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PMC514490_pbio-0020261-g009_278.jpg | What stands out most in this visual? | Immunolocalisation of Rabankyrin-5 in the Mouse KidneyMouse kidney cortex was processed for frozen section immunoelectron microscopy. Sections were (A and B) single labelled for Rabankyrin-5 (arrowheads, 10 nm) or (C and D) double labelled (arrows, 5 nm) for Rabankyrin-5 and LAMP-1.(A) Low-magnification view of the apical region of two proximal tubule cells demonstrates low labelling for Rabankyrin-5 on apical microvilli (M) but stronger labelling (arrowheads) of large subapical electron-lucent vesicular structures (asterisks). One of these structures is shown at higher magnification in (B). L, lateral membrane.(C) Rabankyrin-5 labels LAMP-1–negative subapical structures as well as compartments showing low LAMP-1 labelling (arrows and asterisk).(D) Rabankyrin-5 (arrowheads) associates with compartments, which show no or weak labelling for LAMP-1 (asterisks). In addition, low Rabankyrin-5 labelling is associated with more strongly labelled LAMP-1–positive compartments. Note that there is some nonspecific labelling of mitochondria (m). Scale bars represent 500 nm. |
PMC514499_F4_283.jpg | What is the central feature of this picture? | Echocardiographic apical four-chamber images (end-systolic frames) from two patients with and without contractile reserve. |
PMC514499_F4_286.jpg | What object or scene is depicted here? | Echocardiographic apical four-chamber images (end-systolic frames) from two patients with and without contractile reserve. |
PMC514499_F4_282.jpg | What stands out most in this visual? | Echocardiographic apical four-chamber images (end-systolic frames) from two patients with and without contractile reserve. |
PMC514525_F1_290.jpg | What stands out most in this visual? | US of 65 years old male presented to emergency room with bilateral flank pain, nausea and vomiting for the past 1 week. He had an ultrasound in a peripheral hospital, which identified hydronephrosis on the right side, and percutaneous nephrostomy tube was placed. His left kidney showed hydronephrosis with renal stone (upper picture). This scan shows small-scarred right kidney (middle picture), pigtail catheter could be identified (arrow) and a proximal ureteric stone could also be seen (lower picture). |
PMC514525_F1_289.jpg | What does this image primarily show? | US of 65 years old male presented to emergency room with bilateral flank pain, nausea and vomiting for the past 1 week. He had an ultrasound in a peripheral hospital, which identified hydronephrosis on the right side, and percutaneous nephrostomy tube was placed. His left kidney showed hydronephrosis with renal stone (upper picture). This scan shows small-scarred right kidney (middle picture), pigtail catheter could be identified (arrow) and a proximal ureteric stone could also be seen (lower picture). |
PMC514525_F1_288.jpg | Describe the main subject of this image. | US of 65 years old male presented to emergency room with bilateral flank pain, nausea and vomiting for the past 1 week. He had an ultrasound in a peripheral hospital, which identified hydronephrosis on the right side, and percutaneous nephrostomy tube was placed. His left kidney showed hydronephrosis with renal stone (upper picture). This scan shows small-scarred right kidney (middle picture), pigtail catheter could be identified (arrow) and a proximal ureteric stone could also be seen (lower picture). |
PMC514537_pbio-0020288-g007_294.jpg | Can you identify the primary element in this image? | Increased Muscle Damage in HIF-1α KOs Following Repeated Exercise(A) WT mice and HIF-1α KOs underwent a 4-d endurance test, in which animals were run to exhaustion on each of four successive days with a minimum of 22 h rest between trials. HIF-1α KOs demonstrated initially greater endurance under the protocol; however, by the second day, their endurance advantage was eliminated, and by the fourth day, HIF-1α KOs were running for a significantly shorter time (**p < 0.01) than on the first day, while WT animals were running for approximately similar times as on the first day. Repeated measures ANOVA revealed that the decrease in performance on each successive day was unique to HIF-1α KOs (p < 0.05).(B) Example of hematoxylin and eosin staining of gastrocnemius muscles after 1 d of recovery by mice after the 4-d endurance test. Evidence of greater damage can be seen in HIF-1α KO muscles compared to WT muscles.(C) Example of PCNA staining of gastrocnemius muscles from exercised mice, demonstrating increased levels of muscle regeneration in HIF-1α KOs.(D) Number of PCNA-positive nuclei per square millimeter in gastrocnemius muscles of WT mice (n = 5) and HIF-1α KOs (n = 7) that ran repeatedly for 4 d. Although HIF-1α KOs have almost twice as many PCNA-positive nuclei per square millimeter, the difference is not significant, because of wild variations in that population. F-test analysis of the data reveals that the variance is much greater in the HIF-1α KO population than the WT population (p < 0.05). |
PMC514537_pbio-0020288-g007_291.jpg | Can you identify the primary element in this image? | Increased Muscle Damage in HIF-1α KOs Following Repeated Exercise(A) WT mice and HIF-1α KOs underwent a 4-d endurance test, in which animals were run to exhaustion on each of four successive days with a minimum of 22 h rest between trials. HIF-1α KOs demonstrated initially greater endurance under the protocol; however, by the second day, their endurance advantage was eliminated, and by the fourth day, HIF-1α KOs were running for a significantly shorter time (**p < 0.01) than on the first day, while WT animals were running for approximately similar times as on the first day. Repeated measures ANOVA revealed that the decrease in performance on each successive day was unique to HIF-1α KOs (p < 0.05).(B) Example of hematoxylin and eosin staining of gastrocnemius muscles after 1 d of recovery by mice after the 4-d endurance test. Evidence of greater damage can be seen in HIF-1α KO muscles compared to WT muscles.(C) Example of PCNA staining of gastrocnemius muscles from exercised mice, demonstrating increased levels of muscle regeneration in HIF-1α KOs.(D) Number of PCNA-positive nuclei per square millimeter in gastrocnemius muscles of WT mice (n = 5) and HIF-1α KOs (n = 7) that ran repeatedly for 4 d. Although HIF-1α KOs have almost twice as many PCNA-positive nuclei per square millimeter, the difference is not significant, because of wild variations in that population. F-test analysis of the data reveals that the variance is much greater in the HIF-1α KO population than the WT population (p < 0.05). |
PMC514537_pbio-0020288-g007_295.jpg | What is being portrayed in this visual content? | Increased Muscle Damage in HIF-1α KOs Following Repeated Exercise(A) WT mice and HIF-1α KOs underwent a 4-d endurance test, in which animals were run to exhaustion on each of four successive days with a minimum of 22 h rest between trials. HIF-1α KOs demonstrated initially greater endurance under the protocol; however, by the second day, their endurance advantage was eliminated, and by the fourth day, HIF-1α KOs were running for a significantly shorter time (**p < 0.01) than on the first day, while WT animals were running for approximately similar times as on the first day. Repeated measures ANOVA revealed that the decrease in performance on each successive day was unique to HIF-1α KOs (p < 0.05).(B) Example of hematoxylin and eosin staining of gastrocnemius muscles after 1 d of recovery by mice after the 4-d endurance test. Evidence of greater damage can be seen in HIF-1α KO muscles compared to WT muscles.(C) Example of PCNA staining of gastrocnemius muscles from exercised mice, demonstrating increased levels of muscle regeneration in HIF-1α KOs.(D) Number of PCNA-positive nuclei per square millimeter in gastrocnemius muscles of WT mice (n = 5) and HIF-1α KOs (n = 7) that ran repeatedly for 4 d. Although HIF-1α KOs have almost twice as many PCNA-positive nuclei per square millimeter, the difference is not significant, because of wild variations in that population. F-test analysis of the data reveals that the variance is much greater in the HIF-1α KO population than the WT population (p < 0.05). |
PMC514537_pbio-0020288-g007_292.jpg | What does this image primarily show? | Increased Muscle Damage in HIF-1α KOs Following Repeated Exercise(A) WT mice and HIF-1α KOs underwent a 4-d endurance test, in which animals were run to exhaustion on each of four successive days with a minimum of 22 h rest between trials. HIF-1α KOs demonstrated initially greater endurance under the protocol; however, by the second day, their endurance advantage was eliminated, and by the fourth day, HIF-1α KOs were running for a significantly shorter time (**p < 0.01) than on the first day, while WT animals were running for approximately similar times as on the first day. Repeated measures ANOVA revealed that the decrease in performance on each successive day was unique to HIF-1α KOs (p < 0.05).(B) Example of hematoxylin and eosin staining of gastrocnemius muscles after 1 d of recovery by mice after the 4-d endurance test. Evidence of greater damage can be seen in HIF-1α KO muscles compared to WT muscles.(C) Example of PCNA staining of gastrocnemius muscles from exercised mice, demonstrating increased levels of muscle regeneration in HIF-1α KOs.(D) Number of PCNA-positive nuclei per square millimeter in gastrocnemius muscles of WT mice (n = 5) and HIF-1α KOs (n = 7) that ran repeatedly for 4 d. Although HIF-1α KOs have almost twice as many PCNA-positive nuclei per square millimeter, the difference is not significant, because of wild variations in that population. F-test analysis of the data reveals that the variance is much greater in the HIF-1α KO population than the WT population (p < 0.05). |
