung endothelium from an Arctic beluga. (B) CYP1A1 expression in bladder endothelium from an arteriole from an Arctic beluga. (C) CYP1A1 expression in lung endothelium from an Arctic beluga. (D) Serial section from Arctic beluga shown in (C) was labeled using the nonspecific antibody UPC-10. Magnification: A, C, D, 400×; B, 200×. |
PMC1310924_f2-ehp0113-001594_4120.jpg | What key item or scene is captured in this photo? | CYP1A1 expression in lung and bladder endothelium from beluga whale. CYP1A1 is labeled pink to dark red; arrows indicate cells with labeling and the identical cell type without labeling. (A) CYP1A1 expression in lung endothelium from an Arctic beluga. (B) CYP1A1 expression in bladder endothelium from an arteriole from an Arctic beluga. (C) CYP1A1 expression in lung endothelium from an Arctic beluga. (D) Serial section from Arctic beluga shown in (C) was labeled using the nonspecific antibody UPC-10. Magnification: A, C, D, 400×; B, 200×. |
PMC1310924_f2-ehp0113-001594_4117.jpg | What can you see in this picture? | CYP1A1 expression in lung and bladder endothelium from beluga whale. CYP1A1 is labeled pink to dark red; arrows indicate cells with labeling and the identical cell type without labeling. (A) CYP1A1 expression in lung endothelium from an Arctic beluga. (B) CYP1A1 expression in bladder endothelium from an arteriole from an Arctic beluga. (C) CYP1A1 expression in lung endothelium from an Arctic beluga. (D) Serial section from Arctic beluga shown in (C) was labeled using the nonspecific antibody UPC-10. Magnification: A, C, D, 400×; B, 200×. |
PMC1310924_f2-ehp0113-001594_4118.jpg | What is the principal component of this image? | CYP1A1 expression in lung and bladder endothelium from beluga whale. CYP1A1 is labeled pink to dark red; arrows indicate cells with labeling and the identical cell type without labeling. (A) CYP1A1 expression in lung endothelium from an Arctic beluga. (B) CYP1A1 expression in bladder endothelium from an arteriole from an Arctic beluga. (C) CYP1A1 expression in lung endothelium from an Arctic beluga. (D) Serial section from Arctic beluga shown in (C) was labeled using the nonspecific antibody UPC-10. Magnification: A, C, D, 400×; B, 200×. |
PMC1310924_f3-ehp0113-001594_4122.jpg | Describe the main subject of this image. | CYP1A1 expression in transitional epithelium from the bladder of Arctic beluga whale. CYP1A1 is labeled pink to dark red; arrows indicate cells with labeling and the identical cell type without labeling. (A) CYP1A1 expression in the transitional epithelium of bladder; labeling is most intense in the umbrella cells. (B) Serial section from beluga shown in (A) labeled using the nonspecific antibody UPC-10. Magnification, 400×. |
PMC1310924_f3-ehp0113-001594_4121.jpg | What is being portrayed in this visual content? | CYP1A1 expression in transitional epithelium from the bladder of Arctic beluga whale. CYP1A1 is labeled pink to dark red; arrows indicate cells with labeling and the identical cell type without labeling. (A) CYP1A1 expression in the transitional epithelium of bladder; labeling is most intense in the umbrella cells. (B) Serial section from beluga shown in (A) labeled using the nonspecific antibody UPC-10. Magnification, 400×. |
PMC1311140_ppat-0010042-g005_4129.jpg | What is the dominant medical problem in this image? | Heightened Binding of Dectin-1 to A. fumigatus SCA soluble fusion protein consisting of the extracellular carbohydrate recognition domain of dectin-1 fused with the Fc portion of murine IgG1 (s-dectin-mFc) was constructed and incubated with live A. fumigatus RC and SC. Binding of s-dectin-mFc was detected by Cy3-conjugated, goat anti-mouse IgG antibody followed by imaging with a Zeiss Axioplan 2 upright fluorescent deconvolution microscope (Zeiss), and images were captured using 3i Slidebook Version 4.0 software (Optical Analysis). Representative micrographs show s-dectin-mFc binding to A. fumigatus grown for 2 h (A), 6 h (B), 10 h (C), and 24 h (D). Left lane images are differential interference contrast (DIC) images, and right lane images are Cy3 staining. Magnification is 630 × oil emersion for all frames. |
