Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mortality from acute myocardial infarction (MI) over the 5 year period 1982-1987 in Brown County, Wisconsin, was analyzed to assess the relationship with environmental temperature. Deaths occurring on the day of and the day following a significant snowfall as well as deaths occurring in health care facilities were eliminated from consideration because the focus was upon temperature, not snowfall or events within a hospital. These criteria resulted in the inclusion of 1,802 days and 926 cases of acute MI. The mean temperature on the day of death was obtained from climatological data and were grouped into six categories covering a range of temperatures from less than -17.8 degrees C (0 degrees F) to 16.1 degrees C (61 degrees F). The number of deaths in each category was tabulated. The effect of temperature, sex, and age were analyzed by regression analysis. The results indicated a linear increase in mortality as mean daily temperature decreased over the temperature range. The inverse temperature effect was most pronounced in males over the age of 60. These results indicate that cold temperatures appear to be associated with an increased mortality from myocardial infarction.
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PMID:Environmental temperature and mortality from acute myocardial infarction. 292 68

Identification of a characteristic morphology of a coronary stenosis likely to result in myocardial infarction would facilitate the prospective evaluation of infarct prevention strategies and identification of high-risk patients. We postulated that coronary lesions associated with recent myocardial infarction or unstable angina would have an angiographic morphology suggesting disruption of an atherosclerotic plaque and would appear morphologically different from lesions associated with chronic stable angina. To test this hypothesis, quantitative coronary angiography (Brown-Dodge method) was performed in 15 patients 4 to 30 days after myocardial infarction, in 10 patients with the abrupt onset of unstable angina and single-vessel coronary disease, and in 15 patients with chronic stable angina without prior myocardial infarction. Serial arterial diameters (20 to 40) within each lesion were determined and the degree of luminal irregularity was quantitated by calculation of an "ulceration" index. The majority of all lesions analyzed resulted in severe luminal stenosis (mean 78% area stenosis, all groups). Despite small differences in mean lesion severity among groups, overlap in the degree of luminal compromise prevented precise classification of lesions associated with myocardial infarction or unstable angina based on percent stenosis or minimum luminal cross-sectional area. The mean ulceration index of lesions in patients with unstable angina and in the infarct-related vessel in those with acute myocardial infarction was 0.62 +/- 0.05 (+/- SEM) and 0.61 +/- 0.03, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative angiographic morphology of coronary stenoses leading to myocardial infarction or unstable angina. 394 63

Tissue kallikrein exerts various biological functions through kinin formation with subsequent kinin B2 receptor activation. Recent studies showed that tissue kallikrein directly activates kinin B2 receptor in cultured cells expressing human kinin B2 receptor. In the present study, we investigated the role of tissue kallikrein in protection against cardiac injury through direct kinin B2 receptor activation using kininogen-deficient Brown Norway Katholiek rats after acute myocardial infarction. Tissue kallikrein was injected locally into the myocardium of Brown Norway Katholiek rats after coronary artery ligation with and without coinjection of icatibant (a kinin B2 receptor antagonist) and N(omega)-nitro-L-arginine methylester (an NO synthase inhibitor). One day after myocardial infarction, tissue kallikrein treatment significantly improved cardiac contractility and reduced myocardial infarct size and left ventricle end diastolic pressure in Brown Norway Katholiek rats. Kallikrein attenuated ischemia-induced apoptosis and monocyte/macrophage accumulation in the ischemic myocardium in conjunction with increased NO levels and reduced myeloperoxidase activity. Icatibant and N(omega)-nitro-L-arginine methylester abolished kallikrein's effects, indicating a kinin B2 receptor NO-mediated event. Moreover, inactive kallikrein had no beneficial effects in cardiac function, myocardial infarction, apoptosis, or inflammatory cell infiltration after myocardial infarction. In primary cardiomyocytes derived from Brown Norway Katholiek rats under serum-free conditions, active, but not inactive, kallikrein reduced hypoxia/reoxygenation-induced apoptosis and caspase-3 activity, and the effects were mediated by kinin B2 receptor/nitric oxide formation. This is the first study to demonstrate that tissue kallikrein directly activates kinin B2 receptor in the absence of kininogen to reduce infarct size, apoptosis, and inflammation and improve cardiac performance of infarcted hearts.
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PMID:Tissue kallikrein elicits cardioprotection by direct kinin b2 receptor activation independent of kinin formation. 1876