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)

Disturbances of coagulation and fibrinolytic pathways were studied in 53 young patients with cerebral ischemia. Upon admission 26 of 53 patients had abnormality in at least one of the antithrombin-III, protein C, protein S activities or in activated protein C (APC) ratios. Three months after the first examination the majority of the previously detected abnormalities returned to normal values and the most frequent alterations were decrease in protein S activity (3 patients) and APC resistance (3 patients). Conditions resulting in impaired fibrinolysis were frequently detected upon admission. Elevation of plasminogen activator inhibitor-1, lipoprotein (a), and alpha-2-antiplasmin was present in 23, 10, and 4 cases, respectively. It is concluded that abnormalities of coagulation as well as of the fibrinolytic systems are prevalent in the acute phase of cerebral ischemia, however, the results may be significantly influenced by the disease process or the acute phase effect.
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PMID:Natural coagulation inhibitor proteins in young patients with cerebral ischemia. 1172 Oct 97

Protein C (PC), protein S (PS), and antithrombin III (AT-III) are vital thrombin antagonists in circulation. However, the prevalence of these natural inhibitors for cerebral ischemia is barely mentioned in the Chinese population. The prevalence of PC, PS, and AT-III deficiency in Chinese adults with cerebral ischemia is reported. The study subjects were free of antiphospholipid antibody syndrome or systemic lupus erythematosus. Cardiac, liver, and renal function were normal. An overall rate of thrombophilia was 27%. PS deficiency was the most common disorder, followed by PC with PS and PC deficiency. There was only one patient with AT-III deficiency. No gender was specific for thrombophilia. However, PS deficiency was predilected in young adults. A positive correlation between PC and AT-III was achieved in patients with a normal PC activity but not PC deficiency. There was no correlation between AT-III or PS. The odds ratios of PC and PS were 5.29 and 2.86, respectively. Accordingly, an inability for thrombin antagonization by the PC/PS axis may relate to the occurrence of cerebral ischemia in the Chinese population. AT-III seems to display a minor role only.
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PMID:The prevalence of protein C, protein S, and antithrombin III deficiency in non-APS/SLE Chinese adults with noncardiac cerebral ischemia. 1281 86

The study of biomarkers associated with stroke has proved to be of considerable utility. The astroglial protein S-100b is a candidate marker for cerebral tissue damage. We used a rat embolic model produced by injection of microspheres to demonstrate that serum S-100b is a useful biochemical marker for ischemic brain injury. Serum S-100b levels were significantly increased following microsphere injection, which was closely correlated with the development of brain edema. We found that structurally and mechanistically independent neuroprotective agents, such as 3-[2-[4-(3-chloro-2-methylphenylmethyl)-1-piperazinyl]ethyl]-5,6-dimethoxy-1-(4-imidazolylmethyl)-1H-indazole dihydrochloride 3.5 hydrate (DY-9760e), a novel calmodulin antagonist, and the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801, are capable of attenuating increased serum S-100b levels and brain edema. In contrast, the hyperosmolar agent glycerol, which has no direct neuroprotective action, had little effect on serum S-100b levels, despite a significant decrease in brain water content. These results suggest that lowering of serum S-100b is mediated by neuroprotection against ischemic brain injury. Thus, serum S-100b reflects the extent of brain damage following cerebral ischemia and serves as a useful biomarker for the assessment of neuroprotectants.
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PMID:Serum S-100b protein as a biomarker for the assessment of neuroprotectants. 1534 63

S-100 protein, described initially by Moore, constitutes a large family of at least 20 proteins with calcium binding ability. It is found as homo- or hetero-dimers of two different subunits (A and B). Types S-100AB and S-100BB are described as S-100B protein and are shown to be highly specific for nervous tissue. It is present in the cytosol of glial and Schwann cells, and also in adipocytes and chondrocytes, although in very low concentrations in the latter two. The role of protein S-100B is not yet fully understood. It is suggested that it has intracellular and extracellular neurotropic as well as neurotoxic function. At nanomolar levels, S-100B stimulates neurite outgrowth and enhances survival of neurons. However, at micromolar levels it stimulates the expression of inflammatory cytokines and induces apoptosis. Recently, serum S-100B protein has been proved to be an attractive surrogate marker of primary severe brain injury and secondary insults. It can be measured in the arterial and venous serum; it is not affected by haemolysis and remains stable for several hours without the need for immediate analysis. Its short half-life makes measurements crucial in the emergency and intensive care settings. This review summarises published findings on S-100B regarding its role as a serum biochemical marker of brain injury, i.e., after severe, moderate or mild neuro-trauma, subarachnoid haemorrhage, thrombo-embolic stroke, cerebral ischaemia and brain tumours, as well as extracranial trauma, neurodegenerative and psychiatric disorders.
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PMID:Serum S-100B protein as a biochemical marker of brain injury: a review of current concepts. 1716 33

Overproduction of nitric oxide (NO) can cause neuronal damage, contributing to the pathogenesis of several neurodegenerative diseases and stroke (i.e., focal cerebral ischemia). NO can mediate neurotoxic effects at least in part via protein S-nitrosylation, a reaction that covalently attaches NO to a cysteine thiol (or thiolate anion) to form an S-nitrosothiol. Recently, the tyrosine phosphatase Src homology region 2-containing protein tyrosine phosphatase-2 (SHP-2) and its downstream pathways have emerged as important mediators of cell survival. Here we report that in neurons and brain tissue NO can S-nitrosylate SHP-2 at its active site cysteine, forming S-nitrosylated SHP-2 (SNO-SHP-2). We found that NMDA exposure in vitro and transient focal cerebral ischemia in vivo resulted in increased levels of SNO-SHP-2. S-Nitrosylation of SHP-2 inhibited its phosphatase activity, blocking downstream activation of the neuroprotective physiological ERK1/2 pathway, thus increasing susceptibility to NMDA receptor-mediated excitotoxicity. These findings suggest that formation of SNO-SHP-2 represents a key chemical reaction contributing to excitotoxic damage in stroke and potentially other neurological disorders.
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PMID:S-nitrosylated SHP-2 contributes to NMDA receptor-mediated excitotoxicity in acute ischemic stroke. 2338 82

The superficial temporal artery (STA) to the middle cerebral artery (MCA) bypass is the most common bypass type for revascularization to treat cerebral ischemia. If the ipsilateral STA is not available for anastomosis, various options for bypass conduits can be exercised. When the entire ipsilateral external carotid and its branches are not available, the contralateral STA may be used as a donor artery through an interposition graft. This technique is known as a "bonnet bypass." In this video, we demonstrate the utilization of a bonnet bypass in a 48-yr-old man with protein S deficiency, and right carotid artery occlusion with recurrent strokes and transient ischemic attacks (TIA). After exhausting nonsurgical options by treating with 2 antiplatelet drugs and supportive lifestyle changes, the patient continued to experience TIAs and watershed strokes in the right hemisphere. Angiography showed that the right anterior artery and the MCA were filled through the Circle of Willis, but the ipsilateral STA and entire external and common carotid arteries were not patent for potential use as a bypass donor. Since the ipsilateral bypass options were not available, we elected to perform a bypass from the contralateral STA trunk to the ipsilateral M2 with a saphenous vein interposition graft, for a so-called bonnet bypass. The patient did well after surgery and has remained symptom-free for 19 mo post bypass. The surgical technique and each step in performing this bonnet bypass are demonstrated in this 3-dimensional video. The patient consented to the publication of his operative video.
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PMID:Revascularization for Cerebral Ischemia, Step-by-Step Demonstration of Bonnet Bypass: 3-Dimensional Operative Video. 3069 Apr 94


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