Biomedical subjects

H Vidal

Publications and source records attributed to H Vidal.

130 records · Page 8Linked to original sources

PubMedDate not supplied

Subcutaneous adipose tissue expression of plasminogen activator inhibitor-1 (PAI-1) in nondiabetic and Type 2 diabetic subjects.

OBJECTIVE: Increased plasma levels of plasminogen activator inhibitor-1 (PAI-1) have been suggested to be a part of the insulin resistance syndrome, and recent data suggest that adipose tissue participates in the production of PAI-1. We examined the expression and insulin regulation of subcutaneous adipose tissue PAI-1 mRNA and its relationship to insulin sensitivity. DESIGN: A cross-sectional study involving five lean (60.0+/-3.1 years, BMI 23.5+/-0.5 kg/m(2)) and six obese nondiabetic men (56.0+/-3.1 years, BMI 30.4+/-0.7 kg/m(2)), and six obese Type 2 diabetic men (61.4+/-3.2 years, BMI 31.8+/-1.0 kg/m(2)). MEASUREMENTS: Subcutaneous adipose tissue PAI-1 mRNA and insulin sensitivity were quantified using RT-competitive PCR and euglycemic hyperinsulinemic clamp technique, respectively. RESULTS: Subcutaneous adipose tissue PAI-1 mRNA levels were higher in obese nondiabetic and Type 2 diabetic men than in lean nondiabetic men. PAI-1 mRNA levels decreased in the three groups during a 240-min euglycemic hyperinsulinemic clamp (P<0.05 for all groups), and a similar reduction was observed during a 240-min saline control study indicating that adipose tissue PAI-1 gene expression has diurnal variation and is not acutely controlled by hyperinsulinemia. The basal PAI-1 mRNA levels correlated positively with BMI, and waist-to-hip ratio; and negatively with whole-body glucose disposal rate in nondiabetic men. CONCLUSIONS: Subcutaneous adipose tissue PAI-1 mRNA expression is increased in obese nondiabetic or in Type 2 diabetic men. Subcutaneous adipose tissue PAI-1 mRNA expression is increased in proportion to visceral obesity and to the level of whole-body insulin resistance. Subcutaneous adipose tissue PAI-1 mRNA expression is not acutely regulated by insulin, and it is subject to a diurnal variation.

Adipose Tissue↗

PubMedDate not supplied

Ricin A-chain cytotoxicity depends on its presentation to the cell membrane.

Anti-ricin-A-chain monoclonal antibodies (mAbs) were raised in order to study epitopes of the A-chain involved in the initiation of its transmembrane passage. Five nonoverlapping epitopes were selected by cluster formation using a cross-inhibition assay of mAbs from 172 specific hybridomas. For each cluster, representative high affinity mAbs were selected. These mAbs were disulfide-linked to F(ab')2 fragments of a mAb directed against the CD5 antigen. The cytotoxicity of ricin A-chain bound by affinity through different epitopes to these hybrid mAbs was explored on the CD5-positive CEM cells. Without any enhancer, the hybrids displayed cytotoxicity varying in IC50 within a range of 1-10; in the presence of the enhancer NH4Cl, this variation of activity was maintained ranging from 1 to 20; with the enhancer monensin, the variation of cytotoxicity of hybrids extended over a 1-80-fold range. These differences of cytotoxicity were not correlated with mAb properties such as the inhibition of A-chain enzymatic activity, the A-chain binding affinity, the capacity for releasing A-chain at low pH, or the capacity of hybrids for delivering A-chain on the cell surface. This lack of correlation strongly suggests that the different presentations of A-chain epitopes to the cell membrane may be the essential reason for cytotoxicity variations.

Ammonium Chloride↗

PubMedDate not supplied

[Validation of a version in Spanish of the Yale-Brown Obsessive-Compulsive Scale].

INTRODUCTION: The objective of this study is to validate a version in Spanish of the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS). METHOD: We administered to 20 patients with obsessive-compulsive disorder (OCD) the Maudsley Obsessive-Compulsive Inventory (MOI) and a version in Spanish of the Y-BOCS. The application of the last one was performed by an interviewer, filmed, and then watched and rated by other 4 observers. In addition, the opinion of the treating psychiatrist about the severity of the patient's symptoms was registered. The interviewer and the observers were named raters. RESULTS: The mean scores of the Y-BOCS assigned by the 4 observers were from 18.35 to 19.55; the maximum scores, from 34 to 35; and the minimum scores, from 1 to 5. The Pearson's correlations between raters were significant for all cases (r>0.86 and p<0.001). For all raters, Y-BOCS scores significantly correlated with MOI scores (p<0.001) and the opinion of the treating psychiatrist (p<0.05). We did not find significant correlation between the last one and MOI scores. The Cronbach's coefficients ranged from 0.8789 to 0.9488. CONCLUSIONS: The Spanish version of the Y-BOCS is reliable, homogeneous and valid for quantification of the obsessive-compulsive symptoms, and has more correlation with the opinion of the treating psychiatrist than the MOI.

Adolescent↗

PubMedDate not supplied

Metabolic and drug distribution studies do not support direct inhibitory effects of metformin on intestinal glucose absorption.

In an attempt to clarify the question of an involvement of the inhibition of intestinal glucose absorption in the mechanism of action of Metformin, we used several experimental approaches: 1 glucose/lactate measurement in rat portal blood in vivo and 2 in the venous effluent of an isolated perfused rat intestinal segment; 3 metabolism of freshly isolated enterocytes in vitro and tissue distribution of 3H-labeled Metformin was investigated both in vivo and in vitro. Metformin applied intraluminally had no significant effect on portal glycaemia after a glucose load, but lactate increased, whereas in vivo only a high Metformin dosage reduced portal glucose appearance significantly. Although high Metformin concentrations were found in gut biopsies, precise histological analysis in the isolated intestine revealed that it was absent from enterocytes; however the drug accumulated in villous lacteals. Intrarterially applied Metformin decreased glucose absorption in the isolated perfused ileo-jejunal segment. These data suggested that vascular Metformin boosted intestinal anaerobic glucose metabolism. Biochemical measurements performed on freshly isolated enterocytes showed that even high Metformin levels did not interfere with cell respiration or with Na+/K+ ATPase activity. Thus, our data agree with other recent reports, suggesting that even at nontherapeutic concentrations Metformin has no relevant inhibitory effect on intestinal glucose absorption. The data are discussed in the frame of previous divergent observations. The results suggest however that Metformin of vascular origin stimulates glucose consumption by the intestine, which then increases lactate output from the gut.

Animals↗