Disease relevance of Cerebral Infarction

• We conducted a randomized, double-blind, placebo-controlled study to evaluate low-intensity anticoagulation with warfarin (prothrombin-time ratio, 1.2 to 1.5) in 571 men with chronic nonrheumatic atrial fibrillation; 525 patients had not previously had a cerebral infarction, whereas 46 patients had previously had such an event [1].
• Intraoperative cerebral infarction after desmopressin administration in infant with end-stage renal disease [2].
• Activated protein C resistance in cases of cerebral infarction [3].
• Tumor necrosis factor (TNF)-alpha overexpression has been related to experimental ischemic tolerance when transient ischemia precedes cerebral infarction [4].
• Diabetes, ischemic heart disease, and elevated serum total cholesterol level all favored cerebral infarction as opposed to intracerebral hemorrhage [5].

Psychiatry related information on Cerebral Infarction

• Differential expression of TGF-beta 1, 2 and 3 isotypes in Alzheimer's disease: a comparative immunohistochemical study with cerebral infarction, aged human and mouse control brains [6].
• When do strokes cause dementia? Effects of subcortical cerebral infarction on cortical glucose metabolism and cognitive function [7].
• DESIGN: Mild cognitive impairment was determined for the subjects of the prospective National Heart, Lung, and Blood Institute Twin Study. Quantitative measures of brain, white matter hyperintensity, cerebral infarction, apolipoprotein E genotype, and psychometric testing were obtained [8].
• RESULTS: Stroke animals receiving inosine pretreatment demonstrated a higher level of locomotor activity and less cerebral infarction [9].
• Ganglioside GD3 (II3a(NeuAca2-8NeuAc)-LacCer, GD3) in reactive astrocytes from autopsied patients with Creutzfeldt-Jakob disease (CJD) and old cerebral infarction was investigated immunocytochemically, using mouse IgM anti-GD3 monoclonal antibody (DSG-1) [10].

High impact information on Cerebral Infarction

• Prostacyclin in cerebral infarction [11].
• Cerebral blood flow is regulated by endothelium-derived nitric oxide (NO), and endothelial NO synthase-deficient (eNOS-deficient; eNOS(-/-)) mice develop larger cerebral infarctions following middle cerebral artery (MCA) occlusion [12].
• Inhibition of vascular Rho guanosine-5'-triphosphate binding activity by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor simvastatin increased cerebral blood flow to ischemic regions of the brain, and mice treated with simvastatin, C3 transferase, or cytochalasin D showed smaller cerebral infarctions following MCA occlusion [12].
• Multiple subcortical infarction: CADASIL in context. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy [13].
• Cerebral infarction, cerebral haemorrhage, and ABO blood-groups [14].

Chemical compound and disease context of Cerebral Infarction

• Among the patients with no history of stroke, cerebral infarction occurred in 19 of the 265 patients in the placebo group during an average follow-up of 1.7 years (4.3 percent per year) and in 4 of the 260 patients in the warfarin group during an average follow-up of 1.8 years (0.9 percent per year) [1].
• Letter: Glycerol v. dexamethasone in acute cerebral infarction [15].
• A novel variant of antithrombin III (AT III) that lacks affinity for heparin was found in a 33-year-old man who suffered from recurrent cerebral infarction [16].
• We studied the relation of serum glucose level measured in the first 12 hours of symptoms to the clinical findings, results of computed tomography (CT), and patterns of cerebral metabolism in 39 patients who had acute ischemic cerebral infarction [17].
• At any period of this neonatal model, brain lactate levels did not exceed the toxic level, which is postulated to be responsible for cerebral infarction in adult ischemic models [18].

