ARS Component B: structural characterization, tissue expression and regulation of the gene and protein (SLURP-1) associated with Mal de Meleda.

The ARS Component B gene (EMBL ID: HSARS81S, AC: X99977) encodes a 9 kD non-glycosylated polypeptide (also known as SLURP-1, SwissProt/TrEMBL: P55000), a soluble member of the human Ly6/uPAR superfamily. ARS Component B gene mutations have been implicated in Mal de Meleda. In this study we show by immunohistochemistry that SLURP-1 (secreted Ly-6/uPAR related protein, the protein product of the ARS Component B gene) is localized to human skin, exocervix, gums, stomach and esophagus.

Pharmacokinetics and acute tolerance of a double virus inactivated plasma derived factor VIII concentrate.

To further reduce the risk of possible viral disease transmission, an additional virucidal step was performed in the manufacturing process of a solvent/detergent treated factor VIII concentrate, which consisted of heating the lyophilized preparation at 100 degrees C for 30 min (Emoclot DI; ISI, Italy). Because thermal treatment may modify factor VIII bioavailability, the pharmacokinetic parameters and the acute tolerance of the single viral inactivated concentrate (preparation A) were compared with that of the double viral inactivated one (preparation B). Fifteen patients with severe haemophilia A and positive for HAV Ab were enrolled in a double-blind cross-over study and injected with 32.

Myocardial fatty acid pattern in rats fed on an erucic acid enriched diet.

Individual lipid classes and their fatty acid pattern in myocardium of rats fed on a diet containing 10% erucic acid ethyl ester (cis-13-docosenoic acid ethyl ester) were investigated and compared to rats fed on a normal diet. Two groups of rats were treated for 10 consecutive days with the erucic acid ethyl ester diet and the standard diet, respectively. After extracting total lipids from the myocardium of the rats, the individual lipid classes and the percentage of fatty acids in phospholipids, free fatty acids, diglycerides and triglycerides were measured.

Effect of prolonged treatment with propionyl-L-carnitine on erucic acid-induced myocardial dysfunction in rats.

The aim of this study was to evaluate the ability of propionyl-L-carnitine to prevent cardiac damage induced by erucic acid. Rats were fed for 10 days with normal or 10% erucic acid-enriched diets with or without propionyl-L-carnitine intraperitoneally injected, (1 mM/kg daily, for 10 days). The erucic acid diet produced increases in triglycerides (from 5.

Misleading results in studying pharmacodynamic interaction with oral anticoagulant.

We described an experimental condition, in which the i.p. administration of rats of irritants produces a misleading increase of the anticoagulant effect of warfarin.