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PMC545075_F2_1087.jpg | What is shown in this image? | Identification of septal, outflow tract, and aortic arch malformations using multi-embryo MRI (a – e') Images of transverse sections from 5 Cited2-/- embryos obtained using the multi-embryo technique (a–e) compared with images from the same embryos obtained subsequently using the single embryo technique (a'–e'). (a, a') Section showing left and right atria and ventricles (la, ram, live, rave). The atria are separated by the primary atria septum (pas), which is deficient at its ventral margin creating an osmium premium type of atria septal defect (ASD-P). (b, b') Section showing a ventricular septal defect (VSD) in the interventricular septum (ivs). (c, c') Section showing double outlet right ventricle, wherein the ascending aorta (a-ao) and the pulmonary artery (pa) both arise from the right ventricle (rv). The aortic valve (ao-v) is indicated. (d, d') Section showing a right-sided aortic arch (ao-a) passing to the right of the trachea (tr) and the esophagus (es). (e, e') Section showing bilateral aortic arches (ao-a) forming a vascular ring around the trachea (tr) and the esophagus (es). Also indicated are the thymus (th) and the right superior vena cava (r-svc). (f – j) Serial transverse sections through a wild-type heart obtained using single embryo MRI, demonstrating corresponding normal structures, including the systemic venous sinus (svs), left superior vena cava (l-svc), pulmonary vein (pvn), descending aorta (d-ao), mitral and tricuspid valves (mv, tv), the secondary atrial septum (sas), left and right ventricular outflow tracts (lvot, rvot), pulmonary valve (pv), and arterial duct (ad) of the pulmonary artery. Scale bars = 635 μm for multi-embryo, and 317 μm for single embryo images; axes: d – dorsal; v – ventral; r – right; l – left. |
PMC545075_F2_1090.jpg | What does this image primarily show? | Identification of septal, outflow tract, and aortic arch malformations using multi-embryo MRI (a – e') Images of transverse sections from 5 Cited2-/- embryos obtained using the multi-embryo technique (a–e) compared with images from the same embryos obtained subsequently using the single embryo technique (a'–e'). (a, a') Section showing left and right atria and ventricles (la, ram, live, rave). The atria are separated by the primary atria septum (pas), which is deficient at its ventral margin creating an osmium premium type of atria septal defect (ASD-P). (b, b') Section showing a ventricular septal defect (VSD) in the interventricular septum (ivs). (c, c') Section showing double outlet right ventricle, wherein the ascending aorta (a-ao) and the pulmonary artery (pa) both arise from the right ventricle (rv). The aortic valve (ao-v) is indicated. (d, d') Section showing a right-sided aortic arch (ao-a) passing to the right of the trachea (tr) and the esophagus (es). (e, e') Section showing bilateral aortic arches (ao-a) forming a vascular ring around the trachea (tr) and the esophagus (es). Also indicated are the thymus (th) and the right superior vena cava (r-svc). (f – j) Serial transverse sections through a wild-type heart obtained using single embryo MRI, demonstrating corresponding normal structures, including the systemic venous sinus (svs), left superior vena cava (l-svc), pulmonary vein (pvn), descending aorta (d-ao), mitral and tricuspid valves (mv, tv), the secondary atrial septum (sas), left and right ventricular outflow tracts (lvot, rvot), pulmonary valve (pv), and arterial duct (ad) of the pulmonary artery. Scale bars = 635 μm for multi-embryo, and 317 μm for single embryo images; axes: d – dorsal; v – ventral; r – right; l – left. |
PMC545075_F2_1081.jpg | What is the main focus of this visual representation? | Identification of septal, outflow tract, and aortic arch malformations using multi-embryo MRI (a – e') Images of transverse sections from 5 Cited2-/- embryos obtained using the multi-embryo technique (a–e) compared with images from the same embryos obtained subsequently using the single embryo technique (a'–e'). (a, a') Section showing left and right atria and ventricles (la, ram, live, rave). The atria are separated by the primary atria septum (pas), which is deficient at its ventral margin creating an osmium premium type of atria septal defect (ASD-P). (b, b') Section showing a ventricular septal defect (VSD) in the interventricular septum (ivs). (c, c') Section showing double outlet right ventricle, wherein the ascending aorta (a-ao) and the pulmonary artery (pa) both arise from the right ventricle (rv). The aortic valve (ao-v) is indicated. (d, d') Section showing a right-sided aortic arch (ao-a) passing to the right of the trachea (tr) and the esophagus (es). (e, e') Section showing bilateral aortic arches (ao-a) forming a vascular ring around the trachea (tr) and the esophagus (es). Also indicated are the thymus (th) and the right superior vena cava (r-svc). (f – j) Serial transverse sections through a wild-type heart obtained using single embryo MRI, demonstrating corresponding normal structures, including the systemic venous sinus (svs), left superior vena cava (l-svc), pulmonary vein (pvn), descending aorta (d-ao), mitral and tricuspid valves (mv, tv), the secondary atrial septum (sas), left and right ventricular outflow tracts (lvot, rvot), pulmonary valve (pv), and arterial duct (ad) of the pulmonary artery. Scale bars = 635 μm for multi-embryo, and 317 μm for single embryo images; axes: d – dorsal; v – ventral; r – right; l – left. |
PMC545075_F2_1082.jpg | What does this image primarily show? | Identification of septal, outflow tract, and aortic arch malformations using multi-embryo MRI (a – e') Images of transverse sections from 5 Cited2-/- embryos obtained using the multi-embryo technique (a–e) compared with images from the same embryos obtained subsequently using the single embryo technique (a'–e'). (a, a') Section showing left and right atria and ventricles (la, ram, live, rave). The atria are separated by the primary atria septum (pas), which is deficient at its ventral margin creating an osmium premium type of atria septal defect (ASD-P). (b, b') Section showing a ventricular septal defect (VSD) in the interventricular septum (ivs). (c, c') Section showing double outlet right ventricle, wherein the ascending aorta (a-ao) and the pulmonary artery (pa) both arise from the right ventricle (rv). The aortic valve (ao-v) is indicated. (d, d') Section showing a right-sided aortic arch (ao-a) passing to the right of the trachea (tr) and the esophagus (es). (e, e') Section showing bilateral aortic arches (ao-a) forming a vascular ring around the trachea (tr) and the esophagus (es). Also indicated are the thymus (th) and the right superior vena cava (r-svc). (f – j) Serial transverse sections through a wild-type heart obtained using single embryo MRI, demonstrating corresponding normal structures, including the systemic venous sinus (svs), left superior vena cava (l-svc), pulmonary vein (pvn), descending aorta (d-ao), mitral and tricuspid valves (mv, tv), the secondary atrial septum (sas), left and right ventricular outflow tracts (lvot, rvot), pulmonary valve (pv), and arterial duct (ad) of the pulmonary artery. Scale bars = 635 μm for multi-embryo, and 317 μm for single embryo images; axes: d – dorsal; v – ventral; r – right; l – left. |
PMC545075_F2_1088.jpg | Can you identify the primary element in this image? | Identification of septal, outflow tract, and aortic arch malformations using multi-embryo MRI (a – e') Images of transverse sections from 5 Cited2-/- embryos obtained using the multi-embryo technique (a–e) compared with images from the same embryos obtained subsequently using the single embryo technique (a'–e'). (a, a') Section showing left and right atria and ventricles (la, ram, live, rave). The atria are separated by the primary atria septum (pas), which is deficient at its ventral margin creating an osmium premium type of atria septal defect (ASD-P). (b, b') Section showing a ventricular septal defect (VSD) in the interventricular septum (ivs). (c, c') Section showing double outlet right ventricle, wherein the ascending aorta (a-ao) and the pulmonary artery (pa) both arise from the right ventricle (rv). The aortic valve (ao-v) is indicated. (d, d') Section showing a right-sided aortic arch (ao-a) passing to the right of the trachea (tr) and the esophagus (es). (e, e') Section showing bilateral aortic arches (ao-a) forming a vascular ring around the trachea (tr) and the esophagus (es). Also indicated are the thymus (th) and the right superior vena cava (r-svc). (f – j) Serial transverse sections through a wild-type heart obtained using single embryo MRI, demonstrating corresponding normal structures, including the systemic venous sinus (svs), left superior vena cava (l-svc), pulmonary vein (pvn), descending aorta (d-ao), mitral and tricuspid valves (mv, tv), the secondary atrial septum (sas), left and right ventricular outflow tracts (lvot, rvot), pulmonary valve (pv), and arterial duct (ad) of the pulmonary artery. Scale bars = 635 μm for multi-embryo, and 317 μm for single embryo images; axes: d – dorsal; v – ventral; r – right; l – left. |
