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Biomedical subjects

P Boni

Publications and source records attributed to P Boni.

At least 55 records · Page 3Linked to original sources
PubMed1979

Lack of hypotensive and brain catecholamine depleting effects by erythro- and threo-alpha-methyl DOPS.

An investigation was carried out to ascertain whether erythro- and threo-alpha-methyl-dihydroxy-phenyl-serine were able of depleting cerebral and peripheral norepinephrine (NE) through their metabolization to alpha-mNE. The results show that the alpha-methyl-aminoacids were decarboxylated only at the periphery and that the threo-form caused depletion in cardiac NE. In any case, both isomers were unable to cross the blood-brain barrier leaving the cerebral NE unaffected. Consequently the use of alpha-mDOPS as alternative tool to alpha-mDOPA in the therapy for hypertension seems unlikely to occur. The results also provide evidence for differences in the pharmacokinetics of the two isomers.

Animals↗
PubMed1978

A rapid chromatographic method for quantitation of high molecular weight fibrinogen derivatives in plasma.

High molecular weight fibrinogen derivatives were precipitated from 3 ml of plasma by 0.88 M ammonium sulphate. The resuspended precipitate was analyzed by chromatography on a 2.5 x 30 cm glass bead Bio-Gel 5 M column by using a flow rate of 60 cm/hr and continuous effluent monitoring at O. D. 280 nm. Complete elution of fibrinogen occurred in 50 min. Elution profile was handled according to the chromatographic plate theory analysis. Results obtained by our method were not significantly different from those obtained by conventional chromatography.

Alanine↗
PubMed1977

Circulating anticoagulant against factor XI and thrombocytopenia with platelet aggregation inhibition in systemic lupus erythematosus.

In a patient with systemic lupus erythematosus, anticoagulant activity directed against factor XI was found together with thrombocytopenia. In the serum globulin fraction, antiplatelet antibodies and an activity-inhibiting platelet aggregation could also be found. A possible correlation between the inhibition of platelet aggregation and the anticoagulant activity directed against factor XI is discussed.

Adult↗
PubMed1976

Platelet aggregation by thimerosal: role of ADP and SH groups.

Thimerosal, a sulphydryl inhibitor, induces aggregation of normal platelet rich plasma over a wide range of concentrations. Low doses induce a monophasic response preceded by a lag phase, high doses produce an immediate biphasic response. Thimerosal induces platelet aggregation through its binding by sulphydryl groups. Thimerosal induced aggregation is not mediated by ADP, it is not influenced by fibrinogen, von Willebrand factor, calcium, and magnesium ions of the medium. Thimerosal induced platelet aggregation is normal in patients affected by thrombocytopathia (defect of ADP release) but not in patients affected by Glanzmann's thrombasthenia. Mercaptopropionglycine, a substance which tends to preserve SH groups, inhibits platelet aggregation induced by thimerosal, thrombin, collagen, and ADP. A mechanism is proposed for thimerosal induced aggregation and the role of SH groups also in ADP, thrombin and collagen induced aggregation is indicated.

Adenosine Diphosphate↗