PMC514603_F2_300.jpg | What key item or scene is captured in this photo? | Cytotoxicity and OAS1 induction with RNAi vectors. In A, morphology was observed using phase contrast microscopy of non-transduced IS-1 cells, or cells six days after transduction with vectors leading to expression of no shRNA (U6PT), a 25 mer shRNA targeting PAI-2 (sh325) and a scrambled 25 mer control shRNA (sh325scr). B shows comparison of OAS1 expression in non-transduced cells or cells four days after transduction with U6PT, sh325 and sh325scr vectors, by QRT-PCR. Each target gene was detected in duplicate, error bars represent the standard deviation of mean values. |
PMC514603_F2_298.jpg | What is being portrayed in this visual content? | Cytotoxicity and OAS1 induction with RNAi vectors. In A, morphology was observed using phase contrast microscopy of non-transduced IS-1 cells, or cells six days after transduction with vectors leading to expression of no shRNA (U6PT), a 25 mer shRNA targeting PAI-2 (sh325) and a scrambled 25 mer control shRNA (sh325scr). B shows comparison of OAS1 expression in non-transduced cells or cells four days after transduction with U6PT, sh325 and sh325scr vectors, by QRT-PCR. Each target gene was detected in duplicate, error bars represent the standard deviation of mean values. |
PMC514603_F2_299.jpg | What's the most prominent thing you notice in this picture? | Cytotoxicity and OAS1 induction with RNAi vectors. In A, morphology was observed using phase contrast microscopy of non-transduced IS-1 cells, or cells six days after transduction with vectors leading to expression of no shRNA (U6PT), a 25 mer shRNA targeting PAI-2 (sh325) and a scrambled 25 mer control shRNA (sh325scr). B shows comparison of OAS1 expression in non-transduced cells or cells four days after transduction with U6PT, sh325 and sh325scr vectors, by QRT-PCR. Each target gene was detected in duplicate, error bars represent the standard deviation of mean values. |
PMC514603_F2_297.jpg | What is the main focus of this visual representation? | Cytotoxicity and OAS1 induction with RNAi vectors. In A, morphology was observed using phase contrast microscopy of non-transduced IS-1 cells, or cells six days after transduction with vectors leading to expression of no shRNA (U6PT), a 25 mer shRNA targeting PAI-2 (sh325) and a scrambled 25 mer control shRNA (sh325scr). B shows comparison of OAS1 expression in non-transduced cells or cells four days after transduction with U6PT, sh325 and sh325scr vectors, by QRT-PCR. Each target gene was detected in duplicate, error bars represent the standard deviation of mean values. |
PMC514604_F1_303.jpg | What does this image primarily show? | CS17 OPT model (a). still shot from movie of 3D OPT model of a CS17 human embryo (approximately 41 days of development). bv, blood vessel; drg, dorsal root ganglion; h, heart; H, hindbrain; l, liver; T, telencephalon; v, vertebrae. (b; Additional file 1) Mpeg movie of 3D CS17 OPT model. |
PMC514604_F3_307.jpg | What's the most prominent thing you notice in this picture? | Painted anatomical domains. Fourteen regions of the central nervous system in the CS17 specimen have been defined and painted. Forebrain, red (secondary prosencephalon), dark orange (prosomere 3 including ventral thalamus), light orange (prosomere 2 including dorsal thalamus) and yellow (prosomere 1 including pretectum); midbrain, light green; hindbrain; isthmus, dark green; various shades of blue and purple indicate rhombomeres 1–6 and the caudal medulla oblongata; spinal cord, dark red. (a; Additional file 2) In the Mpeg movie sagittal and transverse views of the painted model are shown, together with a representation of the 3D domains. The model is first sectioned in the transverse plane. This section plane has been matched to that of the histology sections shown in fig 2. As the section is moved through the model the corresponding position is displayed in the 3D box, and by a line on the sagittal section. The model is then moved through the sagittal plane, and the position shown by a line on the transverse section. A snapshot of the fourteen 3D anatomical domains (b), and two examples of painted sections that intersect several anatomic domains (i.e., are topologically nearly horizontal to the reconstructed transverse boundaries) (c). The position of the two digital transverse sections is indicated by white lines on the 3D view. |
PMC514604_F5_305.jpg | What is the core subject represented in this visual? | 3 dimensional gene expression domains. A surface rendered model of the 3D expression pattern of PAX6. Separate gene expression domains in the forebrain and hindbrain are shown in green. For reference the neural tube has been painted pale grey and the eye dark grey. The diencephalon/midbrain (D/M) boundary, the absence of staining in the zona limitans intrathalamica (zli), plus the forebrain alar-basal boundary and the striatopallidal boundary in the basal telencephalon can be seen by viewing the 3D model at various angles (a, frontal and b, lateral). (c; Additional file 3) Mpeg movie of the PAX6 expression domain. |
PMC514604_F5_304.jpg | What is the core subject represented in this visual? | 3 dimensional gene expression domains. A surface rendered model of the 3D expression pattern of PAX6. Separate gene expression domains in the forebrain and hindbrain are shown in green. For reference the neural tube has been painted pale grey and the eye dark grey. The diencephalon/midbrain (D/M) boundary, the absence of staining in the zona limitans intrathalamica (zli), plus the forebrain alar-basal boundary and the striatopallidal boundary in the basal telencephalon can be seen by viewing the 3D model at various angles (a, frontal and b, lateral). (c; Additional file 3) Mpeg movie of the PAX6 expression domain. |
PMC514614_F7_308.jpg | What is the main focus of this visual representation? | Biopsy form grafted area of the lower eyelid. Hematoxylene-eosin staining, × 100 magnification. |
PMC514615_F1_309.jpg | What is the dominant medical problem in this image? | (a) Duodenoscopy showing a 3 × 3 cm protruding tumor with two ulcerations located opposite the ampulla of Vater in the second portion of the duodenum. (b) Hypotonic duodenography showing the donuts-shape tumor in the duodenum. |
PMC514615_F1_310.jpg | What key item or scene is captured in this photo? | (a) Duodenoscopy showing a 3 × 3 cm protruding tumor with two ulcerations located opposite the ampulla of Vater in the second portion of the duodenum. (b) Hypotonic duodenography showing the donuts-shape tumor in the duodenum. |
PMC514615_F2_311.jpg | What is the main focus of this visual representation? | Macroscopic and microscopic findings of the tumor. (a) Gross appearance of the tumor. The tumor was divided into two components, component A (round shape) and B (crescent shape). (b) Photomicrograph of the gross appearance of the tumor (Hematoxylin and eosin X 2). (c) Photomicrograph of the component A showing fibrous tissue, small nuclei, and clear nucleoli. (Hematoxylin and Eosin X 40). (d) Photomicrograph of the component B showing more anaplastic features typical of small-cell carcinoma, such as sheets of tightly packed anaplastic cells with round nuclei and scanty cytoplasm. (Hematoxylin and Eosin X 40). |
PMC514615_F2_312.jpg | Describe the main subject of this image. | Macroscopic and microscopic findings of the tumor. (a) Gross appearance of the tumor. The tumor was divided into two components, component A (round shape) and B (crescent shape). (b) Photomicrograph of the gross appearance of the tumor (Hematoxylin and eosin X 2). (c) Photomicrograph of the component A showing fibrous tissue, small nuclei, and clear nucleoli. (Hematoxylin and Eosin X 40). (d) Photomicrograph of the component B showing more anaplastic features typical of small-cell carcinoma, such as sheets of tightly packed anaplastic cells with round nuclei and scanty cytoplasm. (Hematoxylin and Eosin X 40). |