PMC545075_F2_1089.jpg | What is the main focus of this visual representation? | Identification of septal, outflow tract, and aortic arch malformations using multi-embryo MRI (a – e') Images of transverse sections from 5 Cited2-/- embryos obtained using the multi-embryo technique (a–e) compared with images from the same embryos obtained subsequently using the single embryo technique (a'–e'). (a, a') Section showing left and right atria and ventricles (la, ram, live, rave). The atria are separated by the primary atria septum (pas), which is deficient at its ventral margin creating an osmium premium type of atria septal defect (ASD-P). (b, b') Section showing a ventricular septal defect (VSD) in the interventricular septum (ivs). (c, c') Section showing double outlet right ventricle, wherein the ascending aorta (a-ao) and the pulmonary artery (pa) both arise from the right ventricle (rv). The aortic valve (ao-v) is indicated. (d, d') Section showing a right-sided aortic arch (ao-a) passing to the right of the trachea (tr) and the esophagus (es). (e, e') Section showing bilateral aortic arches (ao-a) forming a vascular ring around the trachea (tr) and the esophagus (es). Also indicated are the thymus (th) and the right superior vena cava (r-svc). (f – j) Serial transverse sections through a wild-type heart obtained using single embryo MRI, demonstrating corresponding normal structures, including the systemic venous sinus (svs), left superior vena cava (l-svc), pulmonary vein (pvn), descending aorta (d-ao), mitral and tricuspid valves (mv, tv), the secondary atrial septum (sas), left and right ventricular outflow tracts (lvot, rvot), pulmonary valve (pv), and arterial duct (ad) of the pulmonary artery. Scale bars = 635 μm for multi-embryo, and 317 μm for single embryo images; axes: d – dorsal; v – ventral; r – right; l – left. |
PMC545075_F2_1079.jpg | What is the dominant medical problem in this image? | Identification of septal, outflow tract, and aortic arch malformations using multi-embryo MRI (a – e') Images of transverse sections from 5 Cited2-/- embryos obtained using the multi-embryo technique (a–e) compared with images from the same embryos obtained subsequently using the single embryo technique (a'–e'). (a, a') Section showing left and right atria and ventricles (la, ram, live, rave). The atria are separated by the primary atria septum (pas), which is deficient at its ventral margin creating an osmium premium type of atria septal defect (ASD-P). (b, b') Section showing a ventricular septal defect (VSD) in the interventricular septum (ivs). (c, c') Section showing double outlet right ventricle, wherein the ascending aorta (a-ao) and the pulmonary artery (pa) both arise from the right ventricle (rv). The aortic valve (ao-v) is indicated. (d, d') Section showing a right-sided aortic arch (ao-a) passing to the right of the trachea (tr) and the esophagus (es). (e, e') Section showing bilateral aortic arches (ao-a) forming a vascular ring around the trachea (tr) and the esophagus (es). Also indicated are the thymus (th) and the right superior vena cava (r-svc). (f – j) Serial transverse sections through a wild-type heart obtained using single embryo MRI, demonstrating corresponding normal structures, including the systemic venous sinus (svs), left superior vena cava (l-svc), pulmonary vein (pvn), descending aorta (d-ao), mitral and tricuspid valves (mv, tv), the secondary atrial septum (sas), left and right ventricular outflow tracts (lvot, rvot), pulmonary valve (pv), and arterial duct (ad) of the pulmonary artery. Scale bars = 635 μm for multi-embryo, and 317 μm for single embryo images; axes: d – dorsal; v – ventral; r – right; l – left. |
PMC545075_F3_1068.jpg | What is the principal component of this image? | Identification of adrenal agenesis using multi-embryo MRI Images of coronal sections from 2 embryos obtained using the multi-embryo technique (a, b) compared with images from the same embryos obtained subsequently using the single embryo technique (a', b'). (a, a') Normal right adrenal gland (rad) anterior to the right kidney (rk) in a wild-type embryo. The right lung (rl) is indicated. (b, b') Agenesis of right adrenal gland in a Cited2-/- embryo. Scale bars = 635 μm for multi-embryo, and 317 μm for single embryo images; axes: d – dorsal; v – ventral; a – anterior, p – posterior. |
PMC545075_F3_1067.jpg | What is shown in this image? | Identification of adrenal agenesis using multi-embryo MRI Images of coronal sections from 2 embryos obtained using the multi-embryo technique (a, b) compared with images from the same embryos obtained subsequently using the single embryo technique (a', b'). (a, a') Normal right adrenal gland (rad) anterior to the right kidney (rk) in a wild-type embryo. The right lung (rl) is indicated. (b, b') Agenesis of right adrenal gland in a Cited2-/- embryo. Scale bars = 635 μm for multi-embryo, and 317 μm for single embryo images; axes: d – dorsal; v – ventral; a – anterior, p – posterior. |
PMC545075_F5_1075.jpg | What object or scene is depicted here? | Identification of cardiac malformations in Ptdsr-/- embryos using multi-embryo MRI (a–e) Transverse thoracic sections showing the heart of heterozygous or wild-type control embryos from each litter. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra) are also indicated, separated by the primary atrial septum (pas). (f–i) Corresponding sections through littermate Ptdsr-/- embryos, showing ventricular septal defects (VSD). Scale bar = 635 μm; axes: d – dorsal; v – ventral; r – right; l – left; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F5_1078.jpg | What is the core subject represented in this visual? | Identification of cardiac malformations in Ptdsr-/- embryos using multi-embryo MRI (a–e) Transverse thoracic sections showing the heart of heterozygous or wild-type control embryos from each litter. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra) are also indicated, separated by the primary atrial septum (pas). (f–i) Corresponding sections through littermate Ptdsr-/- embryos, showing ventricular septal defects (VSD). Scale bar = 635 μm; axes: d – dorsal; v – ventral; r – right; l – left; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F5_1074.jpg | What is the main focus of this visual representation? | Identification of cardiac malformations in Ptdsr-/- embryos using multi-embryo MRI (a–e) Transverse thoracic sections showing the heart of heterozygous or wild-type control embryos from each litter. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra) are also indicated, separated by the primary atrial septum (pas). (f–i) Corresponding sections through littermate Ptdsr-/- embryos, showing ventricular septal defects (VSD). Scale bar = 635 μm; axes: d – dorsal; v – ventral; r – right; l – left; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F5_1069.jpg | What is the principal component of this image? | Identification of cardiac malformations in Ptdsr-/- embryos using multi-embryo MRI (a–e) Transverse thoracic sections showing the heart of heterozygous or wild-type control embryos from each litter. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra) are also indicated, separated by the primary atrial septum (pas). (f–i) Corresponding sections through littermate Ptdsr-/- embryos, showing ventricular septal defects (VSD). Scale bar = 635 μm; axes: d – dorsal; v – ventral; r – right; l – left; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F5_1070.jpg | What's the most prominent thing you notice in this picture? | Identification of cardiac malformations in Ptdsr-/- embryos using multi-embryo MRI (a–e) Transverse thoracic sections showing the heart of heterozygous or wild-type control embryos from each litter. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra) are also indicated, separated by the primary atrial septum (pas). (f–i) Corresponding sections through littermate Ptdsr-/- embryos, showing ventricular septal defects (VSD). Scale bar = 635 μm; axes: d – dorsal; v – ventral; r – right; l – left; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F5_1077.jpg | What can you see in this picture? | Identification of cardiac malformations in Ptdsr-/- embryos using multi-embryo MRI (a–e) Transverse thoracic sections showing the heart of heterozygous or wild-type control embryos from each litter. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra) are also indicated, separated by the primary atrial septum (pas). (f–i) Corresponding sections through littermate Ptdsr-/- embryos, showing ventricular septal defects (VSD). Scale bar = 635 μm; axes: d – dorsal; v – ventral; r – right; l – left; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F5_1072.jpg | What is the focal point of this photograph? | Identification of cardiac malformations in Ptdsr-/- embryos using multi-embryo MRI (a–e) Transverse thoracic sections showing the heart of heterozygous or wild-type control embryos from each litter. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra) are also indicated, separated by the primary atrial septum (pas). (f–i) Corresponding sections through littermate Ptdsr-/- embryos, showing ventricular septal defects (VSD). Scale bar = 635 μm; axes: d – dorsal; v – ventral; r – right; l – left; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F5_1071.jpg | What is being portrayed in this visual content? | Identification of cardiac malformations in Ptdsr-/- embryos using multi-embryo MRI (a–e) Transverse thoracic sections showing the heart of heterozygous or wild-type control embryos from each litter. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra) are also indicated, separated by the primary atrial septum (pas). (f–i) Corresponding sections through littermate Ptdsr-/- embryos, showing ventricular septal defects (VSD). Scale bar = 635 μm; axes: d – dorsal; v – ventral; r – right; l – left; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F5_1073.jpg | What is the principal component of this image? | Identification of cardiac malformations in Ptdsr-/- embryos using multi-embryo MRI (a–e) Transverse thoracic sections showing the heart of heterozygous or wild-type control embryos from each litter. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra) are also indicated, separated by the primary atrial septum (pas). (f–i) Corresponding sections through littermate Ptdsr-/- embryos, showing ventricular septal defects (VSD). Scale bar = 635 μm; axes: d – dorsal; v – ventral; r – right; l – left; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1117.jpg | What's the most prominent thing you notice in this picture? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1109.jpg | What is the focal point of this photograph? