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PMC1697826_F3_7912.jpg | What is the central feature of this picture? | Immunohistochemical analysis. Representative sections of a melanoma biopsy immunostained with anti-HLA-DR (left panel, 20×), and anti-IL4R mAbs (right panel, 20×). |
PMC1697826_F3_7913.jpg | Can you identify the primary element in this image? | Immunohistochemical analysis. Representative sections of a melanoma biopsy immunostained with anti-HLA-DR (left panel, 20×), and anti-IL4R mAbs (right panel, 20×). |
PMC1698139_F1_7915.jpg | Describe the main subject of this image. | The radiological appearance of her right hip following
previous TB, arthrodesis, subsequent lymphoma, and
radiotherapy—and there is now a radiation induced sarcoma
involving the right hemiplevis! Note that the left hip is
normal. |
PMC1698139_F2_7914.jpg | What stands out most in this visual? | AP X-ray of the pelvis showing the result 9 years following
hindquarter amputation, the marked degenerative changes of the
spine, and the severe osteoarthritis changes of the left hip. It
is apparent that the whole pelvis is tilted to the left. |
PMC1698139_F4_7917.jpg | Can you identify the primary element in this image? | The radiological appearance of her pelvis 4 years after the
total hip replacement. There has been some migration of the
cemented cup but the hip causes her no pain. |
PMC1698140_F2_7918.jpg | What is the principal component of this image? | Cardiac mass on CT scan after chemotherapy. |
PMC1698141_F3_7919.jpg | What is the main focus of this visual representation? | Biopsy of proximal femoral lesion showing high-grade
intramedullary osteosarcoma. |
PMC1698144_F1_7920.jpg | What is shown in this image? | An MRI of the elbow showing a soft tissue tumour. |
PMC1698498_F8_7921.jpg | What is the main focus of this visual representation? | Bronchial biopsies in asthma and chronic obstructive pulmonary disease. (a) Bronchial biopsy in a nonsmoker with mild asthma. Note thickening of the epithelial reticular basement membrane in comparison with (b). (b) Bronchial biopsy in a smoker with chronic obstructive pulmonary disease (alkaline phosphatase antialkaline phosphatase, original ×240). Reprinted with permission from Jeffery [66]. |
PMC1698505_pbio-0050002-g007_7926.jpg | Can you identify the primary element in this image? | Carbohydrate/Fat Metabolism and IGF1 Serum LevelsIGF1 (A) and glucose (B) in the serum of 7-, 10-, 15-, and 17-d-old wt, Xpa−/−, Csbm/m, and Csbm/m/Xpa−/− mice (n = 6). The levels of IGF1 (ng/ml) and glucose (mmol/l) in the serum of Csbm/m/Xpa−/− mice are significantly lower than that of control littermates (p < 0.0004 and p < 0.04, respectively). (C) PAS staining for glycogen and Oil Red O staining for triglycerides in livers of 15-d-old wt and Csbm/m/Xpa−/− mice and 96-wk-old wt mice. Pictures were taken at 100× magnification. Note the large polyploid nuclei in the 96-wk-old wt mouse liver and the reduced glycogen levels in the Csbm/m/Xpa−/− liver after overnight fasting. |
PMC1698505_pbio-0050002-g007_7931.jpg | What does this image primarily show? | Carbohydrate/Fat Metabolism and IGF1 Serum LevelsIGF1 (A) and glucose (B) in the serum of 7-, 10-, 15-, and 17-d-old wt, Xpa−/−, Csbm/m, and Csbm/m/Xpa−/− mice (n = 6). The levels of IGF1 (ng/ml) and glucose (mmol/l) in the serum of Csbm/m/Xpa−/− mice are significantly lower than that of control littermates (p < 0.0004 and p < 0.04, respectively). (C) PAS staining for glycogen and Oil Red O staining for triglycerides in livers of 15-d-old wt and Csbm/m/Xpa−/− mice and 96-wk-old wt mice. Pictures were taken at 100× magnification. Note the large polyploid nuclei in the 96-wk-old wt mouse liver and the reduced glycogen levels in the Csbm/m/Xpa−/− liver after overnight fasting. |
PMC1698505_pbio-0050002-g007_7927.jpg | What is the focal point of this photograph? | Carbohydrate/Fat Metabolism and IGF1 Serum LevelsIGF1 (A) and glucose (B) in the serum of 7-, 10-, 15-, and 17-d-old wt, Xpa−/−, Csbm/m, and Csbm/m/Xpa−/− mice (n = 6). The levels of IGF1 (ng/ml) and glucose (mmol/l) in the serum of Csbm/m/Xpa−/− mice are significantly lower than that of control littermates (p < 0.0004 and p < 0.04, respectively). (C) PAS staining for glycogen and Oil Red O staining for triglycerides in livers of 15-d-old wt and Csbm/m/Xpa−/− mice and 96-wk-old wt mice. Pictures were taken at 100× magnification. Note the large polyploid nuclei in the 96-wk-old wt mouse liver and the reduced glycogen levels in the Csbm/m/Xpa−/− liver after overnight fasting. |
PMC1698505_pbio-0050002-g007_7923.jpg | What is shown in this image? | Carbohydrate/Fat Metabolism and IGF1 Serum LevelsIGF1 (A) and glucose (B) in the serum of 7-, 10-, 15-, and 17-d-old wt, Xpa−/−, Csbm/m, and Csbm/m/Xpa−/− mice (n = 6). The levels of IGF1 (ng/ml) and glucose (mmol/l) in the serum of Csbm/m/Xpa−/− mice are significantly lower than that of control littermates (p < 0.0004 and p < 0.04, respectively). (C) PAS staining for glycogen and Oil Red O staining for triglycerides in livers of 15-d-old wt and Csbm/m/Xpa−/− mice and 96-wk-old wt mice. Pictures were taken at 100× magnification. Note the large polyploid nuclei in the 96-wk-old wt mouse liver and the reduced glycogen levels in the Csbm/m/Xpa−/− liver after overnight fasting. |
PMC1698505_pbio-0050002-g007_7924.jpg | What is shown in this image? | Carbohydrate/Fat Metabolism and IGF1 Serum LevelsIGF1 (A) and glucose (B) in the serum of 7-, 10-, 15-, and 17-d-old wt, Xpa−/−, Csbm/m, and Csbm/m/Xpa−/− mice (n = 6). The levels of IGF1 (ng/ml) and glucose (mmol/l) in the serum of Csbm/m/Xpa−/− mice are significantly lower than that of control littermates (p < 0.0004 and p < 0.04, respectively). (C) PAS staining for glycogen and Oil Red O staining for triglycerides in livers of 15-d-old wt and Csbm/m/Xpa−/− mice and 96-wk-old wt mice. Pictures were taken at 100× magnification. Note the large polyploid nuclei in the 96-wk-old wt mouse liver and the reduced glycogen levels in the Csbm/m/Xpa−/− liver after overnight fasting. |
PMC1698505_pbio-0050002-g007_7925.jpg | What is being portrayed in this visual content? | Carbohydrate/Fat Metabolism and IGF1 Serum LevelsIGF1 (A) and glucose (B) in the serum of 7-, 10-, 15-, and 17-d-old wt, Xpa−/−, Csbm/m, and Csbm/m/Xpa−/− mice (n = 6). The levels of IGF1 (ng/ml) and glucose (mmol/l) in the serum of Csbm/m/Xpa−/− mice are significantly lower than that of control littermates (p < 0.0004 and p < 0.04, respectively). (C) PAS staining for glycogen and Oil Red O staining for triglycerides in livers of 15-d-old wt and Csbm/m/Xpa−/− mice and 96-wk-old wt mice. Pictures were taken at 100× magnification. Note the large polyploid nuclei in the 96-wk-old wt mouse liver and the reduced glycogen levels in the Csbm/m/Xpa−/− liver after overnight fasting. |
PMC1698505_pbio-0050002-g007_7928.jpg | What key item or scene is captured in this photo? | Carbohydrate/Fat Metabolism and IGF1 Serum LevelsIGF1 (A) and glucose (B) in the serum of 7-, 10-, 15-, and 17-d-old wt, Xpa−/−, Csbm/m, and Csbm/m/Xpa−/− mice (n = 6). The levels of IGF1 (ng/ml) and glucose (mmol/l) in the serum of Csbm/m/Xpa−/− mice are significantly lower than that of control littermates (p < 0.0004 and p < 0.04, respectively). (C) PAS staining for glycogen and Oil Red O staining for triglycerides in livers of 15-d-old wt and Csbm/m/Xpa−/− mice and 96-wk-old wt mice. Pictures were taken at 100× magnification. Note the large polyploid nuclei in the 96-wk-old wt mouse liver and the reduced glycogen levels in the Csbm/m/Xpa−/− liver after overnight fasting. |
PMC1698919_F1_7933.jpg | What is shown in this image? | Barium enema study showing leakage of barium from the hepatic flexure into duodenum. |
PMC1698931_F4_7943.jpg | Describe the main subject of this image. | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7946.jpg | What is the central feature of this picture? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7950.jpg | What key item or scene is captured in this photo? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7936.jpg | What object or scene is depicted here? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7945.jpg | What is the core subject represented in this visual? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7944.jpg | What key item or scene is captured in this photo? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7938.jpg | What stands out most in this visual? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7939.jpg | What key item or scene is captured in this photo? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7935.jpg | What does this image primarily show? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7937.jpg | What object or scene is depicted here? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7949.jpg | What is shown in this image? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7934.jpg | What is the central feature of this picture? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7940.jpg | What key item or scene is captured in this photo? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7948.jpg | What is being portrayed in this visual content? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F4_7941.jpg | What's the most prominent thing you notice in this picture? | Echogenicity in CXMDJ A: Sequential studies in echogenicity with advancing age by two-dimensional echocardiography in a normal dog III-301MN, and a CXMDJ dog III-302MA, at 6–21 months of age. Hyperechoic lesions (arrowheads) of the left ventricular posterior wall were detected in the CXMDJ dog at 12 months of age and older.B: Two-dimensional echocardiograms of a normal dog III-301MN at 6 months of age, and four CXMDJ dogs III-D53MA, III-D55MA, III-1803MA, and III-D08MA at 6 to 7 months of age. The hyperechoic lesion (arrowhead) was detected only in the left ventricular posterior wall of III-D08MA. |