PMC514652_F4_315.jpg | What object or scene is depicted here? | Computational models of wild type S1P4 and its E3.29(122)Q mutant with S1P and LPA species. Computational models of the complexes between the wild type S1P4 or its E3.29(122)Q mutant with S1P or various LPA species generated by Autodock 3.0 and minimised using the MMFF94 forcefield in the MOE program. Complexes in each panel are shown from the same viewpoint with the extracellular end of the receptors oriented to the top of the figure. Standard element color codes are used with grey, white red, blue and magenta representing carbon, hydrogen, oxygen, nitrogen and phosphorous. Ribbons are shaded from red at the amino-terminus to blue at the carboxy-terminus. (A) Model of the complex between S1P (spacefilling) and the wild type S1P4 receptor. Residues in the receptor involved in ion pairs with S1P are shown as stick models and labelled. (B) Superimposition of the wild type S1P4 complex with S1P (orange) and the E3.29(122)Q S1P4 mutant complex with 14:0 LPA (green). For clarity, the only position at which the modelled amino acid position is shown for both receptor models is 3.29(122). Other residues had very similar optimised positions in the two model structures. (C) Superimposition of wild type S1P4 complexes with 18:1 LPA (cyan), 16:0 LPA (yellow) and 14:0 LPA (green) on E3.29(122)Q mutant complexes with 18:1 LPA (blue-green), 16:0 LPA (gold) and S1P (orange). For clarity, the only position at which modelled amino acid position is shown for both the wild type and mutant receptor models is 3.29(122). Other residues had very similar optimised positions in all model structures. (D) Space-filling models which represent the minimised extended conformation of each structure were constructed using SYBYL 6.9 software (Tripos Inc., St. Louis, MO., U.S.A.). The distance between phosphorus and terminal carbon atoms was predicted for each structure listed from top to bottom: 18:1 LPA, 27.0 Å; 16:0 LPA, 26.7 Å; 14:0 LPA, 24.2 Å; S1P, 24.0 Å. |
PMC514652_F4_314.jpg | What's the most prominent thing you notice in this picture? | Computational models of wild type S1P4 and its E3.29(122)Q mutant with S1P and LPA species. Computational models of the complexes between the wild type S1P4 or its E3.29(122)Q mutant with S1P or various LPA species generated by Autodock 3.0 and minimised using the MMFF94 forcefield in the MOE program. Complexes in each panel are shown from the same viewpoint with the extracellular end of the receptors oriented to the top of the figure. Standard element color codes are used with grey, white red, blue and magenta representing carbon, hydrogen, oxygen, nitrogen and phosphorous. Ribbons are shaded from red at the amino-terminus to blue at the carboxy-terminus. (A) Model of the complex between S1P (spacefilling) and the wild type S1P4 receptor. Residues in the receptor involved in ion pairs with S1P are shown as stick models and labelled. (B) Superimposition of the wild type S1P4 complex with S1P (orange) and the E3.29(122)Q S1P4 mutant complex with 14:0 LPA (green). For clarity, the only position at which the modelled amino acid position is shown for both receptor models is 3.29(122). Other residues had very similar optimised positions in the two model structures. (C) Superimposition of wild type S1P4 complexes with 18:1 LPA (cyan), 16:0 LPA (yellow) and 14:0 LPA (green) on E3.29(122)Q mutant complexes with 18:1 LPA (blue-green), 16:0 LPA (gold) and S1P (orange). For clarity, the only position at which modelled amino acid position is shown for both the wild type and mutant receptor models is 3.29(122). Other residues had very similar optimised positions in all model structures. (D) Space-filling models which represent the minimised extended conformation of each structure were constructed using SYBYL 6.9 software (Tripos Inc., St. Louis, MO., U.S.A.). The distance between phosphorus and terminal carbon atoms was predicted for each structure listed from top to bottom: 18:1 LPA, 27.0 Å; 16:0 LPA, 26.7 Å; 14:0 LPA, 24.2 Å; S1P, 24.0 Å. |
PMC514703_F4_322.jpg | What is the dominant medical problem in this image? | Expression pattern of a bas-1::GFP reporter fusion in transgenic Roller worms. (Panels A-C are from the same adult hermaphrodite. Ventral is down and anterior to the right.) A. Ventral, slightly oblique view of the head, showing NSMs, CEPDs, ADEL and likely AIMs. B. Same head, higher (more dorsal) focal plane, showing CEPDs and ADER. C. Photomontage showing ventral oblique view of HSNs and their processes in the ventral nerve cord; note also apparent labeling of muscles associated with the vulva. A second worm is immediately adjacent above, obscuring the edge of the worm shown. (Panels D-F: Anterior is to the left.) D. Adult hermaphrodite head, ventral view, chosen to show the characteristic highly varicose processes of the NSM cells within the isthmus of the pharynx. E. Larval head, ventral view with fluorescence and brightfield. This clearly shows the location of the NSM somata in the ventral pharynx, anterior bulb; it also shows the serotonergic ADF neurons not seen in A, B. CEPDs would be seen in a dorsal focal plane in this worm. F. Adult hermaphrodite lateral view of body wall. Ventral is down. Shows HSN and PDE; note PDE process extending ventrally toward the ventral nerve cord and dendrite extending dorsally into postdeirid sensillum. Twisting of the body axis associated with Roller phenotype makes HSN and PDE somata appear at the same lateral level when HSN is actually located sublateral and PDE subdorsal; twisting also takes ventral nerve cord out of plane of focus in the right of the panel. (Panels G – I are from males; anterior is to the right.) G. Late L4 male tail showing ray neurons (RNs) with processes extending into the rays. In some males we saw spicule cell staining likely belonging to spicule socket cells (SpSo). Ventral, slightly oblique view. H. Adult male tail showing RNs and their neurites in rays 7 and 9 on the right side, view ventral, slightly oblique. I. Male-specific ventral nerve cord motoneurons CP5 and CP6, the CP neurons most commonly expressing the transgene. The PDE soma in the lateral body wall is out of the plane of focus. |
PMC514703_F4_319.jpg | Describe the main subject of this image. | Expression pattern of a bas-1::GFP reporter fusion in transgenic Roller worms. (Panels A-C are from the same adult hermaphrodite. Ventral is down and anterior to the right.) A. Ventral, slightly oblique view of the head, showing NSMs, CEPDs, ADEL and likely AIMs. B. Same head, higher (more dorsal) focal plane, showing CEPDs and ADER. C. Photomontage showing ventral oblique view of HSNs and their processes in the ventral nerve cord; note also apparent labeling of muscles associated with the vulva. A second worm is immediately adjacent above, obscuring the edge of the worm shown. (Panels D-F: Anterior is to the left.) D. Adult hermaphrodite head, ventral view, chosen to show the characteristic highly varicose processes of the NSM cells within the isthmus of the pharynx. E. Larval head, ventral view with fluorescence and brightfield. This clearly shows the location of the NSM somata in the ventral pharynx, anterior bulb; it also shows the serotonergic ADF neurons not seen in A, B. CEPDs would be seen in a dorsal focal plane in this worm. F. Adult hermaphrodite lateral view of body wall. Ventral is down. Shows HSN and PDE; note PDE process extending ventrally toward the ventral nerve cord and dendrite extending dorsally into postdeirid sensillum. Twisting of the body axis associated with Roller phenotype makes HSN and PDE somata appear at the same lateral level when HSN is actually located sublateral and PDE subdorsal; twisting also takes ventral nerve cord out of plane of focus in the right of the panel. (Panels G – I are from males; anterior is to the right.) G. Late L4 male tail showing ray neurons (RNs) with processes extending into the rays. In some males we saw spicule cell staining likely belonging to spicule socket cells (SpSo). Ventral, slightly oblique view. H. Adult male tail showing RNs and their neurites in rays 7 and 9 on the right side, view ventral, slightly oblique. I. Male-specific ventral nerve cord motoneurons CP5 and CP6, the CP neurons most commonly expressing the transgene. The PDE soma in the lateral body wall is out of the plane of focus. |
PMC514703_F4_323.jpg | What stands out most in this visual? | Expression pattern of a bas-1::GFP reporter fusion in transgenic Roller worms. (Panels A-C are from the same adult hermaphrodite. Ventral is down and anterior to the right.) A. Ventral, slightly oblique view of the head, showing NSMs, CEPDs, ADEL and likely AIMs. B. Same head, higher (more dorsal) focal plane, showing CEPDs and ADER. C. Photomontage showing ventral oblique view of HSNs and their processes in the ventral nerve cord; note also apparent labeling of muscles associated with the vulva. A second worm is immediately adjacent above, obscuring the edge of the worm shown. (Panels D-F: Anterior is to the left.) D. Adult hermaphrodite head, ventral view, chosen to show the characteristic highly varicose processes of the NSM cells within the isthmus of the pharynx. E. Larval head, ventral view with fluorescence and brightfield. This clearly shows the location of the NSM somata in the ventral pharynx, anterior bulb; it also shows the serotonergic ADF neurons not seen in A, B. CEPDs would be seen in a dorsal focal plane in this worm. F. Adult hermaphrodite lateral view of body wall. Ventral is down. Shows HSN and PDE; note PDE process extending ventrally toward the ventral nerve cord and dendrite extending dorsally into postdeirid sensillum. Twisting of the body axis associated with Roller phenotype makes HSN and PDE somata appear at the same lateral level when HSN is actually located sublateral and PDE subdorsal; twisting also takes ventral nerve cord out of plane of focus in the right of the panel. (Panels G – I are from males; anterior is to the right.) G. Late L4 male tail showing ray neurons (RNs) with processes extending into the rays. In some males we saw spicule cell staining likely belonging to spicule socket cells (SpSo). Ventral, slightly oblique view. H. Adult male tail showing RNs and their neurites in rays 7 and 9 on the right side, view ventral, slightly oblique. I. Male-specific ventral nerve cord motoneurons CP5 and CP6, the CP neurons most commonly expressing the transgene. The PDE soma in the lateral body wall is out of the plane of focus. |
