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Biomedical subjects

M R Malinow

Publications and source records attributed to M R Malinow.

158 records · Page 9Linked to original sources
PubMedDate not supplied

Removal of plasma cholesterol by adsorption chromatography.

Batch and column chromatography with porous glass decreased the plasma concentration of cholesterol. Extracorporeal circulation of blood through a column filled with porous glass, as well as exchange transfusion with blood made hypocholesterolemic by passage of its plasma through a column filled with porous glass, temporarily reduced plasma cholesterol concentration in rats.

Adsorption↗
PubMedDate not supplied

Effects of alpha- and beta-tigogenin cellobiosides on cholesterol absorption.

We have synthesized alpha- and beta-anomers of tigogenin cellobioside and have determined their effects on intestinal absorption of [1,2-3H]cholesterol in rats. We demonstrated that the loss of tritium label likely to occur in the conversion of cholesterol to coprostanone was minimal. Dose response studies showed that both anomers depressed intestinal absorption of cholesterol but the depression was greater with the beta-anomer.

Animals↗
PubMedDate not supplied

Prevalence of familial hyperhomocyst(e)inemia in men with premature coronary artery disease.

Elevated plasma levels of homocyst(e)ine have been reported to be more prevalent in patients with coronary artery disease (CAD) than in controls. The purpose of this study was to determine whether this elevation was genetic. We determined homocyst(e)ine levels in 176 men with premature CAD (greater than 50% stenosis of a major epicardial coronary artery occurring before the age of 60 years) and in 255 controls free of cardiovascular disease. Homocyst(e)ine levels were higher in the CAD group compared with controls (13.9 +/- 6.7 versus 10.9 +/- 4.9 nmol/ml, p less than 0.001); in addition, 28% of CAD patients had homocyst(e)ine levels above the 90th percentile of controls. Statistical analysis revealed that homocyst(e)ine levels were not related to the presence of hypertension or diabetes, smoking, or plasma levels of lipoprotein cholesterol and apolipoproteins A-I and B. The families of 71 CAD patients were sampled (selected on the basis of availability of relatives) and included 60 spouses and 239 first-degree relatives; 370 subjects were thus sampled. Spearman correlations between probands and spouses (r = 0.264, p = 0.041) and between mean values for parent and offspring (r = 0.356, p = 0.002) for homocyst(e)ine levels indicated that homocyst(e)ine levels are in part genetically determined. In 20 families (28.2%), the proband had homocyst(e)ine levels greater than the 90th percentile; familial segregation was observed in 10 of these kindreds. Therefore, 14% of CAD patients had familial hyperhomocyst(e)inemia. In conclusion, our data suggest that plasma homocyst(e)ine is a risk factor for the development of CAD, independent of other cardiovascular risk factors, and that this elevation is in part genetically determined.

Adolescent↗