Elderly donors (60 to 87 years) in renal transplantation: good results after 5 years.
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Biomedical subjects
Publications and source records attributed to R Sola.
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This paper describes an oxidative process of human high-density lipoproteins (HDL) based upon the action of oxygenated free radicals produced by water radiolysis (OH. and OH./O2.- free radicals at pH 7), monitored by both biochemical and physical markers. Classical biochemical markers (vitamin E, thiobarbituric acid-reactive substances (TBARS), conjugated dienes and differential fluorescence) were studied as a function of the radiation dose (from 0 to 800 Gy; dose rate = 2.7 x 10(-2) Gy.s(-1)). The fluorescence polarization anisotropy (r) was measured with 1,6-diphenylhexatriene (DPH). Vitamin E decrease and formation of lipid peroxidation products (thiobarbituric acid-reactive substances and conjugated dienes) were concomitant in the case of OH. free radicals alone, whereas these products appeared after a small threshold dose when OH. and O2.- free radicals were simultaneously produced in solution. At high radiation doses, TBARS concentrations have reached plateau values (approx. 2 or 7 nmol/mg lipid with OH. or OH./O2.- free radicals, respectively) which were much lower than those obtained after copper oxidation (approx. 15 or 29 nmol/mg lipid after 12 and 24 h incubation, respectively). The free radical-induced oxidative process has led to a rigidification of the HDL and was associated with low values of cholesterol effluxing capacities when these oxidized HDL were incubated with cholesterol-loaded human fibroblasts. Similar results were obtained with copper-oxidized HDL, under our experimental conditions. Consequently, these two kinds of oxidative modification of HDL resulted both in a loss of their capacity to remove cellular cholesterol, which could be explained by the fact that this ability was under the dependence of a HDL optimum fluidity.
AIM: To investigate the effect of dexfenfluramine (dF) on Energy Expenditure (EE). DESIGN: 20 obese females were studied in a double-blind design. Pre-diet and at 14 and 28 days of VLCD and dF treatment (30 mg/d) or placebo, Resting Metabolic Rate (RMR), 3 h-Thermic Effect of Food (3 h-TEF) and body composition were determined. EE and body composition were measured by indirect calorimetry and bioelectrical impedance, respectively. RESULTS: No differences between groups were observed in relation to weight loss, body composition changes or RMR. At 3 h postprandial, the EE was still elevated in both groups. No changes on TEF were observed in the placebo group during VLCD. In contrast, TEF decreased in dF group during VLCD (P < 0.05). No significant differences in TEF at the end of the study were observed between groups. CONCLUSION: These results suggest that dF modifies 3 h-TEF but not RMR in obese patients during VLCD administration.
BACKGROUND: The equations available for the prediction of basal energy expenditure (BEE) may not be applicable in morbid obese individuals since the contribution of the fat free mass (FFM) over the BEE is not constant. The aim of this study was to obtain new equations for the prediction of BEE which are specific for patients with morbid obesity. METHODS: In 26 women with morbid obesity age, weight, body composition by bioelectric impedance and BEE by open circuit indirect calorimetry were determined. The BEE observed was compared with that estimated from the previously described equations. The multiple regression method was used to obtain the BEE prediction equations. RESULTS: Upon comparison of the BEE observed with the BEE estimated by the described equations a significant relation was found between both parameters. The differences were also significant except when the Harris-Benedict equation was used. Multiple regression analysis demonstrated that when the variables of body composition were included, the FFM explained 75% of the variation in BEE and on forcing the entrance of fatty mass, the explanation increased to 79%. When only the anthropometric variables were included, weight explained 69% of the variation. CONCLUSIONS: In morbid obesity, most of the equations described for estimating basal energy expenditure are not applicable. New equations are reported for the prediction of energy expenditure.
To assess the effects of oxidative modification, human HDL was oxidised in vitro for 12 h (Ox-HDL12) and 24 h (Ox-HDL24) under similar conditions to those commonly used for LDL. The procedure resulted in: an increase in thiobarbituric acid reactive substances but with marginal change in electronegativity; protein denaturation accounting for 16% and 45% loss of immunoreactive apoprotein A-I in the Ox-HDL12 and Ox-HDL24 respectively relative to the non-oxidised, native HDL (Nat-HDL); a decrease in the polyunsaturated fatty acids of the triglyceride, cholesterol ester and phospholipid components of the lipoprotein; an increase in the proportion of short chain saturated fatty acids while the monounsaturated fatty acids remained relatively unchanged. Studies with human macrophages demonstrated: a decrease of 16% and 30% in the capacity of the Ox-HDL12 and Ox-HDL24 respectively to efflux intracellular free cholesterol; 125I-Ox-HDL24 uptake and degradation was directly comparable with that of 125I-Ac-LDL; the addition of excess unlabelled Ox-HDL24, Ac-LDL, Ox-LDL24 and Nat-HDL resulted in 74%, 67%, 69% and 19% displacement of the 125I-Ox-HDL24 respectively; fucoidin and dextran sulphate displaced 125I-Ox-HDL by 20% and 40% respectively; intracellular free and esterified cholesterol was increased 2.5-fold and 4-fold respectively relative to Nat-HDL on incubation with Ox-HDL24. These findings suggest that HDL is susceptible to oxidative modification leading to recognition by the scavenger receptor of macrophages and subsequent intracellular cholesterol accumulation. As such, the in vivo protective role of HDL in cardiovascular disease can be reversed in those circumstances in which HDL, like LDL, undergoes oxidative modification.
