Search PubMed⌕ Search

Biomedical subjects

Y Stein

Publications and source records attributed to Y Stein.

At least 163 records · Page 9Linked to original sources
PubMed1982

Nutrient intake in Jerusalem--consumption in 17-year-olds.

The food intake of 17-yr-old Jerusalem residents was assessed in a random sample, including 627 males and 551 females, by a 24-h dietary recall method. The intake of energy in boys and girls was lower than the recommended energy intake for this age, but the intake relative to body weight was low only in girls. In boys and girls, the intakes of fat relative to energy were 32.4 and 33.7%, respectively; those of saturated fatty acids (SFA) (9.8 and 10.5%) were lower and those of carbohydrates (53.9 and 52.5%) were higher than intakes found in other Western countries. The P:S (polyunsaturated to saturated fatty acids) ratio of their diets was high and ranged from 0.79 to 1.29 in various sex and origin groups. Intake of cholesterol per 1,000 kcal was similar to that in Western countries. There were marked differences in nutrient intake of subjects whose fathers had immigrated from different countries. Boys whose fathers were born in Israel or Europe had higher intakes of fat and cholesterol, and both boys and girls had a higher intake of SFA and a lower intake of carbohydrates and starch as well as a lower P:S ratio than did their counterparts whose fathers were born in Asia and North Africa. Thus, the nutrient intake of youngsters in Jerusalem differs markedly from that of populations in other Western countries.

Adolescent↗
PubMed1982

Nutrient intake in Jerusalem--consumption in adults.

During 1976-80, nutrient intake was assessed in a cross-sectional sample of 1,589 middle-aged Jerusalem residents (1,028 males and 561 females) using the protocols and methods of the North American Lipid Research Clinics (LRCs) Prevalence Studies. All subjects were parents of 17-yr-old youngsters studied previously. Energy intake in both males and females was lower than the recommended energy intake for this age-group. Intake of fat relative to energy in males and females was 32.1 and 34.0%, of saturated fatty acids (SFA) 10.0 and 11.0%, and of total carbohydrates 50.2 and 49.9%, respectively. Cholesterol consumption was 210 and 238 mg/1,000 kcal in males and females, respectively. The mean polyunsaturated to saturated fatty acids (P:S) ratio of the diet was 0.95 in males and 0.84 in females. There were marked differences in the nutrient intake of subjects of different ethnic origin. Subjects from Israel and Europe consumed more total fat and SFA and less total carbohydrates than did their counterparts from Asia and North Africa. Consumption of polyunsaturated fatty acids (PFA) was highest in subjects from Israel. The P:S ratio of the diet was highest in the North African group, followed by the Israeli group, and lowest in subjects from Europe. The highest sucrose intake was found in subjects from North Africa and the highest cholesterol intake in immigrants from Europe. Nutrient intake of Jerusalem adults differed markedly from that of populations in other Western countries.

Adult↗
PubMed1982

Nutrient intake in Jerusalem--effects of origin, social class and education.

The independent association of ethnic group, social class and education with nutrient intake was studied in a sample of 1,294 adults in the Jerusalem Lipid Research Clinic (LRC) population. By univariate analysis, intake of fat and saturated fatty acids (SFA) was higher (P less than or equal to 0.05) in males and females of the upper social classes (classified by the occupation of the head of the family) than in the lower classes, while the opposite trend was found for the consumption of carbohydrates and starch. In men, an association between social class and the intakes of protein and other carbohydrates (i.e., other than sucrose and starch) and the ratio of polyunsaturated fatty acids (PFA) to SFA (P:S ratio) was also found. In both sexes, the mean intakes of SFA and other carbohydrates were higher and that of starch lower in subjects with a higher level of education (P less than or equal to 0.05). Education was also associated with the consumption of protein and fat in males and with that of carbohydrates and sucrose in females. Country of origin was related (P less than or equal to 0.05) to the intake of fat, SFA and other carbohydrates in both sexes, to that of protein and cholesterol in males and to that of carbohydrates, sucrose and starch in females. The P:S ratio of the diet of male subjects was also associated with origin. Using various models of analysis of variance, it was shown that origin was associated with nutrient intake (P less than or equal to 0.10), independent of the effect of social class and education for protein, fat, SFA, cholesterol, sucrose and other carbohydrates in males, and for fat, SFA, PFA and other carbohydrates in females. The P:S ratio of the male diet was also associated with origin. The level of education was independently related (P less than or equal to 0.10) to the intake of fat, SFA, starch and other carbohydrates in males and to that of sucrose in females, while social class was associated independently with carbohydrate consumption in males only. After prior adjustment for origin, education had a stronger residual effect than did social class in males, while in females the associations of social class and education with nutrient intake were almost identical.

