image stringlengths 20 66 | question stringclasses 16
values | answer stringlengths 3 10.7k |
|---|---|---|
PMC1751061_F2_8064.jpg | What is being portrayed in this visual content? | Early and late magnetic resonance imaging (MRI) findings of heterotopic ossification (HO). HO in the right knee of a 35-year-old male patient hospitalised in the intensive care unit for traumatic brain injury. (a-d) First MRI performed on clinical suspicion of HO. (a) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows high signal of the innermost part of the vastus medialis muscle (arrows) and edema of the subcutaneous fat (arrowhead). (b) Sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (arrows). (c) Coronal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (white arrow) and vastus lateralis muscle (black arrow). (d) Mid-sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows joint effusion and synovial enhancement. (e-h) Follow-up MRI (e-g) and x-rays (h) performed 3 weeks later. (e) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). Sagittal (f) and coronal (g) contrast-enhanced fat-suppressed T1-weighted spin-echo MR images (650/17) show heterogeneous enhancement of the innermost part of the vastus medialis muscle (arrows). (h) Anteroposterior x-ray depicts a calcified mass at the anatomic position of the vastus medialis muscle (arrow). |
PMC1751061_F2_8063.jpg | What key item or scene is captured in this photo? | Early and late magnetic resonance imaging (MRI) findings of heterotopic ossification (HO). HO in the right knee of a 35-year-old male patient hospitalised in the intensive care unit for traumatic brain injury. (a-d) First MRI performed on clinical suspicion of HO. (a) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows high signal of the innermost part of the vastus medialis muscle (arrows) and edema of the subcutaneous fat (arrowhead). (b) Sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (arrows). (c) Coronal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (white arrow) and vastus lateralis muscle (black arrow). (d) Mid-sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows joint effusion and synovial enhancement. (e-h) Follow-up MRI (e-g) and x-rays (h) performed 3 weeks later. (e) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). Sagittal (f) and coronal (g) contrast-enhanced fat-suppressed T1-weighted spin-echo MR images (650/17) show heterogeneous enhancement of the innermost part of the vastus medialis muscle (arrows). (h) Anteroposterior x-ray depicts a calcified mass at the anatomic position of the vastus medialis muscle (arrow). |
PMC1751061_F2_8065.jpg | What key item or scene is captured in this photo? | Early and late magnetic resonance imaging (MRI) findings of heterotopic ossification (HO). HO in the right knee of a 35-year-old male patient hospitalised in the intensive care unit for traumatic brain injury. (a-d) First MRI performed on clinical suspicion of HO. (a) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows high signal of the innermost part of the vastus medialis muscle (arrows) and edema of the subcutaneous fat (arrowhead). (b) Sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (arrows). (c) Coronal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (white arrow) and vastus lateralis muscle (black arrow). (d) Mid-sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows joint effusion and synovial enhancement. (e-h) Follow-up MRI (e-g) and x-rays (h) performed 3 weeks later. (e) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). Sagittal (f) and coronal (g) contrast-enhanced fat-suppressed T1-weighted spin-echo MR images (650/17) show heterogeneous enhancement of the innermost part of the vastus medialis muscle (arrows). (h) Anteroposterior x-ray depicts a calcified mass at the anatomic position of the vastus medialis muscle (arrow). |
PMC1751061_F2_8061.jpg | What stands out most in this visual? | Early and late magnetic resonance imaging (MRI) findings of heterotopic ossification (HO). HO in the right knee of a 35-year-old male patient hospitalised in the intensive care unit for traumatic brain injury. (a-d) First MRI performed on clinical suspicion of HO. (a) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows high signal of the innermost part of the vastus medialis muscle (arrows) and edema of the subcutaneous fat (arrowhead). (b) Sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (arrows). (c) Coronal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (white arrow) and vastus lateralis muscle (black arrow). (d) Mid-sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows joint effusion and synovial enhancement. (e-h) Follow-up MRI (e-g) and x-rays (h) performed 3 weeks later. (e) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). Sagittal (f) and coronal (g) contrast-enhanced fat-suppressed T1-weighted spin-echo MR images (650/17) show heterogeneous enhancement of the innermost part of the vastus medialis muscle (arrows). (h) Anteroposterior x-ray depicts a calcified mass at the anatomic position of the vastus medialis muscle (arrow). |
PMC1751061_F2_8062.jpg | Can you identify the primary element in this image? | Early and late magnetic resonance imaging (MRI) findings of heterotopic ossification (HO). HO in the right knee of a 35-year-old male patient hospitalised in the intensive care unit for traumatic brain injury. (a-d) First MRI performed on clinical suspicion of HO. (a) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows high signal of the innermost part of the vastus medialis muscle (arrows) and edema of the subcutaneous fat (arrowhead). (b) Sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (arrows). (c) Coronal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (white arrow) and vastus lateralis muscle (black arrow). (d) Mid-sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows joint effusion and synovial enhancement. (e-h) Follow-up MRI (e-g) and x-rays (h) performed 3 weeks later. (e) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). Sagittal (f) and coronal (g) contrast-enhanced fat-suppressed T1-weighted spin-echo MR images (650/17) show heterogeneous enhancement of the innermost part of the vastus medialis muscle (arrows). (h) Anteroposterior x-ray depicts a calcified mass at the anatomic position of the vastus medialis muscle (arrow). |
PMC1751061_F2_8068.jpg | What's the most prominent thing you notice in this picture? | Early and late magnetic resonance imaging (MRI) findings of heterotopic ossification (HO). HO in the right knee of a 35-year-old male patient hospitalised in the intensive care unit for traumatic brain injury. (a-d) First MRI performed on clinical suspicion of HO. (a) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows high signal of the innermost part of the vastus medialis muscle (arrows) and edema of the subcutaneous fat (arrowhead). (b) Sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (arrows). (c) Coronal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (white arrow) and vastus lateralis muscle (black arrow). (d) Mid-sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows joint effusion and synovial enhancement. (e-h) Follow-up MRI (e-g) and x-rays (h) performed 3 weeks later. (e) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). Sagittal (f) and coronal (g) contrast-enhanced fat-suppressed T1-weighted spin-echo MR images (650/17) show heterogeneous enhancement of the innermost part of the vastus medialis muscle (arrows). (h) Anteroposterior x-ray depicts a calcified mass at the anatomic position of the vastus medialis muscle (arrow). |
PMC1751061_F2_8066.jpg | What is the main focus of this visual representation? | Early and late magnetic resonance imaging (MRI) findings of heterotopic ossification (HO). HO in the right knee of a 35-year-old male patient hospitalised in the intensive care unit for traumatic brain injury. (a-d) First MRI performed on clinical suspicion of HO. (a) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows high signal of the innermost part of the vastus medialis muscle (arrows) and edema of the subcutaneous fat (arrowhead). (b) Sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (arrows). (c) Coronal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (white arrow) and vastus lateralis muscle (black arrow). (d) Mid-sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows joint effusion and synovial enhancement. (e-h) Follow-up MRI (e-g) and x-rays (h) performed 3 weeks later. (e) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). Sagittal (f) and coronal (g) contrast-enhanced fat-suppressed T1-weighted spin-echo MR images (650/17) show heterogeneous enhancement of the innermost part of the vastus medialis muscle (arrows). (h) Anteroposterior x-ray depicts a calcified mass at the anatomic position of the vastus medialis muscle (arrow). |
PMC1751061_F2_8067.jpg | Describe the main subject of this image. | Early and late magnetic resonance imaging (MRI) findings of heterotopic ossification (HO). HO in the right knee of a 35-year-old male patient hospitalised in the intensive care unit for traumatic brain injury. (a-d) First MRI performed on clinical suspicion of HO. (a) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows high signal of the innermost part of the vastus medialis muscle (arrows) and edema of the subcutaneous fat (arrowhead). (b) Sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (arrows). (c) Coronal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows a 'lacy pattern' of the innermost part of the vastus medialis muscle (white arrow) and vastus lateralis muscle (black arrow). (d) Mid-sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows joint effusion and synovial enhancement. (e-h) Follow-up MRI (e-g) and x-rays (h) performed 3 weeks later. (e) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). Sagittal (f) and coronal (g) contrast-enhanced fat-suppressed T1-weighted spin-echo MR images (650/17) show heterogeneous enhancement of the innermost part of the vastus medialis muscle (arrows). (h) Anteroposterior x-ray depicts a calcified mass at the anatomic position of the vastus medialis muscle (arrow). |
PMC1751061_F3_8059.jpg | What is the main focus of this visual representation? | Late magnetic resonance imaging (MRI) findings of heterotopic ossification (HO). HO in the left knee of a 32-year-old male patient hospitalised in the intensive care unit for traumatic brain injury. MRI performed 4 weeks after clinical suspicion of HO. (a) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). (b) Sagittal T1-weighted spin-echo MR image (650/17) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). (c) Sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows heterogeneous enhancement of the innermost part of the vastus medialis muscle (arrow). |
