Étude de la viscosité relative des electrolytes 1:1 en solution aqueuse à 25 [degré] C

L'aspect expérimental de ce travail consiste â mesurer les viscosités relatives des solutions d'électrolytes 1:1 en solution aqueuse à 25OC, dans un domaine de concentration s'étendant de 0.1 jusqu'à1 molaire. Tous les résultats expérimentaux s'expriment par une équation du type: nr = n/no = 1 + Anc1/2 + Bnc + Dnc2 Le terme An représente la contribution des forces coulombiennes à longue portée . Le terme est fonction de la dimension de l'ion et de son hydratation. En associant ce terme avec le volume partiel molaire V , la différence — 0.0025 -vo devient une mesure des interactions soluté-solvant. On choisit l'ion tétraethylammonium comme particule idéale obéissant à la relation d'Einstein et permettant alors d'obtenir une échelle ionique absolue pour le coefficient Bn. Enfin le terme est complexe, puisque sa valeur est à la fois fonction: 1) d'un terme supérieur du développement de l'effet hydrodynamique, 2) des interactions structurales soluté-solute',3) d'un terme supérieur du développement des forces coulombiennes à longue portée. De plus, dans la partie expérimentale, au niveau du calcul de la viscosité, des valeurs précises de densité s'avéraient nécessaires pour les sels quaternaires d'ammonium , il fallut vérifier la validité des données existantes et compléter les valeurs manquantes

Apparent Molal Volumes and Heat Capacities of Alkaline Earth Chlorides in Water at 25 °C

The densities and volumetric specific heats of the alkaline earth chlorides have been measured in water at 25 °C in the concentration range 0.01 to 0.4 M with a flow densimeter and a flow microcalorimeter. Apparent molal volumes and heat capacities have been derived

Apparent Molal Volumes and Heat Capacities of some Sulfates and Carbonates in Water at 25 °C

The densities and volumetric specific heats of Na2SO4, K2SO4, MgSO4, Na2CO3, NaHCO3, and NaOH were measured up to an ionic strength of 1 in water at 25 °C with a flow densimeter and a flow microcalorimeter. From these data, the heat capacity for the formation of the ion pair MgSO40was evaluated as 84.9 J K−1 mol−1. There is an anomalous increase in the apparent molal heat capacities of Na2CO3 at low concentration but the apparent molal volumes are normal. This anomaly can be suppressed with NaOH. Attempts to account quantitatively for this behavior by an hydrolysis correction were not successful

Contribution of receptor negative versus receptor defective mutations in the LDL-receptor gene to angiographically assessed coronary artery disease among young (25–49 years) versus middle-aged (50–64 years) men

Elevated plasma LDL-cholesterol (LDL-C) levels are associated with an increased risk of coronary artery disease (CAD). Familial hypercholesterolemia (FH), a monogenic trait due to mutations in the LDL-receptor (R) gene is characterized by raised plasma LDL-C levels and premature CAD. The aim of the present investigation, derived from the study of a population of 1465 unrelated men aged 25 to 64 years, was to compare the expression of CAD assessed by coronary angiography in young (aged 25–49 years) versus middle-aged (50–64 years) heterozygous FH patients of French Canadian descent. Furthermore, the relationship of binding-defective versus receptor negative mutations in the LDL-R to premature CAD (B50 years) was examined and compared with men displaying a normal plasma lipoprotein-lipid profile. From the original study sample, a total of 100 men met the clinical criteria of heterozygous FH. Among them, 30 were carriers of a receptor negative mutation (deletion \15 kb or point mutations Y468X or R329X) whereas 64 were carriers of a receptor defective mutation (W66G, E207K or C646Y). As expected, in both age groups (25–49 years vs. 50–64 years), carriers of a receptor negative mutation had higher plasma cholesterol and LDL-C levels than carriers of a defective allele or men with a normal plasma lipoprotein-lipid profile. In addition, the mean number of diseased vessels (with\50% stenosis) was higher in men aged 50–64 years compared to those aged 25–49 years. In the two age groups, FH patients were characterized by a higher number of stenosed coronary vessels than the normal phenotype group. Within each group (either receptor negative, receptor defective or normal phenotype) plasma cholesterol, LDL-C, HDL-C, triglyceride and apolipoprotein B levels were similar irrespective of age (25–49 years vs. 50–64 years). Finally, multiple logistic regression analyses revealed that compared to non-FH men, the relative odds of being affected by CAD before the age of 50 years was 7.3-fold higher for carriers of a receptor negative mutation and 2.7-fold higher for men with a receptor defective mutation at the LDL-R locus. These results suggest that CAD could be an earlier event among heterozygous FH subjects bearing a receptor negative mutation compared to LDL-R defective patients. It also suggest that the selective screening for mutations in the LDL-R gene may allow a better assessment of the individual risk and facilitate the development of family-based preventive strategies or intervention programs in FH

