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universal imaging inc computerized video analysis system image 1/fl
Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a <t>computerized</t> <t>video</t> <t>analysis</t> of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).
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1) Product Images from "Novel mechanisms and signaling pathways of esophageal ulcer healing: the role of prostaglandin EP2 receptors, cAMP, and pCREB"

Article Title: Novel mechanisms and signaling pathways of esophageal ulcer healing: the role of prostaglandin EP2 receptors, cAMP, and pCREB

Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

doi: 10.1152/ajpgi.00177.2014

Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a computerized video analysis of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).
Figure Legend Snippet: Misoprostol accelerates esophageal ulcer healing and stimulates angiogenesis. Rats were treated intragastrically twice daily with either 50 μg/kg misoprostol or its vehicle for 3 or 6 days starting 3 days after ulcer induction. A: ulcer healing dynamics. Ulcer area was measured by a computerized video analysis of the ulcer images. The results are expressed as a percentage of ulcer area at day 3. Misoprostol treatment significantly reduced ulcer area, reflecting increased esophageal ulcer healing in rats. B: microvessel density in granulation tissue at the ulcer base. The results are expressed as the number of microvessels per square millimeter of granulation tissue section (n/mm2). Misoprostol treatment significantly increased microvessel density (reflecting angiogenesis) in granulation tissue at the esophageal ulcer base. C: proliferating cell nuclear antigen (PCNA) labeling index (LI) in the epithelium at the ulcer margin. The results are expressed as the percentage of increase in the number of labeled cells in the epithelium of the ulcer margin over the number of labeled cells in the epithelium distant from the ulcer. Misoprostol treatment slightly increased epithelial cell proliferation at the esophageal ulcer margin. NS, not significant. Values are means ± SD. For each column (n = 6).

Techniques Used: Labeling

Related Articles

Labeling:

Article Title: Abnormal PTEN expression in portal hypertensive gastric mucosa: a key to impaired PI 3-kinase/Akt activation and delayed injury healing?
Article Snippet: Phosphatase and tensin homologue deleted on chromosome ten (PTEN) is a dual-specificity phosphatase that has activity toward both phosphorylated peptides and phospholipids.. PTEN inhibits activation of Akt, the downstream effector of PI 3-kinase, which is integral to cell proliferation, migration, survival, and angiogenesis essential for tissue injury healing.. PTEN expression and activation during injury healing remain unexplored.

Article Title: Novel mechanisms and signaling pathways of esophageal ulcer healing: the role of prostaglandin EP2 receptors, cAMP, and pCREB
Article Snippet: The ulcer area was measured using a computerized video analysis system (Image 1/FL; Universal Imaging, Westchester, PA).

Article Title: Esophageal ulceration triggers expression of hypoxia-inducible factor-1 alpha and activates vascular endothelial growth factor gene: implications for angiogenesis and ulcer healing.
Article Snippet: The area of mucosal defect (ulcer area) was measured using a computerized video analysis system (Image 1/FL; Universal Imaging Corp., Westchester, PA), and a 1-cm-long segment of the esophagus (including ulcer) was excised and fixed in 10% formalin for immunohistochemical staining.

Article Title: Selective Cyclooxygenase-2 Blocker Delays Healing of Esophageal Ulcers in Rats and Inhibits Ulceration-Triggered c-Met/Hepatocyte Growth Factor Receptor Induction and Extracellular Signal-Regulated Kinase 2 Activation
Article Snippet: The ulcer area was measured using a computerized video-image analysis system (Image 1/FL; Universal Imaging Corp., Westchester, PA).

Article Title: Selective cyclooxygenase (COX) inhibition causes damage to portal hypertensive gastric mucosa: roles of nitric oxide and NF-kappaB.
Article Snippet: Portal hypertension (PHT) is associated with increased susceptibility of the gastric mucosa to injury by a variety of factors, including nonsteroidal anti-inflammatory drugs (NSAIDs) that nonselectively inhibit both isoforms of cyclooxygenase (COX-1 and -2).. PHT gastric mucosa also has excessive nitric oxide (NO) production that contributes to the general increased susceptibility to injury.. Using a rat model of PHT, we studied whether selective COX inhibition, which does not damage normal (normotensive) gastric mucosa, is sufficient to cause PHT gastric damage and, if so, whether and how excessive NO is involved.

