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PMC1635561_F5_7647.jpg | What is shown in this image? | Two-color fluorescence detection of actin (red) and PRRSV antigen (green) in MARC-145 cells. A. Uninfected control, 20 μm; B.18 h p.i. with PRRSV, 20 μm; C. Control at 42 h p.i. with PRRSV, 50 μm; D. Drug vehicle control at 42 h p.i. with PRRSV, 50 μm. E. Colchicine-treated, 5 μM, 42 h p.i. (arrow indicates PRRSV-positive doublet; see Figure 6, A, C and D for higher magnification), 50 μm; F. AK-2 treated, 250 μm; (Length of scale bar is indicated for each panel) |
PMC1635696_F2_7650.jpg | What is the focal point of this photograph? | Transgene sites in 3D interphase nuclei of wheat (A), rice (B) and tobacco (C) root tissue sections. The wheat line (A) is homozygous and carries two transgene copies per homologue at a single site in the metaphase chromosome [2], each homologue is indicated by arrows. The rice line (B) was labeled with the plasmids SCM11, K1, H28, J1 [64], which were all co-bombarded. The tobacco line (C) contains 7 copies of the GUS gene and is a double haploid [63]. Confocal image stacks were recorded with a section spacing of 1 μm and a projection of two confocal sections is shown. Hybridization signals are indicated by arrows and show two single dots one for each homologue. Each dot can include multiple copies of the transgene. Bars, 10 μm. |
PMC1635696_F2_7649.jpg | Can you identify the primary element in this image? | Transgene sites in 3D interphase nuclei of wheat (A), rice (B) and tobacco (C) root tissue sections. The wheat line (A) is homozygous and carries two transgene copies per homologue at a single site in the metaphase chromosome [2], each homologue is indicated by arrows. The rice line (B) was labeled with the plasmids SCM11, K1, H28, J1 [64], which were all co-bombarded. The tobacco line (C) contains 7 copies of the GUS gene and is a double haploid [63]. Confocal image stacks were recorded with a section spacing of 1 μm and a projection of two confocal sections is shown. Hybridization signals are indicated by arrows and show two single dots one for each homologue. Each dot can include multiple copies of the transgene. Bars, 10 μm. |
PMC1635696_F3_7655.jpg | What is the dominant medical problem in this image? | Transgene sites visualized in tobacco isolated nuclei. In panels A and B a single nucleus is shown, stained with DAPI (3A), and labeled by FISH (3B). This nucleus originates from a double haploid tobacco transgenic plant line that contains 7 copies of the GUS gene [63]; two signals, each corresponding to a homologous chromosome, are clearly visible (arrows). In panels C and D two isolated nuclei from independent NT1 tobacco suspension cell lines expressing luciferase are shown [65]. Panel C demonstrates the detection of a single copy luciferase gene using a luc fragment probe. Panel D shows a nucleus with multiple insertions in a total of 48 transgene copies. Bar, 10 μm. |
PMC1635696_F3_7654.jpg | What's the most prominent thing you notice in this picture? | Transgene sites visualized in tobacco isolated nuclei. In panels A and B a single nucleus is shown, stained with DAPI (3A), and labeled by FISH (3B). This nucleus originates from a double haploid tobacco transgenic plant line that contains 7 copies of the GUS gene [63]; two signals, each corresponding to a homologous chromosome, are clearly visible (arrows). In panels C and D two isolated nuclei from independent NT1 tobacco suspension cell lines expressing luciferase are shown [65]. Panel C demonstrates the detection of a single copy luciferase gene using a luc fragment probe. Panel D shows a nucleus with multiple insertions in a total of 48 transgene copies. Bar, 10 μm. |
PMC1635715_F2_7656.jpg | What is the central feature of this picture? | The prostate model. From the Visible Human Project®, a photographic image of a prostate slice shows a transverse (axial, yz-plane) cross section of the prostate gland. |
PMC1635716_F2_7659.jpg | What is the central feature of this picture? | Segmentation results. From left to right: (a) 3D MR angiogram of the TAA of Patient A; (b) aneurysm shape from the segmentation of the image set A1 (wall contours cW in blue and lumen contours cLH in red); (c) lumen of the aneurysm from the segmentation of image set A2 (lumen contours cLM in magenta) (Units in mm). |
PMC1635716_F5_7658.jpg | What does this image primarily show? | Wall thickness retrieval. Example of the wall thickness measurement (Patient B). |
PMC1635716_F5_7657.jpg | What is the focal point of this photograph? | Wall thickness retrieval. Example of the wall thickness measurement (Patient B). |
PMC1635722_F1_7662.jpg | What is the main focus of this visual representation? | One slice from a confocal-microscopy data set for a live MCF-7 cell. (a) Composite of red, green and blue channels. (b) Red channel, corresponding to the confocal image without fluorescence. (c) Green channel, corresponding to the quantum dots. (d) Blue channel, corresponding to the nucleus. |
PMC1635722_F1_7664.jpg | What is the core subject represented in this visual? | One slice from a confocal-microscopy data set for a live MCF-7 cell. (a) Composite of red, green and blue channels. (b) Red channel, corresponding to the confocal image without fluorescence. (c) Green channel, corresponding to the quantum dots. (d) Blue channel, corresponding to the nucleus. |
PMC1635722_F1_7663.jpg | Describe the main subject of this image. | One slice from a confocal-microscopy data set for a live MCF-7 cell. (a) Composite of red, green and blue channels. (b) Red channel, corresponding to the confocal image without fluorescence. (c) Green channel, corresponding to the quantum dots. (d) Blue channel, corresponding to the nucleus. |
PMC1635735_F5_7666.jpg | What can you see in this picture? | LAK cell binding of MDA-MB-231 breast carcinoma cells. 1 × 105 LAK cells (0.1 ml) and 1 × 105 target cells (0.1 ml) were mixed in the same tube, centrifuged for 2 min at 500 g and incubated at 37°C for 10 min. The cells stained with trypan blue were observed under phase contrast microscope. A LAK cell was observed to form a conjugate with a blue-dead tumor cell. Two blue-dead tumor cells are also seen in this picture. |
PMC1635741_pmed-0030446-g003_7667.jpg | What is the main focus of this visual representation? | Immunofluorescence of Placental Cryosections from First-Time Mothers Showing VEGFR1 Extracellular Domain (Green), Trophoblast (Red), and Nuclear DNA (Blue)All fields are 200X magnification. Cryosections from (A) PM-negative normotensive pregnancy; (B) PM-positive normotensive pregnancy with intervillous inflammation; (C) PM-positive hypertensive pregnancy. |
