Search PubMed⌕ Search

Biomedical subjects

M de Vries

Publications and source records attributed to M de Vries.

41 records · Page 3Linked to original sources
PubMed1967

Isolation and properties of polyribosomes and fragments of the endoplasmic reticulum from rat liver.

1. A centrifugation method for the fractionation of the postmitochondrial fraction from rat-liver homogenates is described. The technique, in which no detergent is used, may be used as a tool to discriminate between two classes of ribosomes. One class is firmly bound to membranes and the other consists either of free polysomes or of ribosomes attached by weaker forces to the membranes of the endoplasmic reticulum. 2. Electron-micrograph studies revealed that the polysomes were not contaminated with bound ribosomes or with membranous fragments. 3. The separated fractions were characterized by their RNA, protein, ribonuclease and phospholipid content. 4. The influence of starvation on the RNA and protein contents of the different fractions was investigated. 5. Labelling of the various centrifugal fractions in vivo revealed no difference in uptake of radioactive amino acid between the two classes of ribosomes. 6. Incorporation of radioactive leucine in vitro and the polyuridylic acid-directed phenylalanine incorporation were similar for both classes of ribosomes.

Animals↗
PubMedDate not supplied

Effects of 2-week ingestion of (-)-hydroxycitrate and (-)-hydroxycitrate combined with medium-chain triglycerides on satiety and food intake.

The aim of this study was to assess the effects of 2 weeks of supplementation with (-)-hydroxycitrate (HCA) and HCA combined with medium-chain triglycerides (MCT) on satiety and energy intake. The experimental design consisted of three intervention periods of 2 weeks separated by washout periods of 2 or 6 weeks in a double-blind, placebo-controlled, randomized, and crossover design. Seven male and 14 female normal to moderately obese subjects (mean+/-S.D.; age, 43+/-10 years; body mass index, 27.6+/-2.0 kg/m(2)) participated in this study. Subjects consumed three self-selected meals and four isoenergetic snacks daily with either no supplementation (PLA), with 500 mg HCA (HCA), or 500 mg HCA and 3 g MCT (HCA+MCT). Each intervention period ended with a test day, consisting of a standardized breakfast and ad libitum a lunch and a dinner. There was a significant body weight (BW) loss during the 2 weeks of intervention (PLA, -0.5+/-0.3 kg, P<.05; HCA, -0.4+/-0.2 kg, P<.05; HCA+MCT, -0.7+/-0.2 kg, P<.01), but this reduction was not different between treatments. Twenty-four-hour energy intake (PLA, 8.1+/-0.3 MJ; HCA, 8.3+/-0.3 MJ; HCA+MCT, 8.4+/-0.3 MJ) and the area under the curve of the appetite-related parameters during the test day were similar for all treatments. Two weeks of supplementation with HCA and HCA combined with MCT did not result in increased satiety or decreased energy intake compared to placebo in subjects losing BW.

Adult↗
PubMedDate not supplied

Inherited congenital extrahepatic portosystemic shunts in Cairn terriers.

The pathogenesis of congenital portosystemic shunt (CPSS) in dogs still is incompletely understood. In Irish Wolfhounds and Yorkshire Terriers, CPSS is reported to be hereditary. The aim of this study was to investigate a possible genetic basis and the mode of inheritance of CPSS in Cairn Terriers. Between July 1990 and July 2001, 6-week-old pups of the Dutch Cairn Terrier population were screened by measuring venous ammonia concentrations and in the presence of hyperammonemia by ultrasonography, autopsy, portal vein angiography, or exploratory celiotomy. The same successfully operated female was used 3 times in test matings with an unrelated affected male, her unaffected sire, and an affected offspring. The prevalence of CPSS in the general Cairn Terrier population, the direct progeny of frequently used males, and the offspring of the test matings were tested for significant differences. In total, 6,367 Cairn Terriers were screened; 32 males and 26 females had CPSS. In 3 large family groups, significantly higher prevalences were found compared with the general population (P < .0001, P < .0001, and P < .044). The prevalence of CPSS in the offspring of the test matings was significantly higher (P < .002) than in the general population. No sex predisposition occurred among the affected dogs. The higher prevalence of CPSS in the test matings and the 3 family groups compared with the general population indicates that CPSS in Cairn Terriers is a genetic disease. The inheritance is autosomal and most likely polygenic or monogenic with variable expression.

Animals↗