PMC514703_F4_320.jpg | What is the focal point of this photograph? | Expression pattern of a bas-1::GFP reporter fusion in transgenic Roller worms. (Panels A-C are from the same adult hermaphrodite. Ventral is down and anterior to the right.) A. Ventral, slightly oblique view of the head, showing NSMs, CEPDs, ADEL and likely AIMs. B. Same head, higher (more dorsal) focal plane, showing CEPDs and ADER. C. Photomontage showing ventral oblique view of HSNs and their processes in the ventral nerve cord; note also apparent labeling of muscles associated with the vulva. A second worm is immediately adjacent above, obscuring the edge of the worm shown. (Panels D-F: Anterior is to the left.) D. Adult hermaphrodite head, ventral view, chosen to show the characteristic highly varicose processes of the NSM cells within the isthmus of the pharynx. E. Larval head, ventral view with fluorescence and brightfield. This clearly shows the location of the NSM somata in the ventral pharynx, anterior bulb; it also shows the serotonergic ADF neurons not seen in A, B. CEPDs would be seen in a dorsal focal plane in this worm. F. Adult hermaphrodite lateral view of body wall. Ventral is down. Shows HSN and PDE; note PDE process extending ventrally toward the ventral nerve cord and dendrite extending dorsally into postdeirid sensillum. Twisting of the body axis associated with Roller phenotype makes HSN and PDE somata appear at the same lateral level when HSN is actually located sublateral and PDE subdorsal; twisting also takes ventral nerve cord out of plane of focus in the right of the panel. (Panels G – I are from males; anterior is to the right.) G. Late L4 male tail showing ray neurons (RNs) with processes extending into the rays. In some males we saw spicule cell staining likely belonging to spicule socket cells (SpSo). Ventral, slightly oblique view. H. Adult male tail showing RNs and their neurites in rays 7 and 9 on the right side, view ventral, slightly oblique. I. Male-specific ventral nerve cord motoneurons CP5 and CP6, the CP neurons most commonly expressing the transgene. The PDE soma in the lateral body wall is out of the plane of focus. |
PMC514711_F2_329.jpg | What key item or scene is captured in this photo? | In-frame <EYOR> transposition events in the voltage sensitive integral membrane motor protein, Prestin. Visual screening of transiently transfected HEK-293 cells revealed truncated Prestin-YFP fusion proteins generated by in-frame <EYOR> transpositions (A) (scale bar = 20 μm). Alternate digestion and re-ligation of an in-frame clone with either Srf I or Asc I produces identical full-length YFP- (B) and CFP-fusion proteins (C). In-frame <EYOR> insertions in Prestin are identified by the first of 3 target amino acids duplicated during transposition (D). Redundant insertions are indicated by the number of recovered clones (e.g. 3x). |
PMC514711_F2_330.jpg | What is the core subject represented in this visual? | In-frame <EYOR> transposition events in the voltage sensitive integral membrane motor protein, Prestin. Visual screening of transiently transfected HEK-293 cells revealed truncated Prestin-YFP fusion proteins generated by in-frame <EYOR> transpositions (A) (scale bar = 20 μm). Alternate digestion and re-ligation of an in-frame clone with either Srf I or Asc I produces identical full-length YFP- (B) and CFP-fusion proteins (C). In-frame <EYOR> insertions in Prestin are identified by the first of 3 target amino acids duplicated during transposition (D). Redundant insertions are indicated by the number of recovered clones (e.g. 3x). |
PMC514711_F3_327.jpg | What is being portrayed in this visual content? | Transposition of the type 1 IP3R with the Double Barrel Transposon (<DBT>). Transient expression in HEK-293 cells allows identification of in-frame insertions producing truncated GFP- (A) or DsRed- (B) IP3R fusion proteins. Digestion and subsequent re-ligation produces a full-length fluorescent IP3R fusion protein (C) (Scale bar = 20 μm). |
PMC514711_F3_328.jpg | Can you identify the primary element in this image? | Transposition of the type 1 IP3R with the Double Barrel Transposon (<DBT>). Transient expression in HEK-293 cells allows identification of in-frame insertions producing truncated GFP- (A) or DsRed- (B) IP3R fusion proteins. Digestion and subsequent re-ligation produces a full-length fluorescent IP3R fusion protein (C) (Scale bar = 20 μm). |
PMC514711_F3_326.jpg | What stands out most in this visual? | Transposition of the type 1 IP3R with the Double Barrel Transposon (<DBT>). Transient expression in HEK-293 cells allows identification of in-frame insertions producing truncated GFP- (A) or DsRed- (B) IP3R fusion proteins. Digestion and subsequent re-ligation produces a full-length fluorescent IP3R fusion protein (C) (Scale bar = 20 μm). |
PMC514717_F2_336.jpg | What does this image primarily show? | Intracellular transport of endocytosed ligands. Cultures of LSEC were pulsed with both TRITC-FSA and FITC-AGG for 1 h at 4°C. Chasing was performed after removal of unbound ligand by washing, and transferring of the cultures to 37°C. The cultures were fixed after chase periods of 10 min or 2 h and examined in fluorescence microscope. At 10 min (A) all TRITC-FSA co-localized with FITC-AGG (yellow colour indicates co-localization) in large ring-shaped vesicles (large arrowheads), and some vesicles with only FITC-AGG were observed (small arrowheads). After 2 h (B), co-localization of FITC-AGG and TRITC-FSA in large vesicles (arrows) was observed together with big vesicles with only FITC-AGG (large arrowheads) and small vesicles with only TRITC-FSA (small arrowheads). Controls show a more perinuclear appearance of TRITC-FSA when pulsed and chased for 2 h alone (C). In other experiments, TRITC-FSA was injected intravenously 1.5 h before isolation of the cells. Following an additional 6.5 h of cultivation at 37°C cultures of LSEC were pulsed with FITC-FSA (D-E), FITC-collagen (F-G), or FITC-mannan (H-I) for 1 h at 4°C. Following a 10 min chase, the FITC-ligands were observed to appear in small vesicles (arrowheads), and did not co-localize with TRITC-FSA (D, F and H). After 2 h, the FITC-ligands were transported to perinuclear compartments that co-localized almost completely with TRITC-FSA (small arrows in E, G and I). Other cultures of LSEC were pulsed for 10 min at 37°C with FITC-bHA. Following a 20 min chase, the FITC-bHA was observed in vesicles distributed all over the cell (arrowheads in J), and a similar appearance was observed after 2 h (arrowheads in K). Occasionally, cells that did not take up TRITC-FSA in vivo, but endocytosed FITC-ligands in vitro (big arrow in I), were observed. Scale bars: 10 μm. |
PMC514717_F2_339.jpg | Can you identify the primary element in this image? | Intracellular transport of endocytosed ligands. Cultures of LSEC were pulsed with both TRITC-FSA and FITC-AGG for 1 h at 4°C. Chasing was performed after removal of unbound ligand by washing, and transferring of the cultures to 37°C. The cultures were fixed after chase periods of 10 min or 2 h and examined in fluorescence microscope. At 10 min (A) all TRITC-FSA co-localized with FITC-AGG (yellow colour indicates co-localization) in large ring-shaped vesicles (large arrowheads), and some vesicles with only FITC-AGG were observed (small arrowheads). After 2 h (B), co-localization of FITC-AGG and TRITC-FSA in large vesicles (arrows) was observed together with big vesicles with only FITC-AGG (large arrowheads) and small vesicles with only TRITC-FSA (small arrowheads). Controls show a more perinuclear appearance of TRITC-FSA when pulsed and chased for 2 h alone (C). In other experiments, TRITC-FSA was injected intravenously 1.5 h before isolation of the cells. Following an additional 6.5 h of cultivation at 37°C cultures of LSEC were pulsed with FITC-FSA (D-E), FITC-collagen (F-G), or FITC-mannan (H-I) for 1 h at 4°C. Following a 10 min chase, the FITC-ligands were observed to appear in small vesicles (arrowheads), and did not co-localize with TRITC-FSA (D, F and H). After 2 h, the FITC-ligands were transported to perinuclear compartments that co-localized almost completely with TRITC-FSA (small arrows in E, G and I). Other cultures of LSEC were pulsed for 10 min at 37°C with FITC-bHA. Following a 20 min chase, the FITC-bHA was observed in vesicles distributed all over the cell (arrowheads in J), and a similar appearance was observed after 2 h (arrowheads in K). Occasionally, cells that did not take up TRITC-FSA in vivo, but endocytosed FITC-ligands in vitro (big arrow in I), were observed. Scale bars: 10 μm. |
