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R del Carmine

Publications and source records attributed to R del Carmine.

14 recordsLinked to original sources
PubMed1992

A dual effect of some 5-HT3 receptor antagonists on cisplatin-induced emesis in the pigeon.

In the present study, the emetic effect of the anticancer drug cisplatin, and protective effects of 5-HT3 receptor antagonists against cisplatin emesis were investigated in the pigeon. The experimental setting involved the i.v. administration of drugs and subsequent observation of the percentage of vomiting animals and number of emetic episodes per vomiting animal over a period of 5 h. In some experiments, the 5-HT and 5-HIAA content in tissues was estimated by the HPLC technique. It was observed that cisplatin (2.5-10 mg/kg) is able to induce dose-dependent emesis in the pigeon. 5-HT3 receptor antagonists (500 micrograms/kg) afford partial protection against cisplatin emesis, although some of them, i.e. indolic derivatives and zacopride, display intrinsic emetic activity at doses of 50-500 micrograms/kg. A serotonergic mechanism appears to be involved in both cisplatin- and 5-HT3 receptor antagonist-induced emesis, since pretreatment with an inhibitor of 5-HT synthesis, para-chlorophenylalanine (300 mg/kg x 3 days), is able to hamper vomiting induced by either cisplatin or 5-HT3 receptor antagonists. It is concluded that the intrinsic emetic effects of 5-HT3 receptor antagonists in the pigeon provide pharmacological evidence of species differences in the properties of 5 HT3 receptors.

Animals↗
PubMed1988

Effects of the benzazepine SCH 23390 on prolactin release from isolated pituitary.

The benzazepine, SCH 23390 (10(-5) M), is able to block D2 anterior pituitary receptors and their interaction with a maximal concentration of dopamine (10(-7) M) in an experimental setting involving superfused pituitary slices and prolactin release by lactotrophs as a functional model of such receptors; this finding which correlates nicely with binding studies and drug-induced hyperprolactinaemia supports a SCH 23390 D1 dose-related selectivity; given at doses higher than those inducing behavioural changes, the compound may affect D2 receptor-driven functions, e.g. prolactin secretion.

Animals↗
PubMed1984

Phosphorylation at a tyrosine residue of lipomodulin in mitogen-stimulated murine thymocytes.

When murine thymocytes were stimulated by mitogens such as concanavalin A, the Ca2+ ionophore A23187, or 4 beta-phorbol 12-myristate 13-acetate, there was a marked increase of 32P incorporation into immunoprecipitable lipomodulin, a phospholipase inhibitory protein. These compounds enhanced 45Ca2+ influx into thymocytes, which, in turn, increased protein phosphorylation, probably by Ca2+- and phospholipid-dependent protein kinase (protein kinase C). Cyclic 8-bromo-AMP, an inhibitor of lymphocyte mitogenesis, blocked the mitogen-stimulated phosphorylation of lipomodulin, although it stimulated the protein phosphorylation via cyclic AMP-dependent kinase (protein kinase A). On electrophoresis, the hydrolysates of 32P-labeled lipomodulin showed a single radioactive spot, which comigrated with authentic phosphotyrosine. The partially purified middle-sized tumor antigen was able to phosphorylate lipomodulin after being phosphorylated by protein kinase C but not by the catalytic subunit of protein kinase A. Our findings suggest that the activity of a tyrosine-specific kinase, which phosphorylates lipomodulin in vivo as well as in vitro, is stimulated by protein kinase C and inhibited by protein kinase A.

Animals↗
PubMed1981

Presence of autoantibody for phospholipase inhibitory protein, lipomodulin, in patients with rheumatic diseases.

The activity of phospholipase inhibitory protein, lipomodulin, partially purified from rabbit neutrophils, was markedly decreased after treatment with sera from patients with rheumatic diseases such as systemic lupus erythematosus, rheumatoid arthritis, and dermatomyositis. The decrease of the protein's inhibitory activity on phospholipase A2 paralleled the amount of [35S]methionine-labeled lipomodulin precipitated by the sera. Absorption of patients' sera with anti-human IgM (mu chain) or protein A-agarose, but not with anti-human IgG (gamma chain), decreased their ability to decrease the activity of lipomodulin on phospholipase A2 or to precipitate the radioactive lipomodulin. The IgM fraction of patients' sera could precipitate [35S]methionine-labeled lipomodulin (40,000 daltons) which comigrated with highly purified lipomodulin on gel electrophoresis with sodium dodecyl sulfate. All of these observations suggest that the sera of many patients with rheumatic diseases contain autoantibody against lipomodulin. A monoclonal antibody against lipomodulin was also obtained. Stimulating human fibroblasts with bradykinin in the presence of monoclonal antilipomodulin antibody markedly enhanced arachidonic acid release due to the activation of phospholipase(s) in the intact cells, and this stimulatory effect was blocked by adding purified lipomodulin. These findings suggest that lipomodulin regulates the activity of phospholipase(s) on the cell surface and that autoantibodies against lipomodulin may play a role in certain symptoms of rheumatic diseases, especially by the formation of prostaglandins and other metabolites of arachidonic acid.

Animals↗
PubMed1975

Effect of dietary rapeseed oil on hepatic hexobarbital metabolism in mice.

The effect of dietary rapeseed oil (RSO) on hepatic hexobarbital metabolism has been studied in short-term experiments in mice by measuring both the activity of mixed function oxidase system in microsomal preparations in vitro and the in vivo hexobarbital-induced sleeping time. Moreover, the fatty acid pattern of liver tissue, with particular regard to erucic and gadoleic acids, was analyzed gas-chromatographically. The hexobarbital metabolism in young RSO-fed (RSO containing 52% of erucic acid and 7.4% of gadoleic acid; 50 cal% for 3 days) is lower by about 44% than in controls treated in the same way with peanut oil, independently of sex. RSO did not have a statistically significant effect of hexobarbital metabolism in adult animals of both sexes. As to the dose-response study, the prolongation of the hexobarbital-induced sleeping time in young male is statistically significant when fed with 30 cal% in RSO for 3 days, while it is not more statistically significant in mice fed 15 cal% in RSO. In RSO mice (50 cal%) erucic and gadoleic acid account both for about 10% of the total fatty acids in the liver tissue, while they are quite absent in controls. It causes a relative deficiency of linoleic and arachidonic acids, known to be essential for synthesis and maintenance of the membranes supporting hepatic microsomal enzymes responsible for the metabolism of some drugs.

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