Relative contribution of low-density lipoprotein receptor and lipoprotein lipase gene mutations to angiographically assessed coronary artery disease among French Canadians

Men with low-density lipoprotein receptor gene mutations causing familial hypercholesterolemia (FH) are at high risk of premature coronary artery disease (CAD). The dyslipidemic state found among patients who are heterozygous for mutations in the lipoprotein lipase (LPL) gene may also increase the risk of CAD. In the present study, the association of the heterozygous forms of low-density lipoprotein receptor gene mutations causing FH as well as of LPL gene mutations causing (P207L and G188E) or not causing (D9N and N291S) complete loss of LPL activity with angiographically assessed CAD was estimated in a cohort of 412 French Canadian men aged <60 years who consecutively underwent coronary angiography for the investigation of retrosternal pain. The frequency of FH as well as of LPL gene mutations tended to increase with the number of narrowed coronary arteries. However, CAD occurred earlier in FH patients than in partly LPL-deficient patients. Indeed, the proportion of men affected by FH was of 16.4% in those <45 years of age, and solely 4.3% among those between 56 and 60 years of age (p <0.0001). In contrast, the LPL gene defect was found in only 4.0% of men aged <45 years, whereas this prevalence reached 8.3% among those aged 56 to 60 years. In multivariate analyses, the association of LPL with CAD was not independent of age, high-density lipoprotein cholesterol concentrations, and other covariates included at baseline, and was not affected by the type of mutation in the LPL gene. In contrast, FH was associated with CAD with minimal contribution of other cardiovascular risk factors. However, the relation between FH and CAD was at least partly dependent on plasma apolipoprotein B concentrations. In the different regression models, fasting insulin and plasma high-density lipoprotein cholesterol concentrations were important covariates of CAD, whether or not patients were affected by FH or LPL deficiency. In conclusion, the association of LPL gene mutations with CAD was delayed compared with FH, appeared to be markedly exacerbated by the presence of additional risk factors, and was not affected by the type of mutation in the LPL gene

Comparison of the effect of two low-density lipoprotein receptor class mutations on coronary heart disease among French-Canadian patients heterozygous for familial hypercholesterolaemia

The aim of this study was to compare the age at first elective coronary angiogram and the age at first revascularization (coronary artery bypass grafting or percutaneous transluminal coronary angioplasty) in 102 patients without familial hypercholesterolaemia (FH), who were matched for age and sex with 76 heterozygous FH patients carrying a defective allele at the low‐density lipoprotein (LDL) receptor gene (LDL‐R) and 26 heterozygous FH patients bearing a null mutation at the LDL‐R. The prevalence of diabetes was significantly higher in the non‐FH group than in the two FH groups (P   50% stenosis was higher in null allele carriers than in non‐FH patients and tended to be higher than among defective allele carriers (P  < 0.01). Although no difference in plasma Lp(a) levels were noted between null allele carrier and non‐FH patients, plasma Lp(a) concentrations were higher in the defective allele group than in the other two groups. In summary, the development of coronary artery disease as estimated by the age at first elective coronary angiography or at first revascularization is premature in FH patients carrying a null mutation compared with defective allele carriers or with non‐FH patients. Moreover, the higher number of stenosed vessels among null allele carriers suggests that coronary artery disease was more severe in FH subjects with a null allele at the LDL‐R locus

Low plasma adiponectin exacerbates the risk of premature coronary heart disease in familial hypercholesterolemia

Familial hypercholesterolemia (FH) is characterized by increased risk for premature coronary artery disease (CAD). This risk is exacerbated in the presence of abdominal obesity and insulin resistance. Low adiponectin is part of the clustering of metabolic abnormalities associated with abdominal obesity and insulin resistance. The present study, therefore, aims to examine the relationship between plasma adiponectin and age at CAD diagnosis in FH patients. Plasma adiponectin was measured by ELISA in 568 non-diabetic FH individuals of French-Canadian origin. CAD was defined according to strict clinical criteria. Prior to analyses, patients were grouped according to age and gender-specific tertiles of plasma adiponectin levels. Multivariate Cox proportional hazards regression was used to estimate the association between plasma adiponectin levels and age at diagnosis of CAD. Overall, FH patients in the lowest tertile of plasma adiponectin exhibited CAD at a significantly younger age (hazard ratio = 1.73, confidence interval 95%: [1.19–2.53]; p = 0.004). These results suggest that low plasma adiponectin is associated with an increased risk of premature CAD over and above the already exaggerated risk seen in FH patients