PMC514717_F2_341.jpg | What key item or scene is captured in this photo? | Intracellular transport of endocytosed ligands. Cultures of LSEC were pulsed with both TRITC-FSA and FITC-AGG for 1 h at 4°C. Chasing was performed after removal of unbound ligand by washing, and transferring of the cultures to 37°C. The cultures were fixed after chase periods of 10 min or 2 h and examined in fluorescence microscope. At 10 min (A) all TRITC-FSA co-localized with FITC-AGG (yellow colour indicates co-localization) in large ring-shaped vesicles (large arrowheads), and some vesicles with only FITC-AGG were observed (small arrowheads). After 2 h (B), co-localization of FITC-AGG and TRITC-FSA in large vesicles (arrows) was observed together with big vesicles with only FITC-AGG (large arrowheads) and small vesicles with only TRITC-FSA (small arrowheads). Controls show a more perinuclear appearance of TRITC-FSA when pulsed and chased for 2 h alone (C). In other experiments, TRITC-FSA was injected intravenously 1.5 h before isolation of the cells. Following an additional 6.5 h of cultivation at 37°C cultures of LSEC were pulsed with FITC-FSA (D-E), FITC-collagen (F-G), or FITC-mannan (H-I) for 1 h at 4°C. Following a 10 min chase, the FITC-ligands were observed to appear in small vesicles (arrowheads), and did not co-localize with TRITC-FSA (D, F and H). After 2 h, the FITC-ligands were transported to perinuclear compartments that co-localized almost completely with TRITC-FSA (small arrows in E, G and I). Other cultures of LSEC were pulsed for 10 min at 37°C with FITC-bHA. Following a 20 min chase, the FITC-bHA was observed in vesicles distributed all over the cell (arrowheads in J), and a similar appearance was observed after 2 h (arrowheads in K). Occasionally, cells that did not take up TRITC-FSA in vivo, but endocytosed FITC-ligands in vitro (big arrow in I), were observed. Scale bars: 10 μm. |
PMC514717_F2_343.jpg | What key item or scene is captured in this photo? | Intracellular transport of endocytosed ligands. Cultures of LSEC were pulsed with both TRITC-FSA and FITC-AGG for 1 h at 4°C. Chasing was performed after removal of unbound ligand by washing, and transferring of the cultures to 37°C. The cultures were fixed after chase periods of 10 min or 2 h and examined in fluorescence microscope. At 10 min (A) all TRITC-FSA co-localized with FITC-AGG (yellow colour indicates co-localization) in large ring-shaped vesicles (large arrowheads), and some vesicles with only FITC-AGG were observed (small arrowheads). After 2 h (B), co-localization of FITC-AGG and TRITC-FSA in large vesicles (arrows) was observed together with big vesicles with only FITC-AGG (large arrowheads) and small vesicles with only TRITC-FSA (small arrowheads). Controls show a more perinuclear appearance of TRITC-FSA when pulsed and chased for 2 h alone (C). In other experiments, TRITC-FSA was injected intravenously 1.5 h before isolation of the cells. Following an additional 6.5 h of cultivation at 37°C cultures of LSEC were pulsed with FITC-FSA (D-E), FITC-collagen (F-G), or FITC-mannan (H-I) for 1 h at 4°C. Following a 10 min chase, the FITC-ligands were observed to appear in small vesicles (arrowheads), and did not co-localize with TRITC-FSA (D, F and H). After 2 h, the FITC-ligands were transported to perinuclear compartments that co-localized almost completely with TRITC-FSA (small arrows in E, G and I). Other cultures of LSEC were pulsed for 10 min at 37°C with FITC-bHA. Following a 20 min chase, the FITC-bHA was observed in vesicles distributed all over the cell (arrowheads in J), and a similar appearance was observed after 2 h (arrowheads in K). Occasionally, cells that did not take up TRITC-FSA in vivo, but endocytosed FITC-ligands in vitro (big arrow in I), were observed. Scale bars: 10 μm. |
PMC514717_F2_344.jpg | Can you identify the primary element in this image? | Intracellular transport of endocytosed ligands. Cultures of LSEC were pulsed with both TRITC-FSA and FITC-AGG for 1 h at 4°C. Chasing was performed after removal of unbound ligand by washing, and transferring of the cultures to 37°C. The cultures were fixed after chase periods of 10 min or 2 h and examined in fluorescence microscope. At 10 min (A) all TRITC-FSA co-localized with FITC-AGG (yellow colour indicates co-localization) in large ring-shaped vesicles (large arrowheads), and some vesicles with only FITC-AGG were observed (small arrowheads). After 2 h (B), co-localization of FITC-AGG and TRITC-FSA in large vesicles (arrows) was observed together with big vesicles with only FITC-AGG (large arrowheads) and small vesicles with only TRITC-FSA (small arrowheads). Controls show a more perinuclear appearance of TRITC-FSA when pulsed and chased for 2 h alone (C). In other experiments, TRITC-FSA was injected intravenously 1.5 h before isolation of the cells. Following an additional 6.5 h of cultivation at 37°C cultures of LSEC were pulsed with FITC-FSA (D-E), FITC-collagen (F-G), or FITC-mannan (H-I) for 1 h at 4°C. Following a 10 min chase, the FITC-ligands were observed to appear in small vesicles (arrowheads), and did not co-localize with TRITC-FSA (D, F and H). After 2 h, the FITC-ligands were transported to perinuclear compartments that co-localized almost completely with TRITC-FSA (small arrows in E, G and I). Other cultures of LSEC were pulsed for 10 min at 37°C with FITC-bHA. Following a 20 min chase, the FITC-bHA was observed in vesicles distributed all over the cell (arrowheads in J), and a similar appearance was observed after 2 h (arrowheads in K). Occasionally, cells that did not take up TRITC-FSA in vivo, but endocytosed FITC-ligands in vitro (big arrow in I), were observed. Scale bars: 10 μm. |
PMC514717_F2_340.jpg | Describe the main subject of this image. | Intracellular transport of endocytosed ligands. Cultures of LSEC were pulsed with both TRITC-FSA and FITC-AGG for 1 h at 4°C. Chasing was performed after removal of unbound ligand by washing, and transferring of the cultures to 37°C. The cultures were fixed after chase periods of 10 min or 2 h and examined in fluorescence microscope. At 10 min (A) all TRITC-FSA co-localized with FITC-AGG (yellow colour indicates co-localization) in large ring-shaped vesicles (large arrowheads), and some vesicles with only FITC-AGG were observed (small arrowheads). After 2 h (B), co-localization of FITC-AGG and TRITC-FSA in large vesicles (arrows) was observed together with big vesicles with only FITC-AGG (large arrowheads) and small vesicles with only TRITC-FSA (small arrowheads). Controls show a more perinuclear appearance of TRITC-FSA when pulsed and chased for 2 h alone (C). In other experiments, TRITC-FSA was injected intravenously 1.5 h before isolation of the cells. Following an additional 6.5 h of cultivation at 37°C cultures of LSEC were pulsed with FITC-FSA (D-E), FITC-collagen (F-G), or FITC-mannan (H-I) for 1 h at 4°C. Following a 10 min chase, the FITC-ligands were observed to appear in small vesicles (arrowheads), and did not co-localize with TRITC-FSA (D, F and H). After 2 h, the FITC-ligands were transported to perinuclear compartments that co-localized almost completely with TRITC-FSA (small arrows in E, G and I). Other cultures of LSEC were pulsed for 10 min at 37°C with FITC-bHA. Following a 20 min chase, the FITC-bHA was observed in vesicles distributed all over the cell (arrowheads in J), and a similar appearance was observed after 2 h (arrowheads in K). Occasionally, cells that did not take up TRITC-FSA in vivo, but endocytosed FITC-ligands in vitro (big arrow in I), were observed. Scale bars: 10 μm. |
PMC514717_F2_335.jpg | What is being portrayed in this visual content? | Intracellular transport of endocytosed ligands. Cultures of LSEC were pulsed with both TRITC-FSA and FITC-AGG for 1 h at 4°C. Chasing was performed after removal of unbound ligand by washing, and transferring of the cultures to 37°C. The cultures were fixed after chase periods of 10 min or 2 h and examined in fluorescence microscope. At 10 min (A) all TRITC-FSA co-localized with FITC-AGG (yellow colour indicates co-localization) in large ring-shaped vesicles (large arrowheads), and some vesicles with only FITC-AGG were observed (small arrowheads). After 2 h (B), co-localization of FITC-AGG and TRITC-FSA in large vesicles (arrows) was observed together with big vesicles with only FITC-AGG (large arrowheads) and small vesicles with only TRITC-FSA (small arrowheads). Controls show a more perinuclear appearance of TRITC-FSA when pulsed and chased for 2 h alone (C). In other experiments, TRITC-FSA was injected intravenously 1.5 h before isolation of the cells. Following an additional 6.5 h of cultivation at 37°C cultures of LSEC were pulsed with FITC-FSA (D-E), FITC-collagen (F-G), or FITC-mannan (H-I) for 1 h at 4°C. Following a 10 min chase, the FITC-ligands were observed to appear in small vesicles (arrowheads), and did not co-localize with TRITC-FSA (D, F and H). After 2 h, the FITC-ligands were transported to perinuclear compartments that co-localized almost completely with TRITC-FSA (small arrows in E, G and I). Other cultures of LSEC were pulsed for 10 min at 37°C with FITC-bHA. Following a 20 min chase, the FITC-bHA was observed in vesicles distributed all over the cell (arrowheads in J), and a similar appearance was observed after 2 h (arrowheads in K). Occasionally, cells that did not take up TRITC-FSA in vivo, but endocytosed FITC-ligands in vitro (big arrow in I), were observed. Scale bars: 10 μm. |
