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Biomedical subjects

M Gentile

Publications and source records attributed to M Gentile.

At least 163 records · Page 9Linked to original sources
PubMed1976

A comparison of short and long haemodialysis.

Two groups of patients treated by short (Milan) and long (Newcastle) haemodialysis were compared for incidence of symptoms and biochemical control. Short dialysis corrected urea and creatinine as well but control of potassium and phosphate were similar. The only apparent penalties to be paid by short dialysis patients were a higher incidence of itching, tingling or numbness, impairment of vibratory sense and difficulty in controlling blood pressure. The short dialysis group had higher haemoglobin and less dyspnoea, muscle weakness and dizziness after dialysis.

Adult↗
PubMed1975

A multicenter double blind clinical trial on 3.4.5-trimethoxybenzoiyl-epsilon-aminocaproic acid (C-3) in acute myocardial infarction.

186 out of 391 patients with acute myocardial infarction were treated with C-3 and 205 with placebo in a multicenter, double-blind clinical trial. Ensuing complications were treated in the same way in both groups. C-3 was injected i.v. slowly at the dose of 2 g statim plus 6 g by continuous drip infusion over 24 hrs for 5 days. During treatment, clinical progress was influenced only in regard to cardiac failure since in the C-3 group the improvement was more significant than in the placebo one (P less than 0.0025). Mortality rates were 8.1% and 11.2% for the C-3 and placebo groups, respectively. The difference in mortality was significant (P less than 0.05) for patients treated with C-3 for more than 24 hours. Mortality in male patients treated with C-3 for more than 12 hours was significantly lower (P less than 0.025). In patients less than 60 years old mortality rate was significantly lower (P less than 0.05) and was more so in patients receiving C-3 for more than 12 hours (P less than 0.025). Mortality due to complications was lower in the C-3 group, with arrhythmias (9.8% vs 14.2%), cardiogenic shock (69.2% vs 75%), and cardiac failure (9% vs 19.4%). Results agree with the hypothesis that C-3 may be effective in acute myocardial infarction by improving the action of traditional antiarrhythmic drugs, and augmenting myocardial contraction energy.

Acute Disease↗
PubMedDate not supplied

Endoscopic ultrasound localization of a solitary insulinoma of pancreatic tail misdiagnosed as epilepsy: case report.

A 17-year-old female patient with features of epilepsy was treated with valproic acid. Two years later, hypoglycemia and hyperinsulinemia appeared. Transabdominal ultrasonography, spiral computed tomography, and indium-111 Octreoscan were performed without positive results. Endoscopic ultrasonography identified an oval tumor in the pancreatic tail with a color Doppler hypervascular pattern. Surgical enucleation decreased levels of insulin and C-peptide within 20 min, and the patient became free of symptoms and medications.

Adolescent↗
PubMedDate not supplied

The aminobisphosphonate alendronate inhibits bone loss induced by thyroid hormone in the rat. Comparison between effects on tibiae and vertebrae.

The aims of this study were to develop a rat model of hyperthyroidism and to determine the efficacy of alendronate in the prevention of thyroid hormone-induced bone loss. Ten week-old Sprague-Dawley rats injected with thyroxine 250 micrograms/kg/day (+T4) or vehicle (-T4) were treated with alendronate (+ALN) or vehicle (-ALN) orally 0.5 mg/kg/day. After 3 weeks of treatment histomorphometric parameters of cancellous bone remodeling were assessed in the proximal tibia and in the first lumbar vertebra. In the secondary spongiosa of the tibia T4 treatment caused significant bone loss, associated with increased bone turnover; trabecular bone volume, trabecular thickness and trabecular number were significantly decreased. Osteoid and osteoclast surfaces increased in +T4/-ALN as compared to control. Alendronate prevented the increase in bone turnover and increased bone volume above control values without interfering with the recruitment of osteoclasts. These changes were not apparent in the vertebra. It is concluded that excess thyroid hormone in the rat induces high turnover bone loss in the tibia which can be prevented by alendronate through an inhibition of osteoclastic activity. The lack of effects of thyroid hormone on the vertebra may be ascribed to a lower rate of basal bone turnover at that site.

Alendronate↗
PubMedDate not supplied

Effects of IFN alpha on late stages of HIV-1 replication cycle.

IFN alpha causes a modest reduction of HIV-1 expression in chronically infected monocytoid U937 cells. However, the ratio between cell-associated and shed viral p24 antigen is altered, being the cell-associated fraction dose-dependently enhanced by IFN. Furthermore, a significant decrease of infectivity of both cell-associated and shed material is observed. Transmission electron microscopy of IFN-treated cells revealed virus assembly being strongly inhibited, with the production of morphologically altered (tear-drop shaped) virus particles. Proteolytic processing of gag proteins appeared to be normal in IFN-treated cultures. However, virions shed from IFN-treated cells showed a markedly reduced incorporation of virus-specific gp120 and cell-derived ICAM-1 by the virus envelope. Additionally, these particles showed a significantly decreased ability to become bound to CD4+ target cells, accounting for, at least in part, the observed decrease of infectivity. Taken together, the data suggest that, in chronically infected cells, IFN alpha can affect late stages of HIV-1 replication, by inhibiting virus assembly and release, and by reducing the infectivity of shed virions. The latter effect seems to be due, at least in part, to altered incorporation of surface glycoproteins and defective particle formation. The relationship between impaired gp120 incorporation and altered morphogenesis of HIV-1 virions is under investigation.

Antiviral Agents↗
PubMedDate not supplied

Histamine-induced activation of human lung macrophages.

BACKGROUND: Histamine plays a central role in the pathogenesis of allergic and inflammatory diseases by modulating vascular and airway responses. Increasing evidence suggests that histamine also regulates the function of inflammatory and immune cells. Macrophages are primarily involved in inflammatory diseases of the lung. We explored the ability of low concentrations of histamine to induce the release of proinflammatory mediators from human lung macrophages. METHODS: Macrophages purified (> 95%) from lung parenchyma by Percoll density gradients and adherence to polystyrene dishes were incubated (37 degrees C, 2-24 h) with histamine (10(-9)-10(-6) M). At the end of incubation, the release of beta-glucuronidase and IL-6 was determined. RESULTS: Histamine induced a concentration-dependent release of beta-glucuronidase and IL-6 with a maximum release after 2 and 6 h of incubation, respectively. Exocytosis induced by histamine was noncytotoxic and was Ca(2+)- and temperature-dependent. The effect of histamine was inhibited by the H(1) receptor antagonist fexofenadine but not by the H(2) antagonist ranitidine. CONCLUSIONS: These data indicate that histamine is an effective stimulus for exocytosis and cytokine production from human lung macrophages. These effects are inhibited by pharmacological concentrations of fexofenadine. Our results suggest that histamine may contribute to the long-term evolution of lung inflammation and tissue remodelling in allergic diseases by modulating the production of proinflammatory and immunoregulatory mediators by macrophages.

Cells, Cultured↗