Adolescent↗
PubMed1982

Cigarette smoking and its relation to anthropometric characteristics and biochemical variables in Jerusalem 17-year-olds and adults.

The relationship of weight, height, Quetelet index, hematocrit and blood levels of thyroxine, globulin, bilirubin, creatinine, aspartate aminotransferase, uric acid, alkaline phosphatase and glucose to smoking was studied in a Jerusalem population sample of youngsters aged 17 yr and their parents. Among youngsters, male smokers had a higher body mass index than did male nonsmokers. In adults, both men and women smokers were slightly leaner than ex-smokers and, in women, smokers were clearly leaner than those who had never smoked. Generally, the associations of smoking with the biochemical variables were weaker in youngsters than in adults. In men, lower mean levels of creatinine, bilirubin, aspartate aminotransferase and uric acid were observed among smokers. Hematocrit levels were somewhat higher in both young and adult smokers of both sexes, being more so in adults. Smokers showed consistently lower globulin levels than did nonsmokers. Plasma glucose levels were somewhat lower in youngsters of both sexes who smoked. Serum thyroxine levels were slightly increased in female smokers, suggesting a hormonal effect of smoking. These findings are discussed in light of the published literature.

Adolescent↗
PubMed1982

Calculation of LDL-cholesterol from total cholesterol, triglyceride and HDL-cholesterol: a comparison of methods in the Jerusalem Lipid Research Clinic Prevalence Study.

Methods for estimating the cholesterol content of the plasma very low-density lipoprotein (VLDL-C) and low-density lipoprotein (LDL-C) fractions were examined in an ethnically diverse population sample from the Jerusalem Lipid Research Clinic Prevalence Study. None of these methods required the use of preparative ultracentrifuge. The often-used method for estimating VLDL-C by multiplying the triglyceride (TG) value by 0.20 was compared with two other models in which linear regression functions were computed for VLDL-C (determined by ultracentrifugation) as the dependent variable and TG as the independent variable. Subsequently, the intercept and the slope coefficients were used for estimation of VLDL-C and LDL-C. In the first regression model, overall age and sex regression coefficients were applied, whereas in the second regression model, the coefficients were calculated within different TG ranges. All three models were similar in their predictive accuracy when applied to the total population sample. However, in subjects with high TG levels, the second regression model was preferable.

Adolescent↗
PubMed1981

Interaction between macrophages and aortic smooth muscle cells. Enhancement of cholesterol esterification in smooth muscle cells by media of macrophages incubated with acetylated LDL.

Mouse peritoneal macrophages were cultured for 24 h in Dulbecco-Vogt medium containing 10% calf serum. This medium was replaced with Dulbecco-Vogt medium containing 1% bovine serum albumin to which all subsequent additions were made. Medium changes, accompanied by appropriate additions, were made every 48 or 72 h and the media were used for incubation of aortic smooth muscle cells, prelabeled with [3H]cholesterol. The amount of labeled cholesteryl ester in the smooth muscle cells incubated for 48 h with macrophage media which had been collected 48-144 h after addition of acetylated LDL was increased 3-4 times above that present prior to postincubation. A marked increment in cholesteryl ester mass occurred also after incubation of smooth muscle cells with macrophage media conditioned with acetylated LDL and this effect was shared by maleylated LDL, but not by other negatively charged compounds. The increase in labeled cholesteryl ester in smooth muscle cells was more pronounced with media collected at later time intervals of incubation with macrophages and was evident 8 hr after postincubation. Only the d less than 1.063 fraction of the medium enhanced cholesterol esterification in smooth muscle cells. The acetylated LDL reisolated from macrophage media at d less than 1.063 did not compete with native LDL for degradation by smooth muscle cells. No increase in degradation of 125I-labeled acetylated LDL preincubated with macrophages was observed above that of non-preincubated acetylated LDL. The macrophage medium conditioned with acetylated LDL depressed [14C]acetate incorporation into sterols in smooth muscle cells and this effect was abolished by extraction of the medium with diethyl ether. The ratio of free to total cholesterol in the macrophage media collected after incubation with acetylated LDL increased from 28-70%, and a decrease occurred after incubation with smooth muscle cells. The enhancement of cholesterol esterification could be abolished by addition of high density apolipoprotein/sphingomyelin mixture during incubation with macrophages, even though excretion of free cholesterol into the medium increased 3-fold. It is proposed that when smooth muscle cells are presented with a lipoprotein in which an increase in the free to esterified cholesterol ratio occurred, and which is not recognized by a specific receptor, the enhancement of cellular cholesterol esterification is due mostly to a surface transfer of lipoprotein-free cholesterol. The present results offer another view of the possible interactions between macrophages and smooth muscle cells. A modified lipoprotein, not recognized by smooth muscle cells, is ingested by macrophages, which leads to accumulation of esterified cholesterol. Part of the esterified cholesterol undergoes hydrolysis and is excreted back into the medium, leading to enrichment of the lipoproteins in the medium with free cholesterol. This enrichment with free cholesterol promotes cholesterol esterification in smooth muscle cells.