PMC514717_F2_342.jpg | What is the principal component of this image? | Intracellular transport of endocytosed ligands. Cultures of LSEC were pulsed with both TRITC-FSA and FITC-AGG for 1 h at 4°C. Chasing was performed after removal of unbound ligand by washing, and transferring of the cultures to 37°C. The cultures were fixed after chase periods of 10 min or 2 h and examined in fluorescence microscope. At 10 min (A) all TRITC-FSA co-localized with FITC-AGG (yellow colour indicates co-localization) in large ring-shaped vesicles (large arrowheads), and some vesicles with only FITC-AGG were observed (small arrowheads). After 2 h (B), co-localization of FITC-AGG and TRITC-FSA in large vesicles (arrows) was observed together with big vesicles with only FITC-AGG (large arrowheads) and small vesicles with only TRITC-FSA (small arrowheads). Controls show a more perinuclear appearance of TRITC-FSA when pulsed and chased for 2 h alone (C). In other experiments, TRITC-FSA was injected intravenously 1.5 h before isolation of the cells. Following an additional 6.5 h of cultivation at 37°C cultures of LSEC were pulsed with FITC-FSA (D-E), FITC-collagen (F-G), or FITC-mannan (H-I) for 1 h at 4°C. Following a 10 min chase, the FITC-ligands were observed to appear in small vesicles (arrowheads), and did not co-localize with TRITC-FSA (D, F and H). After 2 h, the FITC-ligands were transported to perinuclear compartments that co-localized almost completely with TRITC-FSA (small arrows in E, G and I). Other cultures of LSEC were pulsed for 10 min at 37°C with FITC-bHA. Following a 20 min chase, the FITC-bHA was observed in vesicles distributed all over the cell (arrowheads in J), and a similar appearance was observed after 2 h (arrowheads in K). Occasionally, cells that did not take up TRITC-FSA in vivo, but endocytosed FITC-ligands in vitro (big arrow in I), were observed. Scale bars: 10 μm. |
PMC514718_F2_333.jpg | Describe the main subject of this image. | Echocardiography (45 months) long axis view. Myxoma in the left atrium prolapsing into the left ventricle. LV = left ventricle, My = myxoma |
PMC514718_F5_334.jpg | What object or scene is depicted here? | Right coronary artery (RCA) in 60 degree LAO position (45 months, pre-operative coronary angiography). White arrow = atypical vessels in the interatrial septum |
PMC514883_pbio-0020257-g010_346.jpg | What key item or scene is captured in this photo? | The Expressions of elo-5 and lpd-1 Reporter Constructs Are Spatially Similar(A and B) Nomarski and GFP-filtered images of an adult animal containing the lpd-1Prom::GFP construct, showing strong expression in two symmetrical head neurons, each of which has processes to the nose and around a nerve ring. Scale bars, 10 μm.(C) DiI staining of amphid neurons in lpd-1Prom::GFP (dsRed filter). Arrows indicate neuronal nuclei shown in (D). Scale bar, 10 μm.(D) GFP expression in the animal shown in (C). Scale bar, 10 μm.(E and F) Nomarski and GFP-filtered images of an animal containing elo-5Prom::GFP, revealing fluorescence in the similar amphid neuron. Scale bar, 7.5 μm.(G and H) The intestinal and intestinal-muscle GFP expression in (G) lpd-1Prom::GFP and (H) elo-5Prom::GFP constructs. Scale bar, 7.5 μm. |
PMC514883_pbio-0020257-g010_350.jpg | What is the focal point of this photograph? | The Expressions of elo-5 and lpd-1 Reporter Constructs Are Spatially Similar(A and B) Nomarski and GFP-filtered images of an adult animal containing the lpd-1Prom::GFP construct, showing strong expression in two symmetrical head neurons, each of which has processes to the nose and around a nerve ring. Scale bars, 10 μm.(C) DiI staining of amphid neurons in lpd-1Prom::GFP (dsRed filter). Arrows indicate neuronal nuclei shown in (D). Scale bar, 10 μm.(D) GFP expression in the animal shown in (C). Scale bar, 10 μm.(E and F) Nomarski and GFP-filtered images of an animal containing elo-5Prom::GFP, revealing fluorescence in the similar amphid neuron. Scale bar, 7.5 μm.(G and H) The intestinal and intestinal-muscle GFP expression in (G) lpd-1Prom::GFP and (H) elo-5Prom::GFP constructs. Scale bar, 7.5 μm. |
PMC514883_pbio-0020257-g010_345.jpg | What is being portrayed in this visual content? | The Expressions of elo-5 and lpd-1 Reporter Constructs Are Spatially Similar(A and B) Nomarski and GFP-filtered images of an adult animal containing the lpd-1Prom::GFP construct, showing strong expression in two symmetrical head neurons, each of which has processes to the nose and around a nerve ring. Scale bars, 10 μm.(C) DiI staining of amphid neurons in lpd-1Prom::GFP (dsRed filter). Arrows indicate neuronal nuclei shown in (D). Scale bar, 10 μm.(D) GFP expression in the animal shown in (C). Scale bar, 10 μm.(E and F) Nomarski and GFP-filtered images of an animal containing elo-5Prom::GFP, revealing fluorescence in the similar amphid neuron. Scale bar, 7.5 μm.(G and H) The intestinal and intestinal-muscle GFP expression in (G) lpd-1Prom::GFP and (H) elo-5Prom::GFP constructs. Scale bar, 7.5 μm. |
PMC514883_pbio-0020257-g010_351.jpg | What is the core subject represented in this visual? | The Expressions of elo-5 and lpd-1 Reporter Constructs Are Spatially Similar(A and B) Nomarski and GFP-filtered images of an adult animal containing the lpd-1Prom::GFP construct, showing strong expression in two symmetrical head neurons, each of which has processes to the nose and around a nerve ring. Scale bars, 10 μm.(C) DiI staining of amphid neurons in lpd-1Prom::GFP (dsRed filter). Arrows indicate neuronal nuclei shown in (D). Scale bar, 10 μm.(D) GFP expression in the animal shown in (C). Scale bar, 10 μm.(E and F) Nomarski and GFP-filtered images of an animal containing elo-5Prom::GFP, revealing fluorescence in the similar amphid neuron. Scale bar, 7.5 μm.(G and H) The intestinal and intestinal-muscle GFP expression in (G) lpd-1Prom::GFP and (H) elo-5Prom::GFP constructs. Scale bar, 7.5 μm. |
PMC514883_pbio-0020257-g010_349.jpg | What is the principal component of this image? | The Expressions of elo-5 and lpd-1 Reporter Constructs Are Spatially Similar(A and B) Nomarski and GFP-filtered images of an adult animal containing the lpd-1Prom::GFP construct, showing strong expression in two symmetrical head neurons, each of which has processes to the nose and around a nerve ring. Scale bars, 10 μm.(C) DiI staining of amphid neurons in lpd-1Prom::GFP (dsRed filter). Arrows indicate neuronal nuclei shown in (D). Scale bar, 10 μm.(D) GFP expression in the animal shown in (C). Scale bar, 10 μm.(E and F) Nomarski and GFP-filtered images of an animal containing elo-5Prom::GFP, revealing fluorescence in the similar amphid neuron. Scale bar, 7.5 μm.(G and H) The intestinal and intestinal-muscle GFP expression in (G) lpd-1Prom::GFP and (H) elo-5Prom::GFP constructs. Scale bar, 7.5 μm. |
PMC514883_pbio-0020257-g011_355.jpg | What is being portrayed in this visual content? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC514883_pbio-0020257-g011_359.jpg | What is being portrayed in this visual content? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC514883_pbio-0020257-g011_353.jpg | What key item or scene is captured in this photo? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC514883_pbio-0020257-g011_365.jpg | What is shown in this image? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC514883_pbio-0020257-g011_366.jpg | What does this image primarily show? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC514883_pbio-0020257-g011_364.jpg | What is the central feature of this picture? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC514883_pbio-0020257-g011_361.jpg | What stands out most in this visual? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC514883_pbio-0020257-g011_362.jpg | What is the focal point of this photograph? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC514883_pbio-0020257-g011_358.jpg | What is the dominant medical problem in this image? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC514883_pbio-0020257-g011_354.jpg | Can you identify the primary element in this image? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC514883_pbio-0020257-g011_363.jpg | What is the main focus of this visual representation? | The Expression of GFP Fusion Constructs Suggests the Involvement of lpd-1, acs-1, and pnk-1 in mmBCFA Biosynthesis(A–D) elo-5Prom::GFP expression is downregulated in the lpd-1(RNAi) background. Scale bars, 100 μm.(A and C) GFP-filtered images of (A) elo-5Prom::GFP and (C) elo-6Prom::GFP in wild-type animals, showing the characteristic bright intestinal fluorescence.(B and D) GFP-filtered images of (B) elo-5Prom::GFP and (D) elo-5Prom::GFP in lpd-1(RNAi) animals, revealing diminished fluorescence in the gut.(E–H) lpd-1 expression is upregulated in neurons of the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Scale bars, 15 μm.(E and F) Nomarski and GFP images of wild-type L1 larvae containing lpd-1Prom::GFP.