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1106.jpg | What is the core subject represented in this visual? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1110.jpg | What is the focal point of this photograph? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1115.jpg | What is the dominant medical problem in this image? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1105.jpg | What does this image primarily show? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1111.jpg | Can you identify the primary element in this image? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1113.jpg | What is the principal component of this image? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1108.jpg | What is the principal component of this image? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1107.jpg | What is the principal component of this image? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F6_1116.jpg | What is being portrayed in this visual content? | Cardiac malformations and thymus hypoplasia in Ptdsr-/- embryos. (a–c) Transverse and oblique (through the plane of the ascending aorta) sections, and 3D reconstruction (left-ventral oblique view) of a heart of a wild-type embryo at 15.5 dpc. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The left and right atria (la, ra), and the trachea (tr) are also indicated. The ascending aorta (a-ao) arises from the left ventricular outflow tract (lvot), via the aortic valve (ao-v), and continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricular outflow tract (rvot), and continues as the arterial duct (ad), which joins the descending aorta. (d–f) Corresponding images of a Ptdsr-/- embryo, showing a smaller heart with a ventricular septal defect (VSD). The aorta arises from the right ventricle. The pulmonary artery is small and its connection to the descending aorta (arterial duct) could not be identified. (g–i) Corresponding images of another Ptdsr-/- embryo, showing a ventricular septal defect (VSD). The aorta overrides the VSD resulting in a double-outlet right ventricle. (j, k) Coronal sections of Ptdsr+/+ and Ptdsr-/- embryos, showing the two lobes of the thymus (th). The arterial duct of the pulmonary artery in the Ptdsr-/- embryo is narrowed. (l) Correlation between embryo weight and volume. Scattergram of embryo weight versus embryo volume measured from multi-embryo MRI datasets for 16 embryos using Amira. The co-efficient of regression (r) is indicated. (m, n,) Absolute embryo and thymus volumes (μl) were measured from the MRI datasets from 5 wild-type (wt), 3 heterozygote (h), and 8 Ptdsr-/- (m) embryos at 15.5 dpc. There was no significant difference in the wild-type and heterozygote data, which were therefore pooled together (wt/h). (o) Relative thymus volumes (% of embryo volume) were calculated as Ptdsr-/- embryos were slightly smaller than littermate wild-type embryos. The data are represented as mean ± S.D. The probability of a type I error (P) is indicated. Scale bars = 317 μm; axes: r – right; l – left; d – dorsal; v – ventral; a – anterior, p – posterior. Individual embryos are indicated by number. |
PMC545075_F7_1097.jpg | What is the dominant medical problem in this image? | Cardiac malformations in Ptdsr-/- embryos: analysis using histology Embryos analyzed by MRI (Figure 3) were sectioned transversely and stained with hematoxylin and eosin. (a–c) Serial caudal to cranial sections of the wild-type embryo showing normal cardiac and vascular anatomy. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The ascending aorta (a-ao) arises from the left ventricle, continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricle via the pulmonary valve (pv) and continues as the arterial duct (ad), which joins the descending aorta. The left and right atria (la, ra), trachea (tr), right main bronchus (rmb) and esophagus (es) are indicated. (d) Section through embryo 33 indicating the ventricular septal defect (VSD). (e, f) Sections through embryo 55 showing that both aorta and pulmonary artery arise from the right ventricle (double outlet right ventricle), and that the arterial duct of the pulmonary artery is narrow in comparison to the aorta – indicating pulmonary artery hypoplasia. The aortic valve (aov) is indicated. (g–i) Serial caudal to cranial sections through embryo 35 showing a VSD, aorta arising from the right ventricle (double outlet right ventricle), and a severely narrowed arterial duct. Scale bars = 500 μm; axes: r – right; l – left; d – dorsal; v – ventral. Individual embryos are indicated by number. |
PMC545075_F7_1096.jpg | What object or scene is depicted here? | Cardiac malformations in Ptdsr-/- embryos: analysis using histology Embryos analyzed by MRI (Figure 3) were sectioned transversely and stained with hematoxylin and eosin. (a–c) Serial caudal to cranial sections of the wild-type embryo showing normal cardiac and vascular anatomy. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The ascending aorta (a-ao) arises from the left ventricle, continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricle via the pulmonary valve (pv) and continues as the arterial duct (ad), which joins the descending aorta. The left and right atria (la, ra), trachea (tr), right main bronchus (rmb) and esophagus (es) are indicated. (d) Section through embryo 33 indicating the ventricular septal defect (VSD). (e, f) Sections through embryo 55 showing that both aorta and pulmonary artery arise from the right ventricle (double outlet right ventricle), and that the arterial duct of the pulmonary artery is narrow in comparison to the aorta – indicating pulmonary artery hypoplasia. The aortic valve (aov) is indicated. (g–i) Serial caudal to cranial sections through embryo 35 showing a VSD, aorta arising from the right ventricle (double outlet right ventricle), and a severely narrowed arterial duct. Scale bars = 500 μm; axes: r – right; l – left; d – dorsal; v – ventral. Individual embryos are indicated by number. |
PMC545075_F7_1099.jpg | What is the focal point of this photograph? | Cardiac malformations in Ptdsr-/- embryos: analysis using histology Embryos analyzed by MRI (Figure 3) were sectioned transversely and stained with hematoxylin and eosin. (a–c) Serial caudal to cranial sections of the wild-type embryo showing normal cardiac and vascular anatomy. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The ascending aorta (a-ao) arises from the left ventricle, continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricle via the pulmonary valve (pv) and continues as the arterial duct (ad), which joins the descending aorta. The left and right atria (la, ra), trachea (tr), right main bronchus (rmb) and esophagus (es) are indicated. (d) Section through embryo 33 indicating the ventricular septal defect (VSD). (e, f) Sections through embryo 55 showing that both aorta and pulmonary artery arise from the right ventricle (double outlet right ventricle), and that the arterial duct of the pulmonary artery is narrow in comparison to the aorta – indicating pulmonary artery hypoplasia. The aortic valve (aov) is indicated. (g–i) Serial caudal to cranial sections through embryo 35 showing a VSD, aorta arising from the right ventricle (double outlet right ventricle), and a severely narrowed arterial duct. Scale bars = 500 μm; axes: r – right; l – left; d – dorsal; v – ventral. Individual embryos are indicated by number. |
PMC545075_F7_1100.jpg | What is the core subject represented in this visual? | Cardiac malformations in Ptdsr-/- embryos: analysis using histology Embryos analyzed by MRI (Figure 3) were sectioned transversely and stained with hematoxylin and eosin. (a–c) Serial caudal to cranial sections of the wild-type embryo showing normal cardiac and vascular anatomy. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The ascending aorta (a-ao) arises from the left ventricle, continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricle via the pulmonary valve (pv) and continues as the arterial duct (ad), which joins the descending aorta. The left and right atria (la, ra), trachea (tr), right main bronchus (rmb) and esophagus (es) are indicated. (d) Section through embryo 33 indicating the ventricular septal defect (VSD). (e, f) Sections through embryo 55 showing that both aorta and pulmonary artery arise from the right ventricle (double outlet right ventricle), and that the arterial duct of the pulmonary artery is narrow in comparison to the aorta – indicating pulmonary artery hypoplasia. The aortic valve (aov) is indicated. (g–i) Serial caudal to cranial sections through embryo 35 showing a VSD, aorta arising from the right ventricle (double outlet right ventricle), and a severely narrowed arterial duct. Scale bars = 500 μm; axes: r – right; l – left; d – dorsal; v – ventral. Individual embryos are indicated by number. |
PMC545075_F7_1098.jpg | What can you see in this picture? | Cardiac malformations in Ptdsr-/- embryos: analysis using histology Embryos analyzed by MRI (Figure 3) were sectioned transversely and stained with hematoxylin and eosin. (a–c) Serial caudal to cranial sections of the wild-type embryo showing normal cardiac and vascular anatomy. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The ascending aorta (a-ao) arises from the left ventricle, continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricle via the pulmonary valve (pv) and continues as the arterial duct (ad), which joins the descending aorta. The left and right atria (la, ra), trachea (tr), right main bronchus (rmb) and esophagus (es) are indicated. (d) Section through embryo 33 indicating the ventricular septal defect (VSD). (e, f) Sections through embryo 55 showing that both aorta and pulmonary artery arise from the right ventricle (double outlet right ventricle), and that the arterial duct of the pulmonary artery is narrow in comparison to the aorta – indicating pulmonary artery hypoplasia. The aortic valve (aov) is indicated. (g–i) Serial caudal to cranial sections through embryo 35 showing a VSD, aorta arising from the right ventricle (double outlet right ventricle), and a severely narrowed arterial duct. Scale bars = 500 μm; axes: r – right; l – left; d – dorsal; v – ventral. Individual embryos are indicated by number. |