BACKGROUND: This study was performed to investigate the risk factors for a first episode of spontaneous bacterial peritonitis in cirrhotic patients. METHODS: One hundred ten cirrhotics with sterile ascites, without previous spontaneous bacterial peritonitis (SBP), were included from March 1988 to October 1989 and followed up until October 1990 (follow-up, 46 +/- 3.5 weeks; range, 4-120 weeks). RESULTS: Twenty-eight patients (25.45%) suffered SBP. In multivariate analysis (Cox's regression model) including only variables commonly used in clinical practice, ascitic fluid protein concentration and serum bilirubin level independently correlated with first SBP development. Using these two variables the relative risk of a first SBP episode was calculated for each patient. According to the median relative risk coefficient (1.2), a low-risk group (relative risk, < 1.2) and a high-risk group (relative risk, > 1.2) were established. Kaplan-Meier estimates of patients free of SBP were significantly higher in the low-risk group. CONCLUSIONS: The probability of a first SBP episode is significantly influenced by the antimicrobial capacity of ascitic fluid and hepatic function.
This study was designed to determine whether modifications induced by dietary fats on the high-density lipoprotein3 (HDL3) physicochemical characteristics could affect cholesterol efflux and intracellular cholesterol content, leading to upregulation of low-density lipoprotein (LDL) receptor activity from cultured fibroblasts. Serum HDL3S were obtained from 12 healthy women aged 26 to 49 years who adhered to four 7-week isocaloric diets containing 30% of the caloric intake as fat. Of the total calories, 15.6% of each diet was provided by (1) milk fats, rich in saturated fatty acids; (2) sunflower oil, rich in n-6 polyunsaturated fatty acids; (3) olive oil, rich in monounsaturated fatty acids; and (4) rapeseed oil, rich in n-3 polyunsaturated fatty acids. HDL3 isolated after the monounsaturated fatty acid diet induced the greatest cellular [3H]free cholesterol efflux, reduced the content of intracellular cholesterol, and enhanced 125I-LDL degradation. Univariate regression analyses suggested that the increased capacity of HDL3 to promote cellular [3H]free cholesterol efflux was in part due to its greater fluidity, higher cholesteryl ester content, elevated linoleic to linolenic acid ratio in phospholipids, and its smaller size. In conclusion dietary fats induced physicochemical changes in HDL3, which strongly modulated cellular cholesterol homeostasis in vitro. These data also suggest a novel mechanism by which dietary fats exert their effect on atherosclerosis.
The effects on plasma lipoproteins of four fat-modified diets were assessed in 11 nuns in a contemplative order in the Mediterranean region of Spain. Diet 1 [high polyunsaturated fatty acid (PUFA), low monounsaturated fatty acid (MUFA), low ratio of PUFAs to saturated fatty acids (P:S)] and diet 3 (low PUFA, high MUFA, low P:S) induced significant, directly comparable reductions in total plasma (12% and 13%, respectively) and low-density-lipoprotein (LDL) cholesterol (24% and 19%, respectively). Diet 2 [high PUFA, high MUFA, low saturated fatty acid (SFA), high P:S] induced greater decrements (23% and 30% in total plasma and LDL cholesterol, respectively). Diet 4 (low PUFA, low MUFA, high SFA, low P:S) induced a significant increase in LDL cholesterol of 11%. No significant changes in high-density-lipoprotein cholesterol were observed with these diets. Because the effects of PUFAs and MUFAs are comparable, no recommendations on modifying the habitual, high-MUFA-containing Mediterranean diet need be made other than, perhaps, a reduction in the overall intake of SFAs.
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The present study was undertaken to analyze whether the changes induced by dietary manipulations in the chemical composition of HDL, particularly in total phospholipids, phosphatidylcholine and sphingomyelin fatty acid composition, modified their fluidity. 12 healthy women, aged 26-49 years were studied. They consumed, over periods of 5 weeks, various isocaloric diets, each containing 30% of the calories as fat. 15.6% of the total calories were provided successively by olive oil, soybean oil, corn oil, and milk fats. The HDL fluorescence anisotropy was measured with 1,6-diphenyl-1,3,5-hexatriene (DPH) by fluorescence polarization. The HDL from the monounsaturated diet, olive oil, were the most fluid particles. The HDL fluorescence anisotropy was positively correlated with their free cholesterol percentage and negatively correlated with their triacylglycerol content and their triacylglycerol/phospholipid ratio. Moreover, the HDL fluorescence anisotropy was negatively correlated with the percentage of oleic acid in their total phospholipids and particularly in the phosphatidylcholine. These results suggest that the percentages of triacylglycerol and oleic acid in phospholipids of HDL have a fluidifying effect on these lipoproteins.
A case of renal transplantation during the 12th week of pregnancy is presented. An episode of rejection 6 days after surgery was treated satisfactorily. At the 18th week, the patient showed a mild hypertension which was treated by hidralazine. At the 30th week a fetal pyelouretheral stenosis with celiciar dilatation was diagnosed and the mother had another rejection episode. At the 33rd week a cesarean section was performed after a pathological NST. Neonatal and maternal developmental courses were good.
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