Search PubMed⌕ Search

Biomedical subjects

A Melis

Publications and source records attributed to A Melis.

79 records · Page 5Linked to original sources
PubMedDate not supplied

Quenching of chlorophyll fluorescence and photochemical activity of chloroplasts at low temperature.

Fluorescence kinetics and emission spectra of pea and spinach chloroplasts were studied between 294 and 4.2 K. In the presence of MgCl2 the fluorescence-induction curves were sigmoidal between 294 and 180 K but they lost their inflection points at lower temperature. In the absence as well as in the presence of Mg2+ ions, analysis of the kinetics of the area over the induction curve revealed two different components, indicating the existence of two different types of reaction centres at all temperatures. The 'rate constants' for these centres were nearly independent of temperature between 294 and 200 K, but showed a sharp decrease on further cooling. Emission spectra at low temperature showed the previously observed bands at 685, 695 and 735 nm. All three bands showed a considerable increase on cooling between 180 and 4.2 K, but with different temperature-dependence. The amplitude of the 695 band became constant below about 50 K, whereas the 685 emission increased markedly in this region. The relative proportion of the socalled variable fluorescence was almost the same at 685 and 695 nm, both at 80 and at 5 K. The data are discussed in terms of changes of energy-transfer rates on cooling.

Chlorophyll↗
PubMedDate not supplied

Tumour necrosis factor alpha and cellular proliferation in primary biliary cirrhosis.

AIMS: 1) To evaluate serum levels and tissue expression of Tumour necrosis factor alpha in primary biliary cirrhosis: 2) to correlate serum tumour necrosis factor alpha levels and cellular proliferation with the severity and prognosis of liver disease. METHODS: Twenty-nine primary biliary cirrhosis patients (6 stage I, 8 II, 8 III, and 7 IV) entered the study. Serum tumour necrosis factor alpha was measured by EIA (Innogenetics, Antwerp, Belgium). Tissue tumour necrosis factor alpha and Ki-67 were tested by indirect immunoperoxidase staining on liver sections. RESULTS: Serum tumour necrosis factor alpha increased with the severity of histological stage (from 10.8 +/- 11 pg/ml in stage II to 17.1 +/- 10 in stage III and 22.8 +/- 8.7 in stage IV, p < 0.036). A positive correlation was also found between tumour necrosis factor alpha serum levels and the Mayo score (p < 0.05). A weak and sporadic expression of tumour necrosis factor alpha was observed in the inflammatory infiltrate around the bile ducts. Tissue Ki-67 (expressed as the labelling index in the hepatocellular nuclei) was evaluated in all stages of the disease (1.09 +/- 0.6% in stage I, 1.14 +/- 0.6% in stage II, 2.11 +/- 1.9% in stage III, and 2.67 +/- 2.8% in stage IV; the labelling index was significantly lower in early stages (I/II) than in late stages (III/IV), p < 0.05. A strong correlation between Ki-67 and the Mayo score was observed (p < 0.0005). CONCLUSIONS: 1) tumour necrosis factor alpha production seems related to the severity and the prognosis of primary biliary cirrhosis; 2) liver mononuclear cells in the inflammatory infiltrate do not seem to be the major site of tumour necrosis factor alpha release; 3) cellular proliferation is correlated with the severity of liver disease.

Adult↗
PubMedDate not supplied

Oxygen-derived free radical production by peripheral blood neutrophils in chronic cholestatic liver diseases.

BACKGROUND/AIMS: Patients with chronic cholestasis, particularly those with associated cirrhosis, are susceptible to infectious complications. From animal models it has been postulated that cholestasis affects systemic polymorphonuclear leukocyte (PMNL) function by impeding chemotaxis, phagocytosis and superoxide release, which are necessary for an adequate immune response. The aim of this study was to evaluate neutrophil activity in the production of oxygen-derived free radicals in chronic cholestatic liver diseases. METHODOLOGY: The following groups were included in the study: 27 primary biliary cirrhosis (PBC) patients, 12 primary sclerosing cholangitis (PSC) patients, and 3 control groups (29 healthy subjects, 19 patients with HCV-related cirrhosis and 23 ulcerative colitis (UC) patients). Peripheral neutrophils were isolated from heparinized blood samples and PMNL activity was measured by free radical production, using a chemiluminometer, after stimulation with fMLP, PMA and Zymosan. The effect of liver disease severity and degree of cholestasis on PMNL function was also evaluated. RESULTS: Both PBC and PSC patients exhibited a normal PMNL activity compared to healthy subjects after the three stimuli used. In PBC patients only (but not in PSC patients), the histological stage of the disease seems to positively influence ROS production. Stage IV PBC patients showed a significantly higher PMNL activity compared to HCV-related cirrhotic patients. PSC patients failed to show any difference according to the association with UC. CONCLUSIONS: The increased susceptibility to bacterial infections in patients with chronic cholestatic liver disease is not related to an impaired PMNL activity. However, our findings may support the influence of biohumoral factors (cytokines?) on PMNL activation.