PMC1751061_F3_8058.jpg | Can you identify the primary element in this image? | Late magnetic resonance imaging (MRI) findings of heterotopic ossification (HO). HO in the left knee of a 32-year-old male patient hospitalised in the intensive care unit for traumatic brain injury. MRI performed 4 weeks after clinical suspicion of HO. (a) Sagittal fast spin-echo short inversion-recovery MR image (3,000/80; inversion time, 165 milliseconds) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). (b) Sagittal T1-weighted spin-echo MR image (650/17) shows heterogeneous high signal of the innermost part of the vastus medialis muscle (arrow). (c) Sagittal contrast-enhanced fat-suppressed T1-weighted spin-echo MR image (650/17) shows heterogeneous enhancement of the innermost part of the vastus medialis muscle (arrow). |
PMC1751121_pmed-0030516-g009_8073.jpg | What is the main focus of this visual representation? | Expression of Human Wild-Type and P239S Mutant Palladin Constructs in HeLa Cells(A and B) When HeLa cells were transfected with the human wild-type (WT) palladin construct, filamentous bundles (A) clearly colocalized with the F-actin (B).(C and D) In contrast, expression of the mutant P239S Family X (FX) construct resulted in large palladin flower-shaped structures (arrows) in which the center, but not the petals of the flower, colocalizes with actin.(E and F) Expression of Family X constructs can also cause small cytoplasmic flecks of palladin that do not colocalize with actin.HeLa cells overexpressing the empty GFP vector displayed uniform distribution of GFP in the whole cells that did not colocalize with F-actin (unpublished data). Green, GFP-palladin; red, F-actin; blue, nucleus; yellow, colocalized palladin and F-actin. All figures are at 100× magnification. |
PMC1751121_pmed-0030516-g009_8070.jpg | What is the principal component of this image? | Expression of Human Wild-Type and P239S Mutant Palladin Constructs in HeLa Cells(A and B) When HeLa cells were transfected with the human wild-type (WT) palladin construct, filamentous bundles (A) clearly colocalized with the F-actin (B).(C and D) In contrast, expression of the mutant P239S Family X (FX) construct resulted in large palladin flower-shaped structures (arrows) in which the center, but not the petals of the flower, colocalizes with actin.(E and F) Expression of Family X constructs can also cause small cytoplasmic flecks of palladin that do not colocalize with actin.HeLa cells overexpressing the empty GFP vector displayed uniform distribution of GFP in the whole cells that did not colocalize with F-actin (unpublished data). Green, GFP-palladin; red, F-actin; blue, nucleus; yellow, colocalized palladin and F-actin. All figures are at 100× magnification. |
PMC1751121_pmed-0030516-g009_8069.jpg | What is the main focus of this visual representation? | Expression of Human Wild-Type and P239S Mutant Palladin Constructs in HeLa Cells(A and B) When HeLa cells were transfected with the human wild-type (WT) palladin construct, filamentous bundles (A) clearly colocalized with the F-actin (B).(C and D) In contrast, expression of the mutant P239S Family X (FX) construct resulted in large palladin flower-shaped structures (arrows) in which the center, but not the petals of the flower, colocalizes with actin.(E and F) Expression of Family X constructs can also cause small cytoplasmic flecks of palladin that do not colocalize with actin.HeLa cells overexpressing the empty GFP vector displayed uniform distribution of GFP in the whole cells that did not colocalize with F-actin (unpublished data). Green, GFP-palladin; red, F-actin; blue, nucleus; yellow, colocalized palladin and F-actin. All figures are at 100× magnification. |
PMC1751121_pmed-0030516-g009_8074.jpg | What does this image primarily show? | Expression of Human Wild-Type and P239S Mutant Palladin Constructs in HeLa Cells(A and B) When HeLa cells were transfected with the human wild-type (WT) palladin construct, filamentous bundles (A) clearly colocalized with the F-actin (B).(C and D) In contrast, expression of the mutant P239S Family X (FX) construct resulted in large palladin flower-shaped structures (arrows) in which the center, but not the petals of the flower, colocalizes with actin.(E and F) Expression of Family X constructs can also cause small cytoplasmic flecks of palladin that do not colocalize with actin.HeLa cells overexpressing the empty GFP vector displayed uniform distribution of GFP in the whole cells that did not colocalize with F-actin (unpublished data). Green, GFP-palladin; red, F-actin; blue, nucleus; yellow, colocalized palladin and F-actin. All figures are at 100× magnification. |
PMC1751121_pmed-0030516-g009_8071.jpg | What is shown in this image? | Expression of Human Wild-Type and P239S Mutant Palladin Constructs in HeLa Cells(A and B) When HeLa cells were transfected with the human wild-type (WT) palladin construct, filamentous bundles (A) clearly colocalized with the F-actin (B).(C and D) In contrast, expression of the mutant P239S Family X (FX) construct resulted in large palladin flower-shaped structures (arrows) in which the center, but not the petals of the flower, colocalizes with actin.(E and F) Expression of Family X constructs can also cause small cytoplasmic flecks of palladin that do not colocalize with actin.HeLa cells overexpressing the empty GFP vector displayed uniform distribution of GFP in the whole cells that did not colocalize with F-actin (unpublished data). Green, GFP-palladin; red, F-actin; blue, nucleus; yellow, colocalized palladin and F-actin. All figures are at 100× magnification. |
PMC1751121_pmed-0030516-g009_8072.jpg | Describe the main subject of this image. | Expression of Human Wild-Type and P239S Mutant Palladin Constructs in HeLa Cells(A and B) When HeLa cells were transfected with the human wild-type (WT) palladin construct, filamentous bundles (A) clearly colocalized with the F-actin (B).(C and D) In contrast, expression of the mutant P239S Family X (FX) construct resulted in large palladin flower-shaped structures (arrows) in which the center, but not the petals of the flower, colocalizes with actin.(E and F) Expression of Family X constructs can also cause small cytoplasmic flecks of palladin that do not colocalize with actin.HeLa cells overexpressing the empty GFP vector displayed uniform distribution of GFP in the whole cells that did not colocalize with F-actin (unpublished data). Green, GFP-palladin; red, F-actin; blue, nucleus; yellow, colocalized palladin and F-actin. All figures are at 100× magnification. |
PMC1761133_fig05_8081.jpg | What object or scene is depicted here? | Depletion of Sec16 from human cells disrupts COPII assembly and ER-to-Golgi transportA) Depletion of Sec16 expression using siRNA. HeLa cells were transfected with siRNA duplexes targeting Sec16 [pool of four duplexes (Sec16 pool), lamin A/C, a duplex targeting the 3′ UTR of Sec16 (Sec16 3′ UTR) and a further Sec16 duplex targeting the coding region (Sec16 b)]. Cell lysates were then immunoblotted for Sec16 (250 kD), lamin A/C (84 kD) or GAPDH (as a loading control, 40 kD) as indicated. Note that the duplex termed Sec16b only depletes a subset of splice forms of Sec16. Cells depleted of Sec16 using a pool of four siRNA duplexes were methanol fixed and labelled with antibodies specific for B) Sec24C, C) Sec31A, D) ERGIC-53, E) β’-COP and F) giantin as indicated. Bar (all panels) = 10 μm. |
PMC1761133_fig05_8082.jpg | What's the most prominent thing you notice in this picture? | Depletion of Sec16 from human cells disrupts COPII assembly and ER-to-Golgi transportA) Depletion of Sec16 expression using siRNA. HeLa cells were transfected with siRNA duplexes targeting Sec16 [pool of four duplexes (Sec16 pool), lamin A/C, a duplex targeting the 3′ UTR of Sec16 (Sec16 3′ UTR) and a further Sec16 duplex targeting the coding region (Sec16 b)]. Cell lysates were then immunoblotted for Sec16 (250 kD), lamin A/C (84 kD) or GAPDH (as a loading control, 40 kD) as indicated. Note that the duplex termed Sec16b only depletes a subset of splice forms of Sec16. Cells depleted of Sec16 using a pool of four siRNA duplexes were methanol fixed and labelled with antibodies specific for B) Sec24C, C) Sec31A, D) ERGIC-53, E) β’-COP and F) giantin as indicated. Bar (all panels) = 10 μm. |
PMC1761133_fig05_8078.jpg | What is the central feature of this picture? | Depletion of Sec16 from human cells disrupts COPII assembly and ER-to-Golgi transportA) Depletion of Sec16 expression using siRNA. HeLa cells were transfected with siRNA duplexes targeting Sec16 [pool of four duplexes (Sec16 pool), lamin A/C, a duplex targeting the 3′ UTR of Sec16 (Sec16 3′ UTR) and a further Sec16 duplex targeting the coding region (Sec16 b)]. Cell lysates were then immunoblotted for Sec16 (250 kD), lamin A/C (84 kD) or GAPDH (as a loading control, 40 kD) as indicated. Note that the duplex termed Sec16b only depletes a subset of splice forms of Sec16. Cells depleted of Sec16 using a pool of four siRNA duplexes were methanol fixed and labelled with antibodies specific for B) Sec24C, C) Sec31A, D) ERGIC-53, E) β’-COP and F) giantin as indicated. Bar (all panels) = 10 μm. |
PMC1761133_fig05_8083.jpg | What is the dominant medical problem in this image? | Depletion of Sec16 from human cells disrupts COPII assembly and ER-to-Golgi transportA) Depletion of Sec16 expression using siRNA. HeLa cells were transfected with siRNA duplexes targeting Sec16 [pool of four duplexes (Sec16 pool), lamin A/C, a duplex targeting the 3′ UTR of Sec16 (Sec16 3′ UTR) and a further Sec16 duplex targeting the coding region (Sec16 b)]. Cell lysates were then immunoblotted for Sec16 (250 kD), lamin A/C (84 kD) or GAPDH (as a loading control, 40 kD) as indicated. Note that the duplex termed Sec16b only depletes a subset of splice forms of Sec16. Cells depleted of Sec16 using a pool of four siRNA duplexes were methanol fixed and labelled with antibodies specific for B) Sec24C, C) Sec31A, D) ERGIC-53, E) β’-COP and F) giantin as indicated. Bar (all panels) = 10 μm. |
PMC1761133_fig05_8080.jpg | What is shown in this image? | Depletion of Sec16 from human cells disrupts COPII assembly and ER-to-Golgi transportA) Depletion of Sec16 expression using siRNA. HeLa cells were transfected with siRNA duplexes targeting Sec16 [pool of four duplexes (Sec16 pool), lamin A/C, a duplex targeting the 3′ UTR of Sec16 (Sec16 3′ UTR) and a further Sec16 duplex targeting the coding region (Sec16 b)]. Cell lysates were then immunoblotted for Sec16 (250 kD), lamin A/C (84 kD) or GAPDH (as a loading control, 40 kD) as indicated. Note that the duplex termed Sec16b only depletes a subset of splice forms of Sec16. Cells depleted of Sec16 using a pool of four siRNA duplexes were methanol fixed and labelled with antibodies specific for B) Sec24C, C) Sec31A, D) ERGIC-53, E) β’-COP and F) giantin as indicated. Bar (all panels) = 10 μm. |
PMC1761133_fig05_8079.jpg | What is being portrayed in this visual content? | Depletion of Sec16 from human cells disrupts COPII assembly and ER-to-Golgi transportA) Depletion of Sec16 expression using siRNA. HeLa cells were transfected with siRNA duplexes targeting Sec16 [pool of four duplexes (Sec16 pool), lamin A/C, a duplex targeting the 3′ UTR of Sec16 (Sec16 3′ UTR) and a further Sec16 duplex targeting the coding region (Sec16 b)]. Cell lysates were then immunoblotted for Sec16 (250 kD), lamin A/C (84 kD) or GAPDH (as a loading control, 40 kD) as indicated. Note that the duplex termed Sec16b only depletes a subset of splice forms of Sec16. Cells depleted of Sec16 using a pool of four siRNA duplexes were methanol fixed and labelled with antibodies specific for B) Sec24C, C) Sec31A, D) ERGIC-53, E) β’-COP and F) giantin as indicated. Bar (all panels) = 10 μm. |