(G and H) Nomarski and GFP images of elo-5(RNAi)-treated animals (L1 arrested) containing lpd-1Prom::GFP, showing a visibly brighter fluorescence than that seen in (E) and (F). Circles are centered on the pharyngeal back bulb.(I–K) acs-1Prom::GFP expression is upregulated in the elo-5(RNAi) animals deficient for C15ISO and C17ISO. Panels show GFP images of acs-1Prom::GFP animals grown on the (I) control, (J) elo-5(RNAi), and (K) lpd-1(RNAi) plates. The fluorescence from acs-1Prom::GFP in (J) is significantly stronger than that in (I). Scale bars, 100 μm.(L–N) pnk-1Prom::GFP expression is upregulated by elo-5(RNAi) but downregulated by lpd-1(RNAi). Panels show GFP images of pnk-1Prom::GFP animals grown on the (L) control, (M) elo-5(RNAi), and (N) lpd-1(RNAi) plates. The fluorescence of the fusion construct is stronger in (M) but weaker in (N) than that in the control (L). Scale bars, 100 μm. |
PMC515295_F3_368.jpg | What key item or scene is captured in this photo? | pY504-C3G colocalizes with Hck and shows predominant Golgi and membrane localization. (A) pY504 C3G colocalizes with Hck. Cos-1 cells transfected with Hck and C3G were stained for pY504 C3G (Cy3) and Hck (FITC) and examined using a confocal microscope. Figure shows an optical section for the individual stains as well as that of the merged (Dual) image. (B) Cos-1 cells transfected with Hck and C3G were dual labeled to detect phospho-C3G (Cy3 staining) and C3G using the Flag tag antibody (FITC staining). Panels show optical sections taken using the confocal microscope. (C) pY504 C3G is localized to the Golgi apparatus. Cos-1 cells were transfected with Hck, C3G and VSVG-GFP expression constructs and stained using pY504 primary antibody and Cy3 conjugated secondary. An optical section taken using the apotome is represented. (D) HeLa or Cos-1 cells transfected with Hck and C3G were left untreated (control) or treated with pervanadate (PV) prior to fixation and stained for pY504. Counter staining with Dapi shows cell nuclei. |
PMC515295_F3_369.jpg | What is the dominant medical problem in this image? | pY504-C3G colocalizes with Hck and shows predominant Golgi and membrane localization. (A) pY504 C3G colocalizes with Hck. Cos-1 cells transfected with Hck and C3G were stained for pY504 C3G (Cy3) and Hck (FITC) and examined using a confocal microscope. Figure shows an optical section for the individual stains as well as that of the merged (Dual) image. (B) Cos-1 cells transfected with Hck and C3G were dual labeled to detect phospho-C3G (Cy3 staining) and C3G using the Flag tag antibody (FITC staining). Panels show optical sections taken using the confocal microscope. (C) pY504 C3G is localized to the Golgi apparatus. Cos-1 cells were transfected with Hck, C3G and VSVG-GFP expression constructs and stained using pY504 primary antibody and Cy3 conjugated secondary. An optical section taken using the apotome is represented. (D) HeLa or Cos-1 cells transfected with Hck and C3G were left untreated (control) or treated with pervanadate (PV) prior to fixation and stained for pY504. Counter staining with Dapi shows cell nuclei. |
PMC515295_F3_373.jpg | What does this image primarily show? | pY504-C3G colocalizes with Hck and shows predominant Golgi and membrane localization. (A) pY504 C3G colocalizes with Hck. Cos-1 cells transfected with Hck and C3G were stained for pY504 C3G (Cy3) and Hck (FITC) and examined using a confocal microscope. Figure shows an optical section for the individual stains as well as that of the merged (Dual) image. (B) Cos-1 cells transfected with Hck and C3G were dual labeled to detect phospho-C3G (Cy3 staining) and C3G using the Flag tag antibody (FITC staining). Panels show optical sections taken using the confocal microscope. (C) pY504 C3G is localized to the Golgi apparatus. Cos-1 cells were transfected with Hck, C3G and VSVG-GFP expression constructs and stained using pY504 primary antibody and Cy3 conjugated secondary. An optical section taken using the apotome is represented. (D) HeLa or Cos-1 cells transfected with Hck and C3G were left untreated (control) or treated with pervanadate (PV) prior to fixation and stained for pY504. Counter staining with Dapi shows cell nuclei. |
PMC515295_F3_370.jpg | What can you see in this picture? | pY504-C3G colocalizes with Hck and shows predominant Golgi and membrane localization. (A) pY504 C3G colocalizes with Hck. Cos-1 cells transfected with Hck and C3G were stained for pY504 C3G (Cy3) and Hck (FITC) and examined using a confocal microscope. Figure shows an optical section for the individual stains as well as that of the merged (Dual) image. (B) Cos-1 cells transfected with Hck and C3G were dual labeled to detect phospho-C3G (Cy3 staining) and C3G using the Flag tag antibody (FITC staining). Panels show optical sections taken using the confocal microscope. (C) pY504 C3G is localized to the Golgi apparatus. Cos-1 cells were transfected with Hck, C3G and VSVG-GFP expression constructs and stained using pY504 primary antibody and Cy3 conjugated secondary. An optical section taken using the apotome is represented. (D) HeLa or Cos-1 cells transfected with Hck and C3G were left untreated (control) or treated with pervanadate (PV) prior to fixation and stained for pY504. Counter staining with Dapi shows cell nuclei. |
PMC515295_F3_372.jpg | What is the main focus of this visual representation? | pY504-C3G colocalizes with Hck and shows predominant Golgi and membrane localization. (A) pY504 C3G colocalizes with Hck. Cos-1 cells transfected with Hck and C3G were stained for pY504 C3G (Cy3) and Hck (FITC) and examined using a confocal microscope. Figure shows an optical section for the individual stains as well as that of the merged (Dual) image. (B) Cos-1 cells transfected with Hck and C3G were dual labeled to detect phospho-C3G (Cy3 staining) and C3G using the Flag tag antibody (FITC staining). Panels show optical sections taken using the confocal microscope. (C) pY504 C3G is localized to the Golgi apparatus. Cos-1 cells were transfected with Hck, C3G and VSVG-GFP expression constructs and stained using pY504 primary antibody and Cy3 conjugated secondary. An optical section taken using the apotome is represented. (D) HeLa or Cos-1 cells transfected with Hck and C3G were left untreated (control) or treated with pervanadate (PV) prior to fixation and stained for pY504. Counter staining with Dapi shows cell nuclei. |
PMC515295_F3_371.jpg | What is the dominant medical problem in this image? | pY504-C3G colocalizes with Hck and shows predominant Golgi and membrane localization. (A) pY504 C3G colocalizes with Hck. Cos-1 cells transfected with Hck and C3G were stained for pY504 C3G (Cy3) and Hck (FITC) and examined using a confocal microscope. Figure shows an optical section for the individual stains as well as that of the merged (Dual) image. (B) Cos-1 cells transfected with Hck and C3G were dual labeled to detect phospho-C3G (Cy3 staining) and C3G using the Flag tag antibody (FITC staining). Panels show optical sections taken using the confocal microscope. (C) pY504 C3G is localized to the Golgi apparatus. Cos-1 cells were transfected with Hck, C3G and VSVG-GFP expression constructs and stained using pY504 primary antibody and Cy3 conjugated secondary. An optical section taken using the apotome is represented. (D) HeLa or Cos-1 cells transfected with Hck and C3G were left untreated (control) or treated with pervanadate (PV) prior to fixation and stained for pY504. Counter staining with Dapi shows cell nuclei. |
PMC516018_F2_378.jpg | What is being portrayed in this visual content? | Distribution of keratin IFs and HSP70i in hepatocytes from control and GF-fed C3H mice. A, C, E keratin IFs; B, D, F HSP70i; A, B) control; C, D) 2 week treatment; E, F) 5 month treatment. Arrows in E and F indicate reactive MBs with Troma 1 (anti-K8) and anti-HSP70i, respectively. Scale bar = 20 μm. |
PMC516018_F2_379.jpg | What is the main focus of this visual representation? | Distribution of keratin IFs and HSP70i in hepatocytes from control and GF-fed C3H mice. A, C, E keratin IFs; B, D, F HSP70i; A, B) control; C, D) 2 week treatment; E, F) 5 month treatment. Arrows in E and F indicate reactive MBs with Troma 1 (anti-K8) and anti-HSP70i, respectively. Scale bar = 20 μm. |
PMC516018_F2_383.jpg | Can you identify the primary element in this image? | Distribution of keratin IFs and HSP70i in hepatocytes from control and GF-fed C3H mice. A, C, E keratin IFs; B, D, F HSP70i; A, B) control; C, D) 2 week treatment; E, F) 5 month treatment. Arrows in E and F indicate reactive MBs with Troma 1 (anti-K8) and anti-HSP70i, respectively. Scale bar = 20 μm. |
PMC516018_F2_380.jpg | Can you identify the primary element in this image? | Distribution of keratin IFs and HSP70i in hepatocytes from control and GF-fed C3H mice. A, C, E keratin IFs; B, D, F HSP70i; A, B) control; C, D) 2 week treatment; E, F) 5 month treatment. Arrows in E and F indicate reactive MBs with Troma 1 (anti-K8) and anti-HSP70i, respectively. Scale bar = 20 μm. |