PMC1635741_pmed-0030446-g003_7669.jpg | What is the central feature of this picture? | Immunofluorescence of Placental Cryosections from First-Time Mothers Showing VEGFR1 Extracellular Domain (Green), Trophoblast (Red), and Nuclear DNA (Blue)All fields are 200X magnification. Cryosections from (A) PM-negative normotensive pregnancy; (B) PM-positive normotensive pregnancy with intervillous inflammation; (C) PM-positive hypertensive pregnancy. |
PMC1635984_F2_7671.jpg | What is shown in this image? | Immunostainings of cell clusters in the three-dimensional intestinal epithelial cell differentiation model. The nuclei in undifferentiated T84 epithelial cell clusters were more intensively labeled with c-myc antibody (Fig. 2A) than nuclei in TGFβ-treated cell clusters (Fig. 2B). The staining intensity with cytokeratin 19 was lower in undifferentiated T84 epithelial cell clusters (Fig. 2C) than in TGFβ-treated cell clusters, especially seen in the apical part of the epithelial cells in the lumen of organized cell cultures (Fig. 2D). Scale bar = 20 μm. |
PMC1635984_F2_7673.jpg | What does this image primarily show? | Immunostainings of cell clusters in the three-dimensional intestinal epithelial cell differentiation model. The nuclei in undifferentiated T84 epithelial cell clusters were more intensively labeled with c-myc antibody (Fig. 2A) than nuclei in TGFβ-treated cell clusters (Fig. 2B). The staining intensity with cytokeratin 19 was lower in undifferentiated T84 epithelial cell clusters (Fig. 2C) than in TGFβ-treated cell clusters, especially seen in the apical part of the epithelial cells in the lumen of organized cell cultures (Fig. 2D). Scale bar = 20 μm. |
PMC1635984_F2_7670.jpg | What is the main focus of this visual representation? | Immunostainings of cell clusters in the three-dimensional intestinal epithelial cell differentiation model. The nuclei in undifferentiated T84 epithelial cell clusters were more intensively labeled with c-myc antibody (Fig. 2A) than nuclei in TGFβ-treated cell clusters (Fig. 2B). The staining intensity with cytokeratin 19 was lower in undifferentiated T84 epithelial cell clusters (Fig. 2C) than in TGFβ-treated cell clusters, especially seen in the apical part of the epithelial cells in the lumen of organized cell cultures (Fig. 2D). Scale bar = 20 μm. |
PMC1635984_F2_7672.jpg | What is shown in this image? | Immunostainings of cell clusters in the three-dimensional intestinal epithelial cell differentiation model. The nuclei in undifferentiated T84 epithelial cell clusters were more intensively labeled with c-myc antibody (Fig. 2A) than nuclei in TGFβ-treated cell clusters (Fig. 2B). The staining intensity with cytokeratin 19 was lower in undifferentiated T84 epithelial cell clusters (Fig. 2C) than in TGFβ-treated cell clusters, especially seen in the apical part of the epithelial cells in the lumen of organized cell cultures (Fig. 2D). Scale bar = 20 μm. |
PMC1636028_F2_7674.jpg | What key item or scene is captured in this photo? | The periapical radiograph of the hollow-screw implant with extensive marginal bone loss. |
PMC1636035_F1_7675.jpg | Can you identify the primary element in this image? | A sagittal T2-weighted MRI showing thickening and pathological appearance of the ACL. |
PMC1636036_F1_7678.jpg | What stands out most in this visual? | Radiographs of a 45-year-old man multiply injured who had an open complex injury of his left elbow and an ulnar nerve injury after a road traffic accident. Anteroposterior radiographs show a Monteggia fracture dislocation of the left upper arm with additional comminuted fractures of the distal end of both radius and ulna. |
PMC1636036_F2_7676.jpg | What is being portrayed in this visual content? | Lateral radiographs of his left forearm and wrist revealed the describing injury. |
PMC1636036_F3_7677.jpg | What key item or scene is captured in this photo? | Lateral radiographs of his left elbow showed the Monteggia fracture dislocation. |
PMC1636045_F2_7679.jpg | What is the central feature of this picture? | Postoperative transesophageal echocardiographic long axis view of a restored left ventricle. A conical left ventricle is restored. Arrows show the position of the patch. The new apex is evident. |
PMC1636046_F2_7680.jpg | What can you see in this picture? | Histology demonstrating epithelioid mesothelioma showing positivity for the immunohistochemical marker, calretinin {x 200}. |
PMC1636056_F9_7683.jpg | What is the main focus of this visual representation? | Schematic representation of the 3D model of PhaC1P.sp USM 4–55 with the nucleophile Cys296 (green color) located at the sharp turn between β-strand (arrow) and α-helix (cylinder) that results in having unfavorable phi and psi angles. The mesh is colored based on the electrostatic potential around the active site. |
PMC1636056_F9_7682.jpg | What stands out most in this visual? | Schematic representation of the 3D model of PhaC1P.sp USM 4–55 with the nucleophile Cys296 (green color) located at the sharp turn between β-strand (arrow) and α-helix (cylinder) that results in having unfavorable phi and psi angles. The mesh is colored based on the electrostatic potential around the active site. |
PMC1636057_F4_7684.jpg | Describe the main subject of this image. | Imaging features of osteosarcoma. Panel A is a plain radiograph demonstrating a lytic destructive lesion with malignant new bone formation involving the medial aspect of left distal femur. Panel B is a coronal CT image showing typical periosteal new bone formation with cortical destruction associated with a lytic bony lesion involving the left distal femur. Panel C is an enhanced MR image demonstrating an eccentric left distal femoral metaphyseal mass with a large extra-osseous component. Panel D is an axial image of a CT-guided biopsy sampling of the extra-osseous mass. Panel E is an image from a thallium bone study showing uptake overlying the distal left femur indicative of high grade tumour at this site. |
PMC1636057_F4_7685.jpg | What is shown in this image? | Imaging features of osteosarcoma. Panel A is a plain radiograph demonstrating a lytic destructive lesion with malignant new bone formation involving the medial aspect of left distal femur. Panel B is a coronal CT image showing typical periosteal new bone formation with cortical destruction associated with a lytic bony lesion involving the left distal femur. Panel C is an enhanced MR image demonstrating an eccentric left distal femoral metaphyseal mass with a large extra-osseous component. Panel D is an axial image of a CT-guided biopsy sampling of the extra-osseous mass. Panel E is an image from a thallium bone study showing uptake overlying the distal left femur indicative of high grade tumour at this site. |