PMC1761133_fig05_8075.jpg | What is the principal component of this image? | Depletion of Sec16 from human cells disrupts COPII assembly and ER-to-Golgi transportA) Depletion of Sec16 expression using siRNA. HeLa cells were transfected with siRNA duplexes targeting Sec16 [pool of four duplexes (Sec16 pool), lamin A/C, a duplex targeting the 3′ UTR of Sec16 (Sec16 3′ UTR) and a further Sec16 duplex targeting the coding region (Sec16 b)]. Cell lysates were then immunoblotted for Sec16 (250 kD), lamin A/C (84 kD) or GAPDH (as a loading control, 40 kD) as indicated. Note that the duplex termed Sec16b only depletes a subset of splice forms of Sec16. Cells depleted of Sec16 using a pool of four siRNA duplexes were methanol fixed and labelled with antibodies specific for B) Sec24C, C) Sec31A, D) ERGIC-53, E) β’-COP and F) giantin as indicated. Bar (all panels) = 10 μm. |
PMC1761133_fig05_8077.jpg | What is the focal point of this photograph? | Depletion of Sec16 from human cells disrupts COPII assembly and ER-to-Golgi transportA) Depletion of Sec16 expression using siRNA. HeLa cells were transfected with siRNA duplexes targeting Sec16 [pool of four duplexes (Sec16 pool), lamin A/C, a duplex targeting the 3′ UTR of Sec16 (Sec16 3′ UTR) and a further Sec16 duplex targeting the coding region (Sec16 b)]. Cell lysates were then immunoblotted for Sec16 (250 kD), lamin A/C (84 kD) or GAPDH (as a loading control, 40 kD) as indicated. Note that the duplex termed Sec16b only depletes a subset of splice forms of Sec16. Cells depleted of Sec16 using a pool of four siRNA duplexes were methanol fixed and labelled with antibodies specific for B) Sec24C, C) Sec31A, D) ERGIC-53, E) β’-COP and F) giantin as indicated. Bar (all panels) = 10 μm. |
PMC1761133_fig07_8090.jpg | What can you see in this picture? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8091.jpg | What stands out most in this visual? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8089.jpg | What is shown in this image? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8093.jpg | What is the central feature of this picture? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8103.jpg | What is the main focus of this visual representation? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8092.jpg | What's the most prominent thing you notice in this picture? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8088.jpg | What stands out most in this visual? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8087.jpg | What's the most prominent thing you notice in this picture? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8101.jpg | What is the principal component of this image? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8097.jpg | What is the main focus of this visual representation? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8095.jpg | Describe the main subject of this image. | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8100.jpg | What can you see in this picture? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761133_fig07_8086.jpg | What is the focal point of this photograph? | Sar1-GTP mediates assembly of Sec16 at ERESA) Cells expressing ECFP-Sar1-T39N (GDP restricted, blue in merge) were labelled with antibodies to detect endogenous Sec16 (green) and Sec24C (red). The majority of punctate Sec16 localization is lost; those few punctate spots of Sec16 that remain also label with anti-Sec24C antibodies, as they do in non-transfected cells. B) Cells were transfected with both ECFP-Sar1-T39N (blue in merge) and Venus-Sec16 (green) and immunolabelled for endogenous Sec24C (red). C) Cells transfected with ECFP-Sar1-H79G (blue in merge) were labelled for endogenous Sec16 (green) and Sec24C (red). Sec24C is not present on Sec16-positive structures (arrowheads) D) 3D imaging of paraformaldehyde-fixed cells expressing both ECFP-Sar1-H79G (green in merge) and Venus-Sec16 (red) shows that both proteins localize to large curved and round structures. E) 3D rendering of deconvolved stacks from cells expressing both ECFP-Sar1-H79G and Venus-Sec16 reveal that these objects often form near complete spheres. F) Immunolabelling of ECFP-Sar1-H79G (blue in merge) and Venus-Sec16 (green) labelled structures shows that they do not contain Sec24C (red). Boxed regions show threefold enlargements of selected areas. Representative images are shown from four independent experiments in which a total of 400 cells were inspected visually. All bars = 10 μm. |
PMC1761140_F2_8108.jpg | What is the principal component of this image? | Trafficking of yeast Ste2, human β2AR, and a yeast Ste2/human β 2AR chimera expressed in human HEK293 cells in response stimulation by insulin: analysis by confocal microscopy. HEK293 cells were transiently transfected to express either β2AR-GFP (panels a, b), Ste2-GFP (panels c, d), or the Ste2/β2AR-GFP chimeric receptor (panels e,f). For each of these GPCRs, localization of the receptors in the untreated cells was dominant at the cell membrane (white arrows). Cells were treated without (panels a, c, e) or with (panels b, d, f) insulin (100 nM) for 0.5 h and followed by confocal microscopy. Insulin stimulates internalization of the β2AR-GFP (panel b) and of the Ste2/β2AR-GFP chimeric receptor (panel f), but not of Ste2-GFP (panel d). The images displayed are from a single experiment, representative of more than five replicate, separate experiments. Bar equals 10 μm. |
PMC1761140_F2_8105.jpg | What's the most prominent thing you notice in this picture? | Trafficking of yeast Ste2, human β2AR, and a yeast Ste2/human β 2AR chimera expressed in human HEK293 cells in response stimulation by insulin: analysis by confocal microscopy. HEK293 cells were transiently transfected to express either β2AR-GFP (panels a, b), Ste2-GFP (panels c, d), or the Ste2/β2AR-GFP chimeric receptor (panels e,f). For each of these GPCRs, localization of the receptors in the untreated cells was dominant at the cell membrane (white arrows). Cells were treated without (panels a, c, e) or with (panels b, d, f) insulin (100 nM) for 0.5 h and followed by confocal microscopy. Insulin stimulates internalization of the β2AR-GFP (panel b) and of the Ste2/β2AR-GFP chimeric receptor (panel f), but not of Ste2-GFP (panel d). The images displayed are from a single experiment, representative of more than five replicate, separate experiments. Bar equals 10 μm. |
PMC1761140_F2_8106.jpg | What stands out most in this visual? | Trafficking of yeast Ste2, human β2AR, and a yeast Ste2/human β 2AR chimera expressed in human HEK293 cells in response stimulation by insulin: analysis by confocal microscopy. HEK293 cells were transiently transfected to express either β2AR-GFP (panels a, b), Ste2-GFP (panels c, d), or the Ste2/β2AR-GFP chimeric receptor (panels e,f). For each of these GPCRs, localization of the receptors in the untreated cells was dominant at the cell membrane (white arrows). Cells were treated without (panels a, c, e) or with (panels b, d, f) insulin (100 nM) for 0.5 h and followed by confocal microscopy. Insulin stimulates internalization of the β2AR-GFP (panel b) and of the Ste2/β2AR-GFP chimeric receptor (panel f), but not of Ste2-GFP (panel d). The images displayed are from a single experiment, representative of more than five replicate, separate experiments. Bar equals 10 μm. |
PMC1761140_F2_8109.jpg | Can you identify the primary element in this image? | Trafficking of yeast Ste2, human β2AR, and a yeast Ste2/human β 2AR chimera expressed in human HEK293 cells in response stimulation by insulin: analysis by confocal microscopy. HEK293 cells were transiently transfected to express either β2AR-GFP (panels a, b), Ste2-GFP (panels c, d), or the Ste2/β2AR-GFP chimeric receptor (panels e,f). For each of these GPCRs, localization of the receptors in the untreated cells was dominant at the cell membrane (white arrows). Cells were treated without (panels a, c, e) or with (panels b, d, f) insulin (100 nM) for 0.5 h and followed by confocal microscopy. Insulin stimulates internalization of the β2AR-GFP (panel b) and of the Ste2/β2AR-GFP chimeric receptor (panel f), but not of Ste2-GFP (panel d). The images displayed are from a single experiment, representative of more than five replicate, separate experiments. Bar equals 10 μm. |
PMC1761140_F2_8107.jpg | What object or scene is depicted here? | Trafficking of yeast Ste2, human β2AR, and a yeast Ste2/human β 2AR chimera expressed in human HEK293 cells in response stimulation by insulin: analysis by confocal microscopy. HEK293 cells were transiently transfected to express either β2AR-GFP (panels a, b), Ste2-GFP (panels c, d), or the Ste2/β2AR-GFP chimeric receptor (panels e,f). For each of these GPCRs, localization of the receptors in the untreated cells was dominant at the cell membrane (white arrows). Cells were treated without (panels a, c, e) or with (panels b, d, f) insulin (100 nM) for 0.5 h and followed by confocal microscopy. Insulin stimulates internalization of the β2AR-GFP (panel b) and of the Ste2/β2AR-GFP chimeric receptor (panel f), but not of Ste2-GFP (panel d). The images displayed are from a single experiment, representative of more than five replicate, separate experiments. Bar equals 10 μm. |
PMC1761707_figure5_8110.jpg | What key item or scene is captured in this photo? | Examples for ongoing PlugIn development projects are a general purpose 3D volume segmentation and visualization project |
PMC1761707_figure5_8111.jpg | What is the dominant medical problem in this image? | Examples for ongoing PlugIn development projects are a general purpose 3D volume segmentation and visualization project |
PMC1762022_F6_8112.jpg | What is the core subject represented in this visual? | Singly scattered spindle cells seen in some of the smears (Papanicolaou stain × 280). Inset shows a high power view of the same. |
PMC1762030_F6_8117.jpg | What is the principal component of this image? | Nuclear localization of Ce-GnRHR to the germline and intestinal cells. Permeabilized adult N2 worm probed with anti-Ce-GnRHR antibody (i) and Hoechst stain (ii). Nuclear localization of Ce-GnRHR to oocytes was clearly demonstrated following superimposition of images i and ii (iii). Permeabilized adult N2 worm probed with anti-Ce-GnRHR antibody (iv) and Hoescht stain (v). Nuclear localization of Ce-GnRHR to the intestinal cells was clearly demonstrated following superimposition of images iv and v (vi). A high magnification image of a superimposed nucleus is presented in the insert of vi. A superimposed image of the gonadal arm of an adult N2 worm is shown in vii. Higher magnification images of the gonadal arm stained with anti-Ce-GnRHR antibody (viii), Hoechst stain (ix) and superimposed (x) demonstrates Ce-GnRHR staining is primarily confined to the nuclear membrane. Scale: 50μm. |