PMC1311140_ppat-0010042-g005_4125.jpg | What key item or scene is captured in this photo? | Heightened Binding of Dectin-1 to A. fumigatus SCA soluble fusion protein consisting of the extracellular carbohydrate recognition domain of dectin-1 fused with the Fc portion of murine IgG1 (s-dectin-mFc) was constructed and incubated with live A. fumigatus RC and SC. Binding of s-dectin-mFc was detected by Cy3-conjugated, goat anti-mouse IgG antibody followed by imaging with a Zeiss Axioplan 2 upright fluorescent deconvolution microscope (Zeiss), and images were captured using 3i Slidebook Version 4.0 software (Optical Analysis). Representative micrographs show s-dectin-mFc binding to A. fumigatus grown for 2 h (A), 6 h (B), 10 h (C), and 24 h (D). Left lane images are differential interference contrast (DIC) images, and right lane images are Cy3 staining. Magnification is 630 × oil emersion for all frames. |
PMC1311140_ppat-0010042-g005_4123.jpg | Can you identify the primary element in this image? | Heightened Binding of Dectin-1 to A. fumigatus SCA soluble fusion protein consisting of the extracellular carbohydrate recognition domain of dectin-1 fused with the Fc portion of murine IgG1 (s-dectin-mFc) was constructed and incubated with live A. fumigatus RC and SC. Binding of s-dectin-mFc was detected by Cy3-conjugated, goat anti-mouse IgG antibody followed by imaging with a Zeiss Axioplan 2 upright fluorescent deconvolution microscope (Zeiss), and images were captured using 3i Slidebook Version 4.0 software (Optical Analysis). Representative micrographs show s-dectin-mFc binding to A. fumigatus grown for 2 h (A), 6 h (B), 10 h (C), and 24 h (D). Left lane images are differential interference contrast (DIC) images, and right lane images are Cy3 staining. Magnification is 630 × oil emersion for all frames. |
PMC1311140_ppat-0010042-g005_4124.jpg | What can you see in this picture? | Heightened Binding of Dectin-1 to A. fumigatus SCA soluble fusion protein consisting of the extracellular carbohydrate recognition domain of dectin-1 fused with the Fc portion of murine IgG1 (s-dectin-mFc) was constructed and incubated with live A. fumigatus RC and SC. Binding of s-dectin-mFc was detected by Cy3-conjugated, goat anti-mouse IgG antibody followed by imaging with a Zeiss Axioplan 2 upright fluorescent deconvolution microscope (Zeiss), and images were captured using 3i Slidebook Version 4.0 software (Optical Analysis). Representative micrographs show s-dectin-mFc binding to A. fumigatus grown for 2 h (A), 6 h (B), 10 h (C), and 24 h (D). Left lane images are differential interference contrast (DIC) images, and right lane images are Cy3 staining. Magnification is 630 × oil emersion for all frames. |
PMC1311140_ppat-0010042-g005_4127.jpg | What object or scene is depicted here? | Heightened Binding of Dectin-1 to A. fumigatus SCA soluble fusion protein consisting of the extracellular carbohydrate recognition domain of dectin-1 fused with the Fc portion of murine IgG1 (s-dectin-mFc) was constructed and incubated with live A. fumigatus RC and SC. Binding of s-dectin-mFc was detected by Cy3-conjugated, goat anti-mouse IgG antibody followed by imaging with a Zeiss Axioplan 2 upright fluorescent deconvolution microscope (Zeiss), and images were captured using 3i Slidebook Version 4.0 software (Optical Analysis). Representative micrographs show s-dectin-mFc binding to A. fumigatus grown for 2 h (A), 6 h (B), 10 h (C), and 24 h (D). Left lane images are differential interference contrast (DIC) images, and right lane images are Cy3 staining. Magnification is 630 × oil emersion for all frames. |
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