Biomedical subjects

G T Malcom

Publications and source records attributed to G T Malcom.

77 records · Page 5Linked to original sources

PubMedDate not supplied

Regression of experimental atherosclerotic lesions in rhesus monkeys consuming a high saturated fat diet.

Atherosclerotic lesions were induced in rhesus monkeys by feeding them a high-fat, high-cholesterol diet for 2 years. Arteries were examined after autopsy of a subgroup of animals (group P) and cholesterol was removed from the diet of the remaining animals. Lesions were examined in other subgroups after 30 weeks (group R1) and after 52 weeks (group R2). A control group (group C) was fed the diet without cholesterol throughout the study. The mean total serum cholesterol concentration before, during, and after lesion induction was 151, 390, and 157 mg/dl, respectively. The mean percent of surface area with fatty streak or fibrous plaque and the free and esterified cholesterol content of the artery increased in all six arterial segments examined in group P. The means for percent of surface with fatty streak and for arterial cholesterol content or concentration (but not for extent of surface with fibrous plaque) were consistently less in groups R1 and R2 than in group P, although they remained greater in groups R1 and R2 than in group C. The mean intimal thickness for coronary arteries was 10-fold greater in group P than in group C and 60 percent less in groups R1 and R2 than in group P; there was, however, much variability among animals and these differences among groups were not statistically significant. By using several measures in several arterial systems, we have shown that there was regression of diet-induced atherosclerotic lesions in rhesus monkeys while they were fed a diet high in saturated fat but without cholesterol for 30 or 52 weeks.

Animals↗

PubMedDate not supplied

Effect of cholesterol feeding on lipolytic activities in high- and low-responding rhesus monkeys.

We compared the activities of lipoprotein (LPL) and hepatic lipase (HL) in postheparin plasma in groups of high- and low-responding rhesus monkeys fed a low cholesterol diet followed by a high cholesterol diet. Cholesterol feeding resulted in a two-phase response in lipolytic activities: an initial phase lasting about 21 days that was similar in the two groups, followed by the second phase in which major differences became apparent between the groups. In the initial phase, LPL and HL activities increased along with plasma cholesterol and high density lipoprotein (HDL) cholesterol, but there was no change in plasma triglycerides or apolipoprotein (apo) A-I levels. These changes suggest that both high and low responders respond in a similar manner to metabolize an increased lipid load and that both groups continue to remove triglyceride efficiently while cholesterol accumulation begins. The second phase (between 21 and 42 days and thereafter) in high responders was characterized by a decrease in LPL and HL activities along with plasma HDL cholesterol and apo A-I levels, continued increase in plasma cholesterol, and a slow increase in plasma triglycerides. In low responders, LPL activity was maintained at a high level, HL activity decreased to the basal level, and plasma lipids were unchanged. All changes occurred simultaneously, suggesting metabolic relationships between plasma lipolytic activities, plasma lipids, and apolipoprotein.

Animals↗

PubMedDate not supplied

Cytomegalovirus and other herpesviruses: do they have a role in the development of accelerated coronary arterial disease in human heart allografts?

In conclusion, a great deal of indirect and inferential data point to herpesviruses as having a role in atherogenesis. It has been shown that the herpesviruses are able to remain within vascular tissue in a latent state, allowing for reactivation to occur with subsequent sequelae of an active infection. Herpesviruses affect the cellular metabolic activity of cells, induce the accumulation of lipids, and inhibit the production of matrix proteins. They have the ability to inhibit endothelial cell binding to the basement membrane. It is also known that the herpesviruses, particularly CMV, can initiate a variety of immunologic responses that may contribute to endothelial damage, precipitating atherogenesis. We are only beginning to understand how CMV may participate in ACAD. Greater attention must be focused on the exact cause-and-effect relationship between CMV infection and ACAD. Even the presence of CMV genomes in arterial walls of allografts must be viewed conservatively in the knowledge of CMV ubiquity and other probable contributions to ACAD. If CMV is involved in the development of ACAD, as an active or latent infection, directly or indirectly, it probably involves numerous coexistent mechanisms (Figure 5).

Coronary Artery Disease↗

PubMedDate not supplied

Effect of beta-carotene supplementation on serum alpha-tocopherol concentration.

Conflicting reports of the effects of beta-carotene supplementation on serum alpha-tocopherol concentration led us to evaluated serum alpha-tocopherol in subjects with and without beta-carotene (30 mg/day) supplementation for up to 2 years duration in an ongoing chemoprevention trial. No adverse effect has been observed at any of the time periods examined.

Adult↗

PubMedDate not supplied

Racial comparison of p53 alterations in breast cancer: difference in prognostic value.

A significant difference in breast cancer survival between blacks and whites has been observed in the United States. Biological variation between races has been suggested to explain the difference. We investigated the difference by comparing the prognostic value of p53 alterations (mutations and protein accumulation) between black and white breast cancer patients. Black, but not white, patients with p53 mutations had a significantly poorer survival than those without p53 mutations (p < 0.05). In contrast, white, but not black, patients having tumors with p53 protein accumulation tended to have a poorer survival than those without accumulation of p53 protein (p = 0.058). Among patients who died of breast cancer, blacks were often to have p53 mutations without protein accumulation, and whites frequently had p53 protein accumulation without mutations. The racial disparities in the associations of p53 alterations with breast cancer survival could have clinical implications in terms of treatment management.

Black People↗