PMC545075_F7_1102.jpg | What is the main focus of this visual representation? | Cardiac malformations in Ptdsr-/- embryos: analysis using histology Embryos analyzed by MRI (Figure 3) were sectioned transversely and stained with hematoxylin and eosin. (a–c) Serial caudal to cranial sections of the wild-type embryo showing normal cardiac and vascular anatomy. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The ascending aorta (a-ao) arises from the left ventricle, continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricle via the pulmonary valve (pv) and continues as the arterial duct (ad), which joins the descending aorta. The left and right atria (la, ra), trachea (tr), right main bronchus (rmb) and esophagus (es) are indicated. (d) Section through embryo 33 indicating the ventricular septal defect (VSD). (e, f) Sections through embryo 55 showing that both aorta and pulmonary artery arise from the right ventricle (double outlet right ventricle), and that the arterial duct of the pulmonary artery is narrow in comparison to the aorta – indicating pulmonary artery hypoplasia. The aortic valve (aov) is indicated. (g–i) Serial caudal to cranial sections through embryo 35 showing a VSD, aorta arising from the right ventricle (double outlet right ventricle), and a severely narrowed arterial duct. Scale bars = 500 μm; axes: r – right; l – left; d – dorsal; v – ventral. Individual embryos are indicated by number. |
PMC545075_F7_1104.jpg | What's the most prominent thing you notice in this picture? | Cardiac malformations in Ptdsr-/- embryos: analysis using histology Embryos analyzed by MRI (Figure 3) were sectioned transversely and stained with hematoxylin and eosin. (a–c) Serial caudal to cranial sections of the wild-type embryo showing normal cardiac and vascular anatomy. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The ascending aorta (a-ao) arises from the left ventricle, continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricle via the pulmonary valve (pv) and continues as the arterial duct (ad), which joins the descending aorta. The left and right atria (la, ra), trachea (tr), right main bronchus (rmb) and esophagus (es) are indicated. (d) Section through embryo 33 indicating the ventricular septal defect (VSD). (e, f) Sections through embryo 55 showing that both aorta and pulmonary artery arise from the right ventricle (double outlet right ventricle), and that the arterial duct of the pulmonary artery is narrow in comparison to the aorta – indicating pulmonary artery hypoplasia. The aortic valve (aov) is indicated. (g–i) Serial caudal to cranial sections through embryo 35 showing a VSD, aorta arising from the right ventricle (double outlet right ventricle), and a severely narrowed arterial duct. Scale bars = 500 μm; axes: r – right; l – left; d – dorsal; v – ventral. Individual embryos are indicated by number. |
PMC545075_F7_1103.jpg | What is the focal point of this photograph? | Cardiac malformations in Ptdsr-/- embryos: analysis using histology Embryos analyzed by MRI (Figure 3) were sectioned transversely and stained with hematoxylin and eosin. (a–c) Serial caudal to cranial sections of the wild-type embryo showing normal cardiac and vascular anatomy. The left and right ventricles (lv, rv) are separated by the interventricular septum (ivs). The ascending aorta (a-ao) arises from the left ventricle, continues on as the aortic arch (ao-a), which joins the descending aorta (d-ao). The pulmonary artery (pa) arises from the right ventricle via the pulmonary valve (pv) and continues as the arterial duct (ad), which joins the descending aorta. The left and right atria (la, ra), trachea (tr), right main bronchus (rmb) and esophagus (es) are indicated. (d) Section through embryo 33 indicating the ventricular septal defect (VSD). (e, f) Sections through embryo 55 showing that both aorta and pulmonary artery arise from the right ventricle (double outlet right ventricle), and that the arterial duct of the pulmonary artery is narrow in comparison to the aorta – indicating pulmonary artery hypoplasia. The aortic valve (aov) is indicated. (g–i) Serial caudal to cranial sections through embryo 35 showing a VSD, aorta arising from the right ventricle (double outlet right ventricle), and a severely narrowed arterial duct. Scale bars = 500 μm; axes: r – right; l – left; d – dorsal; v – ventral. Individual embryos are indicated by number. |
PMC545077_F4_1095.jpg | What is the central feature of this picture? | The corneal stroma in a case of fungal keratitis shows diffuse TUNEL positivity in the zone of inflammation (*) as well as discrete positive staining in the peripheral keratocytes away from zone of inflammation (arrow head) (TUNEL, ×250) [Left]. The higher magnification of the same shows TUNEL positive nuclei of the keratocyte (Arrow) in a clean background, free of inflammatory cells. (TUNEL staining, ×500) (TUNEL ×400) [Right] |
PMC545077_F4_1094.jpg | What's the most prominent thing you notice in this picture? | The corneal stroma in a case of fungal keratitis shows diffuse TUNEL positivity in the zone of inflammation (*) as well as discrete positive staining in the peripheral keratocytes away from zone of inflammation (arrow head) (TUNEL, ×250) [Left]. The higher magnification of the same shows TUNEL positive nuclei of the keratocyte (Arrow) in a clean background, free of inflammatory cells. (TUNEL staining, ×500) (TUNEL ×400) [Right] |
PMC545208_pmed-0020019-g003_1119.jpg | Describe the main subject of this image. | T2-Weighted Magnetic Resonance Imaging Showing Blood in the Arterial Wall and Narrowing of the Lumen of the Left Internal Carotid ArteryThis is also known as the “crescent sign,” a hallmark of internal carotid artery dissection. |
PMC545208_pmed-0020019-g003_1118.jpg | What is the focal point of this photograph? | T2-Weighted Magnetic Resonance Imaging Showing Blood in the Arterial Wall and Narrowing of the Lumen of the Left Internal Carotid ArteryThis is also known as the “crescent sign,” a hallmark of internal carotid artery dissection. |
PMC545597_F1_1121.jpg | What does this image primarily show? | Circular representation of the B. licheniformis ATCC 14580 chromosome. Circles are numbered from 1 (outermost) to 7 (innermost). Circles 1 and 2 show the locations of predicted CDSs on the + and - strands, respectively; circle 3, %G+C; circle 4, GC skew ((G-C/G+C)); circle 5, homology with B. subtilis 168; circle 6, homology with B. halodurans; circle 7 shows positions of nine copies of insertion sequence element IS3Bli1 and a putative transposase gene; small green bars inside circle 7 denote the positions of possible prophage elements. |
PMC545800_F2_1129.jpg | What is the principal component of this image? | Targeting of GFP-MRP7 and GFP-GSA to peroxisomes in yeast cells. Fluorescence of CB80 yeast cells expressing (a) GFP and DsRed-SKL; (b) GFP-SKL and DsRed-SKL; (c) GFP-MRP7 and DsRed-SKL; or (d) GFP-GSA and DsRed-SKL. Transformed cells were cultured on oleate and observed live for fluorescence. Control experiments (a) show that GFP co-localizes with Ds-Red-SKL only when the sequence -SKL is appended at its extreme carboxyl terminus (b). The figures reveal a punctuate fluorescence pattern for GFP fused to the yeast mitochondrial ribosomal protein L2 encoded by MRP7 (c) or to the bacterial enzyme glutamate-1-semialdehyde 2,1-aminomutase (GSA) (d). Both fusion proteins co-localize with DsRed-SKL in yeast peroxisomes. GFP fused to GSA without its carboxy-terminal -AKL gave rise to a diffuse (cytosolic) fluorescence pattern (data not shown). |
PMC545800_F2_1122.jpg | Describe the main subject of this image. | Targeting of GFP-MRP7 and GFP-GSA to peroxisomes in yeast cells. Fluorescence of CB80 yeast cells expressing (a) GFP and DsRed-SKL; (b) GFP-SKL and DsRed-SKL; (c) GFP-MRP7 and DsRed-SKL; or (d) GFP-GSA and DsRed-SKL. Transformed cells were cultured on oleate and observed live for fluorescence. Control experiments (a) show that GFP co-localizes with Ds-Red-SKL only when the sequence -SKL is appended at its extreme carboxyl terminus (b). The figures reveal a punctuate fluorescence pattern for GFP fused to the yeast mitochondrial ribosomal protein L2 encoded by MRP7 (c) or to the bacterial enzyme glutamate-1-semialdehyde 2,1-aminomutase (GSA) (d). Both fusion proteins co-localize with DsRed-SKL in yeast peroxisomes. GFP fused to GSA without its carboxy-terminal -AKL gave rise to a diffuse (cytosolic) fluorescence pattern (data not shown). |
PMC545800_F2_1123.jpg | What is the core subject represented in this visual? | Targeting of GFP-MRP7 and GFP-GSA to peroxisomes in yeast cells. Fluorescence of CB80 yeast cells expressing (a) GFP and DsRed-SKL; (b) GFP-SKL and DsRed-SKL; (c) GFP-MRP7 and DsRed-SKL; or (d) GFP-GSA and DsRed-SKL. Transformed cells were cultured on oleate and observed live for fluorescence. Control experiments (a) show that GFP co-localizes with Ds-Red-SKL only when the sequence -SKL is appended at its extreme carboxyl terminus (b). The figures reveal a punctuate fluorescence pattern for GFP fused to the yeast mitochondrial ribosomal protein L2 encoded by MRP7 (c) or to the bacterial enzyme glutamate-1-semialdehyde 2,1-aminomutase (GSA) (d). Both fusion proteins co-localize with DsRed-SKL in yeast peroxisomes. GFP fused to GSA without its carboxy-terminal -AKL gave rise to a diffuse (cytosolic) fluorescence pattern (data not shown). |