PMC1698931_F5_7951.jpg | What stands out most in this visual? | Macroscopic and histopathological findings in CXMDJ hearts A. Macroscopic examinations of the base of the formalin-fixed hearts of a normal littermate III-301MN at 21 months and CXMDJ dogs, III-1803MA at 7 months and III-302MA at 21 months of age. *Aortic valve. Bar shows 1 cm. B. Hematoxylin and eosin (H&E) and Masson's trichrome (MT) staining for histopathological evaluation of the left ventricular posterior wall in a normal littermate, III-301MN at 21 months and the CXMDJ dogs, III-1803MA at 7 months, III-D55MA at 9 months, III-D02MA at 15 months, and III-302MA at 21 months of age. Posterior walls of left ventricles of both III-D55MA and III-D02MA were macroscopically normal (data not shown). Bar shows 200 μm. |
PMC1702346_F4_7962.jpg | What does this image primarily show? | Subcellular targeting of the I/LWEQ modules of Talin-a and Talin-b. HeLa cells were transiently transfected with either the dsRed-Talin-a.2341–2531 or the dsRed-Talin-b.2341–2531 fusion construct (I/LWEQ module) and counterstained with vinculin to independently label focal adhesions or fluorescein-phalloidin to label F-actin, as previously described [13]. The Talin-a I/LWEQ module targeted to focal adhesions, where the fluorescence signals for dsRed-Talin-a.2341–2531 and the focal adhesion component vinculin overlap (Column 1, overlay). The Talin-a I/LWEQ module did not preferentially localize to actin stress fibers (Column 2). In contrast to Talin-a, the Talin-b I/LWEQ module was not targeted to focal adhesions (Column 3). However, dsRed-Talin-b.2341–2531 did colocalize with actin stress fibers, as shown by the colocalization of the fluorescence signals of dsRed-Talin-b.2341–2531 with phalloidin-stained F-actin (Column 4, overlay). |
PMC1702346_F4_7964.jpg | What is the focal point of this photograph? | Subcellular targeting of the I/LWEQ modules of Talin-a and Talin-b. HeLa cells were transiently transfected with either the dsRed-Talin-a.2341–2531 or the dsRed-Talin-b.2341–2531 fusion construct (I/LWEQ module) and counterstained with vinculin to independently label focal adhesions or fluorescein-phalloidin to label F-actin, as previously described [13]. The Talin-a I/LWEQ module targeted to focal adhesions, where the fluorescence signals for dsRed-Talin-a.2341–2531 and the focal adhesion component vinculin overlap (Column 1, overlay). The Talin-a I/LWEQ module did not preferentially localize to actin stress fibers (Column 2). In contrast to Talin-a, the Talin-b I/LWEQ module was not targeted to focal adhesions (Column 3). However, dsRed-Talin-b.2341–2531 did colocalize with actin stress fibers, as shown by the colocalization of the fluorescence signals of dsRed-Talin-b.2341–2531 with phalloidin-stained F-actin (Column 4, overlay). |
PMC1702346_F4_7960.jpg | What is the focal point of this photograph? | Subcellular targeting of the I/LWEQ modules of Talin-a and Talin-b. HeLa cells were transiently transfected with either the dsRed-Talin-a.2341–2531 or the dsRed-Talin-b.2341–2531 fusion construct (I/LWEQ module) and counterstained with vinculin to independently label focal adhesions or fluorescein-phalloidin to label F-actin, as previously described [13]. The Talin-a I/LWEQ module targeted to focal adhesions, where the fluorescence signals for dsRed-Talin-a.2341–2531 and the focal adhesion component vinculin overlap (Column 1, overlay). The Talin-a I/LWEQ module did not preferentially localize to actin stress fibers (Column 2). In contrast to Talin-a, the Talin-b I/LWEQ module was not targeted to focal adhesions (Column 3). However, dsRed-Talin-b.2341–2531 did colocalize with actin stress fibers, as shown by the colocalization of the fluorescence signals of dsRed-Talin-b.2341–2531 with phalloidin-stained F-actin (Column 4, overlay). |
PMC1702346_F4_7956.jpg | What is the core subject represented in this visual? | Subcellular targeting of the I/LWEQ modules of Talin-a and Talin-b. HeLa cells were transiently transfected with either the dsRed-Talin-a.2341–2531 or the dsRed-Talin-b.2341–2531 fusion construct (I/LWEQ module) and counterstained with vinculin to independently label focal adhesions or fluorescein-phalloidin to label F-actin, as previously described [13]. The Talin-a I/LWEQ module targeted to focal adhesions, where the fluorescence signals for dsRed-Talin-a.2341–2531 and the focal adhesion component vinculin overlap (Column 1, overlay). The Talin-a I/LWEQ module did not preferentially localize to actin stress fibers (Column 2). In contrast to Talin-a, the Talin-b I/LWEQ module was not targeted to focal adhesions (Column 3). However, dsRed-Talin-b.2341–2531 did colocalize with actin stress fibers, as shown by the colocalization of the fluorescence signals of dsRed-Talin-b.2341–2531 with phalloidin-stained F-actin (Column 4, overlay). |
PMC1702346_F4_7954.jpg | What can you see in this picture? | Subcellular targeting of the I/LWEQ modules of Talin-a and Talin-b. HeLa cells were transiently transfected with either the dsRed-Talin-a.2341–2531 or the dsRed-Talin-b.2341–2531 fusion construct (I/LWEQ module) and counterstained with vinculin to independently label focal adhesions or fluorescein-phalloidin to label F-actin, as previously described [13]. The Talin-a I/LWEQ module targeted to focal adhesions, where the fluorescence signals for dsRed-Talin-a.2341–2531 and the focal adhesion component vinculin overlap (Column 1, overlay). The Talin-a I/LWEQ module did not preferentially localize to actin stress fibers (Column 2). In contrast to Talin-a, the Talin-b I/LWEQ module was not targeted to focal adhesions (Column 3). However, dsRed-Talin-b.2341–2531 did colocalize with actin stress fibers, as shown by the colocalization of the fluorescence signals of dsRed-Talin-b.2341–2531 with phalloidin-stained F-actin (Column 4, overlay). |
PMC1702346_F4_7957.jpg | What stands out most in this visual? | Subcellular targeting of the I/LWEQ modules of Talin-a and Talin-b. HeLa cells were transiently transfected with either the dsRed-Talin-a.2341–2531 or the dsRed-Talin-b.2341–2531 fusion construct (I/LWEQ module) and counterstained with vinculin to independently label focal adhesions or fluorescein-phalloidin to label F-actin, as previously described [13]. The Talin-a I/LWEQ module targeted to focal adhesions, where the fluorescence signals for dsRed-Talin-a.2341–2531 and the focal adhesion component vinculin overlap (Column 1, overlay). The Talin-a I/LWEQ module did not preferentially localize to actin stress fibers (Column 2). In contrast to Talin-a, the Talin-b I/LWEQ module was not targeted to focal adhesions (Column 3). However, dsRed-Talin-b.2341–2531 did colocalize with actin stress fibers, as shown by the colocalization of the fluorescence signals of dsRed-Talin-b.2341–2531 with phalloidin-stained F-actin (Column 4, overlay). |
PMC1702346_F4_7959.jpg | What is the central feature of this picture? | Subcellular targeting of the I/LWEQ modules of Talin-a and Talin-b. HeLa cells were transiently transfected with either the dsRed-Talin-a.2341–2531 or the dsRed-Talin-b.2341–2531 fusion construct (I/LWEQ module) and counterstained with vinculin to independently label focal adhesions or fluorescein-phalloidin to label F-actin, as previously described [13]. The Talin-a I/LWEQ module targeted to focal adhesions, where the fluorescence signals for dsRed-Talin-a.2341–2531 and the focal adhesion component vinculin overlap (Column 1, overlay). The Talin-a I/LWEQ module did not preferentially localize to actin stress fibers (Column 2). In contrast to Talin-a, the Talin-b I/LWEQ module was not targeted to focal adhesions (Column 3). However, dsRed-Talin-b.2341–2531 did colocalize with actin stress fibers, as shown by the colocalization of the fluorescence signals of dsRed-Talin-b.2341–2531 with phalloidin-stained F-actin (Column 4, overlay). |