PMC1636057_F4_7686.jpg | What is the core subject represented in this visual? | Imaging features of osteosarcoma. Panel A is a plain radiograph demonstrating a lytic destructive lesion with malignant new bone formation involving the medial aspect of left distal femur. Panel B is a coronal CT image showing typical periosteal new bone formation with cortical destruction associated with a lytic bony lesion involving the left distal femur. Panel C is an enhanced MR image demonstrating an eccentric left distal femoral metaphyseal mass with a large extra-osseous component. Panel D is an axial image of a CT-guided biopsy sampling of the extra-osseous mass. Panel E is an image from a thallium bone study showing uptake overlying the distal left femur indicative of high grade tumour at this site. |
PMC1636071_F3_7689.jpg | What is being portrayed in this visual content? | Transoesophageal Colour-Doppler image of severe aortic regurgitation associated with the quadricuspid aortic valve in this case. |
PMC1636295_F3_7690.jpg | What is the dominant medical problem in this image? | Increased axonal vacuolisation degeneration is seen at longitidunal section of sciatic nerve (I/R group, score 3), Hematoxylen esozine 40× magnification. |
PMC1636295_F4_7692.jpg | Describe the main subject of this image. | Mild vacuolisation in axons of sciatic nerve (ischemic preconditioning group, score 2), Hematoxylen esozine 40× magnification. |
PMC1636330_F1_7697.jpg | What is shown in this image? | Retinal ganglion cells (RGCs) polarize in vitro after a period of plastic behavior. (a) Time-lapse analysis of dissociated ath5:gfp-expressing retinal cells in culture (Additional file 1). At the start of the time-lapse, cell 'a' expressed a higher level of GFP and was already in late stage 1 of differentiation (namely forming long filopodia), whereas cell 'b' showed a lower fluorescence and was at early stage 1. A short time later cell 'a' started to generate short processes ('neurites'; arrowheads), indicating the onset of stage 2. One of the neurites formed a growth cone at time point 4 minutes 30 seconds and started to grow faster at the beginning of stage 3. After the cell bodies made contact, near the end of the sequence, cell 'b' also seemed to extend an axon-like neurite. Time is shown in hours:minutes. Scale bar, 15 μm. (b) Graphic representation of the timing of in vitro differentiation of zebrafish RGCs, where 30 cells were followed by time-lapse video microscopy. The horizontal lines in the middle of the bar represent the standard deviation from the transitions between stages 1 and 2 and between stages 2 and 3. (c) Analysis of the morphology of the RGCs (Zn5-positive cells) after 24 hours in culture. n = 100 cells, in three independent cell-culture experiments. 'Long neurites' are longer than three cell diameters. (d, e) Cultured RGCs at stage 4 (24 hours in vitro), labeled with the RGC-specific antibody Zn-5 (red), an anti-Tau-1 antibody (green) and 4',6-diamidino-2-phenylindole in (e). Scale bars, 30 μm (d) and 10 μm (e). |
PMC1636330_F1_7693.jpg | Can you identify the primary element in this image? | Retinal ganglion cells (RGCs) polarize in vitro after a period of plastic behavior. (a) Time-lapse analysis of dissociated ath5:gfp-expressing retinal cells in culture (Additional file 1). At the start of the time-lapse, cell 'a' expressed a higher level of GFP and was already in late stage 1 of differentiation (namely forming long filopodia), whereas cell 'b' showed a lower fluorescence and was at early stage 1. A short time later cell 'a' started to generate short processes ('neurites'; arrowheads), indicating the onset of stage 2. One of the neurites formed a growth cone at time point 4 minutes 30 seconds and started to grow faster at the beginning of stage 3. After the cell bodies made contact, near the end of the sequence, cell 'b' also seemed to extend an axon-like neurite. Time is shown in hours:minutes. Scale bar, 15 μm. (b) Graphic representation of the timing of in vitro differentiation of zebrafish RGCs, where 30 cells were followed by time-lapse video microscopy. The horizontal lines in the middle of the bar represent the standard deviation from the transitions between stages 1 and 2 and between stages 2 and 3. (c) Analysis of the morphology of the RGCs (Zn5-positive cells) after 24 hours in culture. n = 100 cells, in three independent cell-culture experiments. 'Long neurites' are longer than three cell diameters. (d, e) Cultured RGCs at stage 4 (24 hours in vitro), labeled with the RGC-specific antibody Zn-5 (red), an anti-Tau-1 antibody (green) and 4',6-diamidino-2-phenylindole in (e). Scale bars, 30 μm (d) and 10 μm (e). |
PMC1636330_F1_7695.jpg | What is being portrayed in this visual content? | Retinal ganglion cells (RGCs) polarize in vitro after a period of plastic behavior. (a) Time-lapse analysis of dissociated ath5:gfp-expressing retinal cells in culture (Additional file 1). At the start of the time-lapse, cell 'a' expressed a higher level of GFP and was already in late stage 1 of differentiation (namely forming long filopodia), whereas cell 'b' showed a lower fluorescence and was at early stage 1. A short time later cell 'a' started to generate short processes ('neurites'; arrowheads), indicating the onset of stage 2. One of the neurites formed a growth cone at time point 4 minutes 30 seconds and started to grow faster at the beginning of stage 3. After the cell bodies made contact, near the end of the sequence, cell 'b' also seemed to extend an axon-like neurite. Time is shown in hours:minutes. Scale bar, 15 μm. (b) Graphic representation of the timing of in vitro differentiation of zebrafish RGCs, where 30 cells were followed by time-lapse video microscopy. The horizontal lines in the middle of the bar represent the standard deviation from the transitions between stages 1 and 2 and between stages 2 and 3. (c) Analysis of the morphology of the RGCs (Zn5-positive cells) after 24 hours in culture. n = 100 cells, in three independent cell-culture experiments. 'Long neurites' are longer than three cell diameters. (d, e) Cultured RGCs at stage 4 (24 hours in vitro), labeled with the RGC-specific antibody Zn-5 (red), an anti-Tau-1 antibody (green) and 4',6-diamidino-2-phenylindole in (e). Scale bars, 30 μm (d) and 10 μm (e). |