PMC1762030_F6_8119.jpg | What is the core subject represented in this visual? | Nuclear localization of Ce-GnRHR to the germline and intestinal cells. Permeabilized adult N2 worm probed with anti-Ce-GnRHR antibody (i) and Hoechst stain (ii). Nuclear localization of Ce-GnRHR to oocytes was clearly demonstrated following superimposition of images i and ii (iii). Permeabilized adult N2 worm probed with anti-Ce-GnRHR antibody (iv) and Hoescht stain (v). Nuclear localization of Ce-GnRHR to the intestinal cells was clearly demonstrated following superimposition of images iv and v (vi). A high magnification image of a superimposed nucleus is presented in the insert of vi. A superimposed image of the gonadal arm of an adult N2 worm is shown in vii. Higher magnification images of the gonadal arm stained with anti-Ce-GnRHR antibody (viii), Hoechst stain (ix) and superimposed (x) demonstrates Ce-GnRHR staining is primarily confined to the nuclear membrane. Scale: 50μm. |
PMC1762030_F6_8115.jpg | What is the core subject represented in this visual? | Nuclear localization of Ce-GnRHR to the germline and intestinal cells. Permeabilized adult N2 worm probed with anti-Ce-GnRHR antibody (i) and Hoechst stain (ii). Nuclear localization of Ce-GnRHR to oocytes was clearly demonstrated following superimposition of images i and ii (iii). Permeabilized adult N2 worm probed with anti-Ce-GnRHR antibody (iv) and Hoescht stain (v). Nuclear localization of Ce-GnRHR to the intestinal cells was clearly demonstrated following superimposition of images iv and v (vi). A high magnification image of a superimposed nucleus is presented in the insert of vi. A superimposed image of the gonadal arm of an adult N2 worm is shown in vii. Higher magnification images of the gonadal arm stained with anti-Ce-GnRHR antibody (viii), Hoechst stain (ix) and superimposed (x) demonstrates Ce-GnRHR staining is primarily confined to the nuclear membrane. Scale: 50μm. |
PMC1762085_pmed-0030484-g002_8124.jpg | What stands out most in this visual? | Effector Sites (LP) of the GI Tract Showing Persistent CD4+ T Cell Depletion during HAARTImmunohistochemical characterization of immune-inductive and effector sites in rectal biopsies. Using a PC-based image-analysis system (KS 4000, Kontron) a standard area was set by the image analyzer. For the LP, a total of between ten and 15 consecutive nonoverlapping fields were analyzed for each staining. For the OLT, between two and five representative areas were chosen.(A) CD4+ T cells per unit area were determined in OLT (left panel) and LP (right panel). Mean CD4+ T cell numbers were compared between HIV-uninfected (white boxes), AEI (light grey boxes), and patients treated for up to 1 y (hatched boxes), 1–3 y (speckled boxes) and 3–7 y (dark grey boxes). In these plots, the boxes extend from the first to the third quartiles, enclosing the middle 50% of the data. The middle line within each box indicates the median of the data, whereas the vertical line extends from the 10th to the 90th percentile. Means of the data are represented by filled-in squares.(B) A biopsy section (viewed at 40× magnification) from an HIV-uninfected control participant, showing CD4+ T cells (stained red) within the GI LP (panel I). In contrast, a pronounced reduction in LP CD4+ T cells is noted in a patient with AEI (patient no. 131) in panel II which does not correct despite antiretroviral therapy for 2 y in the same patient (panel III). Another representative study patient (no. 142) is presented, where LP CD4+ T cell depletion during AEI (panel IV) does not correct after antiretroviral therapy for 1 y (panel V). |
PMC1762085_pmed-0030484-g002_8120.jpg | Describe the main subject of this image. | Effector Sites (LP) of the GI Tract Showing Persistent CD4+ T Cell Depletion during HAARTImmunohistochemical characterization of immune-inductive and effector sites in rectal biopsies. Using a PC-based image-analysis system (KS 4000, Kontron) a standard area was set by the image analyzer. For the LP, a total of between ten and 15 consecutive nonoverlapping fields were analyzed for each staining. For the OLT, between two and five representative areas were chosen.(A) CD4+ T cells per unit area were determined in OLT (left panel) and LP (right panel). Mean CD4+ T cell numbers were compared between HIV-uninfected (white boxes), AEI (light grey boxes), and patients treated for up to 1 y (hatched boxes), 1–3 y (speckled boxes) and 3–7 y (dark grey boxes). In these plots, the boxes extend from the first to the third quartiles, enclosing the middle 50% of the data. The middle line within each box indicates the median of the data, whereas the vertical line extends from the 10th to the 90th percentile. Means of the data are represented by filled-in squares.(B) A biopsy section (viewed at 40× magnification) from an HIV-uninfected control participant, showing CD4+ T cells (stained red) within the GI LP (panel I). In contrast, a pronounced reduction in LP CD4+ T cells is noted in a patient with AEI (patient no. 131) in panel II which does not correct despite antiretroviral therapy for 2 y in the same patient (panel III). Another representative study patient (no. 142) is presented, where LP CD4+ T cell depletion during AEI (panel IV) does not correct after antiretroviral therapy for 1 y (panel V). |
PMC1762085_pmed-0030484-g002_8122.jpg | What's the most prominent thing you notice in this picture? | Effector Sites (LP) of the GI Tract Showing Persistent CD4+ T Cell Depletion during HAARTImmunohistochemical characterization of immune-inductive and effector sites in rectal biopsies. Using a PC-based image-analysis system (KS 4000, Kontron) a standard area was set by the image analyzer. For the LP, a total of between ten and 15 consecutive nonoverlapping fields were analyzed for each staining. For the OLT, between two and five representative areas were chosen.(A) CD4+ T cells per unit area were determined in OLT (left panel) and LP (right panel). Mean CD4+ T cell numbers were compared between HIV-uninfected (white boxes), AEI (light grey boxes), and patients treated for up to 1 y (hatched boxes), 1–3 y (speckled boxes) and 3–7 y (dark grey boxes). In these plots, the boxes extend from the first to the third quartiles, enclosing the middle 50% of the data. The middle line within each box indicates the median of the data, whereas the vertical line extends from the 10th to the 90th percentile. Means of the data are represented by filled-in squares.(B) A biopsy section (viewed at 40× magnification) from an HIV-uninfected control participant, showing CD4+ T cells (stained red) within the GI LP (panel I). In contrast, a pronounced reduction in LP CD4+ T cells is noted in a patient with AEI (patient no. 131) in panel II which does not correct despite antiretroviral therapy for 2 y in the same patient (panel III). Another representative study patient (no. 142) is presented, where LP CD4+ T cell depletion during AEI (panel IV) does not correct after antiretroviral therapy for 1 y (panel V). |
PMC1762085_pmed-0030484-g002_8125.jpg | What is the core subject represented in this visual? | Effector Sites (LP) of the GI Tract Showing Persistent CD4+ T Cell Depletion during HAARTImmunohistochemical characterization of immune-inductive and effector sites in rectal biopsies. Using a PC-based image-analysis system (KS 4000, Kontron) a standard area was set by the image analyzer. For the LP, a total of between ten and 15 consecutive nonoverlapping fields were analyzed for each staining. For the OLT, between two and five representative areas were chosen.(A) CD4+ T cells per unit area were determined in OLT (left panel) and LP (right panel). Mean CD4+ T cell numbers were compared between HIV-uninfected (white boxes), AEI (light grey boxes), and patients treated for up to 1 y (hatched boxes), 1–3 y (speckled boxes) and 3–7 y (dark grey boxes). In these plots, the boxes extend from the first to the third quartiles, enclosing the middle 50% of the data. The middle line within each box indicates the median of the data, whereas the vertical line extends from the 10th to the 90th percentile. Means of the data are represented by filled-in squares.(B) A biopsy section (viewed at 40× magnification) from an HIV-uninfected control participant, showing CD4+ T cells (stained red) within the GI LP (panel I). In contrast, a pronounced reduction in LP CD4+ T cells is noted in a patient with AEI (patient no. 131) in panel II which does not correct despite antiretroviral therapy for 2 y in the same patient (panel III). Another representative study patient (no. 142) is presented, where LP CD4+ T cell depletion during AEI (panel IV) does not correct after antiretroviral therapy for 1 y (panel V). |
PMC1762085_pmed-0030484-g002_8121.jpg | What is the core subject represented in this visual? | Effector Sites (LP) of the GI Tract Showing Persistent CD4+ T Cell Depletion during HAARTImmunohistochemical characterization of immune-inductive and effector sites in rectal biopsies. Using a PC-based image-analysis system (KS 4000, Kontron) a standard area was set by the image analyzer. For the LP, a total of between ten and 15 consecutive nonoverlapping fields were analyzed for each staining. For the OLT, between two and five representative areas were chosen.(A) CD4+ T cells per unit area were determined in OLT (left panel) and LP (right panel). Mean CD4+ T cell numbers were compared between HIV-uninfected (white boxes), AEI (light grey boxes), and patients treated for up to 1 y (hatched boxes), 1–3 y (speckled boxes) and 3–7 y (dark grey boxes). In these plots, the boxes extend from the first to the third quartiles, enclosing the middle 50% of the data. The middle line within each box indicates the median of the data, whereas the vertical line extends from the 10th to the 90th percentile. Means of the data are represented by filled-in squares.(B) A biopsy section (viewed at 40× magnification) from an HIV-uninfected control participant, showing CD4+ T cells (stained red) within the GI LP (panel I). In contrast, a pronounced reduction in LP CD4+ T cells is noted in a patient with AEI (patient no. 131) in panel II which does not correct despite antiretroviral therapy for 2 y in the same patient (panel III). Another representative study patient (no. 142) is presented, where LP CD4+ T cell depletion during AEI (panel IV) does not correct after antiretroviral therapy for 1 y (panel V). |