PMC1702346_F4_7963.jpg | What stands out most in this visual? | Subcellular targeting of the I/LWEQ modules of Talin-a and Talin-b. HeLa cells were transiently transfected with either the dsRed-Talin-a.2341–2531 or the dsRed-Talin-b.2341–2531 fusion construct (I/LWEQ module) and counterstained with vinculin to independently label focal adhesions or fluorescein-phalloidin to label F-actin, as previously described [13]. The Talin-a I/LWEQ module targeted to focal adhesions, where the fluorescence signals for dsRed-Talin-a.2341–2531 and the focal adhesion component vinculin overlap (Column 1, overlay). The Talin-a I/LWEQ module did not preferentially localize to actin stress fibers (Column 2). In contrast to Talin-a, the Talin-b I/LWEQ module was not targeted to focal adhesions (Column 3). However, dsRed-Talin-b.2341–2531 did colocalize with actin stress fibers, as shown by the colocalization of the fluorescence signals of dsRed-Talin-b.2341–2531 with phalloidin-stained F-actin (Column 4, overlay). |
PMC1702559_pmed-0030499-g002_7967.jpg | What does this image primarily show? | Axial T1 Weighted Anatomical MRI Scan Showing Segmentation of the Amygdala (Yellow) and the Hippocampus (Red) |
PMC1712336_F1_7971.jpg | What stands out most in this visual? | Lateral radiogram showed the severe kyphosis. |
PMC1712336_F1_7972.jpg | Describe the main subject of this image. | Lateral radiogram showed the severe kyphosis. |
PMC1712336_F1_7969.jpg | What is the central feature of this picture? | Lateral radiogram showed the severe kyphosis. |
PMC1712336_F3_7974.jpg | What is shown in this image? | End stage of the progressive anterior vertebral fusion and the multi-level anterior fusion with disc space obliteration (T1-T5). There is a massive bony ridge extending anteriorly and in some vertebrae, posteriorly as well. However, (arrow b) note the sparing of the disc space posteriorly, whereas the anterior end plate is totally obliterated (arrow a). Absence of the normal concavity of the anterior body surface. There is a proliferation of sclerotic bone. |
PMC1712336_F4_7973.jpg | What is being portrayed in this visual content? | 3 d reconstruction CT scan showed the massive anterior fusion of (C7-T5) and (T6-T7), and the apparent anterior thick bony ridge (arrow), the latter developed secondary to progressive ossification of the anterior longitudinal ligament. from T7-T12; note the narrowing of the anterior part of the disc space, accompanied by erosion and irregularity of the anterior end plates. |
PMC1712351_F2_7978.jpg | What can you see in this picture? | Transfected neutrophils are responsive to soluble stimuli. Neutrophils were transfected with the expression vector pEGFP-p47phox or with the pEGFP control vector as follows: Neutrophils were resuspended in solution "T" in the presence of the expression vector pEGFP and DNA was transfected using nucleofector program T27. The neutrophils were transferred to a poly-L-lysine – coated chambered glass slide containing 10% FCS-RPMI. Two hours after transfection, the cells were stimulated with PMA (0.1 μg/ml) or fMLP (1 μM) at 37°C for 15 min or 5 min, respectively. The cells were fixed with 3.7% paraformaldehyde and analyzed by confocal microscopy. Transfected neutrophils stimulated with PMA or fMLP can undergo morphological changes represented by the apparition of protrusions of the plasma membrane (arrows). Scale bar = 5 μm. These results are representative of four separate experiments. |
PMC1712351_F2_7977.jpg | What is the dominant medical problem in this image? | Transfected neutrophils are responsive to soluble stimuli. Neutrophils were transfected with the expression vector pEGFP-p47phox or with the pEGFP control vector as follows: Neutrophils were resuspended in solution "T" in the presence of the expression vector pEGFP and DNA was transfected using nucleofector program T27. The neutrophils were transferred to a poly-L-lysine – coated chambered glass slide containing 10% FCS-RPMI. Two hours after transfection, the cells were stimulated with PMA (0.1 μg/ml) or fMLP (1 μM) at 37°C for 15 min or 5 min, respectively. The cells were fixed with 3.7% paraformaldehyde and analyzed by confocal microscopy. Transfected neutrophils stimulated with PMA or fMLP can undergo morphological changes represented by the apparition of protrusions of the plasma membrane (arrows). Scale bar = 5 μm. These results are representative of four separate experiments. |
PMC1712351_F7_7992.jpg | What's the most prominent thing you notice in this picture? | Distribution of exogenously expressed p47phox-PX domain and RhoB during phagocytosis in human neutrophils. Neutrophils were nucleoporated with the expression vectors EGFP-p47-PX or EGFP-RhoB as described in figure 2. After a 2 h recovery period, cells were incubated in the presence of Texas Red-labeled opsonized-zymosan particles at 37°C for 10 or 15 min. Samples were washed, fixed and analyzed by confocal microscopy as described in "Methods." The images were processed and analyzed for the distribution of the fluorescent proteins using the NIH image processing and analysis program IMAGE/J software. The plot profiles, in the right panel, show that EGFP-RhoB is accumulated around the phagosome (red arrows indicating peak of fluorescence intensity) while the plot profiles corresponding to EGFP-p47-PX show a plateau of fluorescence intensity (red lines). The white arrows show the distribution of p47phox-PX domain in membrane protrusions surrounding the opsonized particle at time zero. Scale bar = 3 μm. B, The difference between the fluorescence intensity at the phagosome membrane versus that at the surrounding cytosolic area (ΔFI) was calculated using the NIH image processing and analysis program IMAGE/J software as described under "Methods." The results are mean ± SEM of three phagosomes from different cells. |
PMC1712351_F7_7982.jpg | What is the focal point of this photograph? | Distribution of exogenously expressed p47phox-PX domain and RhoB during phagocytosis in human neutrophils. Neutrophils were nucleoporated with the expression vectors EGFP-p47-PX or EGFP-RhoB as described in figure 2. After a 2 h recovery period, cells were incubated in the presence of Texas Red-labeled opsonized-zymosan particles at 37°C for 10 or 15 min. Samples were washed, fixed and analyzed by confocal microscopy as described in "Methods." The images were processed and analyzed for the distribution of the fluorescent proteins using the NIH image processing and analysis program IMAGE/J software. The plot profiles, in the right panel, show that EGFP-RhoB is accumulated around the phagosome (red arrows indicating peak of fluorescence intensity) while the plot profiles corresponding to EGFP-p47-PX show a plateau of fluorescence intensity (red lines). The white arrows show the distribution of p47phox-PX domain in membrane protrusions surrounding the opsonized particle at time zero. Scale bar = 3 μm. B, The difference between the fluorescence intensity at the phagosome membrane versus that at the surrounding cytosolic area (ΔFI) was calculated using the NIH image processing and analysis program IMAGE/J software as described under "Methods." The results are mean ± SEM of three phagosomes from different cells. |
PMC1712351_F7_7983.jpg | What is the central feature of this picture? | Distribution of exogenously expressed p47phox-PX domain and RhoB during phagocytosis in human neutrophils. Neutrophils were nucleoporated with the expression vectors EGFP-p47-PX or EGFP-RhoB as described in figure 2. After a 2 h recovery period, cells were incubated in the presence of Texas Red-labeled opsonized-zymosan particles at 37°C for 10 or 15 min. Samples were washed, fixed and analyzed by confocal microscopy as described in "Methods." The images were processed and analyzed for the distribution of the fluorescent proteins using the NIH image processing and analysis program IMAGE/J software. The plot profiles, in the right panel, show that EGFP-RhoB is accumulated around the phagosome (red arrows indicating peak of fluorescence intensity) while the plot profiles corresponding to EGFP-p47-PX show a plateau of fluorescence intensity (red lines). The white arrows show the distribution of p47phox-PX domain in membrane protrusions surrounding the opsonized particle at time zero. Scale bar = 3 μm. B, The difference between the fluorescence intensity at the phagosome membrane versus that at the surrounding cytosolic area (ΔFI) was calculated using the NIH image processing and analysis program IMAGE/J software as described under "Methods." The results are mean ± SEM of three phagosomes from different cells. |
