La enuresis. Una manifestación de la regresión en la infancia / Euneresis. A manifestation of regression in infancy

Este artículo refleja el trabajo de un grupo de estudio sobre la relación entre enuresis y regresión. Se considera a la enuresis como síntoma privilegiado que expresa la regresión o el estancamiento en el desarrollo psicosexual del niño y surge la cuestión de cuándo la enuresis puede ser entendida como síntoma de un conflicto y cuándo como un trastorno. Tres viñetas clínicas ilustran tres posibles interpretaciones, no excluyentes, de este síntoma: expresión de hostilidad hacia las figuras parentales, emergente de un conflicto en la relación con los padres y manifestación regresiva (AU)

This article reflects the work of a study group concerning the relationship between enuresis and regression. Enuresis is considered as a privileged symptom which expresses the regression or the stagnation in the sexual development of the individual and the question arises as to what extent enuresis can be understood as conflict or as a disorder. Three clinical vignettes illustrate three possible interpretations not naturally excluded in this symptoms: expression of hostility towards parents, conflict with the relationship with parents and regressive manifestation (AU)

Kinetics of prebeta1 HDL and alphaHDL in type II diabetic patients.

BACKGROUND: The aim of this study was to analyze the recycling of high density lipoprotein (HDL) in six type II diabetic patients compared with six control subjects by endogenous labelling of apolipoprotein A-I (Apo A-I) with stable isotope Apo A. MATERIALS AND METHODS: The -I-HDL kinetics were performed by infusion of (5.5.5-(2)H3)-leucine for 14 h. The prebeta1 and alphaHDL were separated by gel filtration fast protein liquid chromatrography system (FPLC). Kinetics of isotopic enrichment of Apo A-I were analyzed with a multi-compartmental model software (SAAM II, SAAM Institute, Seattle, WA). RESULTS: Plasma Apo A-I concentration was decreased in patients with type II diabetes as a result of a decrease in Apo A-I-alphaHDL (P < 0.05). Diabetic patients were also characterized by an increased relative contribution of Apo A-I in prebeta1 HDL (18.3 +/- 2.8% vs 11.9 +/- 3.7%, P < 0.01). The synthetic rate of prebeta1 HDL was slightly increased in diabetic patients compared with control (NS) and an increase of recycling rate of alpha to prebeta1 HDL was observed (11.67 +/- 3.14 d(-1) vs 7.09 +/- 4.51 d(-1), P < 0.05). The clearance rate of Apo A-I was higher in diabetic patients (P < 0.05 for Apo A-I-prebeta1 HDL and P < 0.005 for Apo A-I-alphaHDL). CONCLUSION: This study suggests that the usual increase in prebeta1 HDL in type II diabetic patients is mainly related to an increased conversion rate of alpha to prebeta1 HDL.

Modulation of the phospholipid transfer protein-mediated transfer of phospholipids by diacylglycerols.

Previous studies have shown that diacylglycerols (DAG) are formed during triglyceride hydrolysis in very low density lipoproteins (VLDL), a process that is accompanied by an elevated phospholipid transfer protein (PLTP)-mediated transfer of phospholipids (PL) from VLDL to high density lipoprotein. Because PLTP has been also shown to transfer DAG, we hypothesized that DAG might modulate PL transfer through a mechanism of competition with respect to PLTP. To address this question we performed in vitro PL transfer assays using specifically designed PL donor particles. These were single bilayer vesicles (SBV) and large (EM-L) or small (EM-S) lipid emulsions, containing various proportions of DAG. The PLTP-mediated transfers of PL decreased as the volumes of the particle cores increased (SBV > EM-S > EM-L). In all cases, these transfers were inhibited by DAG in a concentration-dependent manner. We determined the core-to-surface distribution of DAG and we measured their relative affinity for PLTP by comparison with that of PL. From these parameters, we calculated the theoretical effects of DAG on PL transfers that would result from a competition mechanism. The experimental data showed that the inhibiting effects of DAG on PL transfers were much more important than those predicted from our calculations. Additional data showed that a large part of DAG effects was in fact due to their ability to increase the viscosity of the particle PL surfaces, as calculated from electron spin resonance experiments. These results show that DAG can modulate the PLTP-dependent PL transfers, both by competition with PL and by increasing the viscosity of the particle surfaces. These findings might be physiopathologically relevant in situations where elevated plasma concentrations of DAG might result from hypertriglyceridemia.-Lalanne, F., C. Motta, Y. Pafumi, D. Lairon, and G. Ponsin. Modulation of the phospholipid transfer protein-mediated transfer of phospholipids by diacylglycerols. J. Lipid Res. 2001. 42: 142;-149.

Mechanism of the phospholipid transfer protein-mediated transfer of phospholipids from model lipid vesicles to high density lipoproteins.

To study the effects of the phospholipid transfer protein (PLTP) on the thermodynamic parameters governing the transfer of phospholipids (PL) from single bilayer vesicles (SBV) to high density lipoprotein (HDL), we performed transfer measurements at various temperatures between 4 and 65 degrees C, using a pyrenylphosphatidylcholine (Pyr-PC) as probe. The proportion of excimer (E) to monomer (M) fluorescence of a pyrenyl moiety constitutes a direct measure of its local concentration. The transfers of Pyr-PC were monitored by following the decrease of E/M. The data were used to calculate the rate constants K(+1) for the transfer from SBV to HDL and to generate the corresponding Arrhenius plots. The equilibrium constants, K(eq), for the same reactions were also determined and used to generate Van't Hoff plots. From these data, we calculated the thermodynamic parameters for both the whole transfer reaction and the transition state. Both K(+1) and K(eq) values clearly varied with temperature. PLTP induced very similar decreases in the free energy for the whole reaction (DeltaG) and in that for the transition state (DeltaG(#)). At 37 degrees C, the decreases were of 0.37 and 0.29 kcal/mol, respectively. We studied the thermal denaturation of PLTP between 37 and 65 degrees C, and the effects of denatured PLTP samples on the PL transfer reaction were then determined. In all cases, the changes of DeltaG remained comparable to those of DeltaG(#). Thus the essential action of PLTP is to facilitate the first step of the reaction, which can be considered as the desorption of PL molecules from the surface of donor particles.

