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Biomedical subjects

F Balsano

Publications and source records attributed to F Balsano.

176 records · Page 10Linked to original sources
PubMedDate not supplied

[Changes in the atrial natriuretic factor and the renin-angiotensin-aldosterone axis induced by maximum exertion in subjects with a recent myocardial infarct].

To examine the effect of exercise-induced myocardial ischemia (EIMI) on atrial natriuretic factor (ANF), plasma renin activity (PRA) and aldosterone (PA), a maximal exercise test in 12 patients with recent acute myocardial infarction (AM) was performed. ANF, PRA and PA were measured by radioimmunoassay at baseline, peak-exercise and at 15 min after recovery. Four patients developed EIMI (group I) and 8 patients did not (group II). ANF increased in all patients from baseline to peak-exercise (27.7 +/- 9.5 pg/mL vs 92.7 +/- 26.7 pg/mL, p less than 0.0005) and it was still elevated 15 min after recovery. Baseline ANF was similar in both groups while at peak-exercise it was higher in group. I than in group II (112 +/- 15 pg/mL vs 82 +/- 26 pg/mL p less than 0.05). After 15 min of recovery, ANF was higher in group I than in group II (67 +/- 20 pg/mL vs 32 +/- 10 pg/mL, p less than 0.01), resulting higher than at baseline only in group I (p less than 0.05). PRA and PA also increased during exercise but their values rose more slowly and were the same in both groups. Thus, ANF, PRA and PA increase during exercise in patients after AMI, and EIMI is associated with higher ANF plasma levels.

Adult↗
PubMedDate not supplied

Dipyridamole potentiates the inhibition of platelet aggregation by aspirin (in human platelet rich plasma and whole blood).

This study investigates the influence of dipyridamole on platelet aggregation as evaluated by a single agonist or a pair of agonists in human platelet rich plasma and whole blood. Dipyridamole up to 30 microM was not found to influence the platelet aggregation of platelet rich plasma or whole blood; aspirin (100 microM), on the contrary, did inhibit platelet aggregation. The inhibition of platelet aggregation by aspirin could be reversed by using high concentrations of agonists or pairs of agonists. In this model dipyridamole inhibited platelet aggregation in both platelet rich plasma and whole blood in a dose-dependent fashion. Thromboxane A2 was less than 10% of controls in aspirin-treated PRP stimulated with low or high concentrations of collagen or with a pair of agonists. This study suggests that dipyridamole has direct antiplatelet activity in platelet rich plasma and whole blood when the cyclooxygenase pathway is blocked by aspirin.

Adult↗
PubMedDate not supplied

Clinical use of antiplatelet therapy.

The authors report the principal clinical models in which inhibitors of platelet aggregation were used to prevent the clinical complications of atherosclerosis. The models at risk which were considered include unstable angina, TIAs, myocardial infarction and atherosclerotic vascular disease of the lower limbs. Overall, the studies suggest the value of this therapy for the prevention of cardiovascular accidents. TIAs, unstable angina and myocardial infarction are the models which provide the best evidence for this; however, the effectiveness of this therapy in peripheral vascular disease, while showing positive results, needs to confirmed by further clinical studies. Lastly, therapy with inhibitors of platelet aggregation has been shown to be useful in the prevention of aortocoronary bypass occlusion; however, its efficacy has been shown only when therapy is initiated early.

Animals↗
PubMedDate not supplied

Anticardiolipin antibodies possess anticoagulant activity which is blocked by a monoclonal antibody against a cross reacting idiotype of antiphospholipid antibodies.

Anticardiolipin (aCL) antibodies were isolated from systemic lupus erythematosus serum using cardiolipin liposomes. In a sensitized activated partial thromboplastin time (aPTT) system, low concentrations of aCL were found to significantly prolong aPTT in a dose-dependent fashion. This effect was abolished by adding phosphatidylserine/phosphatidylcholine liposomes to the aPTT system, and could be significantly reduced by a monoclonal antibody against a cross-reacting idiotype of antiphospholipid antibodies (MoAb 5.2) previously incubated with aCL. These results suggest that the anticoagulant properties of aCL are mediated by an interaction with phospholipid components of the coagulation system. The functional block of this activity using monoclonal MoAb 5.2 antibody could be useful for investigating the mechanisms by which aCL is associated with clinical thrombosis.

Antibodies, Anti-Idiotypic↗
PubMedDate not supplied

Autoimmune chronic liver disease as a model of human autoimmunity.

Although clonal deletion and clonal energy have been demonstrated in transgenic mice, the findings that autoreactive B or T cells are present in healthy subjects suggest that they are not the sole mechanisms of tolerance. As regards helper T lymphocytes, tolerance to self-antigens can arise by preventing class II MHC expression on non-lymphoid cells and autoantigen presentation to helper T cells initiating the autoimmune response. Autoimmune chronic active hepatitis (CAH) seems to be a good model of self-tolerance bypass. Hepatocytes are able to express class II molecules and can perform accessory cell functions with respect to T cell clones generated from lymphocytes infiltrating the liver in autoimmune CAH patients. The class II antigen expression on hepatocytes may be modulated by IFN-gamma released by infiltrating T lymphocytes; thus, the activated liver cells can present autoantigens to autoreactive T cell clones. On the other hand, these findings may occur only when the upregulation of IFN-gamma or other lymphokines permits the expression of rare class II antigens on hepatocytes capable of binding particular residues of a liver-autoantigen which are recognized by specific autoreactive T cell clones binding different residues on the same epitope.

