Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Oslo Diet and Exercise Study (ODES) is an unmasked randomized 2 x 2 factorial trial of 1-year duration for each participant. During 1990-1991 219 participants (198 males and 21 females) aged 41-50 were randomized into one of four treatment groups; no treatment (control), dietary changes alone, exercise alone, or a combination of the two treatments. At inclusion, the participants had no overt heart disease, but they had increased body weight; slightly increased blood pressure, serum triglycerides, and total cholesterol, and they had decreased HDL cholesterol. Further, they were all inactive at leisure time. The primary aim of the trial is to compare the isolated and combined effects of the four treatments on the variables fibrinogen, fibrinolytic capacity, coagulation factor VII, and platelet volume. A series of secondary hypotheses will also be tested, such as the effects on other coagulation and fibrinolytic components and activities; lipids and lipoproteins; fatty acids; glucose and insulin response to a glucose load; clinical, physiological, and anthropometric variables; and quality of life. The dietary treatments are adapted according to each participant's risk profile (level of total cholesterol, HDL cholesterol, triglycerides, blood pressure, and body weight). Fish and fish products are recommended. Special emphasis is put on caloric restriction in those who are overweight and those with elevated blood pressure. Exercise sessions take place three times a week under the guidance of highly qualified instructors. The aim is to increase peak oxygen uptake through aerobic endurance training. Adherence to the exercise program is monitored closely.
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PMID:The Oslo Diet and Exercise Study (ODES): design and objectives. 833 52

To study the variation and significance of plasma coagulation factor VII (FVII) in different kinds of ischemia heart disease (IHD) and examine its relation with plasma lipid and gene polymorphism. FVIIa was determined with one stage clotting assay by using a recombinant soluble tissue factor (rsTF). FVIIc was measured with one stage clotting assay. FVIIag was quantified with an enzyme-linked immunosorbent assay (ELISA). Polymorphism was analyzed with PCR-urea-polyacrylamide gel electrophoresis. Our results showed that FVIIa in stable angina (SA), unstable angina (UA), obsolete and acute myocardial infraction (OMI, AMI) patients was higher than those of normal group with the differences being significant within any two groups. FVIIag in UA, OMI and AMI was higher than those in SA and normal groups. There were positive correlations between FVIIa and serum triglycerides, FVIIa and FVIIc, FVIIc and FVIIag. FVII-323 0/10 bp polymorphism analysis was performed in 60 patients and 0/10 bp polymorphism was found in 5 cases. FVIIc and FVIIag were much lower in cases of 0/10 bp groups than those in cases of 0/0 bp groups. It is concluded that there was activation of extrinsic coagulation pathway in every kind of IHD to different extent. FVIIa was the risk factor in the development of IHD, and more sensitive in reflecting the severity of cardiovascular disease than FVIIc or FVIIag. FVIIa was higher in OMI, which may be one of the risk factors of re-infraction. Serum triglyceride may indirectly lead to the development of IHD by increasing the level of FVIIa. FVII-323 0/10 bp polymorphism was present in Chinese patients with IHD and it was correlated with the level of FVIIc, FVIIag in plasma. 10 bp allelomorphic gene was a protective factor against thrombogenesis.
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PMID:Role of coagulation factor VII in pathogenesis of ischemic heart disease. 1735 81