PMC545800_F2_1125.jpg | What object or scene is depicted here? | Targeting of GFP-MRP7 and GFP-GSA to peroxisomes in yeast cells. Fluorescence of CB80 yeast cells expressing (a) GFP and DsRed-SKL; (b) GFP-SKL and DsRed-SKL; (c) GFP-MRP7 and DsRed-SKL; or (d) GFP-GSA and DsRed-SKL. Transformed cells were cultured on oleate and observed live for fluorescence. Control experiments (a) show that GFP co-localizes with Ds-Red-SKL only when the sequence -SKL is appended at its extreme carboxyl terminus (b). The figures reveal a punctuate fluorescence pattern for GFP fused to the yeast mitochondrial ribosomal protein L2 encoded by MRP7 (c) or to the bacterial enzyme glutamate-1-semialdehyde 2,1-aminomutase (GSA) (d). Both fusion proteins co-localize with DsRed-SKL in yeast peroxisomes. GFP fused to GSA without its carboxy-terminal -AKL gave rise to a diffuse (cytosolic) fluorescence pattern (data not shown). |
PMC545800_F2_1126.jpg | Describe the main subject of this image. | Targeting of GFP-MRP7 and GFP-GSA to peroxisomes in yeast cells. Fluorescence of CB80 yeast cells expressing (a) GFP and DsRed-SKL; (b) GFP-SKL and DsRed-SKL; (c) GFP-MRP7 and DsRed-SKL; or (d) GFP-GSA and DsRed-SKL. Transformed cells were cultured on oleate and observed live for fluorescence. Control experiments (a) show that GFP co-localizes with Ds-Red-SKL only when the sequence -SKL is appended at its extreme carboxyl terminus (b). The figures reveal a punctuate fluorescence pattern for GFP fused to the yeast mitochondrial ribosomal protein L2 encoded by MRP7 (c) or to the bacterial enzyme glutamate-1-semialdehyde 2,1-aminomutase (GSA) (d). Both fusion proteins co-localize with DsRed-SKL in yeast peroxisomes. GFP fused to GSA without its carboxy-terminal -AKL gave rise to a diffuse (cytosolic) fluorescence pattern (data not shown). |
PMC545800_F2_1131.jpg | What is the main focus of this visual representation? | Targeting of GFP-MRP7 and GFP-GSA to peroxisomes in yeast cells. Fluorescence of CB80 yeast cells expressing (a) GFP and DsRed-SKL; (b) GFP-SKL and DsRed-SKL; (c) GFP-MRP7 and DsRed-SKL; or (d) GFP-GSA and DsRed-SKL. Transformed cells were cultured on oleate and observed live for fluorescence. Control experiments (a) show that GFP co-localizes with Ds-Red-SKL only when the sequence -SKL is appended at its extreme carboxyl terminus (b). The figures reveal a punctuate fluorescence pattern for GFP fused to the yeast mitochondrial ribosomal protein L2 encoded by MRP7 (c) or to the bacterial enzyme glutamate-1-semialdehyde 2,1-aminomutase (GSA) (d). Both fusion proteins co-localize with DsRed-SKL in yeast peroxisomes. GFP fused to GSA without its carboxy-terminal -AKL gave rise to a diffuse (cytosolic) fluorescence pattern (data not shown). |
PMC545800_F2_1124.jpg | What can you see in this picture? | Targeting of GFP-MRP7 and GFP-GSA to peroxisomes in yeast cells. Fluorescence of CB80 yeast cells expressing (a) GFP and DsRed-SKL; (b) GFP-SKL and DsRed-SKL; (c) GFP-MRP7 and DsRed-SKL; or (d) GFP-GSA and DsRed-SKL. Transformed cells were cultured on oleate and observed live for fluorescence. Control experiments (a) show that GFP co-localizes with Ds-Red-SKL only when the sequence -SKL is appended at its extreme carboxyl terminus (b). The figures reveal a punctuate fluorescence pattern for GFP fused to the yeast mitochondrial ribosomal protein L2 encoded by MRP7 (c) or to the bacterial enzyme glutamate-1-semialdehyde 2,1-aminomutase (GSA) (d). Both fusion proteins co-localize with DsRed-SKL in yeast peroxisomes. GFP fused to GSA without its carboxy-terminal -AKL gave rise to a diffuse (cytosolic) fluorescence pattern (data not shown). |
PMC545935_F4_1137.jpg | What key item or scene is captured in this photo? | Heparin, but not RAP, competes for DiI-apoE-VLDL uptake by adipocytes. Differentiated adipocytes were cultured on glass coverslips and incubated with DiI-labeled apoE-VLDL (4 μg/ml) in the presence or absence (upper panel) of either heparin (500 μg/ml, middle panel) or RAP-GST (50 μg/ml, lower panel) at 37°C for 3 h. Cells were then fixed and processed for fluorescence microscopy. Left panels, phase contrast image; right panels, rhodamine filter set (550 nm excitation-573 nm emission). Magnification, 630×. |
PMC545935_F4_1136.jpg | What is shown in this image? | Heparin, but not RAP, competes for DiI-apoE-VLDL uptake by adipocytes. Differentiated adipocytes were cultured on glass coverslips and incubated with DiI-labeled apoE-VLDL (4 μg/ml) in the presence or absence (upper panel) of either heparin (500 μg/ml, middle panel) or RAP-GST (50 μg/ml, lower panel) at 37°C for 3 h. Cells were then fixed and processed for fluorescence microscopy. Left panels, phase contrast image; right panels, rhodamine filter set (550 nm excitation-573 nm emission). Magnification, 630×. |
PMC545935_F4_1133.jpg | What is the dominant medical problem in this image? | Heparin, but not RAP, competes for DiI-apoE-VLDL uptake by adipocytes. Differentiated adipocytes were cultured on glass coverslips and incubated with DiI-labeled apoE-VLDL (4 μg/ml) in the presence or absence (upper panel) of either heparin (500 μg/ml, middle panel) or RAP-GST (50 μg/ml, lower panel) at 37°C for 3 h. Cells were then fixed and processed for fluorescence microscopy. Left panels, phase contrast image; right panels, rhodamine filter set (550 nm excitation-573 nm emission). Magnification, 630×. |
PMC545935_F4_1132.jpg | What stands out most in this visual? | Heparin, but not RAP, competes for DiI-apoE-VLDL uptake by adipocytes. Differentiated adipocytes were cultured on glass coverslips and incubated with DiI-labeled apoE-VLDL (4 μg/ml) in the presence or absence (upper panel) of either heparin (500 μg/ml, middle panel) or RAP-GST (50 μg/ml, lower panel) at 37°C for 3 h. Cells were then fixed and processed for fluorescence microscopy. Left panels, phase contrast image; right panels, rhodamine filter set (550 nm excitation-573 nm emission). Magnification, 630×. |
PMC545935_F4_1135.jpg | What stands out most in this visual? | Heparin, but not RAP, competes for DiI-apoE-VLDL uptake by adipocytes. Differentiated adipocytes were cultured on glass coverslips and incubated with DiI-labeled apoE-VLDL (4 μg/ml) in the presence or absence (upper panel) of either heparin (500 μg/ml, middle panel) or RAP-GST (50 μg/ml, lower panel) at 37°C for 3 h. Cells were then fixed and processed for fluorescence microscopy. Left panels, phase contrast image; right panels, rhodamine filter set (550 nm excitation-573 nm emission). Magnification, 630×. |
PMC545950_F1_1139.jpg | What is the dominant medical problem in this image? | Phase-contrast photomicrographs of fragile X progenitor cells The figure shows clusters/spheres during the initial stages (2–3 days after plating) of adherence to a fibronectin substrate. (A) 4×; (B) 10×; (C) 20×. Confluent serum- and growth factor-expanded cultures were serum deprived for one week in the presence of growth factors, then lifted with enzyme-free buffers and transferred to new plates with no fibronectin substrate. After growing the resulting clusters/spheres for two weeks, the clusters/spheres were transferred to new fibronectin-coated plates. Clusters/spheres (black arrows) are abundant and are seen adhering to the substrate. Cells (black arrowheads) can be seen streaming from the spheres and spreading out on the substrate. |
PMC545950_F1_1138.jpg | What is the principal component of this image? | Phase-contrast photomicrographs of fragile X progenitor cells The figure shows clusters/spheres during the initial stages (2–3 days after plating) of adherence to a fibronectin substrate. (A) 4×; (B) 10×; (C) 20×. Confluent serum- and growth factor-expanded cultures were serum deprived for one week in the presence of growth factors, then lifted with enzyme-free buffers and transferred to new plates with no fibronectin substrate. After growing the resulting clusters/spheres for two weeks, the clusters/spheres were transferred to new fibronectin-coated plates. Clusters/spheres (black arrows) are abundant and are seen adhering to the substrate. Cells (black arrowheads) can be seen streaming from the spheres and spreading out on the substrate. |
PMC546198_F1_1149.jpg | What's the most prominent thing you notice in this picture? | A Plain radiograph of the right shoulder, showing an irregular, mixed lytic and sclerotic lesion in the glenoid (arrow), that was not appreciated by the reporting radiologist. B Arthrogram performed prior to hydrodilatation. C Coronal TSE post-contrast MR image, showing a diffusely enhansive scapular lesion extending into the inferior aspect of the gleno-humeral joint. D Axial TSE post-contrast MR image showing diffuse enhancement of the tumour extending on either side of the scapular blade with bony destruction. E Bone scan showing increased uptake in the area of the lesion on the delayed static image. F Thallium functional scanning showing retained thallium activity in the glenoid region at 4 hrs. Subsequent biopsy was consistent with Ewing's sarcoma. |
PMC546198_F1_1151.jpg | What key item or scene is captured in this photo? | A Plain radiograph of the right shoulder, showing an irregular, mixed lytic and sclerotic lesion in the glenoid (arrow), that was not appreciated by the reporting radiologist. B Arthrogram performed prior to hydrodilatation. C Coronal TSE post-contrast MR image, showing a diffusely enhansive scapular lesion extending into the inferior aspect of the gleno-humeral joint. D Axial TSE post-contrast MR image showing diffuse enhancement of the tumour extending on either side of the scapular blade with bony destruction. E Bone scan showing increased uptake in the area of the lesion on the delayed static image. F Thallium functional scanning showing retained thallium activity in the glenoid region at 4 hrs. Subsequent biopsy was consistent with Ewing's sarcoma. |
