Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021933 (intussusception)
 3,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an effort to elucidate the molecular mechanisms underlying cerebral vascular alteration after stroke, the authors measured the spatial and temporal profiles of blood-brain barrier (BBB) leakage, angiogenesis, vascular endothelial growth factor (VEGF), associated receptors, and angiopoietins and receptors after embolic stroke in the rat. Two to four hours after onset of ischemia, VEGF mRNA increased, whereas angiopoietin 1 (Ang 1) mRNA decreased. Three-dimensional immunofluorescent analysis revealed spatial coincidence between increases of VEGF immunoreactivity and BBB leakage in the ischemic core. Two to 28 days after the onset of stroke, increased expression of VEGF/VEGF receptors and Ang/Tie2 was detected at the boundary of the ischemic lesion. Concurrently, enlarged and thin-walled vessels were detected at the boundary of the ischemic lesion, and these vessels developed into smaller vessels via sprouting and intussusception. Three-dimensional quantitative analysis of cerebral vessels at the boundary zone 14 days after ischemia revealed a significant (P < 0.05) increase in numbers of vessels (n = 365) compared with numbers (n = 66) in the homologous tissue of the contralateral hemisphere. Furthermore, capillaries in the penumbra had a significantly smaller diameter (4.8 +/- 2.0 microm) than capillaries (5.4 +/- 1.5 microm) in the homologous regions of the contralateral hemisphere. Together, these data suggest that acute alteration of VEGF and Ang 1 in the ischemic core may mediate BBB leakage, whereas upregulation of VEGF/VEGF receptors and Ang/Tie2 at the boundary zone may regulate neovascularization in ischemic brain.
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PMID:Correlation of VEGF and angiopoietin expression with disruption of blood-brain barrier and angiogenesis after focal cerebral ischemia. 1191 9

The landmark publications that gave such impetus to our understanding of proliferative diabetic retinopathy are reviewed in the light of more recent reports. Briefly, confluence of small areas of capillary closure in the midperipheral and peripheral retina results in arteriovenous shunting and abnormal oxygen partial pressure gradients. These gradients embrace a chronic ischaemic penumbra that stimulates neuroglial secretion of angiogenic growth factors and upregulation of their receptors in the retinal venous endothelium and adventitia. The blood shunting produces biomechanical stresses within the veins and induces microvascular intussusception near arteriovenous crossings, giving way to neovascular outgrowths and/or segmental venous lesions (such as omega loops and coils) that penetrate the inner limiting lamina. The lamellar collagenous matrix of the vitreous cortex is then exploited for integrin-dependent rete expansion along chemotactic gradients. During posterior vitreous detachment, haemorrhaging takes place from the arterialised veins as venous neovascular peduncles are avulsed.
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PMID:A chronic grey matter penumbra, lateral microvascular intussusception and venous peduncular avulsion underlie diabetic vitreous haemorrhage. 1744 7