PMC1762316_pone-0000013-g006_8138.jpg | Describe the main subject of this image. | Major changes after 16-months after activation of hVEGF-A165 expression.A. Liver: Encapsulated hepatocellular carcinoma was highly necrotic and focally calcified (Haematoxylin-eosin).B. Lung: Papillary adenocarcinoma. (Haematoxylin-eosin).C. Macroscopical changes in liver (box shows the area of the microscopical sections in F–H).D. Macroscopical changes in spleen, control spleen on the left (microscopical sections in I–K).E. Macroscopical changes in paratubarian area (microscopical sections in L–N).F. Cavernous hemangioma featuring focal hyalinization.G. The same tumor mass area with higher magnification (haematoxylin-eosin).H. Weak focal hVEGF-A165 immunoreactivity was present in the same area (True Blue as a chromogen), arrows indicate positive cells.I–K. Fibrous scars formed by collagenous and elastic fibres surrounded by dilated cystic spaces, focally filled with blood and revealing inconsistently CD34 positive lining.I. Hematoxylin-eosin. (an arrow points to an area shown in K)J. CD34 immunostaining.K. The same area as in I with higher magnification (stained with Masson Trichrom).Asterix in I and J indicate the same area.L. Cystically dilated paratubarian spaces with signs of old haemorrhage and thrombus formation (marked with *), an open circle points to an area which was highly vascularized as shown in M. (CD31 immunostaining) and a box indicates an area which revealed focal hVEGF-A165 immunopositivity shown in N. (hVEGF-A165 immunostaining).Bar: F, I, J - 500 µm, G, H, K - 100 µm, A, B, M, N - 200 µm L - 1000 µm. |
PMC1762316_pone-0000013-g006_8137.jpg | What stands out most in this visual? | Major changes after 16-months after activation of hVEGF-A165 expression.A. Liver: Encapsulated hepatocellular carcinoma was highly necrotic and focally calcified (Haematoxylin-eosin).B. Lung: Papillary adenocarcinoma. (Haematoxylin-eosin).C. Macroscopical changes in liver (box shows the area of the microscopical sections in F–H).D. Macroscopical changes in spleen, control spleen on the left (microscopical sections in I–K).E. Macroscopical changes in paratubarian area (microscopical sections in L–N).F. Cavernous hemangioma featuring focal hyalinization.G. The same tumor mass area with higher magnification (haematoxylin-eosin).H. Weak focal hVEGF-A165 immunoreactivity was present in the same area (True Blue as a chromogen), arrows indicate positive cells.I–K. Fibrous scars formed by collagenous and elastic fibres surrounded by dilated cystic spaces, focally filled with blood and revealing inconsistently CD34 positive lining.I. Hematoxylin-eosin. (an arrow points to an area shown in K)J. CD34 immunostaining.K. The same area as in I with higher magnification (stained with Masson Trichrom).Asterix in I and J indicate the same area.L. Cystically dilated paratubarian spaces with signs of old haemorrhage and thrombus formation (marked with *), an open circle points to an area which was highly vascularized as shown in M. (CD31 immunostaining) and a box indicates an area which revealed focal hVEGF-A165 immunopositivity shown in N. (hVEGF-A165 immunostaining).Bar: F, I, J - 500 µm, G, H, K - 100 µm, A, B, M, N - 200 µm L - 1000 µm. |
PMC1762316_pone-0000013-g006_8131.jpg | What is the main focus of this visual representation? | Major changes after 16-months after activation of hVEGF-A165 expression.A. Liver: Encapsulated hepatocellular carcinoma was highly necrotic and focally calcified (Haematoxylin-eosin).B. Lung: Papillary adenocarcinoma. (Haematoxylin-eosin).C. Macroscopical changes in liver (box shows the area of the microscopical sections in F–H).D. Macroscopical changes in spleen, control spleen on the left (microscopical sections in I–K).E. Macroscopical changes in paratubarian area (microscopical sections in L–N).F. Cavernous hemangioma featuring focal hyalinization.G. The same tumor mass area with higher magnification (haematoxylin-eosin).H. Weak focal hVEGF-A165 immunoreactivity was present in the same area (True Blue as a chromogen), arrows indicate positive cells.I–K. Fibrous scars formed by collagenous and elastic fibres surrounded by dilated cystic spaces, focally filled with blood and revealing inconsistently CD34 positive lining.I. Hematoxylin-eosin. (an arrow points to an area shown in K)J. CD34 immunostaining.K. The same area as in I with higher magnification (stained with Masson Trichrom).Asterix in I and J indicate the same area.L. Cystically dilated paratubarian spaces with signs of old haemorrhage and thrombus formation (marked with *), an open circle points to an area which was highly vascularized as shown in M. (CD31 immunostaining) and a box indicates an area which revealed focal hVEGF-A165 immunopositivity shown in N. (hVEGF-A165 immunostaining).Bar: F, I, J - 500 µm, G, H, K - 100 µm, A, B, M, N - 200 µm L - 1000 µm. |
PMC1762316_pone-0000013-g006_8129.jpg | What object or scene is depicted here? | Major changes after 16-months after activation of hVEGF-A165 expression.A. Liver: Encapsulated hepatocellular carcinoma was highly necrotic and focally calcified (Haematoxylin-eosin).B. Lung: Papillary adenocarcinoma. (Haematoxylin-eosin).C. Macroscopical changes in liver (box shows the area of the microscopical sections in F–H).D. Macroscopical changes in spleen, control spleen on the left (microscopical sections in I–K).E. Macroscopical changes in paratubarian area (microscopical sections in L–N).F. Cavernous hemangioma featuring focal hyalinization.G. The same tumor mass area with higher magnification (haematoxylin-eosin).H. Weak focal hVEGF-A165 immunoreactivity was present in the same area (True Blue as a chromogen), arrows indicate positive cells.I–K. Fibrous scars formed by collagenous and elastic fibres surrounded by dilated cystic spaces, focally filled with blood and revealing inconsistently CD34 positive lining.I. Hematoxylin-eosin. (an arrow points to an area shown in K)J. CD34 immunostaining.K. The same area as in I with higher magnification (stained with Masson Trichrom).Asterix in I and J indicate the same area.L. Cystically dilated paratubarian spaces with signs of old haemorrhage and thrombus formation (marked with *), an open circle points to an area which was highly vascularized as shown in M. (CD31 immunostaining) and a box indicates an area which revealed focal hVEGF-A165 immunopositivity shown in N. (hVEGF-A165 immunostaining).Bar: F, I, J - 500 µm, G, H, K - 100 µm, A, B, M, N - 200 µm L - 1000 µm. |
PMC1762316_pone-0000013-g006_8133.jpg | Describe the main subject of this image. | Major changes after 16-months after activation of hVEGF-A165 expression.A. Liver: Encapsulated hepatocellular carcinoma was highly necrotic and focally calcified (Haematoxylin-eosin).B. Lung: Papillary adenocarcinoma. (Haematoxylin-eosin).C. Macroscopical changes in liver (box shows the area of the microscopical sections in F–H).D. Macroscopical changes in spleen, control spleen on the left (microscopical sections in I–K).E. Macroscopical changes in paratubarian area (microscopical sections in L–N).F. Cavernous hemangioma featuring focal hyalinization.G. The same tumor mass area with higher magnification (haematoxylin-eosin).H. Weak focal hVEGF-A165 immunoreactivity was present in the same area (True Blue as a chromogen), arrows indicate positive cells.I–K. Fibrous scars formed by collagenous and elastic fibres surrounded by dilated cystic spaces, focally filled with blood and revealing inconsistently CD34 positive lining.I. Hematoxylin-eosin. (an arrow points to an area shown in K)J. CD34 immunostaining.K. The same area as in I with higher magnification (stained with Masson Trichrom).Asterix in I and J indicate the same area.L. Cystically dilated paratubarian spaces with signs of old haemorrhage and thrombus formation (marked with *), an open circle points to an area which was highly vascularized as shown in M. (CD31 immunostaining) and a box indicates an area which revealed focal hVEGF-A165 immunopositivity shown in N. (hVEGF-A165 immunostaining).Bar: F, I, J - 500 µm, G, H, K - 100 µm, A, B, M, N - 200 µm L - 1000 µm. |
PMC1762316_pone-0000013-g006_8141.jpg | What is the dominant medical problem in this image? | Major changes after 16-months after activation of hVEGF-A165 expression.A. Liver: Encapsulated hepatocellular carcinoma was highly necrotic and focally calcified (Haematoxylin-eosin).B. Lung: Papillary adenocarcinoma. (Haematoxylin-eosin).C. Macroscopical changes in liver (box shows the area of the microscopical sections in F–H).D. Macroscopical changes in spleen, control spleen on the left (microscopical sections in I–K).E. Macroscopical changes in paratubarian area (microscopical sections in L–N).F. Cavernous hemangioma featuring focal hyalinization.G. The same tumor mass area with higher magnification (haematoxylin-eosin).H. Weak focal hVEGF-A165 immunoreactivity was present in the same area (True Blue as a chromogen), arrows indicate positive cells.I–K. Fibrous scars formed by collagenous and elastic fibres surrounded by dilated cystic spaces, focally filled with blood and revealing inconsistently CD34 positive lining.I. Hematoxylin-eosin. (an arrow points to an area shown in K)J. CD34 immunostaining.K. The same area as in I with higher magnification (stained with Masson Trichrom).Asterix in I and J indicate the same area.L. Cystically dilated paratubarian spaces with signs of old haemorrhage and thrombus formation (marked with *), an open circle points to an area which was highly vascularized as shown in M. (CD31 immunostaining) and a box indicates an area which revealed focal hVEGF-A165 immunopositivity shown in N. (hVEGF-A165 immunostaining).Bar: F, I, J - 500 µm, G, H, K - 100 µm, A, B, M, N - 200 µm L - 1000 µm. |
PMC1762316_pone-0000013-g006_8130.jpg | Can you identify the primary element in this image? | Major changes after 16-months after activation of hVEGF-A165 expression.A. Liver: Encapsulated hepatocellular carcinoma was highly necrotic and focally calcified (Haematoxylin-eosin).B. Lung: Papillary adenocarcinoma. (Haematoxylin-eosin).C. Macroscopical changes in liver (box shows the area of the microscopical sections in F–H).D. Macroscopical changes in spleen, control spleen on the left (microscopical sections in I–K).E. Macroscopical changes in paratubarian area (microscopical sections in L–N).F. Cavernous hemangioma featuring focal hyalinization.G. The same tumor mass area with higher magnification (haematoxylin-eosin).H. Weak focal hVEGF-A165 immunoreactivity was present in the same area (True Blue as a chromogen), arrows indicate positive cells.I–K. Fibrous scars formed by collagenous and elastic fibres surrounded by dilated cystic spaces, focally filled with blood and revealing inconsistently CD34 positive lining.I. Hematoxylin-eosin. (an arrow points to an area shown in K)J. CD34 immunostaining.K. The same area as in I with higher magnification (stained with Masson Trichrom).Asterix in I and J indicate the same area.L. Cystically dilated paratubarian spaces with signs of old haemorrhage and thrombus formation (marked with *), an open circle points to an area which was highly vascularized as shown in M. (CD31 immunostaining) and a box indicates an area which revealed focal hVEGF-A165 immunopositivity shown in N. (hVEGF-A165 immunostaining).Bar: F, I, J - 500 µm, G, H, K - 100 µm, A, B, M, N - 200 µm L - 1000 µm. |
