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Biomedical subjects

A Corsini

Publications and source records attributed to A Corsini.

At least 109 records · Page 6Linked to original sources

In vitro inhibition of rat arterial smooth muscle cell growth by extractive sulfated mucopolysaccharides.

The effect of a sulfated mucopolysaccharide mixture of known composition, extracted from pig duodenum, was studied on the proliferation of rat arterial smooth muscle cells cultured from rat aorta. Cell growth, stimulated by fetal calf serum, was monitored by direct cell count and by determination of the mitotic index. The extractive mixture was studied in comparison with commercial heparin, with heparin with different electrophoretic mobilities in barium acetate and with dermatan and heparan sulfates. Heparins and the extractive mucopolysaccharide mixture inhibited cell growth measured at various time intervals, and in their presence the proliferation of smooth muscle cells plateaued at lower cell densities. Dermatan and heparan sulfates were either inactive or significantly less effective than the other mucopolysaccharides. A short preincubation (3 h) of smooth muscle cells with the extractive mixture, followed by incubation with the growing medium with no mucopolysaccharides added, slowed the cell growing rate, suggesting an interaction of the mixture components with the cell surface.

Animals↗

Nonprotein sulfhydryls as possible components of the protective effect of rosaprostol on the rat gastric mucosa.

Experiments were designed to examine the possibility that nonprotein sulfhydryl groups of the gastric mucosa could participate in the protection of rat gastric mucosa by rosaprostol (the Na salt of 9-hydroxy-8,12 trans-19,20-bis-nor-prostanoic acid). Gastric mucosal lesions and the content of nonprotein sulfhydryls were evaluated after orally administered absolute ethanol. Pretreatment with rosaprostol by gavage prevented gastric lesions and reduced or prevented the decrease of mucosal nonprotein thiols. N-ethylmaleimide, a sulfhydryl blocker, worsened the ethanol-induced gastric lesions and lowered further the non protein thiols. Both variables were improved by the PG analogue and by PGE2. These results suggest a possible role of endogenous nonprotein sulfhydryl groups in the gastric protective effect of rosaprostol.

Animals↗

Preconcentration of cadmium, chromium, copper and lead in drinking water on the polyacrylic ester resin, XAD-7.

The conditions (e.g. pH, resin, particle size, foreign ions) affecting the uptake of Cd(II), Cr(III), Cu(II) and Pb(II) from aqueous solution by the SM-7 (also called XAD-7) resin, were studied. Based on these studies, a two-column method was developed to overcome the effect of complexation by humic substances. The method was successfully tested with the NBS multielement water standard, SRM 1643a, and was subsequently applied to enrich Cd(II), Cr(III), Cu(II) and Pb(II) in 15 drinking water samples from Hamilton, Ontario. The metals were determined using graphite furnace atomic absorption spectrometry. The results for the drinking water samples showed that leaching of copper and lead occurred from the distribution system.

Acrylic Resins↗

Differential effects of in vitro ethanol on prostaglandin E1-sensitive adenylate cyclase from smooth muscle cells and platelets.

In membranes of smooth muscle cells cultured from rabbit mesenteric artery, ethanol dose-dependently activates adenylate cyclase, both basal and PGE1- or GPP(NH)P-sensitive. The alcohol increases the maximal stimulation induced by PGE1 and GPP(NH)P, without greatly affecting their potency. The arrhenius plot displays a discontinuity point, which is only slightly lowered by ethanol. On the contrary, in membranes from human platelets ethanol inhibits basal, GPP(NH)P- and PGE1-sensitive adenylate cyclase, without modification of the prostaglandin or guanine nucleotide potency. The break point present in the Arrhenius plots is definitely lowered by the alcohol. In addition, ethanol decreases the thermostability of the enzyme. Neither in myocytes nor in platelets does ethanol affect the activation energy of the reaction. The data suggest that ethanol probably interacts directly with the membrane proteins, and that its effect is not mediated only through a perturbation of membrane lipid fluidity.

Adenylyl Cyclases↗

6-Keto-prostaglandin E1-sensitive adenylate cyclase and binding sites in membranes from platelets and cultured smooth muscle cells.

6-keto-PGE1 elicits the same biological effects as PGI2 in human platelets and in rabbit aorta and mesenteric artery, being, however, less potent. We report here that 6-keto-PGE1 dose-dependently stimulates adenylate cyclase activity in membranes of human platelets and cultured myocytes from rabbit aorta and mesenteric artery. The extent of stimulation of the enzyme by 6-keto-PGE1 is the same as elicited by PGI2, while the apparent affinity is lower than that of prostacyclin, both in platelets and in vascular smooth muscle cells. At the level of platelet membranes, 6-keto-PGE1 interacts with the binding sites labelled by PGI2. However, in platelets as well as in mesenteric artery myocytes, 6-keto-PGE1 interacts with only one class of sites as demonstrated either by binding or by adenylate cyclase studies, whereas PGI2 in the same conditions recognizes two different classes.

Adenylyl Cyclases↗

Experimental studies on the hypolipidemic activity of chloridarol.

The efficacy of chloridarol (2-benzofuryl-p-chlorophenyl carbinol) as hypolipidemic agent was evaluated in rats and rabbits. In normolipidemic rats chloridarol, at doses ranging from 50 to 200 mg/kg/day, decreased plasma triglycerides without affecting cholesterolemia and fast- or norepinephrine-induced lipolysis. The drug proved effective in reducing fructose-induced hypertriglyceridemia and dietary hypercholesterolemia in rats; in the latter model chloridarol significantly raised both the HDL cholesterol and the HDL/VLDL + LDL cholesterol ratio. In hyperlipidemic rabbits the drug had no effect on plasma cholesterol, but it lowered triglyceridemia. The action of chloridarol on rat liver ultrastructure was also investigated. Treatment for one month induced peroxisome proliferation, less marked, however, than that elicited by clofibrate; after a prolonged chloridarol treatment (9 months), this effect had almost completely disappeared and the ultrastructure of the hepatocytes was close to that of controls.

Animals↗

Solid-phase radioimmunoassay with protein-A-bearing Staphylococcus aureus cells used to assay a protein (ferritin) and a hapten (digoxin).

We compared use of protein-A-containing Staphylococcus aureus bacteria with conventional ammonium sulfate precipitation and second-antibody methods of separating bound and free antigen in the radioimmunoassay of a hapten (digoxin) and protein (ferritin) in human sera. In each case, values obtained with the heat-killed, formalin-fixed bacteria correlated well with those found by established methods. No matrix effects were detected in either hapten or protein measurements. Because of the affinity of S. aureus for rabbit IgG, rabbit antisera could be used with a small number of bacteria to detect antigen in the presence of 50-fold excess human IgG. The availability of S. aureus and ease of handling make this reagent a rapid, economical alternative of general applicability in radioimmunoassay.

Digoxin↗