PMC1712351_F7_7984.jpg | What is the dominant medical problem in this image? | Distribution of exogenously expressed p47phox-PX domain and RhoB during phagocytosis in human neutrophils. Neutrophils were nucleoporated with the expression vectors EGFP-p47-PX or EGFP-RhoB as described in figure 2. After a 2 h recovery period, cells were incubated in the presence of Texas Red-labeled opsonized-zymosan particles at 37°C for 10 or 15 min. Samples were washed, fixed and analyzed by confocal microscopy as described in "Methods." The images were processed and analyzed for the distribution of the fluorescent proteins using the NIH image processing and analysis program IMAGE/J software. The plot profiles, in the right panel, show that EGFP-RhoB is accumulated around the phagosome (red arrows indicating peak of fluorescence intensity) while the plot profiles corresponding to EGFP-p47-PX show a plateau of fluorescence intensity (red lines). The white arrows show the distribution of p47phox-PX domain in membrane protrusions surrounding the opsonized particle at time zero. Scale bar = 3 μm. B, The difference between the fluorescence intensity at the phagosome membrane versus that at the surrounding cytosolic area (ΔFI) was calculated using the NIH image processing and analysis program IMAGE/J software as described under "Methods." The results are mean ± SEM of three phagosomes from different cells. |
PMC1712351_F7_7986.jpg | What object or scene is depicted here? | Distribution of exogenously expressed p47phox-PX domain and RhoB during phagocytosis in human neutrophils. Neutrophils were nucleoporated with the expression vectors EGFP-p47-PX or EGFP-RhoB as described in figure 2. After a 2 h recovery period, cells were incubated in the presence of Texas Red-labeled opsonized-zymosan particles at 37°C for 10 or 15 min. Samples were washed, fixed and analyzed by confocal microscopy as described in "Methods." The images were processed and analyzed for the distribution of the fluorescent proteins using the NIH image processing and analysis program IMAGE/J software. The plot profiles, in the right panel, show that EGFP-RhoB is accumulated around the phagosome (red arrows indicating peak of fluorescence intensity) while the plot profiles corresponding to EGFP-p47-PX show a plateau of fluorescence intensity (red lines). The white arrows show the distribution of p47phox-PX domain in membrane protrusions surrounding the opsonized particle at time zero. Scale bar = 3 μm. B, The difference between the fluorescence intensity at the phagosome membrane versus that at the surrounding cytosolic area (ΔFI) was calculated using the NIH image processing and analysis program IMAGE/J software as described under "Methods." The results are mean ± SEM of three phagosomes from different cells. |
PMC1712351_F7_7985.jpg | What can you see in this picture? | Distribution of exogenously expressed p47phox-PX domain and RhoB during phagocytosis in human neutrophils. Neutrophils were nucleoporated with the expression vectors EGFP-p47-PX or EGFP-RhoB as described in figure 2. After a 2 h recovery period, cells were incubated in the presence of Texas Red-labeled opsonized-zymosan particles at 37°C for 10 or 15 min. Samples were washed, fixed and analyzed by confocal microscopy as described in "Methods." The images were processed and analyzed for the distribution of the fluorescent proteins using the NIH image processing and analysis program IMAGE/J software. The plot profiles, in the right panel, show that EGFP-RhoB is accumulated around the phagosome (red arrows indicating peak of fluorescence intensity) while the plot profiles corresponding to EGFP-p47-PX show a plateau of fluorescence intensity (red lines). The white arrows show the distribution of p47phox-PX domain in membrane protrusions surrounding the opsonized particle at time zero. Scale bar = 3 μm. B, The difference between the fluorescence intensity at the phagosome membrane versus that at the surrounding cytosolic area (ΔFI) was calculated using the NIH image processing and analysis program IMAGE/J software as described under "Methods." The results are mean ± SEM of three phagosomes from different cells. |
PMC1716166_F1_7994.jpg | What does this image primarily show? | X-ray of the pelvis showing no positive findings. |
PMC1716166_F2_7996.jpg | Describe the main subject of this image. | MRI of the pelvis showing effusion with soft tissue swelling and synovial thickening. |
PMC1716167_F1_7997.jpg | Can you identify the primary element in this image? | Fistula injection with small bowel follow-through demonstrating distal obstruction of small bowel. |
PMC1716167_F2_7998.jpg | Can you identify the primary element in this image? | Computed tomogram of the abdomen prior to initiation of cytotoxic chemotherapy demonstrating right-sided abdominal wall soft tissue mass (16 × 9 cm) (arrow), and mesenteric soft tissue mass (7 × 5 cm). |
PMC1716178_F1_8003.jpg | Can you identify the primary element in this image? | Lateral soft tissues X-ray revealing undigested material in the cervical oesophagus. |
PMC1716185_pmed-0030525-g007_8031.jpg | What is being portrayed in this visual content? | Pathogenic Findings Following Homologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 2) taken from an untreated control mouse (A), a VRP-N–vaccinated mouse (B) and (D), a VRP-HA–vaccinated mouse (C), a VRP-S–vaccinated mouse (E), and a VRP-S– and VRP-N–treated mouse (F). No histopathology was evident in (A). A marked mixed inflammatory infiltrate composed mainly of mononuclear leukocytes (lymphocytes and plasma cells) and widely scattered eosinophils are evident in the perivascular and peribronchiolar interstitium (asterisk) in (B). Similar inflammatory cells are also present in bronchiolar (br) airways and alveolar airspaces along with enlarged and vacuolated alveolar macrophages (arrows). The box in (B) denotes the site of the light photomicrograph (D) that was taken at a higher magnification to better illustrate the lymphoplasmacytic inflammatory cell infiltrate with lesser numbers of eosinophils (arrows). Similar, but slightly less severe, perivascular inflammatory infiltrates (asterisk) are also present in (F), but without accompanying alveolitis. Minimal lymphoplasmacytic cell accumulations around the pulmonary arteriole (a) are evident in (C) and (E). All tissues were stained with hematoxylin and eosin. Bars denote the scale of the magnification. a, pulmonary arteriole; ap, alveolar parenchyma; br, bronchiolar lumen; e, surface epithelium of the bronchiole. |
PMC1716185_pmed-0030525-g007_8030.jpg | What does this image primarily show? | Pathogenic Findings Following Homologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 2) taken from an untreated control mouse (A), a VRP-N–vaccinated mouse (B) and (D), a VRP-HA–vaccinated mouse (C), a VRP-S–vaccinated mouse (E), and a VRP-S– and VRP-N–treated mouse (F). No histopathology was evident in (A). A marked mixed inflammatory infiltrate composed mainly of mononuclear leukocytes (lymphocytes and plasma cells) and widely scattered eosinophils are evident in the perivascular and peribronchiolar interstitium (asterisk) in (B). Similar inflammatory cells are also present in bronchiolar (br) airways and alveolar airspaces along with enlarged and vacuolated alveolar macrophages (arrows). The box in (B) denotes the site of the light photomicrograph (D) that was taken at a higher magnification to better illustrate the lymphoplasmacytic inflammatory cell infiltrate with lesser numbers of eosinophils (arrows). Similar, but slightly less severe, perivascular inflammatory infiltrates (asterisk) are also present in (F), but without accompanying alveolitis. Minimal lymphoplasmacytic cell accumulations around the pulmonary arteriole (a) are evident in (C) and (E). All tissues were stained with hematoxylin and eosin. Bars denote the scale of the magnification. a, pulmonary arteriole; ap, alveolar parenchyma; br, bronchiolar lumen; e, surface epithelium of the bronchiole. |
PMC1716185_pmed-0030525-g007_8028.jpg | What does this image primarily show? | Pathogenic Findings Following Homologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 2) taken from an untreated control mouse (A), a VRP-N–vaccinated mouse (B) and (D), a VRP-HA–vaccinated mouse (C), a VRP-S–vaccinated mouse (E), and a VRP-S– and VRP-N–treated mouse (F). No histopathology was evident in (A). A marked mixed inflammatory infiltrate composed mainly of mononuclear leukocytes (lymphocytes and plasma cells) and widely scattered eosinophils are evident in the perivascular and peribronchiolar interstitium (asterisk) in (B). Similar inflammatory cells are also present in bronchiolar (br) airways and alveolar airspaces along with enlarged and vacuolated alveolar macrophages (arrows). The box in (B) denotes the site of the light photomicrograph (D) that was taken at a higher magnification to better illustrate the lymphoplasmacytic inflammatory cell infiltrate with lesser numbers of eosinophils (arrows). Similar, but slightly less severe, perivascular inflammatory infiltrates (asterisk) are also present in (F), but without accompanying alveolitis. Minimal lymphoplasmacytic cell accumulations around the pulmonary arteriole (a) are evident in (C) and (E). All tissues were stained with hematoxylin and eosin. Bars denote the scale of the magnification. a, pulmonary arteriole; ap, alveolar parenchyma; br, bronchiolar lumen; e, surface epithelium of the bronchiole. |