PMC1762316_pone-0000013-g006_8135.jpg | What is the principal component of this image? | Major changes after 16-months after activation of hVEGF-A165 expression.A. Liver: Encapsulated hepatocellular carcinoma was highly necrotic and focally calcified (Haematoxylin-eosin).B. Lung: Papillary adenocarcinoma. (Haematoxylin-eosin).C. Macroscopical changes in liver (box shows the area of the microscopical sections in F–H).D. Macroscopical changes in spleen, control spleen on the left (microscopical sections in I–K).E. Macroscopical changes in paratubarian area (microscopical sections in L–N).F. Cavernous hemangioma featuring focal hyalinization.G. The same tumor mass area with higher magnification (haematoxylin-eosin).H. Weak focal hVEGF-A165 immunoreactivity was present in the same area (True Blue as a chromogen), arrows indicate positive cells.I–K. Fibrous scars formed by collagenous and elastic fibres surrounded by dilated cystic spaces, focally filled with blood and revealing inconsistently CD34 positive lining.I. Hematoxylin-eosin. (an arrow points to an area shown in K)J. CD34 immunostaining.K. The same area as in I with higher magnification (stained with Masson Trichrom).Asterix in I and J indicate the same area.L. Cystically dilated paratubarian spaces with signs of old haemorrhage and thrombus formation (marked with *), an open circle points to an area which was highly vascularized as shown in M. (CD31 immunostaining) and a box indicates an area which revealed focal hVEGF-A165 immunopositivity shown in N. (hVEGF-A165 immunostaining).Bar: F, I, J - 500 µm, G, H, K - 100 µm, A, B, M, N - 200 µm L - 1000 µm. |
PMC1762316_pone-0000013-g006_8134.jpg | Can you identify the primary element in this image? | Major changes after 16-months after activation of hVEGF-A165 expression.A. Liver: Encapsulated hepatocellular carcinoma was highly necrotic and focally calcified (Haematoxylin-eosin).B. Lung: Papillary adenocarcinoma. (Haematoxylin-eosin).C. Macroscopical changes in liver (box shows the area of the microscopical sections in F–H).D. Macroscopical changes in spleen, control spleen on the left (microscopical sections in I–K).E. Macroscopical changes in paratubarian area (microscopical sections in L–N).F. Cavernous hemangioma featuring focal hyalinization.G. The same tumor mass area with higher magnification (haematoxylin-eosin).H. Weak focal hVEGF-A165 immunoreactivity was present in the same area (True Blue as a chromogen), arrows indicate positive cells.I–K. Fibrous scars formed by collagenous and elastic fibres surrounded by dilated cystic spaces, focally filled with blood and revealing inconsistently CD34 positive lining.I. Hematoxylin-eosin. (an arrow points to an area shown in K)J. CD34 immunostaining.K. The same area as in I with higher magnification (stained with Masson Trichrom).Asterix in I and J indicate the same area.L. Cystically dilated paratubarian spaces with signs of old haemorrhage and thrombus formation (marked with *), an open circle points to an area which was highly vascularized as shown in M. (CD31 immunostaining) and a box indicates an area which revealed focal hVEGF-A165 immunopositivity shown in N. (hVEGF-A165 immunostaining).Bar: F, I, J - 500 µm, G, H, K - 100 µm, A, B, M, N - 200 µm L - 1000 µm. |
PMC1762318_pone-0000079-g005_8146.jpg | What is the focal point of this photograph? | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762318_pone-0000079-g005_8145.jpg | What can you see in this picture? | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762318_pone-0000079-g005_8156.jpg | What is shown in this image? | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762318_pone-0000079-g005_8151.jpg | What is the core subject represented in this visual? | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762318_pone-0000079-g005_8149.jpg | What object or scene is depicted here? | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762318_pone-0000079-g005_8155.jpg | What is the central feature of this picture? | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762318_pone-0000079-g005_8153.jpg | Describe the main subject of this image. | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762318_pone-0000079-g005_8148.jpg | What stands out most in this visual? | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762318_pone-0000079-g005_8143.jpg | What is the main focus of this visual representation? | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762318_pone-0000079-g005_8152.jpg | What is the focal point of this photograph? | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762318_pone-0000079-g005_8150.jpg | What is shown in this image? | Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine.(A) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP.(B) Gelfoam containing 10×106 PDLSCs (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle).(C) HA/SCAP-Gelfoam/PDLSCs were implanted into a newly extracted incisor socket.A post channel was pre-created inside the root shape HA carrier (arrow).(D) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step.(E) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months.(F) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel.(G) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure.(H) The exposed section was sutured.(I and J) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows.(K) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image.A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows).(L and M) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M).(N) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*
P = 0.0002), but lower than that in natural swine root dentin (*
P = 0.003) (NR: natural minipig root, BR: newly formed bio-root, HA: original HA carrier). |
PMC1762325_pone-0000015-g001_8157.jpg | What is the main focus of this visual representation? | Cell adhesion, morphology of ES cells on the E-cad-Fc fusion protein-immobilized surface.(A) ES cells (EB3) adhered to E-cad-Fc-coated dishes with equivalent efficiency as to 0.1% gelatin-coated dishes after 3 hours of incubation.(B) ES cells (EB3) were cultured on E-cad-Fc-coated or fibronectin-coated dishes without serum.EGTA (5 mM) was added to the culture medium at 3 hours after seeding (open bar).Detached cells were removed and remaining cells were counted using alamar Blue reagent.*:P<0.05, §:P<0.001 vs. no treated condition (closed bar).(C and D) Morphological observation of ES cells (EB3) on the two different matrices.ES cells were cultured on polystyrene surfaces coated with 0.1% (wt/vol) gelatin (C), or 10 µg/ml E-cad-Fc (D) in the presence of LIF for 2 days.High magnification images are shown in (C′) and (D′).(E) ES cells (EB3 and R1 cells) were cultured on the plates coated with gelatin or E-cad-Fc and differentiation was induced by the withdrawal of LIF.Morphological characteristics were observed as phase contrast images.Bar indicates 100 µm.The data indicate means±SD of 3 separate experiments. |
PMC1762325_pone-0000015-g001_8166.jpg | What key item or scene is captured in this photo? | Cell adhesion, morphology of ES cells on the E-cad-Fc fusion protein-immobilized surface.(A) ES cells (EB3) adhered to E-cad-Fc-coated dishes with equivalent efficiency as to 0.1% gelatin-coated dishes after 3 hours of incubation.(B) ES cells (EB3) were cultured on E-cad-Fc-coated or fibronectin-coated dishes without serum.EGTA (5 mM) was added to the culture medium at 3 hours after seeding (open bar).Detached cells were removed and remaining cells were counted using alamar Blue reagent.*:P<0.05, §:P<0.001 vs. no treated condition (closed bar).(C and D) Morphological observation of ES cells (EB3) on the two different matrices.ES cells were cultured on polystyrene surfaces coated with 0.1% (wt/vol) gelatin (C), or 10 µg/ml E-cad-Fc (D) in the presence of LIF for 2 days.High magnification images are shown in (C′) and (D′).(E) ES cells (EB3 and R1 cells) were cultured on the plates coated with gelatin or E-cad-Fc and differentiation was induced by the withdrawal of LIF.Morphological characteristics were observed as phase contrast images.Bar indicates 100 µm.The data indicate means±SD of 3 separate experiments. |
PMC1762325_pone-0000015-g001_8167.jpg | What object or scene is depicted here? | Cell adhesion, morphology of ES cells on the E-cad-Fc fusion protein-immobilized surface.(A) ES cells (EB3) adhered to E-cad-Fc-coated dishes with equivalent efficiency as to 0.1% gelatin-coated dishes after 3 hours of incubation.(B) ES cells (EB3) were cultured on E-cad-Fc-coated or fibronectin-coated dishes without serum.EGTA (5 mM) was added to the culture medium at 3 hours after seeding (open bar).Detached cells were removed and remaining cells were counted using alamar Blue reagent.*:P<0.05, §:P<0.001 vs. no treated condition (closed bar).(C and D) Morphological observation of ES cells (EB3) on the two different matrices.ES cells were cultured on polystyrene surfaces coated with 0.1% (wt/vol) gelatin (C), or 10 µg/ml E-cad-Fc (D) in the presence of LIF for 2 days.High magnification images are shown in (C′) and (D′).(E) ES cells (EB3 and R1 cells) were cultured on the plates coated with gelatin or E-cad-Fc and differentiation was induced by the withdrawal of LIF.Morphological characteristics were observed as phase contrast images.Bar indicates 100 µm.The data indicate means±SD of 3 separate experiments. |
PMC1762325_pone-0000015-g001_8160.jpg | Describe the main subject of this image. | Cell adhesion, morphology of ES cells on the E-cad-Fc fusion protein-immobilized surface.(A) ES cells (EB3) adhered to E-cad-Fc-coated dishes with equivalent efficiency as to 0.1% gelatin-coated dishes after 3 hours of incubation.(B) ES cells (EB3) were cultured on E-cad-Fc-coated or fibronectin-coated dishes without serum.EGTA (5 mM) was added to the culture medium at 3 hours after seeding (open bar).Detached cells were removed and remaining cells were counted using alamar Blue reagent.*:P<0.05, §:P<0.001 vs. no treated condition (closed bar).(C and D) Morphological observation of ES cells (EB3) on the two different matrices.ES cells were cultured on polystyrene surfaces coated with 0.1% (wt/vol) gelatin (C), or 10 µg/ml E-cad-Fc (D) in the presence of LIF for 2 days.High magnification images are shown in (C′) and (D′).(E) ES cells (EB3 and R1 cells) were cultured on the plates coated with gelatin or E-cad-Fc and differentiation was induced by the withdrawal of LIF.Morphological characteristics were observed as phase contrast images.Bar indicates 100 µm.The data indicate means±SD of 3 separate experiments. |
PMC1762325_pone-0000015-g001_8159.jpg | What's the most prominent thing you notice in this picture? | Cell adhesion, morphology of ES cells on the E-cad-Fc fusion protein-immobilized surface.(A) ES cells (EB3) adhered to E-cad-Fc-coated dishes with equivalent efficiency as to 0.1% gelatin-coated dishes after 3 hours of incubation.(B) ES cells (EB3) were cultured on E-cad-Fc-coated or fibronectin-coated dishes without serum.EGTA (5 mM) was added to the culture medium at 3 hours after seeding (open bar).Detached cells were removed and remaining cells were counted using alamar Blue reagent.*:P<0.05, §:P<0.001 vs. no treated condition (closed bar).(C and D) Morphological observation of ES cells (EB3) on the two different matrices.ES cells were cultured on polystyrene surfaces coated with 0.1% (wt/vol) gelatin (C), or 10 µg/ml E-cad-Fc (D) in the presence of LIF for 2 days.High magnification images are shown in (C′) and (D′).(E) ES cells (EB3 and R1 cells) were cultured on the plates coated with gelatin or E-cad-Fc and differentiation was induced by the withdrawal of LIF.Morphological characteristics were observed as phase contrast images.Bar indicates 100 µm.The data indicate means±SD of 3 separate experiments. |