PMC1636330_F1_7698.jpg | What can you see in this picture? | Retinal ganglion cells (RGCs) polarize in vitro after a period of plastic behavior. (a) Time-lapse analysis of dissociated ath5:gfp-expressing retinal cells in culture (Additional file 1). At the start of the time-lapse, cell 'a' expressed a higher level of GFP and was already in late stage 1 of differentiation (namely forming long filopodia), whereas cell 'b' showed a lower fluorescence and was at early stage 1. A short time later cell 'a' started to generate short processes ('neurites'; arrowheads), indicating the onset of stage 2. One of the neurites formed a growth cone at time point 4 minutes 30 seconds and started to grow faster at the beginning of stage 3. After the cell bodies made contact, near the end of the sequence, cell 'b' also seemed to extend an axon-like neurite. Time is shown in hours:minutes. Scale bar, 15 μm. (b) Graphic representation of the timing of in vitro differentiation of zebrafish RGCs, where 30 cells were followed by time-lapse video microscopy. The horizontal lines in the middle of the bar represent the standard deviation from the transitions between stages 1 and 2 and between stages 2 and 3. (c) Analysis of the morphology of the RGCs (Zn5-positive cells) after 24 hours in culture. n = 100 cells, in three independent cell-culture experiments. 'Long neurites' are longer than three cell diameters. (d, e) Cultured RGCs at stage 4 (24 hours in vitro), labeled with the RGC-specific antibody Zn-5 (red), an anti-Tau-1 antibody (green) and 4',6-diamidino-2-phenylindole in (e). Scale bars, 30 μm (d) and 10 μm (e). |
PMC1636330_F9_7709.jpg | What stands out most in this visual? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636330_F9_7707.jpg | Can you identify the primary element in this image? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636330_F9_7706.jpg | What's the most prominent thing you notice in this picture? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636330_F9_7703.jpg | What is being portrayed in this visual content? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636330_F9_7705.jpg | What key item or scene is captured in this photo? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636330_F9_7710.jpg | What is the dominant medical problem in this image? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636330_F9_7701.jpg | What is being portrayed in this visual content? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636330_F9_7700.jpg | What is the focal point of this photograph? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636330_F9_7704.jpg | What is the main focus of this visual representation? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636330_F9_7702.jpg | What object or scene is depicted here? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636330_F9_7708.jpg | What key item or scene is captured in this photo? | The RPE influences the ability of retinal ganglion cells to polarize in ectopic positions. (a) Head region of wild-type, morphant and mutant embryos, showing the distribution of pigment around the retina. Two examples of nok morpholino-injected embryos (0.17 pmoles per embryo) are shown. (b) Cryosection of the eye from a nok-/-, ath5:gap-gfp transgenic embryo, labeled with an anti-laminin 1 antibody (red). The bright-field image, inverted and pseudo-colored in blue, shows the distribution of the retinal pigment epithelium (RPE). Arrowheads indicate ath5:gap-gfp-positive retinal ganglion cells. D, dorsal; L, lateral; M, medial. Scale bar, 20 μm. (c) Transmission electron micrograph of the apical region of a nok mutant retina, showing the distribution of the RPE cells (dotted lines). Inset, a higher magnification of the boxed region, showing two apparent transverse-sectioned axons (Ax) at the RPE-free apical surface of the retina. Scale bars: low-magnification image, 5 μm; inset, 0.5 μm. (d) Transmission electron micrographs of the apical region of a wild-type (Wt) and a has-/- embryo. The RPE (blue arrows) is a very organized simple epithelium in the wild type, and it seems disrupted in the has mutant. Nevertheless, the picture does not show any actual gap between the RPE cells in the has-/-embryo. Red arrowheads indicate mitotic cells in a normal (apical) position in the wild-type, and in an ectopic position in the mutant. Scale bar, 5 μm. (e) Fluorescence intensity profiles made on confocal sections of 48 hpf ath5:gap-gfp transgenic embryos labeled with an anti-RPE antibody (Zpr-2). For the measurements a 20-pixel wide line was drawn along a radius of the retina as in (f). The intensity profile of the green channel (GFP) was plotted and the values were normalized (maximum intensity) and averaged for each embryo; the resulting plots were then normalized to each other (integrated intensity). To compare the profiles in relation to the distribution of the RPE, we positioned the line either in regions where zpr-2 immunoreactivity was detected (RPE) or not (NO RPE). For the nok mutants, only measurements of areas without detectable RPE were used. Measurements were made in three to ten different areas from one wild-type, five nok mutant, four nok morphant and three has mutant retinas. The inset picture shows a region of a wild-type retina, like those used for the measurements, which is aligned with the profile plot to show the correspondence with the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OFL, optic fiber layer; OPL, outer plexiform layer; PL, photoreceptor layer. (f) Optical sections of wild-type and mutant retinas of ath5:gap-gfp transgenic embryos labeled in red with the Zpr-2 antibody, which stains the RPE. The yellow rectangles show an example of the lines used for the measurements presented in (e). Scale bar, 25 μm. |
PMC1636628_F3_7711.jpg | What can you see in this picture? | a, b. T1 and T2 weight MRI of thoracic spine showed continuous multi-level ossification of ligamentum flavum between T7–12. c. CT scan showed ossified ligamentum flavum, note that there was a thin gap between the ossified ligament and the lamina. |
PMC1636628_F3_7713.jpg | What's the most prominent thing you notice in this picture? | a, b. T1 and T2 weight MRI of thoracic spine showed continuous multi-level ossification of ligamentum flavum between T7–12. c. CT scan showed ossified ligamentum flavum, note that there was a thin gap between the ossified ligament and the lamina. |