PMC1716185_pmed-0030525-g007_8029.jpg | Can you identify the primary element in this image? | Pathogenic Findings Following Homologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 2) taken from an untreated control mouse (A), a VRP-N–vaccinated mouse (B) and (D), a VRP-HA–vaccinated mouse (C), a VRP-S–vaccinated mouse (E), and a VRP-S– and VRP-N–treated mouse (F). No histopathology was evident in (A). A marked mixed inflammatory infiltrate composed mainly of mononuclear leukocytes (lymphocytes and plasma cells) and widely scattered eosinophils are evident in the perivascular and peribronchiolar interstitium (asterisk) in (B). Similar inflammatory cells are also present in bronchiolar (br) airways and alveolar airspaces along with enlarged and vacuolated alveolar macrophages (arrows). The box in (B) denotes the site of the light photomicrograph (D) that was taken at a higher magnification to better illustrate the lymphoplasmacytic inflammatory cell infiltrate with lesser numbers of eosinophils (arrows). Similar, but slightly less severe, perivascular inflammatory infiltrates (asterisk) are also present in (F), but without accompanying alveolitis. Minimal lymphoplasmacytic cell accumulations around the pulmonary arteriole (a) are evident in (C) and (E). All tissues were stained with hematoxylin and eosin. Bars denote the scale of the magnification. a, pulmonary arteriole; ap, alveolar parenchyma; br, bronchiolar lumen; e, surface epithelium of the bronchiole. |
PMC1716185_pmed-0030525-g007_8033.jpg | Can you identify the primary element in this image? | Pathogenic Findings Following Homologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 2) taken from an untreated control mouse (A), a VRP-N–vaccinated mouse (B) and (D), a VRP-HA–vaccinated mouse (C), a VRP-S–vaccinated mouse (E), and a VRP-S– and VRP-N–treated mouse (F). No histopathology was evident in (A). A marked mixed inflammatory infiltrate composed mainly of mononuclear leukocytes (lymphocytes and plasma cells) and widely scattered eosinophils are evident in the perivascular and peribronchiolar interstitium (asterisk) in (B). Similar inflammatory cells are also present in bronchiolar (br) airways and alveolar airspaces along with enlarged and vacuolated alveolar macrophages (arrows). The box in (B) denotes the site of the light photomicrograph (D) that was taken at a higher magnification to better illustrate the lymphoplasmacytic inflammatory cell infiltrate with lesser numbers of eosinophils (arrows). Similar, but slightly less severe, perivascular inflammatory infiltrates (asterisk) are also present in (F), but without accompanying alveolitis. Minimal lymphoplasmacytic cell accumulations around the pulmonary arteriole (a) are evident in (C) and (E). All tissues were stained with hematoxylin and eosin. Bars denote the scale of the magnification. a, pulmonary arteriole; ap, alveolar parenchyma; br, bronchiolar lumen; e, surface epithelium of the bronchiole. |
PMC1716185_pmed-0030525-g008_8005.jpg | What is the dominant medical problem in this image? | Pathogenic Findings Following Heterologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 4) taken from a mock PBS–vaccinated mouse (A) and (B), a VRP-N–vaccinated mouse (C) and (D), a VRP-S–vaccinated mouse (E) and (F), or a VRP-S+N–vaccinated mouse (G) and (H). The boxes in (A), (C), (E), and (G) (200× magnification) denote the site of the light photomicrograph that was taken at a higher magnification (400×) to better illustrate the lymphoplasmacytic inflammatory cell infiltrates including eosinophils (yellow arrows). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g008_8011.jpg | What is the focal point of this photograph? | Pathogenic Findings Following Heterologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 4) taken from a mock PBS–vaccinated mouse (A) and (B), a VRP-N–vaccinated mouse (C) and (D), a VRP-S–vaccinated mouse (E) and (F), or a VRP-S+N–vaccinated mouse (G) and (H). The boxes in (A), (C), (E), and (G) (200× magnification) denote the site of the light photomicrograph that was taken at a higher magnification (400×) to better illustrate the lymphoplasmacytic inflammatory cell infiltrates including eosinophils (yellow arrows). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g008_8007.jpg | What can you see in this picture? | Pathogenic Findings Following Heterologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 4) taken from a mock PBS–vaccinated mouse (A) and (B), a VRP-N–vaccinated mouse (C) and (D), a VRP-S–vaccinated mouse (E) and (F), or a VRP-S+N–vaccinated mouse (G) and (H). The boxes in (A), (C), (E), and (G) (200× magnification) denote the site of the light photomicrograph that was taken at a higher magnification (400×) to better illustrate the lymphoplasmacytic inflammatory cell infiltrates including eosinophils (yellow arrows). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g008_8009.jpg | What does this image primarily show? | Pathogenic Findings Following Heterologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 4) taken from a mock PBS–vaccinated mouse (A) and (B), a VRP-N–vaccinated mouse (C) and (D), a VRP-S–vaccinated mouse (E) and (F), or a VRP-S+N–vaccinated mouse (G) and (H). The boxes in (A), (C), (E), and (G) (200× magnification) denote the site of the light photomicrograph that was taken at a higher magnification (400×) to better illustrate the lymphoplasmacytic inflammatory cell infiltrates including eosinophils (yellow arrows). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g008_8010.jpg | Describe the main subject of this image. | Pathogenic Findings Following Heterologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 4) taken from a mock PBS–vaccinated mouse (A) and (B), a VRP-N–vaccinated mouse (C) and (D), a VRP-S–vaccinated mouse (E) and (F), or a VRP-S+N–vaccinated mouse (G) and (H). The boxes in (A), (C), (E), and (G) (200× magnification) denote the site of the light photomicrograph that was taken at a higher magnification (400×) to better illustrate the lymphoplasmacytic inflammatory cell infiltrates including eosinophils (yellow arrows). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g008_8006.jpg | What is the principal component of this image? | Pathogenic Findings Following Heterologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 4) taken from a mock PBS–vaccinated mouse (A) and (B), a VRP-N–vaccinated mouse (C) and (D), a VRP-S–vaccinated mouse (E) and (F), or a VRP-S+N–vaccinated mouse (G) and (H). The boxes in (A), (C), (E), and (G) (200× magnification) denote the site of the light photomicrograph that was taken at a higher magnification (400×) to better illustrate the lymphoplasmacytic inflammatory cell infiltrates including eosinophils (yellow arrows). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g008_8008.jpg | What is the principal component of this image? | Pathogenic Findings Following Heterologous ChallengeLight photomicrographs of representative histologic lung sections (Table 1, experiment 4) taken from a mock PBS–vaccinated mouse (A) and (B), a VRP-N–vaccinated mouse (C) and (D), a VRP-S–vaccinated mouse (E) and (F), or a VRP-S+N–vaccinated mouse (G) and (H). The boxes in (A), (C), (E), and (G) (200× magnification) denote the site of the light photomicrograph that was taken at a higher magnification (400×) to better illustrate the lymphoplasmacytic inflammatory cell infiltrates including eosinophils (yellow arrows). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g009_8023.jpg | Describe the main subject of this image. | Kinetics of VRP-N–Associated InflammationLight photomicrographs of lung sections taken from VRP-HA– and VRP-N–vaccinated mice harvested at days 2, 4, 7, and 14 post–icSARS-CoV challenge (Table 1, experiment 5). Representative lung sections (200× magnification) comparing pulmonary inflammation between VRP-HA–vaccinated (A), (C), (E), and (G) and VRP-N–vaccinated (B), (D), (F), and (H) mice. Enhanced inflammation was evident by day 2 (A) and (B) in some VRP-N–vaccinated animals relative to lung sections of VRP-HA–inoculated mice. By day 4 post-infection (C) and (D), increased inflammation in VRP-N–vaccinated animals was widely apparent and was maintained through days 7 (E) and (F) and 14 (G) and (H). |
PMC1716185_pmed-0030525-g009_8025.jpg | What is the central feature of this picture? | Kinetics of VRP-N–Associated InflammationLight photomicrographs of lung sections taken from VRP-HA– and VRP-N–vaccinated mice harvested at days 2, 4, 7, and 14 post–icSARS-CoV challenge (Table 1, experiment 5). Representative lung sections (200× magnification) comparing pulmonary inflammation between VRP-HA–vaccinated (A), (C), (E), and (G) and VRP-N–vaccinated (B), (D), (F), and (H) mice. Enhanced inflammation was evident by day 2 (A) and (B) in some VRP-N–vaccinated animals relative to lung sections of VRP-HA–inoculated mice. By day 4 post-infection (C) and (D), increased inflammation in VRP-N–vaccinated animals was widely apparent and was maintained through days 7 (E) and (F) and 14 (G) and (H). |