PMC1762325_pone-0000015-g001_8162.jpg | What can you see in this picture? | Cell adhesion, morphology of ES cells on the E-cad-Fc fusion protein-immobilized surface.(A) ES cells (EB3) adhered to E-cad-Fc-coated dishes with equivalent efficiency as to 0.1% gelatin-coated dishes after 3 hours of incubation.(B) ES cells (EB3) were cultured on E-cad-Fc-coated or fibronectin-coated dishes without serum.EGTA (5 mM) was added to the culture medium at 3 hours after seeding (open bar).Detached cells were removed and remaining cells were counted using alamar Blue reagent.*:P<0.05, §:P<0.001 vs. no treated condition (closed bar).(C and D) Morphological observation of ES cells (EB3) on the two different matrices.ES cells were cultured on polystyrene surfaces coated with 0.1% (wt/vol) gelatin (C), or 10 µg/ml E-cad-Fc (D) in the presence of LIF for 2 days.High magnification images are shown in (C′) and (D′).(E) ES cells (EB3 and R1 cells) were cultured on the plates coated with gelatin or E-cad-Fc and differentiation was induced by the withdrawal of LIF.Morphological characteristics were observed as phase contrast images.Bar indicates 100 µm.The data indicate means±SD of 3 separate experiments. |
PMC1762325_pone-0000015-g001_8163.jpg | What is shown in this image? | Cell adhesion, morphology of ES cells on the E-cad-Fc fusion protein-immobilized surface.(A) ES cells (EB3) adhered to E-cad-Fc-coated dishes with equivalent efficiency as to 0.1% gelatin-coated dishes after 3 hours of incubation.(B) ES cells (EB3) were cultured on E-cad-Fc-coated or fibronectin-coated dishes without serum.EGTA (5 mM) was added to the culture medium at 3 hours after seeding (open bar).Detached cells were removed and remaining cells were counted using alamar Blue reagent.*:P<0.05, §:P<0.001 vs. no treated condition (closed bar).(C and D) Morphological observation of ES cells (EB3) on the two different matrices.ES cells were cultured on polystyrene surfaces coated with 0.1% (wt/vol) gelatin (C), or 10 µg/ml E-cad-Fc (D) in the presence of LIF for 2 days.High magnification images are shown in (C′) and (D′).(E) ES cells (EB3 and R1 cells) were cultured on the plates coated with gelatin or E-cad-Fc and differentiation was induced by the withdrawal of LIF.Morphological characteristics were observed as phase contrast images.Bar indicates 100 µm.The data indicate means±SD of 3 separate experiments. |
PMC1762325_pone-0000015-g001_8165.jpg | What is the main focus of this visual representation? | Cell adhesion, morphology of ES cells on the E-cad-Fc fusion protein-immobilized surface.(A) ES cells (EB3) adhered to E-cad-Fc-coated dishes with equivalent efficiency as to 0.1% gelatin-coated dishes after 3 hours of incubation.(B) ES cells (EB3) were cultured on E-cad-Fc-coated or fibronectin-coated dishes without serum.EGTA (5 mM) was added to the culture medium at 3 hours after seeding (open bar).Detached cells were removed and remaining cells were counted using alamar Blue reagent.*:P<0.05, §:P<0.001 vs. no treated condition (closed bar).(C and D) Morphological observation of ES cells (EB3) on the two different matrices.ES cells were cultured on polystyrene surfaces coated with 0.1% (wt/vol) gelatin (C), or 10 µg/ml E-cad-Fc (D) in the presence of LIF for 2 days.High magnification images are shown in (C′) and (D′).(E) ES cells (EB3 and R1 cells) were cultured on the plates coated with gelatin or E-cad-Fc and differentiation was induced by the withdrawal of LIF.Morphological characteristics were observed as phase contrast images.Bar indicates 100 µm.The data indicate means±SD of 3 separate experiments. |
PMC1762325_pone-0000015-g003_8170.jpg | What stands out most in this visual? | Pluripotency of ES cells on E-cad-Fc-coated surface.(A) R1 cells were maintained on gelatin or E-cad-Fc for 26 days, and then were cultured to form embryoid bodies.After 14 days culture of embryoid bodies, expression of marker genes was analyzed by RT-PCR.Lane 1: undifferentiated cells; lane 2: on gelatin; lane 3: on E-cad-Fc.(B and C) Characterization of teratomas from ES cells (EB3) cultured on an E-cad-Fc-coated surface.(B) H&E staining of teratomas showed the differentiation into ectoderm (epidermis), mesoderm (cartilage, and striated muscle cells) and endoderm (ciliated columnar epithelium, possibly bronchial epithelium).Differentiation into ectoderm was confirmed by specific staining for the neural markers βIII-tubulin, GFAP, Neurofilament-M and GAP-43 (C).Scale bar indicates 50 µm.(D) EB3 cells cultured on gelatin- or E-cad-Fc-coated dishes for 15 days were introduced into approximately 100 blastocysts of C57BL/6 (B6) mice in each group, which yielded 4 and 7 heads of chimera pups, respectively.Furthermore, by mating with wild-type B6 females, 2/4 chimera males from the gelatin-coated group and 3/5 chimera males from the E-cad-Fc-treated group produced offspring with ES cell-derived coat colors, suggesting comparable chimera formation and germ-line transmission abilities in E-cad-Fc-treated ES cells.Germ-line transmission was also verified genetically by DNA microsatellite marker analysis.PCR-based microsatellite marker analysis was performed on a litter mate.The primer sequences for D4Mit72 and D4Mit116 microsatellite markers were obtained from Mouse Microsatellite Data Base of Japan (http://shigen.lab.nig.ac.jp/mouse/mmdbj/top.jsp). |
PMC1762326_pone-0000048-g001_8182.jpg | What is shown in this image? |
A: Short axis high resolution, high field cardiac MRI of a FXIII−/− mouse 2 days after coronary ligation. Arrows: intrathoracic hematoma adjacent to experimental anterolateral infarction.
B: Autopsy confirms a blood clot (asterisk) originating from myocardial rupture at the border zone (arrow) of the myocardial infarct.
C: Histology of 1A shows rupture channel (arrows), filled with blood.
D: In patients with ruptured MI, FXIII levels were significantly reduced (*p<0.01).
E: Color Doppler echo of patient with new ventricular septum defect 7 days after myocardial infarction (arrow).
F: MRI after VSD repair with patch (arrows).
G–I: Explantation site of saphenous veins for CABG surgery displays delayed healing.
J: 73 days after initial surgery, 3 revisions and 2 weeks after i.v. FXIII augmentation, the wound is closed. |
PMC1762326_pone-0000048-g001_8173.jpg | What can you see in this picture? |
A: Short axis high resolution, high field cardiac MRI of a FXIII−/− mouse 2 days after coronary ligation. Arrows: intrathoracic hematoma adjacent to experimental anterolateral infarction.
B: Autopsy confirms a blood clot (asterisk) originating from myocardial rupture at the border zone (arrow) of the myocardial infarct.
C: Histology of 1A shows rupture channel (arrows), filled with blood.
D: In patients with ruptured MI, FXIII levels were significantly reduced (*p<0.01).
E: Color Doppler echo of patient with new ventricular septum defect 7 days after myocardial infarction (arrow).
F: MRI after VSD repair with patch (arrows).
G–I: Explantation site of saphenous veins for CABG surgery displays delayed healing.
J: 73 days after initial surgery, 3 revisions and 2 weeks after i.v. FXIII augmentation, the wound is closed. |
PMC1762326_pone-0000048-g001_8175.jpg | What's the most prominent thing you notice in this picture? |
A: Short axis high resolution, high field cardiac MRI of a FXIII−/− mouse 2 days after coronary ligation. Arrows: intrathoracic hematoma adjacent to experimental anterolateral infarction.
B: Autopsy confirms a blood clot (asterisk) originating from myocardial rupture at the border zone (arrow) of the myocardial infarct.
C: Histology of 1A shows rupture channel (arrows), filled with blood.
D: In patients with ruptured MI, FXIII levels were significantly reduced (*p<0.01).
E: Color Doppler echo of patient with new ventricular septum defect 7 days after myocardial infarction (arrow).
F: MRI after VSD repair with patch (arrows).
G–I: Explantation site of saphenous veins for CABG surgery displays delayed healing.
J: 73 days after initial surgery, 3 revisions and 2 weeks after i.v. FXIII augmentation, the wound is closed. |
PMC1762326_pone-0000048-g001_8174.jpg | What is being portrayed in this visual content? |
A: Short axis high resolution, high field cardiac MRI of a FXIII−/− mouse 2 days after coronary ligation. Arrows: intrathoracic hematoma adjacent to experimental anterolateral infarction.
B: Autopsy confirms a blood clot (asterisk) originating from myocardial rupture at the border zone (arrow) of the myocardial infarct.
C: Histology of 1A shows rupture channel (arrows), filled with blood.
D: In patients with ruptured MI, FXIII levels were significantly reduced (*p<0.01).
E: Color Doppler echo of patient with new ventricular septum defect 7 days after myocardial infarction (arrow).
F: MRI after VSD repair with patch (arrows).
G–I: Explantation site of saphenous veins for CABG surgery displays delayed healing.
J: 73 days after initial surgery, 3 revisions and 2 weeks after i.v. FXIII augmentation, the wound is closed. |
PMC1762326_pone-0000048-g001_8178.jpg | What is the main focus of this visual representation? |
A: Short axis high resolution, high field cardiac MRI of a FXIII−/− mouse 2 days after coronary ligation. Arrows: intrathoracic hematoma adjacent to experimental anterolateral infarction.
B: Autopsy confirms a blood clot (asterisk) originating from myocardial rupture at the border zone (arrow) of the myocardial infarct.
C: Histology of 1A shows rupture channel (arrows), filled with blood.
D: In patients with ruptured MI, FXIII levels were significantly reduced (*p<0.01).
E: Color Doppler echo of patient with new ventricular septum defect 7 days after myocardial infarction (arrow).
F: MRI after VSD repair with patch (arrows).
G–I: Explantation site of saphenous veins for CABG surgery displays delayed healing.
J: 73 days after initial surgery, 3 revisions and 2 weeks after i.v. FXIII augmentation, the wound is closed. |
PMC1762326_pone-0000048-g001_8181.jpg | Describe the main subject of this image. |
A: Short axis high resolution, high field cardiac MRI of a FXIII−/− mouse 2 days after coronary ligation. Arrows: intrathoracic hematoma adjacent to experimental anterolateral infarction.
B: Autopsy confirms a blood clot (asterisk) originating from myocardial rupture at the border zone (arrow) of the myocardial infarct.
C: Histology of 1A shows rupture channel (arrows), filled with blood.
D: In patients with ruptured MI, FXIII levels were significantly reduced (*p<0.01).
E: Color Doppler echo of patient with new ventricular septum defect 7 days after myocardial infarction (arrow).
F: MRI after VSD repair with patch (arrows).
G–I: Explantation site of saphenous veins for CABG surgery displays delayed healing.