Acylation↗
PubMed1981

The fate of cholesteryl linoleyl ether and cholesteryl linoleate in the intact rat after injection of biologically labeled human low density lipoprotein.

In vitro labeling of low density lipoproteins (LDL) with [7 alpha(n)-3H]cholesteryl linoleyl ether, and with [4-14C]cholesteryl linoleate was achieved by a modification of the method developed for labeling of very low density lipoproteins. [3H]Cholesteryl linoleyl ether and [14C]cholesteryl linoleate were cosonicated with partially delipidated high density lipoprotein (HDL) and the HDL was purified by centrifugation at d = 1.063. LDL was labeled by incubation of the labeled HDL in the presence of the d greater than 1.25 fraction of human plasma and reisolated at d = 1.063. The 3H/14C ratio in the labeled LDL was the same as in the HDL. The labeled LDL had the same lipid composition and ultrastructural appearance as the non-incubated LDL. After injection into rats, both labels disappeared at similar rates and the t1/2 between 1-24 h was 7.0 h. Up to 8 h after injection of labeled LDL, 94-97% of 3H and 14C radioactivity in the plasma was precipitable by heparin-manganese. 24 h after injection, 28% of the [3H]cholesteryl linoleyl ether was recovered in the liver, 6% in small intestine and 34% in the carcass, and the rest was distributed among all other organs; total recovery of 3H label was 89 +/- 3.0%. The present findings indicate that as in the rat there is no transfer of esterified cholesterol among plasma lipoproteins, LDL is catabolized by both the liver and extrahepatic tissues.

Animals↗
PubMed1981

Metabolism of cytoplasmic triacylglycerol in cultured aortic smooth muscle cells.

A turnover of cytoplasmic triacylglycerol was studied in cultured rat, rabbit, and bovine aortic smooth muscle cells. Cytoplasmic triacylglycerol was labeled with [3H]glycerol in the presence of oleic acid in the medium and its loss from the cell was studied in the presence of carrier glycerol. Multiple additions of Isuprel or dibutyryl cyclic AMP during the chase period did not enhance the loss of labeled triacylglycerol. The rate of hydrolysis of cellular triacylglycerol was unchanged in the absence or in the presence of 100 microM chloroquine. Modulation of cellular cholesterol content by addition of low density lipoprotein or high density apolipoprotein--sphingomyelin liposomes did not affect the residence time of the cellular triacylglycerol. We conclude that cytoplasmic triacylglycerol in cultured aortic smooth muscle cells is metabolized by an extralysosomal enzyme which is neither catecholamine responsive nor affected by modulation of cellular cholesterol.

Animals↗
PubMed1980

Modulation of cytoplasmic cholesteryl ester of smooth muscle cells in culture derived from rat, rabbit and bovine aorta.

Esterification of cholesterol in smooth muscle cells, isolated from rat, rabbit and bovine aorta, was achieved by incubation with cholesterol enriched medium containing [7(n)-3H]cholesterol. The newly formed cholesteryl ester was readily hydrolyzed when the cells were post-incubated with medium containing lipoprotein deficient serum. The rate of loss of labeled cholesteryl ester was not inhibited by the presence of 100 microM chloroquine. Addition of LDL to the post-incubation medium retarded the decrease in labeled cellular cholesteryl ester in rat smooth muscle cells and this effect of LDL was abolished by chloroquine. In bovine and rabbit smooth muscle cells, enriched in cholesteryl ester, addition of LDL to post-incubation medium resulted in an increase in labeled cholesteryl ester and in cholesteryl ester mass. Retardation in the loss of labeled cellular cholesteryl ester occurred also on addition of oleic acid to the post-incubation medium. In the presence of HDL and especially of high density apolipoprotein-sphingomyelin liposomes there was an efflux of cellular free cholesterol and a reduction in cholesteryl ester. These findings indicate that the catabolism of cytoplasmic cholesteryl ester in aortic smooth muscle cells is catalyzed by extralysosomal enzymes. The cytoplasmic cholesteryl ester hydrolase is apparently not activated by cyclic AMP. The intracellular availability of unesterified cholesterol, which can be modulated by plasma lipoproteins, may determine the residence time of cellular cholesteryl ester. Thus under pathological conditions an increase in extracellular LDL accompanied by a reduction in HDL would prolong the residence time of cholesteryl esters and thus promote their intracellular accretion.

