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Biomedical subjects

S Villa

Publications and source records attributed to S Villa.

At least 109 records · Page 6Linked to original sources
PubMed1979

Platelet aggregation and antithrombin III levels in diabetic children.

We studied platelet function and antithrombrin III levels in 30 insulin-dependent diabetic children with no clinically evident vascular complications. 9 were in-patients and 21 were out-patients. The disease had been discovered within the previous 10 years. 25 control subjects of comparable age and body weight were studied simultaneously. Template bleeding time, threshold concentrations of ADP or adrenaline required to induce irreversible platelet aggregation and plasma antiherparin activity (platelet factor 4) did not differ significantly in control and patient groups. In contrast, the immunological levels of plasma antithrombine III were significantly higher in the diabetic group. These results suggest that diabetic children, with no clinical signs of microanigopathy, show no laboratory changes suggesting increased platelet function. The unxpected increase in the antithrombin III level could reflect a very early defense mechanism against activation of the blood clotting system.

Adenosine Diphosphate↗
PubMed1978

Platelet aggregation: methodology and physiopathology.

The physiopathological role of platelet aggregation in some thromboembolic and atherosclerotic complications is strongly suggested on the basis of many indirect findings. The qualitative methodological approach to this problem generally used until recently is rapidly giving way to a quantitative, biochemical approach. Platelet aggregation, however, even if expressed in terms of nanomoles of a product obtained in a sophisticated reaction system, will continue to deceive investigators and clinicians who fail to view it in the adequate (although still uncertain) context of rheological and vascular interactions.

Animals↗
PubMed1977

Prostacyclin-like activity in rat vascular tissues. Fast, long-lasting inhibition by treatment with lysine acetylsalicylate.

Both arterial and venous tissues obtained from normal rats released prostacyclin (PGI2)-like activity, as marked by its potent inhibitory effect on platelet aggregation. Intraperitoneal or intravenous administration of a single dose of a soluble lysine salt of acetylsalicyclic acid (L-ASA, 1-400 mg/kg) resulted in abolition or substantial reduction of prostacyclin-like activity released from rat vasculature. The inhibitory effect of L-ASA was evident one minute after its i.v. administration to the animals, persisted for at least 24 hours and was still detectable (in venous tissues only) 168 hours later. Venous tissues were inhibited by doses of L-ASA as low as 1 mg/kg, whereas arterial tissues were not inhibited by doses of LA-ASA lower than 10 mg/kg. This difference may possibly be related to the lower prostacyclin-like activity shown by rat venous tissues compared to arterial ones. It is suggested that L-ASA or part of its molecule may bind to and inhibit cyclo-oxygenase in the blood vessel wall in a manner similar to the acetylation of platelt cyclo-oxygenase.

Animals↗
PubMed1977

Bioavailability and platelet aggregation inhibitory activity of solufenum. A comparison with ibuprofen.

Bioavailability and platelet aggregation inhibitory activity of the lysine salt of ibuprofen (solufenum) were compared with those of the parent molecule in 5 healthy male volunteers. The study had a randomized, cross-over design. The average peak plasma level and the area under the curve were higher when solufenum was administered orally as compared to the same preparation given i.m. or as compared to oral ibuprofen. However, the bioavailability of the 3 preparations studied was not significantly different. In contrast, the inhibitory effect on adrenaline-induced platelet aggregation appeared significantly different. In contrast, the inhibitory effect on adrenaline-induced platelet aggregation appeared significantly earlier after the administration of both solufenum than after ibuprofen. The clinical relevance of these findings is discussed.

Adult↗
PubMed1976

Effects of 6-aminochrysene on liver microsomal enzyme activity.

1. No transformation of 6-aminochrysene took place during its incubation with rat liver microsomes under oxygen or anaerobic conditions. 2. 6-Aminochrysene inhibited the hydroxylation of aniline, O-demethylation of p-nitroanisole, and N-demethylation of aminopyrine by rat liver microsomes. 3. Pre-treatment of rats with 6-aminochrysene markedly decreased the N-demethylation in vitro but significantly increased the hydroxylation and the O-demethylation. Similar effects were observed also with microsomal preparations from livers perfused with 6-aminochrysene.

Aminopyrine N-Demethylase↗
PubMed1976

6-Aminochrysene kinetics in isolated perfused liver.

1. New quantitative assays of 6-aminochrysene by spectrophotometric and g.l.c. methods and t.l.c. separation systems are described. 2. The decline in blood levels of the antitumoral agent 6-aminochrysene was due to its distribution rather than to metabolism to polar metabolites, during liver perfusion experiments. 3. No marked changes in kinetics of 6-aminochrysene were observed during perfusion of livers isolated both from normal and from Walker 256 carcinosarcoma-bearing rats.

Animals↗
PubMedDate not supplied

Expression of the T1 (CD5, p67) surface antigen in B-CLL and B-NHL and its correlation with other B-cell differentiation markers.

The T1 surface antigen (CD5,p67) expression on blood lymphocytes (PBL) and lymphoid cells from lymph node biopsies (LN) from 31 patients with B-cell chronic lymphocytic leukemia (B-CLL) and 79 with B non-Hodgkin lymphoma (B-NHL), was detected in 25 B-CLL (80 per cent) and in 11 B-NHL (13 per cent) belonging to the following histologic subtypes: lymphocytic of CLL type (DLWD) one case, lymphoplasmacytoid (DLWD) four cases, centrocytic (DLPD) five cases, immunoblastic (DH) one case. All B-CLL and the T1 + B-NHL were also tested with monoclonal antibodies against the Common Acute Lymphoblastic Leukemia Antigen, B cells (FMC7, FMC8, BA1, Y29-55), T cells (OKT11a), HLA-DR and HLA-DQ monomorphic determinants. All the B-CLL and the T1+ B-NHL were CALLA-, BA1+, Y29.55+. FMC7+ cells were detected in large numbers six B-CLL (three T1+ and three T1-) and in four centrocytic lymphomas. FMC8 reacted with 70 per cent of leukemias (where it stained 30 per cent of neoplastic cells) and with 8/9 T+ B-NHL. HLA-DR and HLA-DQ molecules were detected in 100 per cent and 90 per cent of cases respectively. In vitro treatment of HLA-DQ- or T1- B-CLL with phorbol ester TPA led to the expression of these antigens as well as of the receptors for Interleukin 2 and MLR3 activation antigen. Surface membrane Ig (SIg) was detected in 79 per cent of cases, its density measured by FACS analysis varied, even markedly, from case to case. Among the B-CLL, cells with high SIg content were either T1+ or T1- and more likely FMC7+. The SIg- cases were seven B-CLL (five T1+ and two T1-) and two B-NHL, in which, however, cytoplasmic IgM was detected. This study reveals the existence of four major B-CLL subgroups: T1- SIg-, T1+ SIg+, T1+ SIg+, T1- SIg+. It also indicates that the T1 antigen may be transitionally present during B-cell differentiation and that its expression may precede that of SIg as supported by the in vitro studies. In addition, the finding that some B-NHL are T1+ suggests that they derive similarly to the B-CLL from a common progenitor.

Antibodies, Monoclonal↗