PMC1716185_pmed-0030525-g009_8024.jpg | What's the most prominent thing you notice in this picture? | Kinetics of VRP-N–Associated InflammationLight photomicrographs of lung sections taken from VRP-HA– and VRP-N–vaccinated mice harvested at days 2, 4, 7, and 14 post–icSARS-CoV challenge (Table 1, experiment 5). Representative lung sections (200× magnification) comparing pulmonary inflammation between VRP-HA–vaccinated (A), (C), (E), and (G) and VRP-N–vaccinated (B), (D), (F), and (H) mice. Enhanced inflammation was evident by day 2 (A) and (B) in some VRP-N–vaccinated animals relative to lung sections of VRP-HA–inoculated mice. By day 4 post-infection (C) and (D), increased inflammation in VRP-N–vaccinated animals was widely apparent and was maintained through days 7 (E) and (F) and 14 (G) and (H). |
PMC1716185_pmed-0030525-g009_8027.jpg | What is being portrayed in this visual content? | Kinetics of VRP-N–Associated InflammationLight photomicrographs of lung sections taken from VRP-HA– and VRP-N–vaccinated mice harvested at days 2, 4, 7, and 14 post–icSARS-CoV challenge (Table 1, experiment 5). Representative lung sections (200× magnification) comparing pulmonary inflammation between VRP-HA–vaccinated (A), (C), (E), and (G) and VRP-N–vaccinated (B), (D), (F), and (H) mice. Enhanced inflammation was evident by day 2 (A) and (B) in some VRP-N–vaccinated animals relative to lung sections of VRP-HA–inoculated mice. By day 4 post-infection (C) and (D), increased inflammation in VRP-N–vaccinated animals was widely apparent and was maintained through days 7 (E) and (F) and 14 (G) and (H). |
PMC1716185_pmed-0030525-g010_8016.jpg | Can you identify the primary element in this image? | Identifying Eosinophils among Inflammatory InfiltratesThe 400× magnification comparing eosinophil infiltration within the lung sections of VRP-HA–vaccinated (A), (C), (E), and (G) and VRP-N–vaccinated (B), (D), (F), and (H) mice (Table 1, Experiment 5). At day 2 post-infection (A) and (B), eosinophils are rarely evident in the lungs of either VRP-HA (A) or VRP-N (B) mice. Day 4 post-infection (C) and (D), extensive eosinophils (yellow arrows) are present within the lungs of VRP-N–vaccinated mice. Widespread eosinophils are seen at day 7 post-challenge in VRP-N–vaccinated (F), but not VRP-HA–vaccinated (E) mice. By day 14 (G) and (H), eosinophils are rarely found among inflammatory cells of VRP-N–vaccinated mice. An identical experiment in old animals was performed simultaneously (Table 1, experiment 6), showed results indistinguishable from those of young mice (unpublished data). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g010_8019.jpg | What stands out most in this visual? | Identifying Eosinophils among Inflammatory InfiltratesThe 400× magnification comparing eosinophil infiltration within the lung sections of VRP-HA–vaccinated (A), (C), (E), and (G) and VRP-N–vaccinated (B), (D), (F), and (H) mice (Table 1, Experiment 5). At day 2 post-infection (A) and (B), eosinophils are rarely evident in the lungs of either VRP-HA (A) or VRP-N (B) mice. Day 4 post-infection (C) and (D), extensive eosinophils (yellow arrows) are present within the lungs of VRP-N–vaccinated mice. Widespread eosinophils are seen at day 7 post-challenge in VRP-N–vaccinated (F), but not VRP-HA–vaccinated (E) mice. By day 14 (G) and (H), eosinophils are rarely found among inflammatory cells of VRP-N–vaccinated mice. An identical experiment in old animals was performed simultaneously (Table 1, experiment 6), showed results indistinguishable from those of young mice (unpublished data). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g010_8018.jpg | What key item or scene is captured in this photo? | Identifying Eosinophils among Inflammatory InfiltratesThe 400× magnification comparing eosinophil infiltration within the lung sections of VRP-HA–vaccinated (A), (C), (E), and (G) and VRP-N–vaccinated (B), (D), (F), and (H) mice (Table 1, Experiment 5). At day 2 post-infection (A) and (B), eosinophils are rarely evident in the lungs of either VRP-HA (A) or VRP-N (B) mice. Day 4 post-infection (C) and (D), extensive eosinophils (yellow arrows) are present within the lungs of VRP-N–vaccinated mice. Widespread eosinophils are seen at day 7 post-challenge in VRP-N–vaccinated (F), but not VRP-HA–vaccinated (E) mice. By day 14 (G) and (H), eosinophils are rarely found among inflammatory cells of VRP-N–vaccinated mice. An identical experiment in old animals was performed simultaneously (Table 1, experiment 6), showed results indistinguishable from those of young mice (unpublished data). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g010_8014.jpg | What is the core subject represented in this visual? | Identifying Eosinophils among Inflammatory InfiltratesThe 400× magnification comparing eosinophil infiltration within the lung sections of VRP-HA–vaccinated (A), (C), (E), and (G) and VRP-N–vaccinated (B), (D), (F), and (H) mice (Table 1, Experiment 5). At day 2 post-infection (A) and (B), eosinophils are rarely evident in the lungs of either VRP-HA (A) or VRP-N (B) mice. Day 4 post-infection (C) and (D), extensive eosinophils (yellow arrows) are present within the lungs of VRP-N–vaccinated mice. Widespread eosinophils are seen at day 7 post-challenge in VRP-N–vaccinated (F), but not VRP-HA–vaccinated (E) mice. By day 14 (G) and (H), eosinophils are rarely found among inflammatory cells of VRP-N–vaccinated mice. An identical experiment in old animals was performed simultaneously (Table 1, experiment 6), showed results indistinguishable from those of young mice (unpublished data). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g010_8013.jpg | What is being portrayed in this visual content? | Identifying Eosinophils among Inflammatory InfiltratesThe 400× magnification comparing eosinophil infiltration within the lung sections of VRP-HA–vaccinated (A), (C), (E), and (G) and VRP-N–vaccinated (B), (D), (F), and (H) mice (Table 1, Experiment 5). At day 2 post-infection (A) and (B), eosinophils are rarely evident in the lungs of either VRP-HA (A) or VRP-N (B) mice. Day 4 post-infection (C) and (D), extensive eosinophils (yellow arrows) are present within the lungs of VRP-N–vaccinated mice. Widespread eosinophils are seen at day 7 post-challenge in VRP-N–vaccinated (F), but not VRP-HA–vaccinated (E) mice. By day 14 (G) and (H), eosinophils are rarely found among inflammatory cells of VRP-N–vaccinated mice. An identical experiment in old animals was performed simultaneously (Table 1, experiment 6), showed results indistinguishable from those of young mice (unpublished data). All tissues were stained with hematoxylin and eosin. |
PMC1716185_pmed-0030525-g010_8012.jpg | What's the most prominent thing you notice in this picture? | Identifying Eosinophils among Inflammatory InfiltratesThe 400× magnification comparing eosinophil infiltration within the lung sections of VRP-HA–vaccinated (A), (C), (E), and (G) and VRP-N–vaccinated (B), (D), (F), and (H) mice (Table 1, Experiment 5). At day 2 post-infection (A) and (B), eosinophils are rarely evident in the lungs of either VRP-HA (A) or VRP-N (B) mice. Day 4 post-infection (C) and (D), extensive eosinophils (yellow arrows) are present within the lungs of VRP-N–vaccinated mice. Widespread eosinophils are seen at day 7 post-challenge in VRP-N–vaccinated (F), but not VRP-HA–vaccinated (E) mice. By day 14 (G) and (H), eosinophils are rarely found among inflammatory cells of VRP-N–vaccinated mice. An identical experiment in old animals was performed simultaneously (Table 1, experiment 6), showed results indistinguishable from those of young mice (unpublished data). All tissues were stained with hematoxylin and eosin. |
PMC1716762_F2_8034.jpg | What is the dominant medical problem in this image? | A labial biopsy reveals lobules of small salivary glands and a small, non-necrotic, sarcoid type epithelioid granuloma (arrow). (Haematoxylin & Eosin, original magnification ×100). |
PMC1716762_F3_8035.jpg | Describe the main subject of this image. | A skin biopsy reveals acanthosis of epidermis, with elongated rete ridges, thin suprapapillary epidermal plates, absent granular layer and hyperkeratosis. A Munro microabscess (arrow) is also noticed within the parakeratotic cornified layer. (Haematoxylin & Eosin, original magnification ×100). |