PMC546198_F1_1150.jpg | What stands out most in this visual? | A Plain radiograph of the right shoulder, showing an irregular, mixed lytic and sclerotic lesion in the glenoid (arrow), that was not appreciated by the reporting radiologist. B Arthrogram performed prior to hydrodilatation. C Coronal TSE post-contrast MR image, showing a diffusely enhansive scapular lesion extending into the inferior aspect of the gleno-humeral joint. D Axial TSE post-contrast MR image showing diffuse enhancement of the tumour extending on either side of the scapular blade with bony destruction. E Bone scan showing increased uptake in the area of the lesion on the delayed static image. F Thallium functional scanning showing retained thallium activity in the glenoid region at 4 hrs. Subsequent biopsy was consistent with Ewing's sarcoma. |
PMC546198_F2_1165.jpg | What can you see in this picture? | A Plain radiograph of the left shoulder showing a lytic lesion affecting the proximal humerus, with cortical irregularity medially (arrow), that was not initially recognized. B At the time of arthrographic distension, the lesion (arrow) was more apparent, but remained unnoticed. C Sagittal TSE post-contrast MR image showing an enhancing lesion within the proximal humerus extending outside the bone. D Axial TSE post-contrast MR image showing the tumour destroying the humeral head and extending into the gleno-humeral articulation. E Bone scan showing increased uptake in the area of the lesion on the delayed static image. F Thallium functional scanning showing retained thallium activity in the proximal humerus at 4 hrs. Histological sections from the biopsy and surgical resection specimen were consistent with a malignant fibrous histiocytoma. |
PMC546198_F2_1166.jpg | What can you see in this picture? | A Plain radiograph of the left shoulder showing a lytic lesion affecting the proximal humerus, with cortical irregularity medially (arrow), that was not initially recognized. B At the time of arthrographic distension, the lesion (arrow) was more apparent, but remained unnoticed. C Sagittal TSE post-contrast MR image showing an enhancing lesion within the proximal humerus extending outside the bone. D Axial TSE post-contrast MR image showing the tumour destroying the humeral head and extending into the gleno-humeral articulation. E Bone scan showing increased uptake in the area of the lesion on the delayed static image. F Thallium functional scanning showing retained thallium activity in the proximal humerus at 4 hrs. Histological sections from the biopsy and surgical resection specimen were consistent with a malignant fibrous histiocytoma. |
PMC546198_F2_1162.jpg | What key item or scene is captured in this photo? | A Plain radiograph of the left shoulder showing a lytic lesion affecting the proximal humerus, with cortical irregularity medially (arrow), that was not initially recognized. B At the time of arthrographic distension, the lesion (arrow) was more apparent, but remained unnoticed. C Sagittal TSE post-contrast MR image showing an enhancing lesion within the proximal humerus extending outside the bone. D Axial TSE post-contrast MR image showing the tumour destroying the humeral head and extending into the gleno-humeral articulation. E Bone scan showing increased uptake in the area of the lesion on the delayed static image. F Thallium functional scanning showing retained thallium activity in the proximal humerus at 4 hrs. Histological sections from the biopsy and surgical resection specimen were consistent with a malignant fibrous histiocytoma. |
PMC546198_F3_1158.jpg | Describe the main subject of this image. | A Initial plain radiographs of the shoulder were unremarkable. B Repeat radiographs after two years of failed treatment, showing an irregular mixed lytic and sclerotic lesion destroying the coracoid process of the scapula (arrow), which was not appreciated. C Arthrogram performed prior to hydrodilatation similarly showing the destructive process, which remained unnoticed. D Axial T1-weighted post-contrast MR image showing a heterogenous contrast-enhancing lesion destroying the glenoid and extending into the gleno-humeral joint. The lesion is lobulated and loculated with central areas of lower signal intensity, suggestive of a chondroid lesion. E Bone scan showing increased uptake in the area of the lesion on the delayed static image. F Thallium functional scanning showing no retention of thallium by the lesion at 4 hrs. Biopsy confirmed low-grade chondrosarcoma. |
PMC546198_F3_1155.jpg | What stands out most in this visual? | A Initial plain radiographs of the shoulder were unremarkable. B Repeat radiographs after two years of failed treatment, showing an irregular mixed lytic and sclerotic lesion destroying the coracoid process of the scapula (arrow), which was not appreciated. C Arthrogram performed prior to hydrodilatation similarly showing the destructive process, which remained unnoticed. D Axial T1-weighted post-contrast MR image showing a heterogenous contrast-enhancing lesion destroying the glenoid and extending into the gleno-humeral joint. The lesion is lobulated and loculated with central areas of lower signal intensity, suggestive of a chondroid lesion. E Bone scan showing increased uptake in the area of the lesion on the delayed static image. F Thallium functional scanning showing no retention of thallium by the lesion at 4 hrs. Biopsy confirmed low-grade chondrosarcoma. |
PMC546198_F3_1160.jpg | Describe the main subject of this image. | A Initial plain radiographs of the shoulder were unremarkable. B Repeat radiographs after two years of failed treatment, showing an irregular mixed lytic and sclerotic lesion destroying the coracoid process of the scapula (arrow), which was not appreciated. C Arthrogram performed prior to hydrodilatation similarly showing the destructive process, which remained unnoticed. D Axial T1-weighted post-contrast MR image showing a heterogenous contrast-enhancing lesion destroying the glenoid and extending into the gleno-humeral joint. The lesion is lobulated and loculated with central areas of lower signal intensity, suggestive of a chondroid lesion. E Bone scan showing increased uptake in the area of the lesion on the delayed static image. F Thallium functional scanning showing no retention of thallium by the lesion at 4 hrs. Biopsy confirmed low-grade chondrosarcoma. |
PMC546198_F3_1156.jpg | Can you identify the primary element in this image? | A Initial plain radiographs of the shoulder were unremarkable. B Repeat radiographs after two years of failed treatment, showing an irregular mixed lytic and sclerotic lesion destroying the coracoid process of the scapula (arrow), which was not appreciated. C Arthrogram performed prior to hydrodilatation similarly showing the destructive process, which remained unnoticed. D Axial T1-weighted post-contrast MR image showing a heterogenous contrast-enhancing lesion destroying the glenoid and extending into the gleno-humeral joint. The lesion is lobulated and loculated with central areas of lower signal intensity, suggestive of a chondroid lesion. E Bone scan showing increased uptake in the area of the lesion on the delayed static image. F Thallium functional scanning showing no retention of thallium by the lesion at 4 hrs. Biopsy confirmed low-grade chondrosarcoma. |
PMC546198_F4_1141.jpg | What's the most prominent thing you notice in this picture? | Patient had persistent pain and stiffness following hydrodilatation. A Plain shoulder radiographs were normal. B STIR MR image showing multiple high signal intensity lesions in the supraspinatus muscle. A presumptive diagnosis of metastatic squamous cell carcinoma was made. |
PMC546198_F4_1142.jpg | What is the focal point of this photograph? | Patient had persistent pain and stiffness following hydrodilatation. A Plain shoulder radiographs were normal. B STIR MR image showing multiple high signal intensity lesions in the supraspinatus muscle. A presumptive diagnosis of metastatic squamous cell carcinoma was made. |
PMC546198_F5_1144.jpg | What is being portrayed in this visual content? | A Initial plain radiographs of the right shoulder appeared normal. B CT scan was performed after a year of progressive shoulder pain and stiffness, showing a destructive lesion involving the glenoid (arrow). C Axial T1-weighted and post-contrast (D) MR images showing destruction of the glenoid with an associated soft tissue mass and involvement of the humeral head. E Bone scan showing increased osteoblastic activity involving the coracoid process and right humeral head and relative photopaenia of the glenoid. F CT-guided percutaneous biopsy was able to obtain a histological diagnosis of malignant fibrous histiocytoma. |
PMC546198_F5_1146.jpg | What is the main focus of this visual representation? | A Initial plain radiographs of the right shoulder appeared normal. B CT scan was performed after a year of progressive shoulder pain and stiffness, showing a destructive lesion involving the glenoid (arrow). C Axial T1-weighted and post-contrast (D) MR images showing destruction of the glenoid with an associated soft tissue mass and involvement of the humeral head. E Bone scan showing increased osteoblastic activity involving the coracoid process and right humeral head and relative photopaenia of the glenoid. F CT-guided percutaneous biopsy was able to obtain a histological diagnosis of malignant fibrous histiocytoma. |
PMC546198_F5_1143.jpg | What stands out most in this visual? | A Initial plain radiographs of the right shoulder appeared normal. B CT scan was performed after a year of progressive shoulder pain and stiffness, showing a destructive lesion involving the glenoid (arrow). C Axial T1-weighted and post-contrast (D) MR images showing destruction of the glenoid with an associated soft tissue mass and involvement of the humeral head. E Bone scan showing increased osteoblastic activity involving the coracoid process and right humeral head and relative photopaenia of the glenoid. F CT-guided percutaneous biopsy was able to obtain a histological diagnosis of malignant fibrous histiocytoma. |
