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)

By using ELISA and RIA to measure the levels of Beta-thromboglobulin (beta-TG), platelet factor 4(PF4), thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in plasma of patients with acute cerebral infarction, the authors found that the levels of beta-TG, PF4 and TXB2 in plasma had significantly increased (P less than 0.01), but the level of 6-keto-PGF1 alpha in plasma showed no change (P greater than 0.05). The results of the Ligusticum wallichii (Ligusticum) treatment to the test-group showed that the levels of beta-TG, PF4 and TXB2 in plasma had significantly decreased (P less than 0.01), and the level of 6-keto-PGF1 alpha in plasma had significantly increased (P less than 0.05). This suggested that the Ligusticum treatment could effectively inhibit the platelet activation in vivo and correct the TXA2-PGI2 imbalance in blood of the patients. In this study, some new approaches were explored to explain the mechanisms of Ligusticum for preventing and treating cerebral ischemia.
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PMID:[Effects of Ligusticum wallichii on the plasma levels of beta-thromboglobulin, platelet factor 4, thromboxane B2 and 6-keto-PGF1 alpha in patients with acute cerebral infarction]. 184 Mar 63

By occluding the bilateral carotid arteries of rabbits to produce bilateral partial cerebral ischemia, and by using RIA and ELISA to measure the levels of Beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in plasma, the authors found that the levels of beta-TG, PF4 and TXB2 in plasma had significantly increased (P less than 0.01), but the level of 6-keto-PGF1 alpha in plasma showed no change (P greater than 0.05) after cerebral ischemia appeared. The results of the Ligusticum wallichii (Ligusticum) pre-treatment to the test-group showed that the levels of beta-TG, PF4 and TXB2 in plasma had significantly decreased (P less than 0.01), and the level of 6-keto-PGF1 alpha in plasma had significantly increased (P less than 0.05). This suggested that the Ligusticum treatment could effectively inhibit the platelet activation in vivo and correct the TXA2-PGI2 imbalance in blood after cerebral ischemia. In this study, some new approaches were explored to explain the mechanisms of Ligusticum for preventing and treating cerebral ischemia.
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PMID:[Effects of Ligusticum wallichii on the plasma levels of beta-thromboglobulin, platelet factor 4, thromboxane B2 and 6-keto-PGF1 alpha in rabbits under acute experimental cerebral ischemia]. 214 9

The effect of short and long-term therapy with aspirin (50 mg/day) on platelet alpha granule secretion was studied in 11 healthy controls and 57 patients suffering from transient cerebral ischemic attacks (TIA) with and without accompanying diabetes and hypertension. Plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF 4) were measured as indicators of platelet alpha granule secretion. beta-TG and PF 4 levels were increased following cerebral ischemia. Aspirin treatment failed to suppress plasma levels of both proteins when measured a month and then a year after initiation of treatment. Therefore, these proteins may be poor indicators of platelet inhibition by aspirin.
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PMID:Platelet alpha granule secretion in cerebral ischemia: effect of short and long term low dose aspirin treatment. 245 69

Mitral valve prolapse (MVP) is a predisposing factor for cerebral ischemia, especially in young adults. Cerebral embolization of intracardiac thrombi is the probable mechanism in many cases. Platelets play a key role in the development of thrombi. We found that platelet factor 4, a marker protein of platelet activation, was elevated in 12 of 33 MVP patients (36%) without a history of stroke. This finding indicates that platelets are frequently activated in asymptomatic MVP patients and may allow identification of a subgroup of MVP patients with activated platelets who are at increased risk for emboli.
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PMID:Platelet activation and mitral valve prolapse. 668 86

Heparin-induced thrombocytopenia (HIT) is an adverse effect of heparin therapy which can be responsible for thrombotic events with embolic consequences. Although ischemic stroke is a well known consequence of HIT, few cases of cerebral ischemia of arterial origin have been reported so far. A 38-year-old man was admitted because of acute multiple ischemic strokes and pulmonary embolism which occurred during treatment with low molecular weight heparin as prophylactic therapy for orthopedic surgery. Neuroimaging showed occlusion of the right common carotid artery with multiple acute cerebral infarcts. Testing for anti-platelet factor 4 antibodies confirmed the diagnosis. Systematic review of the literature revealed 55 cases of arterial stroke and three cases of carotid artery occlusion caused by HIT. Although arterial ischemic stroke is a rare complication of HIT, a high level of suspicion and a prompt diagnosis of this coagulation disorder are necessary to avoid life-threatening thromboembolic complications.
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PMID:Thromboembolic complications of heparin-induced thrombocytopenia. 2268 53