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T Uberti

Publications and source records attributed to T Uberti.

8 recordsLinked to original sources
PubMed1994

Platelet-derived growth factor (PDGF) in patients with different degrees of chronic arterial obstructive disease.

Platelet activation and platelet-derived growth factor (PDGF) play a pivotal role in the pathogenesis of atherosclerosis. Evidence has been accumulating that in the evolution of chronic arterial obstructive disease (CAOD) platelets are also crucially important. The aim of the present study was, therefore, to assess plasma levels of PDGF in patients with different degrees of CAOD according to Fontaine. Twenty patients (17 men, 3 women, mean age sixty-eight +/- seven years) with intermittent claudication (Fontaine stage II) entered the study and their PDGF levels were assessed by radioimmunoassay. Ten additional patients (7 men, 3 women, mean age seventy-three +/- seven years) with more severe CAOD (leg pain at rest/skin ulcers) were also studied. Ten healthy subjects (6 men, 4 women, mean age fifty-four +/- six years) comprised the control group. Patients in stage II were reinvestigated after sixty days of a "training" procedure. Patients with both intermittent claudication and more severe disease had higher levels of PDGF than controls (controls 165.9 +/- 119.1 pg/mL; Fontaine stage II 403.5 +/- 218.4; Fontaine stage III/IV 578.1 +/- 637.2: ANOVA P = 0.04) with no difference between the two groups of patients. After the training period, PDGF levels were significantly higher than at baseline (863.7 +/- 819.6 pg/mL vs 403.5 +/- 218.4) but without significant improvement of physical performance. The elevation of PDGF levels in blood from CAOD patients could be the result of marked platelet activation due to interaction with a widely damaged peripheral vasculature. The same was not true for coronary heart disease, in which normal values of PDGF in venous blood were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

t-PA, PAI, and protein C before and after vascular occlusion of the upper limb in patients with Raynaud's phenomenon.

Tissue plasminogen activator (t-PA) and its inhibitor (PAI) were assessed in venous blood drawn before and after venous occlusion (bvo, avo) for 33 patients with Raynaud's phenomenon (RP), 14 with primary RP (PRP), 9 with suspected secondary RP (SSRP), and 10 with definite collagen disease and secondary RP (SRP). There were significant differences in PAI values avo between PRP (and controls), SSRP, and SRP. PAI activity decreased significantly avo only in controls and in PRP, and there was significant t-PA antigen elevation avo in the same groups. In addition, since PAI is neutralized by activated protein C (PC), both PC antigen and PC activity were assessed avo and bvo. PC Ag remained unchanged in all groups, with PC activity significantly lower than controls in SRP and SSRP. Finally the authors looked for interference of anticardiolipin antibodies (ACA) and lupus-like anticoagulant (LAC) with the PC system in collagen disease-associated RP. Specific IgG ACA were found in only 1 patient with SRP. In conclusion, there is an endothelial derangement, involving t-PA release and PAI, in SSRP and SRP patients. The reduced PC activity in these latter groups appears to be due to increased PAI influence rather than to ACA/LAC.

Adult↗
PubMed1991

Antiaggregating therapy in acute myocardial infarction.

The clinical benefit of aspirin in the acute phase of myocardial infarction is dramatically suggested by the results of the ISIS-2 trial. However, the time course of pathophysiological events that lead to such a determining involvement of platelets still appears uncertain and further study is needed to single out exactly how early and how long antiplatelet drugs should be given, since there is a risk of bleeding complications due to the combination of the different antithrombotic therapies. Thrombolytic agents and heparin are in fact widely used for patients with acute myocardial infarction, even if the optimal schedule of treatment, including anti-aggregating therapy, is not yet firmly established. To avoid rethrombosis and to enhance the efficacy of coronary thrombolysis, thus reducing early mortality, several newer antiplatelet agents other than aspirin, such as antibodies against the platelet receptor of adhesive proteins, the glycoprotein IIb/IIIa and the RGD peptides, are currently under investigation.

Aspirin↗
PubMed1987

Ticlopidine administration to patients does not inhibit the ability of their monocytes to form rosettes and to phagocytize erythrocytes in vitro.

Inhibition of monocyte function is known to have important clinical consequences and to be present in a variety of diseases: Accordingly we evaluated the effect of Ticlopidine, a powerful and widely employed inhibitor of platelet aggregation, on the capacity of peripheral blood monocytes to ingest IgG-coated erythrocytes. Our results show that in vivo administration of this drug has no effect on monocyte phagocytosis, when tested with an in vitro assay. This finding suggests that Ticlopidine can be safely used in patients with depressed monocyte function and in those in whom an impairment of monocyte phagocytosis could lead to a deterioration of the clinical picture.

Aged↗
PubMed1985

Bacillus subtilis selectively stimulates the synthesis of membrane bound and secreted IgA.

Peripheral blood lymphocyte subpopulations and IgA production in vitro have been studied in 30 elderly subjects. Fifteen patients were treated with Bacillus subtilis (Enterogermina, Midy) and 15 with a placebo preparation. At the end of the treatment, a significant increase was noticed in lymphocytes bearing membrane IgA and Ia+ cells in the group treated with Bacillus subtilis, but not in the controls. Similarly, a significantly enhanced spontaneous production of IgA in vitro was seen in the treated subjects. The relevance of these findings to the understanding of the mode of action of Bacillus subtilis and its usefulness in different immunodeficiency states is discussed.

Aged↗
PubMedDate not supplied

Effects of ticlopidine and indobufen on platelet aggregation induced by A23187 and adrenaline in the presence of different anticoagulants.

As Ca2+ is known to play a fundamental role in platelet function, the effect of combining two platelet aggregating agents (adrenaline and the ionophore A23187) with different effects on Ca2+ was studied at levels subthreshold for aggregation using platelet-rich plasma from eight atherosclerotic patients. Adrenaline lowered the A23187 threshold required to induce aggregation. The effects of treating patients with the antiplatelet agents, indobufen and ticlopidine, on A23187 and adrenaline induced aggregation of platelets prepared in hirudin or sodium citrate was also evaluated. Aggregation was also studied using platelets resuspended in Ca2(+)-free and Ca2(+)-enriched Tyrode solution. Before treatment hirudin treated platelet-rich plasma, which has physiological extraplatelet Ca2+ levels, was more sensitive to A23187 and adrenaline than was citrated platelet-rich plasma, which has suppressed Ca2+ levels. Ticlopidine significantly raised the concentration of A23187 required to induce aggregation in citrated but not hirudin treated platelet-rich plasma. Indobufen did not significantly affect A23187 induced aggregation. Ticlopidine acts by inhibiting the glycoprotein IIb-IIIa complex on the platelet membranes. Low levels of extracellular Ca2+ and ticlopdine may act synergistically to reduce the aggregatory response of stimulated platelets.

Aged↗