PMC546198_F5_1147.jpg | What is the central feature of this picture? | A Initial plain radiographs of the right shoulder appeared normal. B CT scan was performed after a year of progressive shoulder pain and stiffness, showing a destructive lesion involving the glenoid (arrow). C Axial T1-weighted and post-contrast (D) MR images showing destruction of the glenoid with an associated soft tissue mass and involvement of the humeral head. E Bone scan showing increased osteoblastic activity involving the coracoid process and right humeral head and relative photopaenia of the glenoid. F CT-guided percutaneous biopsy was able to obtain a histological diagnosis of malignant fibrous histiocytoma. |
PMC546198_F5_1145.jpg | What's the most prominent thing you notice in this picture? | A Initial plain radiographs of the right shoulder appeared normal. B CT scan was performed after a year of progressive shoulder pain and stiffness, showing a destructive lesion involving the glenoid (arrow). C Axial T1-weighted and post-contrast (D) MR images showing destruction of the glenoid with an associated soft tissue mass and involvement of the humeral head. E Bone scan showing increased osteoblastic activity involving the coracoid process and right humeral head and relative photopaenia of the glenoid. F CT-guided percutaneous biopsy was able to obtain a histological diagnosis of malignant fibrous histiocytoma. |
PMC546200_F1_1170.jpg | Describe the main subject of this image. | Scanning electron micrograph survey of pumice granules and biofilm development. Before colonisation (A) pumice granules are blank. After 6 month of operation (B), rod shaped cells cover the pumice surface. In the 12 month biofilm, an abundant exopolymeric matrix is visible on pumice granules both at the bottom (C) and top (D) of the column. |
PMC546200_F1_1168.jpg | What's the most prominent thing you notice in this picture? | Scanning electron micrograph survey of pumice granules and biofilm development. Before colonisation (A) pumice granules are blank. After 6 month of operation (B), rod shaped cells cover the pumice surface. In the 12 month biofilm, an abundant exopolymeric matrix is visible on pumice granules both at the bottom (C) and top (D) of the column. |
PMC546208_F4_1173.jpg | What is shown in this image? | Scrib is not localized in focal adhesions in CV-1 cells, and is dispensable for targeting LPP to these structures. Upper panels: CV-1 cells, grown on glass coverslips, were double labelled with Scrib-472 antibodies (left panel) and anti-vinculin antibodies (right panel) used as a marker for focal adhesions. Lower panels: CV-1 cells were transiently transfected with wild-type human LPP (left panel), or LPP with a mutated carboxy-terminus (T610A) (right panel), as GFP-fusions. GFP-fluorescence was visualized by epifluorescence microscopy. |
PMC546208_F4_1174.jpg | What key item or scene is captured in this photo? | Scrib is not localized in focal adhesions in CV-1 cells, and is dispensable for targeting LPP to these structures. Upper panels: CV-1 cells, grown on glass coverslips, were double labelled with Scrib-472 antibodies (left panel) and anti-vinculin antibodies (right panel) used as a marker for focal adhesions. Lower panels: CV-1 cells were transiently transfected with wild-type human LPP (left panel), or LPP with a mutated carboxy-terminus (T610A) (right panel), as GFP-fusions. GFP-fluorescence was visualized by epifluorescence microscopy. |
PMC546208_F4_1171.jpg | What is being portrayed in this visual content? | Scrib is not localized in focal adhesions in CV-1 cells, and is dispensable for targeting LPP to these structures. Upper panels: CV-1 cells, grown on glass coverslips, were double labelled with Scrib-472 antibodies (left panel) and anti-vinculin antibodies (right panel) used as a marker for focal adhesions. Lower panels: CV-1 cells were transiently transfected with wild-type human LPP (left panel), or LPP with a mutated carboxy-terminus (T610A) (right panel), as GFP-fusions. GFP-fluorescence was visualized by epifluorescence microscopy. |
PMC546208_F4_1172.jpg | What is the core subject represented in this visual? | Scrib is not localized in focal adhesions in CV-1 cells, and is dispensable for targeting LPP to these structures. Upper panels: CV-1 cells, grown on glass coverslips, were double labelled with Scrib-472 antibodies (left panel) and anti-vinculin antibodies (right panel) used as a marker for focal adhesions. Lower panels: CV-1 cells were transiently transfected with wild-type human LPP (left panel), or LPP with a mutated carboxy-terminus (T610A) (right panel), as GFP-fusions. GFP-fluorescence was visualized by epifluorescence microscopy. |
PMC546208_F5_1175.jpg | What stands out most in this visual? | Scrib and LPP are localized in cell-cell contacts but are dispensable for targeting each other to these structures. Upper panels: MDCKII cells, grown on glass coverslips, were double labelled with anti-LPP antibodies (left panel) and anti-Scrib antibodies (right panel). Lower panels: MDCKII stable cell lines, expressing GFP-fusion proteins containing wild-type human LPP (upper left panel), LPP with a mutated carboxy-terminus (T610A) (upper right panel), human wild-type Scrib (lower left panel), or Scrib with a deletion of all its PDZ domains (lower right panel), were grown on glass coverslips (Scrib) or on Transwell-Clear polyester membranes (LPP). GFP-fluorescence was visualized by epifluorescence microscopy (Scrib) or by confocal microscopy (LPP). |
PMC546208_F5_1176.jpg | What key item or scene is captured in this photo? | Scrib and LPP are localized in cell-cell contacts but are dispensable for targeting each other to these structures. Upper panels: MDCKII cells, grown on glass coverslips, were double labelled with anti-LPP antibodies (left panel) and anti-Scrib antibodies (right panel). Lower panels: MDCKII stable cell lines, expressing GFP-fusion proteins containing wild-type human LPP (upper left panel), LPP with a mutated carboxy-terminus (T610A) (upper right panel), human wild-type Scrib (lower left panel), or Scrib with a deletion of all its PDZ domains (lower right panel), were grown on glass coverslips (Scrib) or on Transwell-Clear polyester membranes (LPP). GFP-fluorescence was visualized by epifluorescence microscopy (Scrib) or by confocal microscopy (LPP). |
PMC546208_F5_1178.jpg | What is being portrayed in this visual content? | Scrib and LPP are localized in cell-cell contacts but are dispensable for targeting each other to these structures. Upper panels: MDCKII cells, grown on glass coverslips, were double labelled with anti-LPP antibodies (left panel) and anti-Scrib antibodies (right panel). Lower panels: MDCKII stable cell lines, expressing GFP-fusion proteins containing wild-type human LPP (upper left panel), LPP with a mutated carboxy-terminus (T610A) (upper right panel), human wild-type Scrib (lower left panel), or Scrib with a deletion of all its PDZ domains (lower right panel), were grown on glass coverslips (Scrib) or on Transwell-Clear polyester membranes (LPP). GFP-fluorescence was visualized by epifluorescence microscopy (Scrib) or by confocal microscopy (LPP). |
PMC546208_F5_1179.jpg | Describe the main subject of this image. | Scrib and LPP are localized in cell-cell contacts but are dispensable for targeting each other to these structures. Upper panels: MDCKII cells, grown on glass coverslips, were double labelled with anti-LPP antibodies (left panel) and anti-Scrib antibodies (right panel). Lower panels: MDCKII stable cell lines, expressing GFP-fusion proteins containing wild-type human LPP (upper left panel), LPP with a mutated carboxy-terminus (T610A) (upper right panel), human wild-type Scrib (lower left panel), or Scrib with a deletion of all its PDZ domains (lower right panel), were grown on glass coverslips (Scrib) or on Transwell-Clear polyester membranes (LPP). GFP-fluorescence was visualized by epifluorescence microscopy (Scrib) or by confocal microscopy (LPP). |
PMC546208_F5_1177.jpg | Can you identify the primary element in this image? | Scrib and LPP are localized in cell-cell contacts but are dispensable for targeting each other to these structures. Upper panels: MDCKII cells, grown on glass coverslips, were double labelled with anti-LPP antibodies (left panel) and anti-Scrib antibodies (right panel). Lower panels: MDCKII stable cell lines, expressing GFP-fusion proteins containing wild-type human LPP (upper left panel), LPP with a mutated carboxy-terminus (T610A) (upper right panel), human wild-type Scrib (lower left panel), or Scrib with a deletion of all its PDZ domains (lower right panel), were grown on glass coverslips (Scrib) or on Transwell-Clear polyester membranes (LPP). GFP-fluorescence was visualized by epifluorescence microscopy (Scrib) or by confocal microscopy (LPP). |
PMC546208_F5_1180.jpg | What can you see in this picture? | Scrib and LPP are localized in cell-cell contacts but are dispensable for targeting each other to these structures. Upper panels: MDCKII cells, grown on glass coverslips, were double labelled with anti-LPP antibodies (left panel) and anti-Scrib antibodies (right panel). Lower panels: MDCKII stable cell lines, expressing GFP-fusion proteins containing wild-type human LPP (upper left panel), LPP with a mutated carboxy-terminus (T610A) (upper right panel), human wild-type Scrib (lower left panel), or Scrib with a deletion of all its PDZ domains (lower right panel), were grown on glass coverslips (Scrib) or on Transwell-Clear polyester membranes (LPP). GFP-fluorescence was visualized by epifluorescence microscopy (Scrib) or by confocal microscopy (LPP). |
PMC546210_F7_1185.jpg | What is the main focus of this visual representation? | Immunocytochemistry of isolated mouse ventricular myocytes demonstrating the subcellular localization of Kir6.1, Kir6.2, SUR1 and SUR2 subunits. A: Double staining of a ventricular myocyte with the CAF-1 anti-Kir6.1 antibody (A1) and 76A anti-Kir6.2 antibody (A2). Panel A3 is an overlay of panels A1 and A2. Secondary antibodies used were Cy-3 conjugated donkey anti-chicken IgY (red) and Cy-2 conjugated donkey anti-rabbit IgG (green). Yellow in panel C demonstrates areas of co-localization. The image width is 91 μm. B: Ventricular myocyte probed with anti-SUR1 antibodies and detected with Cy-3 conjugated donkey anti goat secondary antibodies. Image width is 148 μm. C: Staining with a pan-SUR2 antibody (detected with Cy-2 conjugated donkey anti-goat IgG). The image width is 229 μm. D: An isolated myocyte was stained with MitoTracker Red (500 nM) before being paraformaldehyde fixed and viewed with confocal microscopy Image width is 47 μm. |