PMC1636628_F3_7712.jpg | What is the focal point of this photograph? | a, b. T1 and T2 weight MRI of thoracic spine showed continuous multi-level ossification of ligamentum flavum between T7–12. c. CT scan showed ossified ligamentum flavum, note that there was a thin gap between the ossified ligament and the lamina. |
PMC1636636_F2_7714.jpg | What is being portrayed in this visual content? | Non-calcified hyaline tissue, approximately 1 mm diameter, (H&E, 100× magnification). |
PMC1636656_F5_7717.jpg | What's the most prominent thing you notice in this picture? | Fluoresence (First column) and their corresponding phase images (Second column) of 786-O cells treated with LnPO4·H2O nanorods. (A): Control 786-O cells with no treatment, slight green color due to auto fluorescence in (A), (B): 786-O cells treated with EuPO4·H2O nanorods, and (C): 786-O cells treated with TbPO4·H2O nanorods, taken by confocal microscope. In few places green fluorescence color of nanorods inside the cells, were marked by white arrow sign. |
PMC1636656_F5_7716.jpg | What is the principal component of this image? | Fluoresence (First column) and their corresponding phase images (Second column) of 786-O cells treated with LnPO4·H2O nanorods. (A): Control 786-O cells with no treatment, slight green color due to auto fluorescence in (A), (B): 786-O cells treated with EuPO4·H2O nanorods, and (C): 786-O cells treated with TbPO4·H2O nanorods, taken by confocal microscope. In few places green fluorescence color of nanorods inside the cells, were marked by white arrow sign. |
PMC1636656_F5_7718.jpg | What is the core subject represented in this visual? | Fluoresence (First column) and their corresponding phase images (Second column) of 786-O cells treated with LnPO4·H2O nanorods. (A): Control 786-O cells with no treatment, slight green color due to auto fluorescence in (A), (B): 786-O cells treated with EuPO4·H2O nanorods, and (C): 786-O cells treated with TbPO4·H2O nanorods, taken by confocal microscope. In few places green fluorescence color of nanorods inside the cells, were marked by white arrow sign. |
PMC1636656_F5_7715.jpg | What is the dominant medical problem in this image? | Fluoresence (First column) and their corresponding phase images (Second column) of 786-O cells treated with LnPO4·H2O nanorods. (A): Control 786-O cells with no treatment, slight green color due to auto fluorescence in (A), (B): 786-O cells treated with EuPO4·H2O nanorods, and (C): 786-O cells treated with TbPO4·H2O nanorods, taken by confocal microscope. In few places green fluorescence color of nanorods inside the cells, were marked by white arrow sign. |
PMC1636656_F5_7720.jpg | What object or scene is depicted here? | Fluoresence (First column) and their corresponding phase images (Second column) of 786-O cells treated with LnPO4·H2O nanorods. (A): Control 786-O cells with no treatment, slight green color due to auto fluorescence in (A), (B): 786-O cells treated with EuPO4·H2O nanorods, and (C): 786-O cells treated with TbPO4·H2O nanorods, taken by confocal microscope. In few places green fluorescence color of nanorods inside the cells, were marked by white arrow sign. |
PMC1636656_F7_7724.jpg | Describe the main subject of this image. | Fluorescent LnPO4·H2O nanorods were visualized by TEM inside the cytoplasmic compartments of HUVEC. (A-C) EuPO4·H2O nanorods and (D-F) TbPO4·H2O nanorodsare observed inside the HUVEC with increasing magnifications. B was the enlarge picture of white block in A, C was the enlarge picture of white block in B. Similarly, E was the enlarge picture of white block in D and F was the enlarge picture of white block in E. |
PMC1636656_F7_7726.jpg | What is the central feature of this picture? | Fluorescent LnPO4·H2O nanorods were visualized by TEM inside the cytoplasmic compartments of HUVEC. (A-C) EuPO4·H2O nanorods and (D-F) TbPO4·H2O nanorodsare observed inside the HUVEC with increasing magnifications. B was the enlarge picture of white block in A, C was the enlarge picture of white block in B. Similarly, E was the enlarge picture of white block in D and F was the enlarge picture of white block in E. |
PMC1636656_F7_7721.jpg | What object or scene is depicted here? | Fluorescent LnPO4·H2O nanorods were visualized by TEM inside the cytoplasmic compartments of HUVEC. (A-C) EuPO4·H2O nanorods and (D-F) TbPO4·H2O nanorodsare observed inside the HUVEC with increasing magnifications. B was the enlarge picture of white block in A, C was the enlarge picture of white block in B. Similarly, E was the enlarge picture of white block in D and F was the enlarge picture of white block in E. |
PMC1636656_F7_7722.jpg | What can you see in this picture? | Fluorescent LnPO4·H2O nanorods were visualized by TEM inside the cytoplasmic compartments of HUVEC. (A-C) EuPO4·H2O nanorods and (D-F) TbPO4·H2O nanorodsare observed inside the HUVEC with increasing magnifications. B was the enlarge picture of white block in A, C was the enlarge picture of white block in B. Similarly, E was the enlarge picture of white block in D and F was the enlarge picture of white block in E. |
PMC1636667_F1_7732.jpg | What's the most prominent thing you notice in this picture? | TSI images in a heart failure patient who deteriorated after CRT. Color bar at the top right of each panel denotes severity of delay in peak contraction during ejection phase, recognized as time interval between aortic valve opening and closure. In TSI, normal myocardium is coded in green. Presence of delay is coded in progressive sequence of green, yellow, orange, and red. Figure shows severe lateral wall (white arrows, A) and posterior wall delay (white arrows, D) which decreased at LV pre-excitation of 20 ms (white arrows, B and E) and was abolished (C and F) at LV pre-excitation of 50 ms is shown. LV outflow velocity times integral (VTI) increased from 10.95 cm at nominal (0) VV delay (G) to 12.36 cm at LV pre-excitation of 50 ms (H). NYHA symptoms improved from class III pre-optimization to class II post optimization. |
PMC1636667_F1_7733.jpg | What is the dominant medical problem in this image? | TSI images in a heart failure patient who deteriorated after CRT. Color bar at the top right of each panel denotes severity of delay in peak contraction during ejection phase, recognized as time interval between aortic valve opening and closure. In TSI, normal myocardium is coded in green. Presence of delay is coded in progressive sequence of green, yellow, orange, and red. Figure shows severe lateral wall (white arrows, A) and posterior wall delay (white arrows, D) which decreased at LV pre-excitation of 20 ms (white arrows, B and E) and was abolished (C and F) at LV pre-excitation of 50 ms is shown. LV outflow velocity times integral (VTI) increased from 10.95 cm at nominal (0) VV delay (G) to 12.36 cm at LV pre-excitation of 50 ms (H). NYHA symptoms improved from class III pre-optimization to class II post optimization. |