Animals↗
PubMed1980

Bovine aortic endothelial cells display macrophage-like properties towards acetylated 125I-labelled low density lipoprotein.

Bovine aortic endothelial cells in culture were shown to take up and degrade acetylated 125I-labelled low density lipoproteins (125I-acetylated LDL) in preference to 125I-labelled low density lipoproteins (LDL). The confluent cultures of endothelial cells had a higher rate of degradation of 125I-acetylated LDL than did subconfluent cells. The ratio of degradation of 125I-acetylated LDL to 125I-LDL was 3--9 in the case of the endothelial cells, 0.06--0.11 for aortic smooth muscle cells and 18 for mouse peritoneal macrophages. The uptake and degradation of acetylated LDL by the endothelial cells was accompanied also by an increase in cellular cholesterol. The present findings indicate that cultured endothelial cells display certain macrophage-like properties towards serum lipoproteins.

Animals↗
PubMed1980

Biological labeling of very low density lipoproteins with cholesteryl linoleyl ether and its fate in the intact rat.

In vitro labeling of very low density lipoproteins (VLDL) with radioactive cholesteryl linoleyl ether, an analog of cholesteryl linoleate, was studied. The protocol which gave the highest efficiency and seemed least injurious to the final product included: (1) sonication of the labeled cholesteryl ether with partially delipidated high density lipoproteins (HDL); (2) transfer of the labeled lipids to VLDL in the presence of lipoprotein-deficient human serum; (3) reisolation of the VLDL by ultracentrifugation. Under optimal conditions 70% of the added labeled lipid was recovered with HDL and 60% were transferred from HDL to VLDL. The labeled cholesteryl linoleyl ether was shown to comigrate with the protein of VLDL on agarose gel electrophoresis. In negatively stained preparations, the labeled VLDl and its unlabeled counterpart had similar appearance. The in vitro labeled VLDL was injected into rats and was cleared from the circulation with a t1/2 comparable to endogenously labeled VLDL. More than 80% of the injected dose was recovered in the liver between 3 and 48 h after injection of VLDL labeled with [3H]cholesteryl linoleyl ether of which 91-97% were in the ether form. On radioautography of fixed frozen sections of liver the bulk of the radioautographic reaction was associated with the cytoplasm of hepatocytes. When the VLDL had been labeled also with [14C]cholesteryl linoleate only 35% of injected dose was present in the liver at 3 h, of which 87% was in unesterified form. The distribution of the labeled cholesteryl linoleyl ether, 3-48 h after injection, expressed as per cent of injected dose per organ was 0.7-1.5 in spleen, 0.2-0.5 in lung, 0.1 in heart and 0.2-0.4 in adrenal. The main advantage of the presently described approach in which a nondegradable analog of cholesteryl ester was introduced into VLDL by a biological procedure is the possibility to study the role of various organs to take up circulating cholesteryl ester, especially in species in which LDL is produced from VLDL.

Animals↗
PubMed1980

Lipoprotein lipase activity in F1 heart cell cultures. Effect of dialyzable serum factors on enzyme stability and enzyme synthesis.

F1 heat cell cultures were grown in F-10 medium containing 20% fetal calf and horse serum and after 6-7 days showed high activity of lipoprotein lipase. When the culture medium contained 20% serum which had been dialyzed against F-10 medium, a 75% decline in lipoprotein lipase activity occurred after 3 h of incubation. Cultures incubated with 20% dialyzed serum and dialysate, obtained after 24 h dialysis of serum against F-10 medium, retained full enzyme activity. Restoration of enzyme activity, lost upon incubation with dialyzed serum, became apparent only 2 h after incubation of the cells with dialysate and dialyzed serum and was complete after 24 h. The effectiveness of the dialysate was not affected by trichloroacetic acid precipitation, ether extraction, exposure to pronase or to 80 degrees C for 10 min; it was retained after chromatography of DEAE cellulose but was lost after elution from CM cellulose colums. Addition of spermidine and spermine to culture media containing dialyzed serum did prevent partially the decline in lipoprotein lipase activity of the heart cell cultures. These polyamines were also able to stabilize lipoprotein lipase activity of heart homogenates incubated at 37 degrees C. However, these compounds were not effective in resoration of enzyme activity of cultured cells lost after exposure to dialyzed serum. It appears that positively charged low molecular weight molecules present in sera of various species are required for the stabilization and synthesis of lipoprotein lipase in heart cell cultures.

Animals↗