PMC546210_F7_1184.jpg | What is the dominant medical problem in this image? | Immunocytochemistry of isolated mouse ventricular myocytes demonstrating the subcellular localization of Kir6.1, Kir6.2, SUR1 and SUR2 subunits. A: Double staining of a ventricular myocyte with the CAF-1 anti-Kir6.1 antibody (A1) and 76A anti-Kir6.2 antibody (A2). Panel A3 is an overlay of panels A1 and A2. Secondary antibodies used were Cy-3 conjugated donkey anti-chicken IgY (red) and Cy-2 conjugated donkey anti-rabbit IgG (green). Yellow in panel C demonstrates areas of co-localization. The image width is 91 μm. B: Ventricular myocyte probed with anti-SUR1 antibodies and detected with Cy-3 conjugated donkey anti goat secondary antibodies. Image width is 148 μm. C: Staining with a pan-SUR2 antibody (detected with Cy-2 conjugated donkey anti-goat IgG). The image width is 229 μm. D: An isolated myocyte was stained with MitoTracker Red (500 nM) before being paraformaldehyde fixed and viewed with confocal microscopy Image width is 47 μm. |
PMC546210_F7_1182.jpg | What is the focal point of this photograph? | Immunocytochemistry of isolated mouse ventricular myocytes demonstrating the subcellular localization of Kir6.1, Kir6.2, SUR1 and SUR2 subunits. A: Double staining of a ventricular myocyte with the CAF-1 anti-Kir6.1 antibody (A1) and 76A anti-Kir6.2 antibody (A2). Panel A3 is an overlay of panels A1 and A2. Secondary antibodies used were Cy-3 conjugated donkey anti-chicken IgY (red) and Cy-2 conjugated donkey anti-rabbit IgG (green). Yellow in panel C demonstrates areas of co-localization. The image width is 91 μm. B: Ventricular myocyte probed with anti-SUR1 antibodies and detected with Cy-3 conjugated donkey anti goat secondary antibodies. Image width is 148 μm. C: Staining with a pan-SUR2 antibody (detected with Cy-2 conjugated donkey anti-goat IgG). The image width is 229 μm. D: An isolated myocyte was stained with MitoTracker Red (500 nM) before being paraformaldehyde fixed and viewed with confocal microscopy Image width is 47 μm. |
PMC546210_F7_1186.jpg | What's the most prominent thing you notice in this picture? | Immunocytochemistry of isolated mouse ventricular myocytes demonstrating the subcellular localization of Kir6.1, Kir6.2, SUR1 and SUR2 subunits. A: Double staining of a ventricular myocyte with the CAF-1 anti-Kir6.1 antibody (A1) and 76A anti-Kir6.2 antibody (A2). Panel A3 is an overlay of panels A1 and A2. Secondary antibodies used were Cy-3 conjugated donkey anti-chicken IgY (red) and Cy-2 conjugated donkey anti-rabbit IgG (green). Yellow in panel C demonstrates areas of co-localization. The image width is 91 μm. B: Ventricular myocyte probed with anti-SUR1 antibodies and detected with Cy-3 conjugated donkey anti goat secondary antibodies. Image width is 148 μm. C: Staining with a pan-SUR2 antibody (detected with Cy-2 conjugated donkey anti-goat IgG). The image width is 229 μm. D: An isolated myocyte was stained with MitoTracker Red (500 nM) before being paraformaldehyde fixed and viewed with confocal microscopy Image width is 47 μm. |
PMC546210_F7_1181.jpg | Describe the main subject of this image. | Immunocytochemistry of isolated mouse ventricular myocytes demonstrating the subcellular localization of Kir6.1, Kir6.2, SUR1 and SUR2 subunits. A: Double staining of a ventricular myocyte with the CAF-1 anti-Kir6.1 antibody (A1) and 76A anti-Kir6.2 antibody (A2). Panel A3 is an overlay of panels A1 and A2. Secondary antibodies used were Cy-3 conjugated donkey anti-chicken IgY (red) and Cy-2 conjugated donkey anti-rabbit IgG (green). Yellow in panel C demonstrates areas of co-localization. The image width is 91 μm. B: Ventricular myocyte probed with anti-SUR1 antibodies and detected with Cy-3 conjugated donkey anti goat secondary antibodies. Image width is 148 μm. C: Staining with a pan-SUR2 antibody (detected with Cy-2 conjugated donkey anti-goat IgG). The image width is 229 μm. D: An isolated myocyte was stained with MitoTracker Red (500 nM) before being paraformaldehyde fixed and viewed with confocal microscopy Image width is 47 μm. |
PMC546210_F7_1183.jpg | What object or scene is depicted here? | Immunocytochemistry of isolated mouse ventricular myocytes demonstrating the subcellular localization of Kir6.1, Kir6.2, SUR1 and SUR2 subunits. A: Double staining of a ventricular myocyte with the CAF-1 anti-Kir6.1 antibody (A1) and 76A anti-Kir6.2 antibody (A2). Panel A3 is an overlay of panels A1 and A2. Secondary antibodies used were Cy-3 conjugated donkey anti-chicken IgY (red) and Cy-2 conjugated donkey anti-rabbit IgG (green). Yellow in panel C demonstrates areas of co-localization. The image width is 91 μm. B: Ventricular myocyte probed with anti-SUR1 antibodies and detected with Cy-3 conjugated donkey anti goat secondary antibodies. Image width is 148 μm. C: Staining with a pan-SUR2 antibody (detected with Cy-2 conjugated donkey anti-goat IgG). The image width is 229 μm. D: An isolated myocyte was stained with MitoTracker Red (500 nM) before being paraformaldehyde fixed and viewed with confocal microscopy Image width is 47 μm. |
PMC546218_F1_1187.jpg | What is the dominant medical problem in this image? | Immunohistochemical studies of ILK in non-neoplastic pulmonary tissue and in NSCLC tissue. a non-neoplastic pulmonary tissue: ILK was not detected in epithelial cells, while ILK expression was found in many stromal cells. |
PMC546218_F2_1188.jpg | Describe the main subject of this image. | well differentiated adenocarcinoma: ILK protein was localized in both cytoplasms and nuclei. (Magnification, ×40 (Figure 1), ×16 (Figure 2), and ×40 (Figure 3)). |
PMC546218_F3_1189.jpg | What is shown in this image? | well differentiated adenocarcinoma: ILK protein was localized in both cytoplasms and nuclei. (Magnification, ×40 (Figure 1), ×16 (Figure 2), and ×40 (Figure 3)). |
PMC546218_F3_1190.jpg | What is being portrayed in this visual content? | well differentiated adenocarcinoma: ILK protein was localized in both cytoplasms and nuclei. (Magnification, ×40 (Figure 1), ×16 (Figure 2), and ×40 (Figure 3)). |
PMC546237_F1_1191.jpg | Describe the main subject of this image. | CT scan image showing the hepatic metastasis in segment VII. |
PMC546237_F2_1192.jpg | What's the most prominent thing you notice in this picture? | CT scan image showing the omental mass adjacent to bowel loop (circle around the omental mass). |
PMC546405_F4_1196.jpg | What's the most prominent thing you notice in this picture? | NaK2Cl cotransporter expression in human CP: Lateral ventricle plexuses were incubated with T4 (not thyroxine) antibody, which stains the secretory isoform 1 of the NaK2Cl (NKCC1) cotransporter protein. The T4 antibody (mouse monoclonal; 1:100) was from the University of Iowa Developmental Studies Hybridoma Bank (Iowa City, IA); the biotinylated secondary was a rat-absorbed horse antibody. Diaminobenzidine was used to develop the brown reaction product. Controls (negative staining results; not shown) involved omission of secondary and/or primary antibody. AD tissues were from patients at Braak stage V/VI (top right) and III/IV (bottom right). Images are representative of 6 CPs analyzed for AD (mean age of 76 yr) and 6 for age-matched controls (mean age of 76 yr). On average, the staining intensity of AD specimens was 50% greater than controls. The text describes staining localization. All photographs are at the same magnification. |
PMC546405_F4_1193.jpg | Can you identify the primary element in this image? | NaK2Cl cotransporter expression in human CP: Lateral ventricle plexuses were incubated with T4 (not thyroxine) antibody, which stains the secretory isoform 1 of the NaK2Cl (NKCC1) cotransporter protein. The T4 antibody (mouse monoclonal; 1:100) was from the University of Iowa Developmental Studies Hybridoma Bank (Iowa City, IA); the biotinylated secondary was a rat-absorbed horse antibody. Diaminobenzidine was used to develop the brown reaction product. Controls (negative staining results; not shown) involved omission of secondary and/or primary antibody. AD tissues were from patients at Braak stage V/VI (top right) and III/IV (bottom right). Images are representative of 6 CPs analyzed for AD (mean age of 76 yr) and 6 for age-matched controls (mean age of 76 yr). On average, the staining intensity of AD specimens was 50% greater than controls. The text describes staining localization. All photographs are at the same magnification. |
PMC546405_F4_1194.jpg | What stands out most in this visual? | NaK2Cl cotransporter expression in human CP: Lateral ventricle plexuses were incubated with T4 (not thyroxine) antibody, which stains the secretory isoform 1 of the NaK2Cl (NKCC1) cotransporter protein. The T4 antibody (mouse monoclonal; 1:100) was from the University of Iowa Developmental Studies Hybridoma Bank (Iowa City, IA); the biotinylated secondary was a rat-absorbed horse antibody. Diaminobenzidine was used to develop the brown reaction product. Controls (negative staining results; not shown) involved omission of secondary and/or primary antibody. AD tissues were from patients at Braak stage V/VI (top right) and III/IV (bottom right). Images are representative of 6 CPs analyzed for AD (mean age of 76 yr) and 6 for age-matched controls (mean age of 76 yr). On average, the staining intensity of AD specimens was 50% greater than controls. The text describes staining localization. All photographs are at the same magnification. |
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