Autoimmune Diseases↗
PubMedDate not supplied

Fate of the patient with chronic leg ischaemia. A review article.

Much has been published on the surgical treatment of leg ischaemia but relatively little is known about the incidence of claudication and the fate of the majority of patients presenting with chronic leg ischaemia who never come to surgery. A review of the available literature suggests the following conclusions: (1) about 1.5% of men under 49 and 5% of men over 50 will develop symptoms of intermittent claudication. The incidence of asymptomatic arterial disease is much higher; (2) the incidence of claudication in women is only slightly less, but the local disease follows a more benign course; (3) compared to the general population of comparable age the mortality of men presenting with chronic leg ischaemia is two to three times higher after 5 years; (4) about 50% of deaths will be due to myocardial ischaemia, 15% to stroke and 10% to vascular disease in the abdomen. In only 25% will the principal cause of death be unconnected with the circulation; (5) there is virtually no reliable information available at the moment on the incidence of non-fatal myocardial infarction or stroke in these patients.

Arteriosclerosis↗
PubMedDate not supplied

Blood lipid abnormalities in patients suffering from peripheral vascular disease.

Blood lipid profile was investigated in 40 patients suffering from peripheral vascular disease (PVD). The most frequent abnormality was the increase of cholesterol and triglycerides. HDL-cholesterol and the subfractions HDL2 and HDL3 were decreased but not significantly. Cholesterol/HDL-cholesterol ratio was significantly increased suggesting an abnormal cholesterol distribution on lipoprotein fractions. Apolipoproteins AI and AII were within normal range while apolipoproteins B, CII, CIII, and E were significantly increased. This study provide further findings on the blood lipid abnormalities in patients affected by PVD.

Aged↗
PubMedDate not supplied

Class II MHC antigen expression on epithelial cells of salivary glands from patients with Sjögren's syndrome.

Class II MHC molecules are two-chain glycoproteins normally expressed only on the membrane of cells involved in the immune response. These molecules are restriction elements for helper T cells. Using indirect immunofluorescence on cryostat sections of biopsied salivary glands we have demonstrated epithelial expression of class II antigens in patients with Sjögren's syndrome. The HLA DR+ epithelial cells were seen in close proximity to lymphocyte infiltrates. The finding that class II molecules are also expressed in salivary glands without focal lymphocytic infiltrates suggests a "modulation" as opposed to "induction" of HLA DR antigens on epithelial cells in Sjögren's syndrome, the distinction being related to the enhancement of low levels of expressions vs. de novo synthesis.

Adult↗
PubMedDate not supplied

[Primary hyperaldosteronism caused by monolateral adrenal hyperplasia].

We have reported two patients with unilateral adrenal hyperplasia as a rare cause of primary aldosteronism, and discussed the literature on this subject. When diagnosed by NMR-CT imaging and selective sampling from adrenal veins, the treatment of this disorder appears to be surgical. Whether its pathogenesis is related to the more common varieties of primary aldosteronism is open to speculation according to metabolic findings.

Adrenal Glands↗
PubMedDate not supplied

[Sodium-modulating hormones and the pressor response to sodium chloride in essential arterial hypertension].

Some predictive markers for NaCl sensitivity, related to the red blood cell membrane or to circulating proteins, have already been described in human essential hypertension. The present study was planned to investigate whether or not some hormones produced by the kidney or acting at the kidney level could be used as new markers for NaCl sensitivity. The study was conducted in 28 not previously treated outpatients affected by uncomplicated mild to moderate essential hypertension. After 15 days on a normal NaCl diet, plasma renin activity (PRA), plasma atrial natriuretic peptide (ANP), and the urinary excretion of active kallikrein were evaluated. The sensitivity of blood pressure to changes in NaCl intake was then assessed in all patients, according to a randomized double blind cross-over design. Each patient was assigned to a high (240 mmol of NaCl/day for 15 days) or low (40 mmol of NaCl/day for 15 days) NaCl intake. During the assessment of NaCl sensitivity, the double blindness was achieved by the use of capsules containing either NaCl or placebo. Fifteen patients (11 males and 4 females) resulted as NaCl-sensitive, while 13 patients (8 males and 5 females) were classified as NaCl-resistant. Our results indicate that PRA levels were significantly lower in the NaCl-sensitive group than in the NaCl-resistant one (0.108 +/- 0.05 ng/L/s vs 0.247 +/- 0.16 ng/L/s, p < 0.007), in the presence of raised levels of plasma ANP in NaCl-sensitive hypertensives (18.08 +/- 4.61 fmol/mL vs 12.45 +/- 3.77 fmol/mL, p < 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Geographical clustering of scleroderma in a rural area in the province of Rome.

A geographical cluster of scleroderma and scleroderma-related features was identified in a rural area in the province of Rome. Two patients with scleroderma, three with CREST syndrome and one with eosinophilic fasciitis were living in a village where the total population included 572 persons of voting age. No kindred relationships were demonstrable among these patients. Clinical features of scleroderma such as Raynaud's phenomenon, bilateral hand edema, and digital scars were detected in an additional 10 cases. A group of apparently healthy subjects with scleroderma-related serological abnormalities (circulating antinuclear and anticentriole autoantibodies) was also identified in the village. No disease-associated HLA antigen in the patients nor genetic differences between patients and healthy subjects living in the same village were detected by HLA typing. Some still unidentified environmental factors acting on genetically predisposed subjects may be responsible for the clustering of the disease seen in this study.

Adolescent↗