J: 73 days after initial surgery, 3 revisions and 2 weeks after i.v. FXIII augmentation, the wound is closed. |
PMC1762337_pone-0000036-g003_8186.jpg | What's the most prominent thing you notice in this picture? | Dissociation of PHOT1 from the plasma membrane in blue-light irradiated cells(A) Stomata blue-light irradiation.Confocal section of the epidermis of a dark-adapted PHOT1-GFP seedling showing all GFP signal attached to the cell surface (left).Section of the same field 3 min after the initial scan (right).The intensity of the GFP signal decreased in the irradiated stoma.No changes were detected in its neighbour epidermal cells.(B) Stomatal neighbour cell irradiation.Epidermal sections before (left) and after (right) the blue-light illumination.The argon laser provided the blue-light source.Scale bar: 3 µm; all images are the same magnification. |
PMC1762337_pone-0000036-g003_8185.jpg | What is the principal component of this image? | Dissociation of PHOT1 from the plasma membrane in blue-light irradiated cells(A) Stomata blue-light irradiation.Confocal section of the epidermis of a dark-adapted PHOT1-GFP seedling showing all GFP signal attached to the cell surface (left).Section of the same field 3 min after the initial scan (right).The intensity of the GFP signal decreased in the irradiated stoma.No changes were detected in its neighbour epidermal cells.(B) Stomatal neighbour cell irradiation.Epidermal sections before (left) and after (right) the blue-light illumination.The argon laser provided the blue-light source.Scale bar: 3 µm; all images are the same magnification. |
PMC1762337_pone-0000036-g003_8183.jpg | What is being portrayed in this visual content? | Dissociation of PHOT1 from the plasma membrane in blue-light irradiated cells(A) Stomata blue-light irradiation.Confocal section of the epidermis of a dark-adapted PHOT1-GFP seedling showing all GFP signal attached to the cell surface (left).Section of the same field 3 min after the initial scan (right).The intensity of the GFP signal decreased in the irradiated stoma.No changes were detected in its neighbour epidermal cells.(B) Stomatal neighbour cell irradiation.Epidermal sections before (left) and after (right) the blue-light illumination.The argon laser provided the blue-light source.Scale bar: 3 µm; all images are the same magnification. |
PMC1762345_pone-0000038-g003_8189.jpg | What stands out most in this visual? | EGFP localization in ocular tissues following intravitreal injection.Direct fluorescence microscopy was utilized to localize EGFP expression in ocular tissues at 2-days post-injection of 0.6 µg of compacted DNA.(A) Retinal autofluorescence was present in the outer segment of all samples including mock- and naked plasmid-injected eyes, however EGFP fluorescence was detected in the GCL of both the AC-GFP and TFA-GFP injected eyes.(B) Upon examination at higher magnification, EGFP expression was confined to the GCL in the AC-GFP-injected eyes, and present in the GCL and IPL of TFA-GFP-injected eyes.(C) Expression of EGFP was also detected in the cornea, trabecular meshwork, and lens following intravitreal injection of both TFA and AC nanoparticles (only AC shown).“FITC” channel imaging was performed as described in the Methods Section.OS: Outer Segment; ONL: Outer Nuclear Layer; INL: Inner Nuclear Layer; IPL: Inner Plexiform Layer; GCL: Ganglion Cell Layer; CO: Cornea; TM: Trabecular Meshwork; LE: Lens.Scale bars, 10 µM. |
PMC1762355_pone-0000043-g002_8194.jpg | What is the dominant medical problem in this image? |
M. tuberculosis accumulates lipid droplets inside adipocytes.3T3-L1 mouse adipocytes (A–C&E) and pre-adipocytes (D) were pulsed with M. tuberculosis MT103 at a MOI of 1 for 4 h, then chased with fresh medium for 24 h and observed by electron microscopy.In A., the arrow indicates a mycobacterial vacuole shown at higher magnification in the inset; LD, lipid droplet; bar = 2 µm.In B., perilipinA/B was immuno-stained with gold-conjugated antibodies.
Mtb, M. tuberculosis; bar = 200 nm.In C, bar = 500 nm.In D&E, bar = 200 nm.
F. Electron micrographs of 2 independent experiments were used to quantified lipid droplet accumulation inside mycobacteria when within adipocytes and pre-adipocytes.An average of 50 mycobacteria were observed in different fields in each sample. |
PMC1762355_pone-0000043-g002_8195.jpg | What is shown in this image? |
M. tuberculosis accumulates lipid droplets inside adipocytes.3T3-L1 mouse adipocytes (A–C&E) and pre-adipocytes (D) were pulsed with M. tuberculosis MT103 at a MOI of 1 for 4 h, then chased with fresh medium for 24 h and observed by electron microscopy.In A., the arrow indicates a mycobacterial vacuole shown at higher magnification in the inset; LD, lipid droplet; bar = 2 µm.In B., perilipinA/B was immuno-stained with gold-conjugated antibodies.
Mtb, M. tuberculosis; bar = 200 nm.In C, bar = 500 nm.In D&E, bar = 200 nm.
F. Electron micrographs of 2 independent experiments were used to quantified lipid droplet accumulation inside mycobacteria when within adipocytes and pre-adipocytes.An average of 50 mycobacteria were observed in different fields in each sample. |
PMC1762355_pone-0000043-g002_8192.jpg | What stands out most in this visual? |
M. tuberculosis accumulates lipid droplets inside adipocytes.3T3-L1 mouse adipocytes (A–C&E) and pre-adipocytes (D) were pulsed with M. tuberculosis MT103 at a MOI of 1 for 4 h, then chased with fresh medium for 24 h and observed by electron microscopy.In A., the arrow indicates a mycobacterial vacuole shown at higher magnification in the inset; LD, lipid droplet; bar = 2 µm.In B., perilipinA/B was immuno-stained with gold-conjugated antibodies.
Mtb, M. tuberculosis; bar = 200 nm.In C, bar = 500 nm.In D&E, bar = 200 nm.
F. Electron micrographs of 2 independent experiments were used to quantified lipid droplet accumulation inside mycobacteria when within adipocytes and pre-adipocytes.An average of 50 mycobacteria were observed in different fields in each sample. |
PMC1762355_pone-0000043-g003_8197.jpg | What is the dominant medical problem in this image? | Detection of M. tuberculosis in adipose tissue from individuals with latent or active TB.
A. Perinodal adipose tissue was taken from biopsy of the mediastinal lymph node from a patient with active TB.Bacilli were immuno-detected using an anti-BCG rabbit hyperimmune serum (right panel).As a control, a serial section was stained with serum from a naïve animal (left panel).
B. Perinodal adipose tissue was taken at autopsy from two individuals (upper and lower panels) with no clinical sign of pulmonary TB.
In situ PCR was used to detect IS6110.In A&B, arrows indicate positive signals. |
PMC1762355_pone-0000043-g003_8200.jpg | What is the principal component of this image? | Detection of M. tuberculosis in adipose tissue from individuals with latent or active TB.
A. Perinodal adipose tissue was taken from biopsy of the mediastinal lymph node from a patient with active TB.Bacilli were immuno-detected using an anti-BCG rabbit hyperimmune serum (right panel).As a control, a serial section was stained with serum from a naïve animal (left panel).
B. Perinodal adipose tissue was taken at autopsy from two individuals (upper and lower panels) with no clinical sign of pulmonary TB.
In situ PCR was used to detect IS6110.In A&B, arrows indicate positive signals. |
PMC1762355_pone-0000043-g003_8198.jpg | What is the main focus of this visual representation? | Detection of M. tuberculosis in adipose tissue from individuals with latent or active TB.
A. Perinodal adipose tissue was taken from biopsy of the mediastinal lymph node from a patient with active TB.Bacilli were immuno-detected using an anti-BCG rabbit hyperimmune serum (right panel).As a control, a serial section was stained with serum from a naïve animal (left panel).
B. Perinodal adipose tissue was taken at autopsy from two individuals (upper and lower panels) with no clinical sign of pulmonary TB.
In situ PCR was used to detect IS6110.In A&B, arrows indicate positive signals. |
PMC1762384_pone-0000018-g005_8204.jpg | What can you see in this picture? | Evolution of JAK2 V617F-induced polycythemia to “spent” phase with myelofibrosis.(A) Box-style plots of hematocrit (red squares, left axis) and reticulocyte counts (blue triangles, right axis) in a cohort (n = 12) of Balb/c recipients of syngeneic JAK2 V617F-transduced BM, followed for over eight months after transplantation.Similar data were observed for a B6 cohort (data not shown).(B) Increasing fibrosis (demonstrated by reticulin staining) in spleen (left panels) and BM (right panels) of representative JAK2 V617F recipients at about 3 months (middle panels) and 7 months (bottom panels) after transplantation.Note the marked increase in reticulin staining at 7 months in the JAK2 V617F recipients, but not in recipients of JAK2 WT-transduced BM (top panels).(C): Efficient transfer of the PV-like MPD by transplantation of BM from primary mice sacrificed either in the early, polycythemic phase (left, n = 3, sacrificed 72–167 days post-transplant) or the late, myelofibrotic phase (right, n = 2, sacrificed 208 days post-transplant), to lethally irradiated syngeneic secondary recipients (n = 6 for early phase and n = 4 for late phase).The graphs depict mean hematocrit (black, left axis), reticulocyte count (white, right axis) and peripheral blood leukocyte count (grey, right axis) of the donors at the time of sacrifice, and of the recipients at day 30–70 post-transplant.For transplants performed in the late phase of the disease, the hematocrit and reticulocyte counts of recipients were significantly higher than of the donors (P = 0.0407 and P = 0.0337, respectively, unpaired t-test), while there was no significant difference between donors and recipients transplanted in the early phase. |
PMC1762384_pone-0000018-g005_8205.jpg | What is the focal point of this photograph? | Evolution of JAK2 V617F-induced polycythemia to “spent” phase with myelofibrosis.(A) Box-style plots of hematocrit (red squares, left axis) and reticulocyte counts (blue triangles, right axis) in a cohort (n = 12) of Balb/c recipients of syngeneic JAK2 V617F-transduced BM, followed for over eight months after transplantation.Similar data were observed for a B6 cohort (data not shown).(B) Increasing fibrosis (demonstrated by reticulin staining) in spleen (left panels) and BM (right panels) of representative JAK2 V617F recipients at about 3 months (middle panels) and 7 months (bottom panels) after transplantation.Note the marked increase in reticulin staining at 7 months in the JAK2 V617F recipients, but not in recipients of JAK2 WT-transduced BM (top panels).(C): Efficient transfer of the PV-like MPD by transplantation of BM from primary mice sacrificed either in the early, polycythemic phase (left, n = 3, sacrificed 72–167 days post-transplant) or the late, myelofibrotic phase (right, n = 2, sacrificed 208 days post-transplant), to lethally irradiated syngeneic secondary recipients (n = 6 for early phase and n = 4 for late phase).The graphs depict mean hematocrit (black, left axis), reticulocyte count (white, right axis) and peripheral blood leukocyte count (grey, right axis) of the donors at the time of sacrifice, and of the recipients at day 30–70 post-transplant.For transplants performed in the late phase of the disease, the hematocrit and reticulocyte counts of recipients were significantly higher than of the donors (P = 0.0407 and P = 0.0337, respectively, unpaired t-test), while there was no significant difference between donors and recipients transplanted in the early phase. |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.