PMC1636667_F1_7730.jpg | What is being portrayed in this visual content? | TSI images in a heart failure patient who deteriorated after CRT. Color bar at the top right of each panel denotes severity of delay in peak contraction during ejection phase, recognized as time interval between aortic valve opening and closure. In TSI, normal myocardium is coded in green. Presence of delay is coded in progressive sequence of green, yellow, orange, and red. Figure shows severe lateral wall (white arrows, A) and posterior wall delay (white arrows, D) which decreased at LV pre-excitation of 20 ms (white arrows, B and E) and was abolished (C and F) at LV pre-excitation of 50 ms is shown. LV outflow velocity times integral (VTI) increased from 10.95 cm at nominal (0) VV delay (G) to 12.36 cm at LV pre-excitation of 50 ms (H). NYHA symptoms improved from class III pre-optimization to class II post optimization. |
PMC1636667_F1_7729.jpg | What can you see in this picture? | TSI images in a heart failure patient who deteriorated after CRT. Color bar at the top right of each panel denotes severity of delay in peak contraction during ejection phase, recognized as time interval between aortic valve opening and closure. In TSI, normal myocardium is coded in green. Presence of delay is coded in progressive sequence of green, yellow, orange, and red. Figure shows severe lateral wall (white arrows, A) and posterior wall delay (white arrows, D) which decreased at LV pre-excitation of 20 ms (white arrows, B and E) and was abolished (C and F) at LV pre-excitation of 50 ms is shown. LV outflow velocity times integral (VTI) increased from 10.95 cm at nominal (0) VV delay (G) to 12.36 cm at LV pre-excitation of 50 ms (H). NYHA symptoms improved from class III pre-optimization to class II post optimization. |
PMC1636667_F1_7735.jpg | Describe the main subject of this image. | TSI images in a heart failure patient who deteriorated after CRT. Color bar at the top right of each panel denotes severity of delay in peak contraction during ejection phase, recognized as time interval between aortic valve opening and closure. In TSI, normal myocardium is coded in green. Presence of delay is coded in progressive sequence of green, yellow, orange, and red. Figure shows severe lateral wall (white arrows, A) and posterior wall delay (white arrows, D) which decreased at LV pre-excitation of 20 ms (white arrows, B and E) and was abolished (C and F) at LV pre-excitation of 50 ms is shown. LV outflow velocity times integral (VTI) increased from 10.95 cm at nominal (0) VV delay (G) to 12.36 cm at LV pre-excitation of 50 ms (H). NYHA symptoms improved from class III pre-optimization to class II post optimization. |
PMC1636667_F7_7727.jpg | What is the core subject represented in this visual? | PW Doppler showing left ventricular outflow tract velocity. Improvement in left ventricular ejection duration is shown in B during LV pre-excitation of 40 ms compared to baseline VV delay of 0 ms in A. |
PMC1636667_F7_7728.jpg | What stands out most in this visual? | PW Doppler showing left ventricular outflow tract velocity. Improvement in left ventricular ejection duration is shown in B during LV pre-excitation of 40 ms compared to baseline VV delay of 0 ms in A. |
PMC1636667_F12_7742.jpg | What is the central feature of this picture? | Tissue velocity (A, B and C) and strain rate (D, E and F) maps in the apical 2 chamber view at baseline pre cardiac resynchronization treatment (A and D), post cardiac resynchronization treatment with LV pre-excitation of 20 ms (B and E) and post optimization with RV pre-excitation of 20 ms (C and F). Note delayed longitudinal contraction (shown by white arrows) in the velocity (A) and strain rate maps (D) at baseline indicated by white arrows that is abolished in all segments in the velocity map in B and in mid inferior segment in the strain rate map in E post cardiac resynchronization treatment. In addition note the marked improvement in synchrony in systole between basal and mid segments post cardiac resynchronization treatment in B and E compared to A and D. RV pre-excitation causes further increase in velocities with establishment of a normal velocity gradient between basal and mid segments and improved synchrony in C, as well as improvement in strain rate velocities, synchrony and a reduction of delayed longitudinal contraction velocities in F. Note different velocity calibration settings between D-F. Yellow line represent basal inferior LV segment, blue represents basal anterior LV segment, red represents mid inferior LV segment and green mid anterior LV segment. |
PMC1636667_F12_7743.jpg | What can you see in this picture? | Tissue velocity (A, B and C) and strain rate (D, E and F) maps in the apical 2 chamber view at baseline pre cardiac resynchronization treatment (A and D), post cardiac resynchronization treatment with LV pre-excitation of 20 ms (B and E) and post optimization with RV pre-excitation of 20 ms (C and F). Note delayed longitudinal contraction (shown by white arrows) in the velocity (A) and strain rate maps (D) at baseline indicated by white arrows that is abolished in all segments in the velocity map in B and in mid inferior segment in the strain rate map in E post cardiac resynchronization treatment. In addition note the marked improvement in synchrony in systole between basal and mid segments post cardiac resynchronization treatment in B and E compared to A and D. RV pre-excitation causes further increase in velocities with establishment of a normal velocity gradient between basal and mid segments and improved synchrony in C, as well as improvement in strain rate velocities, synchrony and a reduction of delayed longitudinal contraction velocities in F. Note different velocity calibration settings between D-F. Yellow line represent basal inferior LV segment, blue represents basal anterior LV segment, red represents mid inferior LV segment and green mid anterior LV segment. |