Polymerase Chain Reaction:

Article Title: Abnormal PTEN expression in portal hypertensive gastric mucosa: a key to impaired PI 3-kinase/Akt activation and delayed injury healing?
Article Snippet: Phosphatase and tensin homologue deleted on chromosome ten (PTEN) is a dual-specificity phosphatase that has activity toward both phosphorylated peptides and phospholipids.. PTEN inhibits activation of Akt, the downstream effector of PI 3-kinase, which is integral to cell proliferation, migration, survival, and angiogenesis essential for tissue injury healing.. PTEN expression and activation during injury healing remain unexplored.

Article Title: Novel mechanisms and signaling pathways of esophageal ulcer healing: the role of prostaglandin EP2 receptors, cAMP, and pCREB
Article Snippet: The ulcer area was measured using a computerized video analysis system (Image 1/FL; Universal Imaging, Westchester, PA).

Article Title: Esophageal ulceration triggers expression of hypoxia-inducible factor-1 alpha and activates vascular endothelial growth factor gene: implications for angiogenesis and ulcer healing.
Article Snippet: The area of mucosal defect (ulcer area) was measured using a computerized video analysis system (Image 1/FL; Universal Imaging Corp., Westchester, PA), and a 1-cm-long segment of the esophagus (including ulcer) was excised and fixed in 10% formalin for immunohistochemical staining.

Article Title: Selective Cyclooxygenase-2 Blocker Delays Healing of Esophageal Ulcers in Rats and Inhibits Ulceration-Triggered c-Met/Hepatocyte Growth Factor Receptor Induction and Extracellular Signal-Regulated Kinase 2 Activation
Article Snippet: The ulcer area was measured using a computerized video-image analysis system (Image 1/FL; Universal Imaging Corp., Westchester, PA).

Article Title: Selective cyclooxygenase (COX) inhibition causes damage to portal hypertensive gastric mucosa: roles of nitric oxide and NF-kappaB.
Article Snippet: Portal hypertension (PHT) is associated with increased susceptibility of the gastric mucosa to injury by a variety of factors, including nonsteroidal anti-inflammatory drugs (NSAIDs) that nonselectively inhibit both isoforms of cyclooxygenase (COX-1 and -2).. PHT gastric mucosa also has excessive nitric oxide (NO) production that contributes to the general increased susceptibility to injury.. Using a rat model of PHT, we studied whether selective COX inhibition, which does not damage normal (normotensive) gastric mucosa, is sufficient to cause PHT gastric damage and, if so, whether and how excessive NO is involved.

Immunohistochemical staining:

Article Title: Abnormal PTEN expression in portal hypertensive gastric mucosa: a key to impaired PI 3-kinase/Akt activation and delayed injury healing?
Article Snippet: Phosphatase and tensin homologue deleted on chromosome ten (PTEN) is a dual-specificity phosphatase that has activity toward both phosphorylated peptides and phospholipids.. PTEN inhibits activation of Akt, the downstream effector of PI 3-kinase, which is integral to cell proliferation, migration, survival, and angiogenesis essential for tissue injury healing.. PTEN expression and activation during injury healing remain unexplored.

Article Title: Novel mechanisms and signaling pathways of esophageal ulcer healing: the role of prostaglandin EP2 receptors, cAMP, and pCREB
Article Snippet: The ulcer area was measured using a computerized video analysis system (Image 1/FL; Universal Imaging, Westchester, PA).