Adult↗
PubMedDate not supplied

Heterogeneous derangement of cellular sodium metabolism in Bartter's syndrome. Description of two cases and review of the literature.

The basic tubular alteration present in Bartter's syndrome is still a subject of controversy. The possibility that a generalized defect in transmembrane ion transport underlies the disease has been extensively investigated. Previous evaluations of cellular sodium metabolism in Bartter's patients showed extremely variable findings. In the present study we have examined in red blood cells of two patients with Bartter's syndrome the intracellular Na+ and K+ concentrations, the activity of ouabain-sensitive Na+/K+ pump, furosemide sensitive Na+/K+ cotransport, Na+/Li+ countertransport, and the rate constant of Na+ and K+ passive permeability. We have compared these values with those of a control group. Ouabain-sensitive Na+/K+ pump activity was decreased in both patients, whereas Na+/Li+ countertransport was activated. One of the patients also exhibited markedly decreased intraerythrocyte K+ concentration and decreased furosemide-sensitive Na+/K+ cotransport. The other had increased Na+/K+ cotransport activity and Na+ passive permeability. Intracellular Na+ and passive permeability to K+ were normal in both subjects. Our results are partially consistent with previously reported observations, and indicate the existence of heterogeneous alterations of erythrocyte sodium transport systems in patients with Bartter's syndrome. Although some of these alterations could be secondary to the electrolyte metabolism derangements of this disease, others might be genetically transmitted and could cause the different renal tubular defects shown in Bartter's disease so far.

Adult↗
PubMedDate not supplied

[Increase of circulating levels of insulin and C-peptide: common factors in essential hypertension and overweight].

The aim of our study was to investigate the hypothesis that insulin resistance is involved in the pathogenesis of essential hypertension, and to explain whether hyperinsulinemia in this condition is the result of either pancreas overproduction or defective hepatic insulin clearance. In 14 lean normotensive, 17 overweight normotensive, 17 lean essential hypertensive, and 20 overweight essential hypertensive subjects, we measured, after overnight fasting, blood glucose, serum insulin, and serum C-peptide, and calculated the glucose/insulin and the insulin/C-peptide ratios, which can be commonly taken as indexes of peripheral sensitivity to insulin and hepatic insulin clearance, respectively. When compared to lean normotensives, overweight and/or hypertensive patients exhibited higher serum insulin and C-peptide concentrations, and a lower glucose/insulin ratio. No difference was found in the insulin/C-peptide ratio between normotensive and hypertensive subjects. Diastolic blood pressure was directly correlated with serum insulin (p less than 0.01) and C-peptide (p less than 0.01), and inversely correlated with the glucose/insulin ratio (p less than 0.02). We conclude that insulin resistance is present in both essential hypertensive and overweight subjects. Considering the normality of the insulin/C-peptide ratio when taken as the hepatic insulin clearance index, we believe that hyperinsulinemia is caused by a beta-cell hypersecretory response to the defective peripheral action of the hormone.

Adult↗
PubMedDate not supplied

Sublingual and intravenous ketanserin versus sublingual nifedipine in the treatment of severe hypertension: a randomized study.

Thirty-seven patients with severe hypertension were randomly assigned to receive 20 mg of ketanserin sublingually, 10 mg of ketanserin intravenously, or 20 mg of nifedipine sublingually. Systolic and diastolic blood pressures fell significantly after the three treatments. The maximum effects were reached 25 minutes after sublingual ketanserin (with decreases of 7.7% in systolic and 7.1% in diastolic blood pressure), six minutes after intravenous ketanserin (decreases of 9.4% and 9.6%, respectively), and 25 minutes after sublingual nifedipine (decreases of 16.9% and 15.9%, respectively). Blood pressure returned to pretreatment levels 20 minutes after intravenous ketanserin. Heart rate increased significantly in the group receiving nifedipine. No changes in plasma aldosterone, sodium, or potassium levels or in erythrocyte sodium and potassium levels were found after ketanserin. It is concluded that even intravenous ketanserin is inferior to sublingual nifedipine in the control of blood pressure.

Administration, Sublingual↗