PMC1636667_F12_7744.jpg | Can you identify the primary element in this image? | Tissue velocity (A, B and C) and strain rate (D, E and F) maps in the apical 2 chamber view at baseline pre cardiac resynchronization treatment (A and D), post cardiac resynchronization treatment with LV pre-excitation of 20 ms (B and E) and post optimization with RV pre-excitation of 20 ms (C and F). Note delayed longitudinal contraction (shown by white arrows) in the velocity (A) and strain rate maps (D) at baseline indicated by white arrows that is abolished in all segments in the velocity map in B and in mid inferior segment in the strain rate map in E post cardiac resynchronization treatment. In addition note the marked improvement in synchrony in systole between basal and mid segments post cardiac resynchronization treatment in B and E compared to A and D. RV pre-excitation causes further increase in velocities with establishment of a normal velocity gradient between basal and mid segments and improved synchrony in C, as well as improvement in strain rate velocities, synchrony and a reduction of delayed longitudinal contraction velocities in F. Note different velocity calibration settings between D-F. Yellow line represent basal inferior LV segment, blue represents basal anterior LV segment, red represents mid inferior LV segment and green mid anterior LV segment. |
PMC1636667_F12_7745.jpg | What is the main focus of this visual representation? | Tissue velocity (A, B and C) and strain rate (D, E and F) maps in the apical 2 chamber view at baseline pre cardiac resynchronization treatment (A and D), post cardiac resynchronization treatment with LV pre-excitation of 20 ms (B and E) and post optimization with RV pre-excitation of 20 ms (C and F). Note delayed longitudinal contraction (shown by white arrows) in the velocity (A) and strain rate maps (D) at baseline indicated by white arrows that is abolished in all segments in the velocity map in B and in mid inferior segment in the strain rate map in E post cardiac resynchronization treatment. In addition note the marked improvement in synchrony in systole between basal and mid segments post cardiac resynchronization treatment in B and E compared to A and D. RV pre-excitation causes further increase in velocities with establishment of a normal velocity gradient between basal and mid segments and improved synchrony in C, as well as improvement in strain rate velocities, synchrony and a reduction of delayed longitudinal contraction velocities in F. Note different velocity calibration settings between D-F. Yellow line represent basal inferior LV segment, blue represents basal anterior LV segment, red represents mid inferior LV segment and green mid anterior LV segment. |
PMC1636667_F13_7736.jpg | What stands out most in this visual? | Panels A-C show color Doppler images of mitral regurgitation in the apical 4 chamber view and D-F show right upper pulmonary vein pulsed wave Doppler, at baseline with an AV of 180 ms and LV pre-excitation of 20 ms (A and D), during an AV delay of 220 ms and VV delay of 0 ms (B and E) and during an AV delay of 210 ms and RV pre-excitation of 20 ms. Inset in panel A shows prolapse of the middle segment of posterior leaflet (white arrow) causing malcoaptation between anterior and posterior leaflets and an eccentric severe anterior mitral regurgitation jet entering the right superior pulmonary vein (white asterisk, A) and panel D shows systolic pulmonary vein flow reversal. Prolonging the AV delay to 220 ms no longer causes MR jet to enter the pulmonary vein (B) which in turn produces a somewhat blunted but upright pulmonary vein S wave (E). Right ventricular pre-excitation causes further reduction in mitral regurgitation severity with a dominant systolic flow entering the left atrium (orange red color marked with a black asterisk in C) and a systolic dominant pulmonary vein S wave in F. |
PMC1636667_F13_7739.jpg | What is the core subject represented in this visual? | Panels A-C show color Doppler images of mitral regurgitation in the apical 4 chamber view and D-F show right upper pulmonary vein pulsed wave Doppler, at baseline with an AV of 180 ms and LV pre-excitation of 20 ms (A and D), during an AV delay of 220 ms and VV delay of 0 ms (B and E) and during an AV delay of 210 ms and RV pre-excitation of 20 ms. Inset in panel A shows prolapse of the middle segment of posterior leaflet (white arrow) causing malcoaptation between anterior and posterior leaflets and an eccentric severe anterior mitral regurgitation jet entering the right superior pulmonary vein (white asterisk, A) and panel D shows systolic pulmonary vein flow reversal. Prolonging the AV delay to 220 ms no longer causes MR jet to enter the pulmonary vein (B) which in turn produces a somewhat blunted but upright pulmonary vein S wave (E). Right ventricular pre-excitation causes further reduction in mitral regurgitation severity with a dominant systolic flow entering the left atrium (orange red color marked with a black asterisk in C) and a systolic dominant pulmonary vein S wave in F. |
PMC1636667_F13_7737.jpg | What's the most prominent thing you notice in this picture? | Panels A-C show color Doppler images of mitral regurgitation in the apical 4 chamber view and D-F show right upper pulmonary vein pulsed wave Doppler, at baseline with an AV of 180 ms and LV pre-excitation of 20 ms (A and D), during an AV delay of 220 ms and VV delay of 0 ms (B and E) and during an AV delay of 210 ms and RV pre-excitation of 20 ms. Inset in panel A shows prolapse of the middle segment of posterior leaflet (white arrow) causing malcoaptation between anterior and posterior leaflets and an eccentric severe anterior mitral regurgitation jet entering the right superior pulmonary vein (white asterisk, A) and panel D shows systolic pulmonary vein flow reversal. Prolonging the AV delay to 220 ms no longer causes MR jet to enter the pulmonary vein (B) which in turn produces a somewhat blunted but upright pulmonary vein S wave (E). Right ventricular pre-excitation causes further reduction in mitral regurgitation severity with a dominant systolic flow entering the left atrium (orange red color marked with a black asterisk in C) and a systolic dominant pulmonary vein S wave in F. |
PMC1636667_F13_7738.jpg | What is the principal component of this image? | Panels A-C show color Doppler images of mitral regurgitation in the apical 4 chamber view and D-F show right upper pulmonary vein pulsed wave Doppler, at baseline with an AV of 180 ms and LV pre-excitation of 20 ms (A and D), during an AV delay of 220 ms and VV delay of 0 ms (B and E) and during an AV delay of 210 ms and RV pre-excitation of 20 ms. Inset in panel A shows prolapse of the middle segment of posterior leaflet (white arrow) causing malcoaptation between anterior and posterior leaflets and an eccentric severe anterior mitral regurgitation jet entering the right superior pulmonary vein (white asterisk, A) and panel D shows systolic pulmonary vein flow reversal. Prolonging the AV delay to 220 ms no longer causes MR jet to enter the pulmonary vein (B) which in turn produces a somewhat blunted but upright pulmonary vein S wave (E). Right ventricular pre-excitation causes further reduction in mitral regurgitation severity with a dominant systolic flow entering the left atrium (orange red color marked with a black asterisk in C) and a systolic dominant pulmonary vein S wave in F. |
