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Biomedical subjects

S R Bates

Publications and source records attributed to S R Bates.

49 records · Page 3Linked to original sources
PubMed1980

Effect of HDL on the interaction of hyperlipemic LDL with monkey smooth muscle cells.

The stimulation of the esterification of cholesterol and the subsequent enrichment of cholesterol esters in arterial smooth muscle cells produced by low density lipoproteins (LDL) from hyperlipemic monkeys was altered by the presence of high density lipoproteins (HDL) isolated from normolipemic monkeys. Increasing concentrations of HDL decreased the rate of cellular cholesterol esterification and cholesterol ester accumulation. This was accompanied by a reduction in the cellular uptake of radioiodinated LDL. At physiological levels of lipoproteins, HDL interfered with the interaction of smooth muscle cells and LDL from hyperlipemic serum.

Animals↗
PubMed1979

Accumulation and loss of cholesterol esters in monkey arterial smooth muscle cells exposed to normal and hyperlipemic serum lipoproteins.

The effects of high low and very low density lipoprotein fractions from normal or hyperlipemic rhesus monkey serum on the accumulation or removal of cholesterol esters from rhesus monkey smooth muscle cells in tissue culture were determined. Serum or serum lipoproteins were labeled with [14C] free cholesterol and adjusted to the same free cholesterol level in the incubation medium. Of the two normal lipoproteins examined, the LDL fraction caused more esterification than the HDL. Cells incubated in hyperlipemic serum showed a 2-fold stimulation in esterification as compared to cells in normal serum. This was contributed by hyperlipemic VLDL and LDL and led to a concomitant increase in cellular cholesterol ester content. Both hyperlipemic LDL and HDL stimulated esterification when compared to their normal counterparts. Cholesterol ester removal was examined by incubating the serum or lipoprotein fractions with cells enriched in cholesterol ester through a prior exposure to hyperlipemic serum. The cells incubated in normal or hyperlipemic HDL or lipoprotein-deficient serum had the lowest cholesterol ester content. Thus, the lipoprotein fractions which caused the lowest levels of cholesterol esterification were also the most efficient in the removal of cellular cholesterol esters.

Animals↗
PubMed1978

Phospholipid metabolism of monkey smooth muscle cells grown in hyperlipemic serum.

The phospholipid content and synthesis of monkey smooth muscle cells grown in tissue culture with normal or hyperlipemic monkey serum were examined. The pattern of incorporation of radioactively labeled inorganic phosphate into the phospholipids of these cells was measured using a 4 h pulse of 32P. Phosphatidylcholine and phosphatidylinositol were the predominant phospholipids labeled. Although phosphatidylcholine constituted 45% of the cellular phospholipid, phosphatidylinositol had the highest specific activity. Exposure of the smooth muscle cells to hyperlipemic monkey serum did not alter the phospholipid content, composition or synthesis of these cells. The total phospholipid content of the smooth muscle cells was independent of the concentration of lipid in the media. The distribution of 32P into the phospholipids of monkey alveolar macrophages, L-cell mouse fibroblasts, and segments of the intima-media from monkey aortas is reported.

Animals↗
PubMed1978

Fatal massive intracerebral hemorrhage complicating cerebral amyloid angiopathy.

A 58-year-old normotensive woman died 24 hours after a stroke. Two months earlier, she had a transient neurological episode consistent with cerebrovascular insufficiency. Necropsy demonstrated a massive recent hemorrhage in the right occipital lobe associated with severe cerebral amyloid angiopathy (CAA). The cerebral cortex showed interstitial and perivascular neuritic plaques but no Alzheimer's tangles. There was no family history of CAA. A review of the literature indicated that only ten cases of such hemorrhage caused by nonfamilial CAA have been reported. Massive intracerebral hemorrhage seems to be more common in patients with familial Icelandic forms of CAA.

Amyloidosis↗
PubMed1976

Effect of hyperlipemic serum on cholesterol accumulation in monkey aortic medial cells.

The effect of hyperlipemic monkey serum on cholesterol ester formation and accumulation in monkey aortic medial cells grown in tissue culture was studied. The cellular incorporation and esterification of free cholesterol was followed using the specific activity of serum labeled with free [14C]cholesterol while the cellular sterol content was analyzed by gas-liquid chromatographic techniqyes. The effects produced by hyperlipemic monkey serum (HMS) and normal monkey serum (NMS) were evaluated at both comparable percentage levels in the media and at equivalent exogenous cholesterol concentrations. When the two sera were adjusted to equal exogenous free cholesterol levels, the incorporation of free cholesterol by the aortic medial cells was related to the free cholesterol concentration of the culture media whether supplied by normal or hyperlipemic serum cholesterol. Under these conditions the total cholesterol content of the HMS-grown cells was 35% greater than that of NMS-grown cells, due to an elevation in free cholesterol of approximately 3 mug/mg cell protein and a 2- to 4-fold increase in esterified cholesterol. At similar percentage levels, the hyperlipemic serum stimulated a greater incorporation of free cholesterol into the monkey medial cells, accompanied by a 2-fold increase in the cellular esterification of this free cholesterol.

