Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.6 (CAD)
 4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postmortem blood lipid and lipoprotein analyses were conducted in a case-controlled study of young adults (ages 22-43) who died suddenly and unexpectedly of atherosclerotic coronary artery disease in Allegheny County, Pennsylvania. None of the individuals in the study group (n = 28 cases) had a significant medical or cardiac history except in the immediate antemortem period. The control group (n = 31) consisted of age- and sex-matched cohorts who died of noncardiac related fatalities and who had no evidence of CAD. The results indicated a male-to-female ratio of nearly 30:1 with a marked predominance of young white men. Mean total cholesterol (241 mg/dL), triglycerides (583 mg/dL), and low-density lipoproteins (LDL) (107 mg/dL) were all significantly elevated in the study group as compared to controls (p < 0.001, p < 0.018, and p < 0.001 for the three parameters, respectively). Mean Apolipoprotein B (98.7 mg/dL) was also significantly elevated compared to control values (p < 0.001). By contrast, mean high-density lipoprotein values (36 mg/dL) were not significantly different from control values (p = 0.35), and mean values of Apolipoproteins A1 (121 mg/dL) and A2 (37.6 mg/dL) were essentially identical to control values (p = 0.44 and p = 0.64, respectively). The differences in these biochemical markers between the two groups could not be explained by differences in postmortem interval or by the presence of recently ingested food. These findings indicate that elevations of plasma cholesterol, triglycerides, LDL, and Apolipoprotein B are important biochemical markers for the development of early and apparently clinically silent yet life-threatening coronary artery disease.
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PMID:A comparison of blood lipid and lipoprotein values in young adults who die suddenly and unexpectedly from atherosclerotic coronary artery disease with other noncardiac deaths. 757 60

Several environmental and genetic factors are associated with high levels of cholesterol. Hypercholesterolemia is the main phenotype of Familial Defective Apolipoprotein B and Familial Hypercholesterolemia that are caused by mutations at the apolipoprotein (apo) B and LDL receptor genes, respectively. Identification of the specific genetic alteration associated with hypercholesterolemia is an important issue in clinical diagnosis of high risk for CAD. Apo B gene mutations and polymorphisms are usually screened by SSCP, DGGE, and heteroduplex, which must be confirmed by DNA sequencing or by direct detection using PCR techniques. In this study, we have optimized a PCR-RFLP procedure for identification of 3500Q and 3531 mutations and MspI polymorphism at the apo B gene. The technique can be performed in a single reaction, using the restriction endonuclease MspI for simultaneous detection of 3500Q mutation and MspI polymorphism, and NsiI for detection of 3531 mutation. The procedure was validated by analysis of control DNA samples from individuals carrying these mutations. Screening of 186 Brazilian hypercholesterolemic individuals showed that the frequency of the M-allele (7.8%) of MspI polymorphism was similar to that found in other individuals with CAD. However, neither 3500Q nor 3531 mutations were detected in this group. In conclusion, this procedure is simple and rapid, being easily introduced in clinical laboratories for direct detection of the more frequent mutations at the apo B gene associated with hypercholesterolemia.
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PMID:Rapid detection of 3500Q and 3531 mutations and MspI polymorphism in exon 26 at the apolipoprotein B gene. 1117 Feb 32

Indian ethnicity by itself is a strong risk factor for development of CAD in Indian postmenopausal women due to lower HDL levels as compared to Whites and women of oriental origin. We evaluated and compared the short-term effects of menopause, estrogen replacement therapy and combined estrogen and progestin replacement therapy on various atherogenic indices. 40 postmenopausal women, both surgical and natural (20 each) were selected. 10 surgical postmenopausal women were given 0.625 mg conjugated estrogens daily for 6 months and 10 natural postmenopausal women were given 0.625 mg conjugated estrogen with 2.5 mg medroxyprogesterone acetate daily. 20 women were included in the control group and given placebo. Fasting venous blood samples were analyzed for extended lipid profile and calculated atherogenic indices before starting the therapy and after 1,3 and 6 months. LDL and Apolipoprotein B increased (p<0.05) and those of Apolipoprotein A1 and HDL decreased in the control groups. In both the study groups levels of serum cholesterol and LDL decreased (p<0.05) and those of HDL and Apolipoprotein A1 increased (p<0.01). LDL/HDL, Apo B/ApoA1, Total Cholesterol/HDL decreased significantly (p<0.05) in both the study groups compared to the control groups. The effect of estrogen alone was more significant as compared to combination therapy. Log Triglycerides (TG)/HDL ratio showed a decrease in women on estrogen alone but the difference was not significant. Our study confirms that short term HRT has a favorable effect on atherogenic indices in Indian postmenopausal women.
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PMID:Effects of short-term hormone replacement on atherogenic indices in Indian postmenopausal women. 2310 68