PMC1636699_pgen-0020193-g015_7758.jpg | What can you see in this picture? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7759.jpg | What key item or scene is captured in this photo? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7763.jpg | What is shown in this image? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7770.jpg | What stands out most in this visual? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7765.jpg | Can you identify the primary element in this image? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7760.jpg | Describe the main subject of this image. | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7750.jpg | What is the dominant medical problem in this image? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7771.jpg | What stands out most in this visual? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7766.jpg | What does this image primarily show? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7756.jpg | What key item or scene is captured in this photo? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7755.jpg | What is the main focus of this visual representation? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7767.jpg | What's the most prominent thing you notice in this picture? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7751.jpg | Describe the main subject of this image. | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7762.jpg | What is the dominant medical problem in this image? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1636699_pgen-0020193-g015_7754.jpg | What is the main focus of this visual representation? | Tests of the Specificities of the Phenotypes Observed in the Gastrula Defects Phenotypic ClassThe specificities of the MOs used to define this phenotypic class were investigated by injecting 10–15 ng of the Gene Tools standard control MO (Column 1); the original antisense MO (Column 2); MO1 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 3); MO1 (or, in the case of Dp71, MO2) with five mismatched bases (Column 4); MO2 (Column 5); MO2 together with 1 ng of a form of the target RNA that lacks the MO target sequence (Column 6).The results of these experiments are summarized in Table 5. In Column 1 (control MO) embryos are shown at the mid-gastrula stage. Embryos in Column 2 (MO1) are at the same stage as those in Column 1, but (with the exception of Dp71) gastrulation is delayed or inhibited. In the case of Dp71, MO1 does not inhibit gastrulation but does cause embryos to develop with a shortened axis. Column 3 indicates that for five of the nine MOs studied, complete or partial rescue of the phenotype was obtained by injection of the cognate RNA. In these experiments, embryos were allowed to develop beyond gastrula stages to tailbud or tadpole stages. In the case of D1LIC, rescue was more complete at tailbud stages (upper panel) than tadpole stages (lower panel). Column 4 shows that for each of the nine MOs, changing five bases caused them to lose the ability to disrupt development.Use of a second site MO usually causes a milder phenotype than is observed with MO1 (Column 5), but the phenotype is usually specific, in the sense that it can frequently be rescued by injection of the cognate RNA (Column 6).MO1, original antisense oligonucleotide; MO2, second site MO. |
PMC1637094_F2_7773.jpg | What is the principal component of this image? | Pulmonary Lymphangiectasia. Chest radiographs, AP views. Radiological findings occurring during the clinical course of PL. A and B: over time progression of hazy perihilar infiltrates on the left lung. C: important bilateral pleural effusion. D: after pleurodesis, bilateral lung hyperinflation with interstitial and septa thickening are evident, and a mild degree of pleural effusion remains. |
PMC1637094_F2_7774.jpg | What is the focal point of this photograph? | Pulmonary Lymphangiectasia. Chest radiographs, AP views. Radiological findings occurring during the clinical course of PL. A and B: over time progression of hazy perihilar infiltrates on the left lung. C: important bilateral pleural effusion. D: after pleurodesis, bilateral lung hyperinflation with interstitial and septa thickening are evident, and a mild degree of pleural effusion remains. |
PMC1637094_F2_7775.jpg | What is being portrayed in this visual content? | Pulmonary Lymphangiectasia. Chest radiographs, AP views. Radiological findings occurring during the clinical course of PL. A and B: over time progression of hazy perihilar infiltrates on the left lung. C: important bilateral pleural effusion. D: after pleurodesis, bilateral lung hyperinflation with interstitial and septa thickening are evident, and a mild degree of pleural effusion remains. |
PMC1637094_F2_7776.jpg | What is the core subject represented in this visual? | Pulmonary Lymphangiectasia. Chest radiographs, AP views. Radiological findings occurring during the clinical course of PL. A and B: over time progression of hazy perihilar infiltrates on the left lung. C: important bilateral pleural effusion. D: after pleurodesis, bilateral lung hyperinflation with interstitial and septa thickening are evident, and a mild degree of pleural effusion remains. |
PMC1637094_F3_7772.jpg | What can you see in this picture? | Pulmonary Lymphangiectasia. High-resolution computed tomography (HRCT). Diffuse thickening of the peribronchovascular interstitium and the interlobular septa (arrowheads), associated with bilateral pleural effusion (*), and peribronchovascular infiltrates (arrows) with bronchogram. |
PMC1637101_F3_7778.jpg | What's the most prominent thing you notice in this picture? | Pretreatment panoramic radiograph of the patient. |
PMC1637101_F4_7779.jpg | What is being portrayed in this visual content? | Pretreatment cephalometric radiograph of the patient. |
PMC1637101_F5_7783.jpg | What is shown in this image? | After distalization intraoral photographs and occlusal radiograph of the patient and intraosseous screw. |
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