PMC1750924_pbio-0040417-g004_8046.jpg | What is shown in this image? | Polyglutamine Aggregates Are Present in Committed Crypt Cells but Absent in Stem Cells in the Small Intestine of SCA3 Patients(A) Schematic representation of an intestinal crypt for visualisation of the different cell types present in this tissue. Light micrographs of a 4-μm (B) and 1-μm (C) section of a crypt from an SCA3 patient showing positive staining for anti-Musashi antibody. Note that stem cells are localised in between and on both sides of the morphologically recognizable Paneth cells residing at the base of the crypt. (D) A light micrograph of a crypt of a SCA3 patient showing positive staining for the anti-polyglutamine antibody IC2 in some epithelial cells (arrowheads). The asterisks (marked E–J) show representative positions of cells analyzed by subsequent electron microscopy. (E–J) show digitally modified, pseudo-coloured images of electron micrographs indicating the polyglutamine staining in blue. Differentiated epithelial cells (E), transit epithelial cells (F and I), and Paneth cells (J) contain polyglutamine aggregates (arrowheads). Stem cells (G) are negative for polyglutamine aggregates but occasionally contain micro-aggregates (H). Note that also some electron dense material is stained blue by this digital processing. In (G and H), contours are provided in black dashed lines to indicate the stem cells. Bars: D, 20 μm; E and H, 2 μm; F, 1 μm; G, I and J, 5 μm. (K) Quantification of cells with aggregates in the crypts of two SCA3 patients. As double labelling for aggregates and stem cells failed, only the stem cells that were adjacent to the Paneth cells were counted, because these could be easily identified on this basis. |
PMC1750924_pbio-0040417-g004_8051.jpg | What is the principal component of this image? | Polyglutamine Aggregates Are Present in Committed Crypt Cells but Absent in Stem Cells in the Small Intestine of SCA3 Patients(A) Schematic representation of an intestinal crypt for visualisation of the different cell types present in this tissue. Light micrographs of a 4-μm (B) and 1-μm (C) section of a crypt from an SCA3 patient showing positive staining for anti-Musashi antibody. Note that stem cells are localised in between and on both sides of the morphologically recognizable Paneth cells residing at the base of the crypt. (D) A light micrograph of a crypt of a SCA3 patient showing positive staining for the anti-polyglutamine antibody IC2 in some epithelial cells (arrowheads). The asterisks (marked E–J) show representative positions of cells analyzed by subsequent electron microscopy. (E–J) show digitally modified, pseudo-coloured images of electron micrographs indicating the polyglutamine staining in blue. Differentiated epithelial cells (E), transit epithelial cells (F and I), and Paneth cells (J) contain polyglutamine aggregates (arrowheads). Stem cells (G) are negative for polyglutamine aggregates but occasionally contain micro-aggregates (H). Note that also some electron dense material is stained blue by this digital processing. In (G and H), contours are provided in black dashed lines to indicate the stem cells. Bars: D, 20 μm; E and H, 2 μm; F, 1 μm; G, I and J, 5 μm. (K) Quantification of cells with aggregates in the crypts of two SCA3 patients. As double labelling for aggregates and stem cells failed, only the stem cells that were adjacent to the Paneth cells were counted, because these could be easily identified on this basis. |
PMC1750924_pbio-0040417-g004_8043.jpg | What is the principal component of this image? | Polyglutamine Aggregates Are Present in Committed Crypt Cells but Absent in Stem Cells in the Small Intestine of SCA3 Patients(A) Schematic representation of an intestinal crypt for visualisation of the different cell types present in this tissue. Light micrographs of a 4-μm (B) and 1-μm (C) section of a crypt from an SCA3 patient showing positive staining for anti-Musashi antibody. Note that stem cells are localised in between and on both sides of the morphologically recognizable Paneth cells residing at the base of the crypt. (D) A light micrograph of a crypt of a SCA3 patient showing positive staining for the anti-polyglutamine antibody IC2 in some epithelial cells (arrowheads). The asterisks (marked E–J) show representative positions of cells analyzed by subsequent electron microscopy. (E–J) show digitally modified, pseudo-coloured images of electron micrographs indicating the polyglutamine staining in blue. Differentiated epithelial cells (E), transit epithelial cells (F and I), and Paneth cells (J) contain polyglutamine aggregates (arrowheads). Stem cells (G) are negative for polyglutamine aggregates but occasionally contain micro-aggregates (H). Note that also some electron dense material is stained blue by this digital processing. In (G and H), contours are provided in black dashed lines to indicate the stem cells. Bars: D, 20 μm; E and H, 2 μm; F, 1 μm; G, I and J, 5 μm. (K) Quantification of cells with aggregates in the crypts of two SCA3 patients. As double labelling for aggregates and stem cells failed, only the stem cells that were adjacent to the Paneth cells were counted, because these could be easily identified on this basis. |
PMC1750924_pbio-0040417-g004_8049.jpg | What is the core subject represented in this visual? | Polyglutamine Aggregates Are Present in Committed Crypt Cells but Absent in Stem Cells in the Small Intestine of SCA3 Patients(A) Schematic representation of an intestinal crypt for visualisation of the different cell types present in this tissue. Light micrographs of a 4-μm (B) and 1-μm (C) section of a crypt from an SCA3 patient showing positive staining for anti-Musashi antibody. Note that stem cells are localised in between and on both sides of the morphologically recognizable Paneth cells residing at the base of the crypt. (D) A light micrograph of a crypt of a SCA3 patient showing positive staining for the anti-polyglutamine antibody IC2 in some epithelial cells (arrowheads). The asterisks (marked E–J) show representative positions of cells analyzed by subsequent electron microscopy. (E–J) show digitally modified, pseudo-coloured images of electron micrographs indicating the polyglutamine staining in blue. Differentiated epithelial cells (E), transit epithelial cells (F and I), and Paneth cells (J) contain polyglutamine aggregates (arrowheads). Stem cells (G) are negative for polyglutamine aggregates but occasionally contain micro-aggregates (H). Note that also some electron dense material is stained blue by this digital processing. In (G and H), contours are provided in black dashed lines to indicate the stem cells. Bars: D, 20 μm; E and H, 2 μm; F, 1 μm; G, I and J, 5 μm. (K) Quantification of cells with aggregates in the crypts of two SCA3 patients. As double labelling for aggregates and stem cells failed, only the stem cells that were adjacent to the Paneth cells were counted, because these could be easily identified on this basis. |
PMC1750924_pbio-0040417-g004_8048.jpg | What is shown in this image? | Polyglutamine Aggregates Are Present in Committed Crypt Cells but Absent in Stem Cells in the Small Intestine of SCA3 Patients(A) Schematic representation of an intestinal crypt for visualisation of the different cell types present in this tissue. Light micrographs of a 4-μm (B) and 1-μm (C) section of a crypt from an SCA3 patient showing positive staining for anti-Musashi antibody. Note that stem cells are localised in between and on both sides of the morphologically recognizable Paneth cells residing at the base of the crypt. (D) A light micrograph of a crypt of a SCA3 patient showing positive staining for the anti-polyglutamine antibody IC2 in some epithelial cells (arrowheads). The asterisks (marked E–J) show representative positions of cells analyzed by subsequent electron microscopy. (E–J) show digitally modified, pseudo-coloured images of electron micrographs indicating the polyglutamine staining in blue. Differentiated epithelial cells (E), transit epithelial cells (F and I), and Paneth cells (J) contain polyglutamine aggregates (arrowheads). Stem cells (G) are negative for polyglutamine aggregates but occasionally contain micro-aggregates (H). Note that also some electron dense material is stained blue by this digital processing. In (G and H), contours are provided in black dashed lines to indicate the stem cells. Bars: D, 20 μm; E and H, 2 μm; F, 1 μm; G, I and J, 5 μm. (K) Quantification of cells with aggregates in the crypts of two SCA3 patients. As double labelling for aggregates and stem cells failed, only the stem cells that were adjacent to the Paneth cells were counted, because these could be easily identified on this basis. |