Article Title: Esophageal ulceration triggers expression of hypoxia-inducible factor-1 alpha and activates vascular endothelial growth factor gene: implications for angiogenesis and ulcer healing.
Article Snippet: The area of mucosal defect (ulcer area) was measured using a computerized video analysis system (Image 1/FL; Universal Imaging Corp., Westchester, PA), and a 1-cm-long segment of the esophagus (including ulcer) was excised and fixed in 10% formalin for immunohistochemical staining.

Article Title: Selective Cyclooxygenase-2 Blocker Delays Healing of Esophageal Ulcers in Rats and Inhibits Ulceration-Triggered c-Met/Hepatocyte Growth Factor Receptor Induction and Extracellular Signal-Regulated Kinase 2 Activation
Article Snippet: The ulcer area was measured using a computerized video-image analysis system (Image 1/FL; Universal Imaging Corp., Westchester, PA).

Article Title: Selective cyclooxygenase (COX) inhibition causes damage to portal hypertensive gastric mucosa: roles of nitric oxide and NF-kappaB.
Article Snippet: Portal hypertension (PHT) is associated with increased susceptibility of the gastric mucosa to injury by a variety of factors, including nonsteroidal anti-inflammatory drugs (NSAIDs) that nonselectively inhibit both isoforms of cyclooxygenase (COX-1 and -2).. PHT gastric mucosa also has excessive nitric oxide (NO) production that contributes to the general increased susceptibility to injury.. Using a rat model of PHT, we studied whether selective COX inhibition, which does not damage normal (normotensive) gastric mucosa, is sufficient to cause PHT gastric damage and, if so, whether and how excessive NO is involved.

Staining:

Article Title: Abnormal PTEN expression in portal hypertensive gastric mucosa: a key to impaired PI 3-kinase/Akt activation and delayed injury healing?
Article Snippet: Phosphatase and tensin homologue deleted on chromosome ten (PTEN) is a dual-specificity phosphatase that has activity toward both phosphorylated peptides and phospholipids.. PTEN inhibits activation of Akt, the downstream effector of PI 3-kinase, which is integral to cell proliferation, migration, survival, and angiogenesis essential for tissue injury healing.. PTEN expression and activation during injury healing remain unexplored.

Article Title: Novel mechanisms and signaling pathways of esophageal ulcer healing: the role of prostaglandin EP2 receptors, cAMP, and pCREB
Article Snippet: The ulcer area was measured using a computerized video analysis system (Image 1/FL; Universal Imaging, Westchester, PA).

Article Title: Esophageal ulceration triggers expression of hypoxia-inducible factor-1 alpha and activates vascular endothelial growth factor gene: implications for angiogenesis and ulcer healing.
Article Snippet: The area of mucosal defect (ulcer area) was measured using a computerized video analysis system (Image 1/FL; Universal Imaging Corp., Westchester, PA), and a 1-cm-long segment of the esophagus (including ulcer) was excised and fixed in 10% formalin for immunohistochemical staining.

Article Title: Selective Cyclooxygenase-2 Blocker Delays Healing of Esophageal Ulcers in Rats and Inhibits Ulceration-Triggered c-Met/Hepatocyte Growth Factor Receptor Induction and Extracellular Signal-Regulated Kinase 2 Activation
Article Snippet: The ulcer area was measured using a computerized video-image analysis system (Image 1/FL; Universal Imaging Corp., Westchester, PA).

Article Title: Selective cyclooxygenase (COX) inhibition causes damage to portal hypertensive gastric mucosa: roles of nitric oxide and NF-kappaB.
Article Snippet: Portal hypertension (PHT) is associated with increased susceptibility of the gastric mucosa to injury by a variety of factors, including nonsteroidal anti-inflammatory drugs (NSAIDs) that nonselectively inhibit both isoforms of cyclooxygenase (COX-1 and -2).. PHT gastric mucosa also has excessive nitric oxide (NO) production that contributes to the general increased susceptibility to injury.. Using a rat model of PHT, we studied whether selective COX inhibition, which does not damage normal (normotensive) gastric mucosa, is sufficient to cause PHT gastric damage and, if so, whether and how excessive NO is involved.



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