VLDL-bound lipoprotein lipase facilitates the cholesteryl ester transfer protein-mediated transfer of cholesteryl esters from HDL to VLDL.

In recent years, it has been established that lipoprotein lipase (LPL) is partly associated with circulating lipoproteins. This report describes the effects of physiological amounts of very low density lipoprotein (VLDL)-bound LPL on the cholesteryl ester transfer protein (CETP)-mediated cholesteryl ester transfer (CET) from high density lipoprotein (HDL) to VLDL. Three patients with severe LPL deficiency exhibited a strong decrease in net mass CET that was more than 80% lower than that of common hypertriglyceridemic subjects. Recombination experiments showed that this was due to an abnormal behavior of the VLDL fraction. Replacement of the latter by normal VLDL totally normalized net mass CET. We therefore prepared VLDL containing controlled amounts of bound LPL that we used as CE acceptors in experiments involving unidirectional radioisotopic CET measurements. These were carried out either in the absence or in the presence of inhibitors of LPL lipolytic activity. When LPL-induced lipolysis was totally blocked, the stimulating effect of the enzyme on the CETP-dependent CET was only reduced by about 50%, showing that it did not entirely result from its lipolytic action. These data were dependent upon neither the type of LPL inhibitor (E600 or THL) nor the source of CETP (delipidated plasma or partially purified CETP). Thus, in addition to the well-known stimulating effect of LPL-dependent lipolysis on CET, our work demonstrates that physiological amounts of VLDL-bound LPL may facilitate CET through a mechanism partially independent of its lipolytic activity.

Distribution of diacylglycerols among plasma lipoproteins in control subjects and in patients with non-insulin-dependent diabetes.

BACKGROUND: Diacylglycerols (DAGs), which are well-known components of insect lipophorins, have been recently recognized as a major glyceride of human high-density lipoprotein (HDL). Moreover, DAGs are good substrates for hepatic lipase and for the phospholipid transfer protein (PLTP). The present work was undertaken to determine the lipoprotein concentrations of DAGs, in control subjects, in non-insulin-dependent diabetic (NIDD) patients and in patients with severe hypertriglyceridaemia. MATERIALS AND METHODS: Lipoproteins were isolated from 11 control subjects, 17 diabetic patients and three hypertriglyceridaemic patients, using a combination of ultracentrifugation and precipitation. After lipid extraction, DAGs were separated by thin-layer chromatography and quantified by a glyceride assay. RESULTS: DAGs were detectable in all lipoprotein fractions of the three groups of subjects. Total DAGs were correlated with total triglycerides (TGs) and even more strikingly with very low-density lipoprotein triglycerides. Although the majority of DAG was recovered in apo B-containing lipoproteins, the proportion of DAG with respect to TG was most elevated in HDL. CONCLUSION: These findings indicate that DAGs are probably formed from TG during lipolysis and that they can be transported to HDL through the action of PLTP. This raises the question whether DAG might act as an inhibitor of phospholipid transfer by competition for binding to PLTP.

Multi-parameter observation of environmental asbestos pollution at the Institut de Physique du Globe de Paris (Jussieu Campus, France).

An original multi-parameter system has been used to study the nature of dust in the ambient air, particularly the total fibers and asbestos fibers, in eight areas of the Institut de Physique de Globe de Paris (France). These analyses provide a detailed case study of environmental pollution by asbestos fibers at low levels. The levels of total fibers with a length greater than 3 microns, measured with a real time fiber analyser monitor (FAM), give a baseline of 2.5 fibers per l., throughout the duration of sampling. The same levels, calculated during periods of effective presence of staff, are smaller than 10 fb per l. During these periods, the instantaneous value can show high peaks, reaching a maximum of 60 fb per l., but more often of about 5 to 10 fb per l. A direct cause and effect relationship exists between fiber concentrations and the presence of people, and indirectly with the variation of the other environmental parameters (temperature, humidity, air velocity). The baseline concentration of asbestos fibers, determined by analytical transmission electron microscopy (ATEM), is about 10(-1) fb per l., with a mean value during the presence of people always less than 1.5 fb per l. The low levels of asbestos fibers do not allow us to establish a precise correlation between the concentration of total fibers and the asbestos concentration, but a rough estimate suggests that asbestos could represent 10-20% of the airborne fibers monitored with the FAM. The statistical study of fiber sizes shows that 70 and 55% of analyzed chrysotile and amosite fibers respectively are smaller than 5 microns. These numbers are 40 and 35% for fibers smaller than 3 microns, which are undetected by the FAM. Amosite, which characterizes most of the asbestos-containing materials (ACM) in the analyzed areas, is detected in the ambient air in quantities ten times less important than chrysotile. The low asbestos levels and the difference between the nature of building asbestos and airborne fibers, show that the mean measured asbestos contents in the ambient air represent the geochemical background of chrysotile asbestos fibers in the Parisian air.