PMC516018_F3_400.jpg | What is shown in this image? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, F, I keratin IFs; B, D, E, G, H, J K8 pS79; A, B) control; C, D, E) 2 week treatment; F, G, H 6 week treatment; I, J 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79. Empty arrowheads in I and J indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F3_401.jpg | What is the central feature of this picture? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, F, I keratin IFs; B, D, E, G, H, J K8 pS79; A, B) control; C, D, E) 2 week treatment; F, G, H 6 week treatment; I, J 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79. Empty arrowheads in I and J indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F3_404.jpg | What does this image primarily show? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, F, I keratin IFs; B, D, E, G, H, J K8 pS79; A, B) control; C, D, E) 2 week treatment; F, G, H 6 week treatment; I, J 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79. Empty arrowheads in I and J indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F3_402.jpg | What object or scene is depicted here? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, F, I keratin IFs; B, D, E, G, H, J K8 pS79; A, B) control; C, D, E) 2 week treatment; F, G, H 6 week treatment; I, J 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79. Empty arrowheads in I and J indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F3_409.jpg | What stands out most in this visual? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, F, I keratin IFs; B, D, E, G, H, J K8 pS79; A, B) control; C, D, E) 2 week treatment; F, G, H 6 week treatment; I, J 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79. Empty arrowheads in I and J indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F3_408.jpg | What is the focal point of this photograph? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, F, I keratin IFs; B, D, E, G, H, J K8 pS79; A, B) control; C, D, E) 2 week treatment; F, G, H 6 week treatment; I, J 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79. Empty arrowheads in I and J indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F3_406.jpg | What is the main focus of this visual representation? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, F, I keratin IFs; B, D, E, G, H, J K8 pS79; A, B) control; C, D, E) 2 week treatment; F, G, H 6 week treatment; I, J 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79. Empty arrowheads in I and J indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F3_405.jpg | What can you see in this picture? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, F, I keratin IFs; B, D, E, G, H, J K8 pS79; A, B) control; C, D, E) 2 week treatment; F, G, H 6 week treatment; I, J 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79. Empty arrowheads in I and J indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F4_396.jpg | What's the most prominent thing you notice in this picture? | Distribution of keratin IFs and K8 pS436 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS436; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H); 5 month treatment. Arrows in D indicate clusters of cells containing K8 pS436. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and 5B3 (anti-K8 pS436), respectively. Scale bar = 20 μm. |
PMC516018_F4_397.jpg | What is the central feature of this picture? | Distribution of keratin IFs and K8 pS436 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS436; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H); 5 month treatment. Arrows in D indicate clusters of cells containing K8 pS436. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and 5B3 (anti-K8 pS436), respectively. Scale bar = 20 μm. |
PMC516018_F4_392.jpg | What is the focal point of this photograph? | Distribution of keratin IFs and K8 pS436 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS436; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H); 5 month treatment. Arrows in D indicate clusters of cells containing K8 pS436. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and 5B3 (anti-K8 pS436), respectively. Scale bar = 20 μm. |
PMC516018_F4_395.jpg | What is the core subject represented in this visual? | Distribution of keratin IFs and K8 pS436 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS436; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H); 5 month treatment. Arrows in D indicate clusters of cells containing K8 pS436. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and 5B3 (anti-K8 pS436), respectively. Scale bar = 20 μm. |
PMC516018_F4_393.jpg | What does this image primarily show? | Distribution of keratin IFs and K8 pS436 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS436; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H); 5 month treatment. Arrows in D indicate clusters of cells containing K8 pS436. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and 5B3 (anti-K8 pS436), respectively. Scale bar = 20 μm. |
PMC516018_F4_398.jpg | What is shown in this image? | Distribution of keratin IFs and K8 pS436 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS436; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H); 5 month treatment. Arrows in D indicate clusters of cells containing K8 pS436. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and 5B3 (anti-K8 pS436), respectively. Scale bar = 20 μm. |
PMC516018_F4_399.jpg | What is the dominant medical problem in this image? | Distribution of keratin IFs and K8 pS436 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS436; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H); 5 month treatment. Arrows in D indicate clusters of cells containing K8 pS436. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and 5B3 (anti-K8 pS436), respectively. Scale bar = 20 μm. |
PMC516018_F5_418.jpg | What is being portrayed in this visual content? | Distribution of keratin IFs and K18 pS33 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K18 pS33; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Asterisk in D shows an hepatocyte containing a high level of K18 pS33; arrow indicates a dilated bile canaliculi. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and Ab8250 (anti-K18 pS33), respectively. Scale bar = 20 μm. |
PMC516018_F5_420.jpg | What can you see in this picture? | Distribution of keratin IFs and K18 pS33 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K18 pS33; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Asterisk in D shows an hepatocyte containing a high level of K18 pS33; arrow indicates a dilated bile canaliculi. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and Ab8250 (anti-K18 pS33), respectively. Scale bar = 20 μm. |
PMC516018_F5_416.jpg | What does this image primarily show? | Distribution of keratin IFs and K18 pS33 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K18 pS33; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Asterisk in D shows an hepatocyte containing a high level of K18 pS33; arrow indicates a dilated bile canaliculi. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and Ab8250 (anti-K18 pS33), respectively. Scale bar = 20 μm. |
PMC516018_F5_422.jpg | Can you identify the primary element in this image? | Distribution of keratin IFs and K18 pS33 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K18 pS33; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Asterisk in D shows an hepatocyte containing a high level of K18 pS33; arrow indicates a dilated bile canaliculi. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and Ab8250 (anti-K18 pS33), respectively. Scale bar = 20 μm. |
PMC516018_F5_415.jpg | What is the main focus of this visual representation? | Distribution of keratin IFs and K18 pS33 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K18 pS33; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Asterisk in D shows an hepatocyte containing a high level of K18 pS33; arrow indicates a dilated bile canaliculi. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and Ab8250 (anti-K18 pS33), respectively. Scale bar = 20 μm. |
PMC516018_F5_421.jpg | What does this image primarily show? | Distribution of keratin IFs and K18 pS33 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K18 pS33; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Asterisk in D shows an hepatocyte containing a high level of K18 pS33; arrow indicates a dilated bile canaliculi. Filled arrowheads in G and H indicate reactive MBs with Troma 1 and Ab8250 (anti-K18 pS33), respectively. Scale bar = 20 μm. |
PMC516018_F7_385.jpg | What is the focal point of this photograph? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS79; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79; asterisk shows a damaged hepatocyte. Filled arrowheads in G and H indicate MBs reactive with Troma 1 and LJ4 (anti-K8 pS79), respectively; empty arrowheads indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F7_388.jpg | What does this image primarily show? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS79; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79; asterisk shows a damaged hepatocyte. Filled arrowheads in G and H indicate MBs reactive with Troma 1 and LJ4 (anti-K8 pS79), respectively; empty arrowheads indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F7_391.jpg | What stands out most in this visual? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS79; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79; asterisk shows a damaged hepatocyte. Filled arrowheads in G and H indicate MBs reactive with Troma 1 and LJ4 (anti-K8 pS79), respectively; empty arrowheads indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F7_390.jpg | What is the central feature of this picture? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS79; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79; asterisk shows a damaged hepatocyte. Filled arrowheads in G and H indicate MBs reactive with Troma 1 and LJ4 (anti-K8 pS79), respectively; empty arrowheads indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F7_389.jpg | What can you see in this picture? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS79; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79; asterisk shows a damaged hepatocyte. Filled arrowheads in G and H indicate MBs reactive with Troma 1 and LJ4 (anti-K8 pS79), respectively; empty arrowheads indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F7_386.jpg | Can you identify the primary element in this image? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS79; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79; asterisk shows a damaged hepatocyte. Filled arrowheads in G and H indicate MBs reactive with Troma 1 and LJ4 (anti-K8 pS79), respectively; empty arrowheads indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F7_384.jpg | What is the dominant medical problem in this image? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS79; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79; asterisk shows a damaged hepatocyte. Filled arrowheads in G and H indicate MBs reactive with Troma 1 and LJ4 (anti-K8 pS79), respectively; empty arrowheads indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
PMC516018_F7_387.jpg | What can you see in this picture? | Distribution of keratin IFs and K8 pS79 in hepatocytes from control and GF-fed C3H mice. A, C, E, G keratin IFs; B, D, F, H K8 pS79; A, B) control; C, D) 2 week treatment; E, F) 6 week treatment; G, H) 5 month treatment. Arrow in D indicates clusters of cells containing K8 pS79; asterisk shows a damaged hepatocyte. Filled arrowheads in G and H indicate MBs reactive with Troma 1 and LJ4 (anti-K8 pS79), respectively; empty arrowheads indicate MBs reactive with Troma 1 but not with LJ4 (anti-K8 pS79), respectively. Scale bar = 20 μm. |
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