Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aortoventriculoplasty is a new method of treatment for left ventricular outflow tract obstructions. The concept is based on creating a surgical defect which is patched in such a way as to provide the largest possible outflow to the left ventricle. The incision of the aorta continues down as far as necessary, with the right ventricular wall, the aortic ring, and the septum being cut. Reconstruction with an inner Dacron patch on the septum is completed by replacing the aortic valve with an adequate prosthesis, covering the aortic incision with the same patch, and patching the right venticular opening with an outer patch. This method was used in 4 children with tunnel-like subaortic stenosis, 3 of whom had had unsuccessful previous surgical attempts. Other associated lesions including parachute mitral valve were also corrected during aortoventriculoplasty. Hemodynamic results were excellent following this operation. Two patients died postoperatively, one from advanced myocardial damage and progressive failure and the other from cerebral ischemia caused by insufficient retrograde perfusion through an aortic coarctation that was not repaired earlier. No arrhythmias were observed following the procedure. The other 2 patients are well 7 and 5 months postoperatively with excellent hemodynamic function.
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PMID:Aortoventriculoplasty: a new technique for the treatment of left ventricular outflow tract obstruction. 13 85

To evaluate the perioperative outcomes and the immediate increases in size after patch closure, 140 carotid endarterectomies were randomized into one of three groups: direct no-patch closure, saphenous vein patch closure, and polytetrafluoroethylene patch closure. Seven patients (4.4%) experienced signs of cerebral ischemia in the immediate postoperative period. In three cases this was transient and reversible. In the other four reexploration was undertaken and carotid thrombosis was corrected by thrombectomy. The condition of one of these patients deteriorated to a permanent stroke, whereas the other patients made a complete recovery. Neurologic complications were more frequent in the no-patch group, but the differences between the groups were not significant. The incidence of perioperative internal carotid stenosis, aneurysmal dilatation, and other morphologic abnormalities was assessed in 131 intravenous digital subtraction angiograms taken before the patient was discharged from the hospital. Eight (17.0%) of the endarterectomies in the no-patch group were narrowed by 30% to 50% diameter stenosis, whereas none of the patched arteries had more than 30% stenosis. In contrast, dilatation of the common or internal carotid artery to more than twice the measured diameter was absent in non-patched arteries but was present in seven (17.0%) saphenous patch closures and four (9.23%) polytetrafluoroethylene patch closures. We conclude that patch closure after carotid endarterectomy is less likely to cause stenosis in the perioperative period. Poly-tetrafluoroethylene patches resist dilatation better than do saphenous vein patches and are less likely to become aneurysmal.
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PMID:Comparison of saphenous vein patch, polytetrafluoroethylene patch, and direct arteriotomy closure after carotid endarterectomy. Part I. Perioperative results. 270 21

Oxidative and cytotoxic damage play an important role in cerebral ischemic pathogenesis and may represent a target for treatment. Recent studies have indicated that sonic hedgehog (Shh) signaling could protect neurons against oxidative stress by increasing superoxide dismutase 1 (SOD1) activity. Glioma-associated oncogene homolog 1 (Gli1) and patched-1 (Ptch1) are both components and transcriptional targets of the Shh pathway. Here, we designed this study to determine the effect of inhibition of Shh pathway on the development of cerebral ischemia injury. Male, Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (pMCAO). Cyclopamine (0.18mg/kg), the classical inhibitor of Shh signaling, was stereotactic injected into the lateral cerebral ventricle immediately after pMCAO. At 24h neurological deficit was evaluated using a modified six point scale; brain water content was measured; infarct size was analyzed with 2,3,5-triphenyltetrazolium chloride (TTC). Immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR), Western Blotting and activity assay were used to analyze the expression of Gli1, Ptch1 and SOD1. Compared with Vehicle group, cyclopamine down-regulated Gli1, Ptch1 and SOD1 in pMCAO-affected brain tissue (P<0.05), and increased infarct volume (P<0.05), brain water content (P<0.05) and behavioral deficits (P<0.05). Collectively, the present results suggest that inhibition of Shh signaling pathway exacerbated rat ischemic damage caused by pMCAO, which may be correlated with down-regulated expression of Gli1, Ptch1 and SOD1.
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PMID:Inhibition of sonic hedgehog signaling aggravates brain damage associated with the down-regulation of Gli1, Ptch1 and SOD1 expression in acute ischemic stroke. 2213 7