PMC1750924_pbio-0040417-g004_8045.jpg | Can you identify the primary element in this image? | Polyglutamine Aggregates Are Present in Committed Crypt Cells but Absent in Stem Cells in the Small Intestine of SCA3 Patients(A) Schematic representation of an intestinal crypt for visualisation of the different cell types present in this tissue. Light micrographs of a 4-μm (B) and 1-μm (C) section of a crypt from an SCA3 patient showing positive staining for anti-Musashi antibody. Note that stem cells are localised in between and on both sides of the morphologically recognizable Paneth cells residing at the base of the crypt. (D) A light micrograph of a crypt of a SCA3 patient showing positive staining for the anti-polyglutamine antibody IC2 in some epithelial cells (arrowheads). The asterisks (marked E–J) show representative positions of cells analyzed by subsequent electron microscopy. (E–J) show digitally modified, pseudo-coloured images of electron micrographs indicating the polyglutamine staining in blue. Differentiated epithelial cells (E), transit epithelial cells (F and I), and Paneth cells (J) contain polyglutamine aggregates (arrowheads). Stem cells (G) are negative for polyglutamine aggregates but occasionally contain micro-aggregates (H). Note that also some electron dense material is stained blue by this digital processing. In (G and H), contours are provided in black dashed lines to indicate the stem cells. Bars: D, 20 μm; E and H, 2 μm; F, 1 μm; G, I and J, 5 μm. (K) Quantification of cells with aggregates in the crypts of two SCA3 patients. As double labelling for aggregates and stem cells failed, only the stem cells that were adjacent to the Paneth cells were counted, because these could be easily identified on this basis. |
PMC1750924_pbio-0040417-g005_8039.jpg | What is shown in this image? | Polyglutamine Aggregates Are Inherited by De Novo Generated Neuroblast Cells after Mitosis in D. Melanogaster
(A) Expression of Htt-Q128 (red) and Pon-GFP (green) was assessed by confocal laser scanning microscopy in whole embryos (Stage 11, in which anterior is at the top). Occasionally, Htt-Q128 aggregates were observed (inset).(B) During mitosis, the aggregated protein Htt-Q128 is associated with only one of the poles in metaphase, anaphase, and telophase, opposing the Pon-GFP crescent, indicative of asymmetric inheritance to de novo generated neuroblast.(C) Spindle pole–associated aggregates were more clearly visualised after α-tubulin (red) staining in Htt-Q128 (cyan), Pon-GFP (green) neuroblasts. DNA is stained with DAPI (blue). |
PMC1750924_pbio-0040417-g005_8036.jpg | What is the main focus of this visual representation? | Polyglutamine Aggregates Are Inherited by De Novo Generated Neuroblast Cells after Mitosis in D. Melanogaster
(A) Expression of Htt-Q128 (red) and Pon-GFP (green) was assessed by confocal laser scanning microscopy in whole embryos (Stage 11, in which anterior is at the top). Occasionally, Htt-Q128 aggregates were observed (inset).(B) During mitosis, the aggregated protein Htt-Q128 is associated with only one of the poles in metaphase, anaphase, and telophase, opposing the Pon-GFP crescent, indicative of asymmetric inheritance to de novo generated neuroblast.(C) Spindle pole–associated aggregates were more clearly visualised after α-tubulin (red) staining in Htt-Q128 (cyan), Pon-GFP (green) neuroblasts. DNA is stained with DAPI (blue). |
PMC1750924_pbio-0040417-g005_8037.jpg | What is the central feature of this picture? | Polyglutamine Aggregates Are Inherited by De Novo Generated Neuroblast Cells after Mitosis in D. Melanogaster
(A) Expression of Htt-Q128 (red) and Pon-GFP (green) was assessed by confocal laser scanning microscopy in whole embryos (Stage 11, in which anterior is at the top). Occasionally, Htt-Q128 aggregates were observed (inset).(B) During mitosis, the aggregated protein Htt-Q128 is associated with only one of the poles in metaphase, anaphase, and telophase, opposing the Pon-GFP crescent, indicative of asymmetric inheritance to de novo generated neuroblast.(C) Spindle pole–associated aggregates were more clearly visualised after α-tubulin (red) staining in Htt-Q128 (cyan), Pon-GFP (green) neuroblasts. DNA is stained with DAPI (blue). |
PMC1750924_pbio-0040417-g005_8040.jpg | What key item or scene is captured in this photo? | Polyglutamine Aggregates Are Inherited by De Novo Generated Neuroblast Cells after Mitosis in D. Melanogaster
(A) Expression of Htt-Q128 (red) and Pon-GFP (green) was assessed by confocal laser scanning microscopy in whole embryos (Stage 11, in which anterior is at the top). Occasionally, Htt-Q128 aggregates were observed (inset).(B) During mitosis, the aggregated protein Htt-Q128 is associated with only one of the poles in metaphase, anaphase, and telophase, opposing the Pon-GFP crescent, indicative of asymmetric inheritance to de novo generated neuroblast.(C) Spindle pole–associated aggregates were more clearly visualised after α-tubulin (red) staining in Htt-Q128 (cyan), Pon-GFP (green) neuroblasts. DNA is stained with DAPI (blue). |
PMC1750924_pbio-0040417-g005_8038.jpg | What can you see in this picture? | Polyglutamine Aggregates Are Inherited by De Novo Generated Neuroblast Cells after Mitosis in D. Melanogaster
(A) Expression of Htt-Q128 (red) and Pon-GFP (green) was assessed by confocal laser scanning microscopy in whole embryos (Stage 11, in which anterior is at the top). Occasionally, Htt-Q128 aggregates were observed (inset).(B) During mitosis, the aggregated protein Htt-Q128 is associated with only one of the poles in metaphase, anaphase, and telophase, opposing the Pon-GFP crescent, indicative of asymmetric inheritance to de novo generated neuroblast.(C) Spindle pole–associated aggregates were more clearly visualised after α-tubulin (red) staining in Htt-Q128 (cyan), Pon-GFP (green) neuroblasts. DNA is stained with DAPI (blue). |
PMC1751015_F1_8054.jpg | What does this image primarily show? | Conventional ultrasonic signs in the lung. (a) The pleural line (black bold arrow) is a roughly horizontal hyper-echoic line between upper and lower ribs, identified by acoustic shadows (white arrow). (b) Lung-sliding is a forward-and-back movement of visceral pleura against parietal pleura in real-time motion. In time-motion mode, it includes motionless parietal tissues over the pleural line and a homogenous granular pattern below it (right image). (c) Comet-tail artifacts (white bold arrows) are hyper-echoic reverberation artifacts arising from the pleural line, laser-beam-like and spreading up to the edge of the screen. |
PMC1751015_F1_8053.jpg | What object or scene is depicted here? | Conventional ultrasonic signs in the lung. (a) The pleural line (black bold arrow) is a roughly horizontal hyper-echoic line between upper and lower ribs, identified by acoustic shadows (white arrow). (b) Lung-sliding is a forward-and-back movement of visceral pleura against parietal pleura in real-time motion. In time-motion mode, it includes motionless parietal tissues over the pleural line and a homogenous granular pattern below it (right image). (c) Comet-tail artifacts (white bold arrows) are hyper-echoic reverberation artifacts arising from the pleural line, laser-beam-like and spreading up to the edge of the screen. |
PMC1751015_F2_8056.jpg | What is the principal component of this image? | A typical patient with pneumothorax correctly diagnosed by US and missed by CXR. This 42 year old male patient sustained injuries from a car accident, and arrived with dyspnea, tachycardia, hypotension and desaturation requiring mechanical ventilation. (a) The supine chest radiograph did not enable a diagnosis of pneumothorax. (b) A rapid exploration of the thorax by US indicated medium left pneumothorax (absence of lung-sliding), associated with left lung contusion and pleural effusion. (c) The diagnosis was confirmed afterwards by chest CT. Arterial oxygenation was improved after chest tube placement. |
PMC1751015_F2_8055.jpg | What can you see in this picture? | A typical patient with pneumothorax correctly diagnosed by US and missed by CXR. This 42 year old male patient sustained injuries from a car accident, and arrived with dyspnea, tachycardia, hypotension and desaturation requiring mechanical ventilation. (a) The supine chest radiograph did not enable a diagnosis of pneumothorax. (b) A rapid exploration of the thorax by US indicated medium left pneumothorax (absence of lung-sliding), associated with left lung contusion and pleural effusion. (c) The diagnosis was confirmed afterwards by chest CT. Arterial oxygenation was improved after chest tube placement. |
PMC1751015_F2_8057.jpg | What is the focal point of this photograph? | A typical patient with pneumothorax correctly diagnosed by US and missed by CXR. This 42 year old male patient sustained injuries from a car accident, and arrived with dyspnea, tachycardia, hypotension and desaturation requiring mechanical ventilation. (a) The supine chest radiograph did not enable a diagnosis of pneumothorax. (b) A rapid exploration of the thorax by US indicated medium left pneumothorax (absence of lung-sliding), associated with left lung contusion and pleural effusion. (c) The diagnosis was confirmed afterwards by chest CT. Arterial oxygenation was improved after chest tube placement. |
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