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

Non-invasive transcranial Doppler US investigation in adult patients was first described by Aaslid et al. (1982). The apparatus consists in a 2 MHz bidirectional pulsed Doppler with spectrum analyser. Middle and anterior cerebral arteries were insonated by transtemporal exploration, basilar artery by occipital foramen. The criteria of identification were: position and angulation of the probe, direction of the flow, depth of sample volume. The authors present a first series of 31 patients, all with cervical CW Doppler and B-mode Echo. The percentage of identification was: MCA 72%; ACA 69%; BA 54%. Some clinical cases are illustrated. The interest of the method is emphasized in spite of constraints depending on probe position and anatomical variability of the circle of Willis: ambulatory and non-invasive methods; assessment of intracranial blood flow in various conditions: cerebral ischemia and infarction, intracerebral angioma; complementarity with other non-invasive and non-expensive techniques: EEG and cervical US investigation.
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PMID:[The transcranial Doppler in the adult. Preliminary results in 31 patients]. 295 May 71

Magnetic resonance imaging of the brain in two infants with Sturge-Weber syndrome has demonstrated a pattern of accelerated myelination in the abnormal cerebral hemisphere. The extent of myelination was most apparent on the T1-weighted inversion recovery sequence while the T2-weighted images demonstrated concomitant changes in hydration of the brain. We propose an explanation for this finding based on cerebral ischemia underlying the leptomeningeal angioma.
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PMID:Accelerated myelination in early Sturge-Weber syndrome demonstrated by MR imaging. 381 19

We report a female patient who had a scalp hemangioma, a cleft uvula, an upper sternal defect, pectus excavatum, arachnodactyly, pes planus, and joint hypermobility. She had rupture of an aortic aneurysm after minor trauma at 11 years of age. At 17 years of age, elective repair of a dilated, ectatic aorta was complicated by cerebral ischemia. Other vascular abnormalities in the proband included an aneurysm of the left subclavian artery, atresia of the right carotid artery, and calcified cerebral aneurysms. We believe that the proband's physical anomalies are best described by the PHACE (posterior fossa brain malformations, hemangiomas, arterial anomalies, coarctation of the aorta and cardiac defects, and eye abnormalities) phenotypic spectrum. This spectrum of physical anomalies also includes sternal clefting and hemagiomas as part of the sternal malformation/vascular dysplasia (SM/VD) association, as found in our patient, and the acronym PHACES has also been used. We consider that the PHACE phenotypic spectrum is likely to be broader than previously recognized and includes orofacial clefting and aortic dilatation and rupture. Our patient also had skeletal anomalies that lead to consideration of Marfan syndrome as a diagnosis. It should be recognized that there is clinical overlap between PHACE syndrome and Marfan syndrome when aortic dilatation is present. We would also like to emphasize the minor nature of the cutaneous findings in our patient despite her severe vascular complications. This is in contrast to previous reports of large or multiple hemangiomas in PHACE syndrome.
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PMID:Report of a child with aortic aneurysm, orofacial clefting, hemangioma, upper sternal defect, and marfanoid features: possible PHACE syndrome. 1211 39

Uncontrolled expression of vascular endothelial growth factor (VEGF) in vivo may cause unexpected side effects, such as brain hemangioma or tumor growth. Because hypoxia-inducible factor-1 (HIF-1) is upregulated during cerebral ischemia and regulates gene expression by binding to a cis-acting hypoxia-responsive element (HRE), we therefore used a novel HRE, originating in the 3'-end of the erythropoietin (Epo) gene, to control gene expression in the ischemic brain. A concatemer of nine copies (H9) of the consensus sequence of HRE was used to mediate hypoxia induction. Three groups of adult CD-1 mice received AAVH9-VEGF, AAVH9-lacZ or saline injection, and then underwent 45 min of transient middle cerebral artery occlusion (tMCAO). Results show that HIF-1 was persistently expressed in the ischemic brain. VEGF was overexpressed in the ischemic perifocal region in AAVH9-VEGF-transduced mice. Double-labeled immunostaining showed that VEGF expressed in neurons and astrocytes but not endothelial cells, suggesting that adeno-associated virus (AAV) vectors transduced neurons and astrocytes predominantly. The total number of microvessels/enlarged microvessels was greatly increased in the AAVH9-VEGF-transduced mice (180+/-29/27+/-4) compared to the AAVH9-lacZ (118+/-19/14+/-3) or saline-treated (119+/-20/14+/-2) mice after tMCAO (P<0.05). Cell proliferation examination demonstrated that these microvessels were newly formed. Regional cerebral blood flow recovery in the AAVH9-VEGF-transduced mice was also better than in AAVH9-lacZ or saline-treated mice (P<0.05). Our data indicated that HRE is a novel trigger for the control of VEGF expression in the ischemic brain. VEGF overexpression through AAVH9-VEGF gene transfer showed stable focal angiogenic effects in post-ischemic repair process, providing an opportunity to rebuild injured brain tissue.
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PMID:Adeno-associated viral vector-mediated hypoxia-regulated VEGF gene transfer promotes angiogenesis following focal cerebral ischemia in mice. 1796 Jan 59