Biological context of Cerebral Infarction

• Circulatory and metabolic effects of glycerol infusion in patients with recent cerebral infarction [19].
• Heparin and heparin plus warfarin were ineffective in reducing the high level of dense body secretion seen in acute cerebral infarction, whereas treatment with aspirin plus dipyridamole inhibited both dense body secretion and platelet aggregation [20].
• The impact of blood pressure, serum cholesterol and triglycerides, and smoking on the risk of cerebral infarction and other stroke was studied by a longitudinal design [21].
• Papaverine and its derivatives (naftidrofuryl, viquidil, YC-93) decreased respiratory control, an effect that might correlate with their capacity to effect a vasodilatation of the cerebral vessels and their inefficacy in models of acute cerebral infarction [22].
• We investigated the putative role of apolipoprotein E phenotypes in cerebral infarction [23].

Anatomical context of Cerebral Infarction

• The molecular weight of the myelin basic protein (BP)-like material appearing in cerebrospinal fluid (CSF) of 2 persons with active-phase multiple sclerosis (MS) and 3 with recent cerebral infarctions was determined by gel filtration chromatography under acidic conditions [24].
• Systemic lupus erythematosus (SLE) can produce profound disturbances in the central nervous system, characterized by encephalopathy, focal neurologic deficits, cerebral infarction, psychosis, and seizures [25].
• RESULTS: beta2 adrenergic receptors were visualized on astrocytes in white matter of controls, and they were prominently expressed in reactive astrocytes at the boundary of cerebral infarctions and in the lateral corticospinal tract in ALS [26].
• Kallikrein gene transfer also reduced ischemia-reperfusion (I/R)-induced cerebral infarction and promoted the survival and migration of glial cells from penumbra to the ischemic core from 3 to 14 days after gene delivery [27].
• Twenty-four hours after the operation, sections of the cerebrum were stained with triphenyltetrazolium chloride, and the area of cerebral infarction was analyzed by a computer [28].

Gene context of Cerebral Infarction

• Local leakage of endothelin-1 may induce severe and prolonged constriction of collateral vessels and may therefore have a deleterious role in the pathogenesis and final outcome of cerebral infarction [29].
• Delivery of GDNF or BMP-7 to brain tissue reduced cerebral infarction and improved motor functions in stroke animals [30].
• Recombinant human interleukin-1 receptor antagonist (rhIL-1ra) markedly protects against focal cerebral ischaemia in the rat, implicating endogenous IL-1 in the events leading to cerebral infarction [31].
• Role of cyclooxygenase-2 in the development of bladder overactivity after cerebral infarction in the rat [32].
• PURPOSE: We investigated the role of cyclooxygenase (COX) isoforms in bladder overactivity induced by cerebral infarction (CI) in rats [32].
• Our results support a role for PRKCH in the pathogenesis of cerebral infarction [33].

Analytical, diagnostic and therapeutic context of Cerebral Infarction

• Plasma HMWFC values were significantly higher (p less than 0.001) in the cerebral infarction patients than in any of the control groups, and plasma fibrinogen, plasminogen, alpha1-antitrypsin and alpha2-macroglobulin also were significiantly higher (p less than 0.001) in the patients [34].
• To demonstrate the BBB break-down on the CT image in the acute stage of cerebral infarction, a 3 hour continuous drip infusion of 200 ml of meglumine amidotrizoate, rather than the conventional bolus injection, was used [35].
• To determine the hemorrhagic potential of thrombolytic therapy in experimental cerebral infarction, we compared a group of tissue plasminogen activator-treated rabbits (n = 4) with 2 groups of streptokinase-treated rabbits (n = 6 in each), as well as with 3 groups of heparin-treated rabbits (n = 5 in each) and untreated controls (n = 12) [36].
• METHODS: Glutamate in CSF was measured by high-performance liquid chromatography in 184 patients with an acute cerebral infarction of less than 24 hours' duration and in 43 control subjects [37].
• METHODS: Free protein S was measured by Laurell rocket immunoelectrophoresis in 94 adults admitted for acute cerebral infarction and in 94 hospitalized control subjects of similar age, sex, and race [38].

References