Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Breddin thrombagglutination test is followed up in patients with hypercoagulation states--atherosclerosis, atherosclerotic myocardiodysthrophia, angina pectoris gravis and acute myocardial infarction and hypocoagulation states--esential and symptomatic thrombopenia. TAT is positive in 88% of the patients with atherosclerosis and in patients with angina pectoris gravis and myocardial infarction TAT is Vth stage in 100%. TAT is zero stage in 91% in patients with thrombopenia and only in 9%-I stage. The term "zero stage" is introduced.
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PMID:[Thrombagglutination test (TAT) in hyper- and hypocoagulation]. 122 97

Oxypangam is a substance applied therapeutically against a number of diseases, such as chronic liver damages, angina pectoris, and psychosomatic disturbances. The mode of action of oxypangam has not yet conclusively been described. The only well-known properties of this substance are its intensive methylating and lipolytic effects. The present paper serves to elucidate the influence of oxypangam on the induction of the tyrosine aminotransferase, on the NAD content and on the activity of the ADPR transferase in the liver. Our studies showed that in normal animals, increasing doses of oxypangam support the induction of tyrosine aminotransferase. Up to a concentration of 100 mg/kg oxypangam enhances also the induction of tyrosine aminotransferase by tryptophan. In both cases, however, it does not work in adrenalectomized animals. Under the influence of oxypangam the NAD content of the liver remained unchanged, while the activity of the ADPR transferase was influenced only slightly.
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PMID:Influence of oxypangam upon the induction of tyrosine aminotransferase, the NAD content and the ADPR transferase activity in several organs of the rat. 288 34

It has been established that inflammation and enhanced pro-coagulant activity are associated with the pathogenesis of atherosclerotic vascular disease. We evaluated and compared the contributions of the factor (F)XIa and tissue factor (TF) activity in plasma of patients with coronary artery disease (CAD). Citrate plasma was obtained prior to therapy from 53 patients with stable angina (29 with a history of previous myocardial infarction; CAD-MI) and 30 with acute coronary syndrome (ACS) within 12 hours from pain onset. Four ACS patients treated with heparin were excluded. FXIa and TF activity were determined in clotting assays based upon the prolongation of clotting time by inhibitory monoclonal antibodies. Twenty-five of 26ACS patients (96%) and 22 of 29 CAD-MI patients (76%) had quantifiable FXIa (50 +/- 33 and 42 +/- 45pM, respectively). Ten of 26 (38%) ACS patients and only three of 53 (6%) stable CAD patients showed TF activity (<0.4pM). No FXIa or TF activity was observed in age-matched healthy controls (n = 12). For both CAD-MI and ACS patients, there were correlations (p < 0.05) between FXIa and interleukin-6 (R(2) = 0.59 and 0.39, respectively) and between FXIa and TAT (R(2) = 0.64 and 0.63, respectively). In conclusion, the majority of ACS and CAD-MI patients have circulating FXIa that correlates with markers of coagulation and inflammation.
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PMID:Factor XIa and tissue factor activity in patients with coronary artery disease. 1821 46