Animals↗
PubMed1972

Incorporation of L cell sterols into vesicular stomatitis virus.

The incorporation of host cell sterol into vesicular stomatitis virus can be effectively studied in an L cell system. The end product of de novo sterol synthesis in the L cell is desmosterol, and as the concentration of cholesterol in the medium is increased the cells incorporate the exogenous cholesterol and the synthesis of desmosterol decreases. L cells which contained desmosterol as their sole sterol produced virus whose sterol content was similarly composed of only desmosterol. Virus grown in L cells which had a constantly changing sterol ratio also contained a mixture of cholesterol and desmosterol, but the virus was found to be more enriched in cholesterol than in the L cells in which it was grown. Viral stability, growth, and plaquing efficiency were tested and found not to be affected by the alteration of its sterol composition, i.e., by partially or completely replacing cholesterol with desmosterol.

Acetates↗
PubMedDate not supplied

Very low density lipoproteins promote triglyceride accumulation in macrophages.

Incubation of mouse peritoneal macrophages with very low density lipoproteins (VLDL) from normal rats or rhesus monkeys markedly increased the levels of intracellular triglycerides by 10- to 56-fold and was accompanied by the production of oil red O positive vacuoles. The stimulation of triglyceride accumulation in macrophages was time- and concentration-dependent and was specific for VLDL. Three possible mechanisms for the VLDL-stimulated triglyceride accumulation in macrophages were explored: receptor-mediated uptake, action of lipoprotein lipase, and phagocytosis. Macrophage uptake and degradation of 125I-monkey and rat VLDL demonstrated saturable and nonsaturable components. Uptake of 125I-VLDL could be inhibited by unlabeled normal VLDL, although hyperlipemic VLDL was more effective. HDL did not compete to a significant extent. Heparin released lipoprotein lipase-like activity from peritoneal macrophages. Addition of heparin with VLDL resulted in a greater, more rapid elevation in intracellular triglycerides, which was partially inhibited by albumin. Free fatty acid and Intralipid also produced triglyceride accumulation in macrophages. The data showed that all three of the mechanisms examined could contribute to the metabolism of VLDL by macrophages and cause the production of triglyceride-rich cells with a "foamy" appearance, although the evidence suggested that the action of lipoprotein lipase was probably the most important in this process.

Animals↗
PubMedDate not supplied

Effect of normolipemic and hyperlipemic serum on biosynthetic response to cyclic stretching of aortic smooth muscle cells.

Arterial smooth muscle cells synthesize matrix macromolecules in response to mechanical stimulation. Exposure to serum lipids also stimulates connective tissue fiber accumulation. To assess the effect of serum lipids on the biosynthetic response to tensile stress, we subjected rabbit aortic smooth muscle cells that were cultured on purified elastin membranes to cyclic stretching and relaxation 50 times per minute in the presence of serum-free medium (SFM), normolipemic serum (NLS), or hyperlipemic serum (HLS). Incorporation of 14C-proline into proline and into hydroxyproline was taken as a measure of protein and collagen synthesis. When cells were grown in plastic Petri dishes, exposure to NLS or HLS increased both protein and collagen production to the same extent compared to synthesis in SFM (1.7 times for NLS and 1.6 times for HLS; p less than 0.001 compared to SFM). For cells grown on stationary elastin membranes, NLS and HLS also increased protein and collagen synthesis compared to SFM. The effect of NLS was 1.35 times that of HLS for protein and 1.43 times greater for collagen (p less than 0.03). Cyclic stretching in SFM doubled synthesis for both protein (p less than 0.002) and collagen (p less than 0.002) compared to stationary controls, but had no effect on synthesis in NLS. In HLS, however, cyclic stretching elevated synthesis to the same level as was found in NLS (p less than 0.003). We conclude that the relative inhibition of synthesis on stationary membranes by HLS was not due to a toxic effect, since HLS increased synthesis both in Petri dishes and on elastin membranes, and the amplifying effect of cyclic stretching in HLS was similar to that seen in SFM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Cardiovascular disease risk factors in an Indochinese population.

One hundred seventeen Indochinese adults were screened for heart disease risk factors at a San Diego community health facility during December 1986. Two levels of excess risk, moderate-high and high, were categorically defined for blood pressure, total cholesterol, cigarette smoking, and obesity. Overall, 61% were at moderate-high or high risk in at least one category, and 34% were at high risk by these criteria. Systolic blood pressure, diastolic blood pressure, and total cholesterol were positively correlated to age, and ethnicity was a significant covariate for cholesterol, body mass index, and cigarette smoking. The Hmong, compared with other Indochinese, had a significantly lower mean cholesterol level, which remained after adjusting for age and body mass. High rates of cigarette smoking were found among Vietnamese men and young Indochinese men. If confirmed, the high prevalence of heart disease risk factors in Indochinese refugees and immigrants suggests that cardiovascular health education programs are appropriate in Indochinese communities.

Adolescent↗