PubMed Health⌕ Search

Biomedical subjects

A Curti

Publications and source records attributed to A Curti.

At least 19 recordsLinked to original sources
PubMed1993

Two years' air mutagenesis monitoring in a northwestern rural area of Italy with an industrial plant.

The mutagenicity of organic extracts from inhalable airborne particles, collected in a northwestern rural area of Italy in which an industrial plant producing chemical intermediates is present, was assessed during the years 1989 and 1990. The Ames plate test with Salmonella strains TA98 and TA100 with and without metabolic activation was used. Eight sites in the first and three sites in the second year were monitored once and twice a month respectively. Results show that the mutagenicity of air particulate matter reaches maximum values in the cold months and is not dependent on plant activities. In addition, a correlation analysis between mutagenicity data and number of vehicles seems to indicate traffic emissions as the main source of mutagens.

Air Pollutants↗
PubMed1984

Erythrocyte sodium transport in acute hypophosphatemia in man.

In 21 patients with acute hypophosphatemia (AHPP), we measured red cell intracellular Na concentration (Nai) and either total (T), ouabain-sensitive (OS) or ouabain-resistant (OR) efflux rate constant of Na (0K Na) in a 'physiological' Na medium. High Nai, normal 0K Na T, reduced 0K Na OS and normal 0K Na OR were found. Total OS and OR unidirectional Na effluxes were increased, normal and increased, respectively. The findings suggest that high Nai in AHPP is due to an impairment of active (OS) red cell Na transport; the increase of total Na efflux is only supported by the OR Na efflux, which, under physiological conditions, is mediated mostly by the 1 Na:1 Na exchange diffusion.

Acute Disease↗
PubMed1984

Skeletal muscle cell abnormalities in acute hypophosphatemia during total parenteral nutrition.

Muscle tissue H2O, Na, K, Mg, Cl and total P were studied in 23 patients with acute hypophosphatemia during P-deficient total parenteral nutrition. Increased muscle extracellular water and low intracellular K and Mg with high intracellular Na were found. These abnormalities were detected either in previously underfed patients with low muscle P or in well-nourished, acutely ill subjects with muscle P near to normal. These findings show that acute depletion of extracellular inorganic P is associated with changes of muscle cell composition independently of muscle cell P content.

Acute Disease↗
PubMed1983

Extracellular water, electrolyte and nitrogen balance after postoperative parenteral nutrition and intracellular involvement in muscle.

Brief periods of fasting or moderate trauma were previously shown to give rise to malnutrition characterized by negative nitrogen balance, reduction of lean body mass and relative increase of body water. The present study aimed to assess the possibility that brief low-calorie, low-protein parenteral fluid regimen after relatively moderate surgical trauma can modify the muscle metabolism and alter the water, electrolyte and protein composition. Well-nourished patients undergoing elective cholecystectomy were studied. During the first four postoperative days, seven patients (group I) received parenteral nutrition adequate as regards water, sodium and potassium but deficient in carbohydrates and without amino acids, while six patients (group II) had adequate parenteral supply of calories and nitrogen. The extracellular balance in regard to water, sodium, potassium, calcium, phosphorus, magnesium and urea was assessed in all 13 patients. Needle biopsy of muscle was performed during surgery and at the end of the observation period in six patients from group I and five from group II, in order to assess the total and the intracellular and extracellular water content and also sodium, chloride, potassium, magnesium, phosphorus and alkali-soluble protein nitrogen. In group I, but not in group II, there was weight loss and negative extracellular balance of all parameters, in particular potassium and nitrogen, and reduction of muscle potassium. The analyses of balance and of muscle cell composition showed considerable loss of lean body mass and indicated 'true' electrolyte disturbance, although clinical symptoms were absent and serum parameters remained normal.

Adult↗
PubMed1982

Muscle tissue electrolytes in burned subjects.

In a group of patients with burns covering at least 20 per cent of their body surface area (BSA), extracellular electrolytes and acid-base status and intracellular electrolytes and nitrogen (muscle needle biopsy) were measured both in the early phase (12-24 hours) and 7-14 days after burn injury. In the acute burn phase, extracellular electrolyte and acid-base disturbances are uncommon, while intracellular data shows increase of muscle sodium, decrease of muscle potassium and magnesium and normal muscle cell nitrogen. In the later burn phase, despite an adequate fluid, electrolyte and protein-calorie supply, the changes of electrolytes appear to be uncorrected; no decrease of muscle cell nitrogen is found. Our data could suggest that defects of the sodium-potassium pump in the cell membrane, which are thought to be the cause phase of burns, do not ameliorate with adequate fluid and protein-calorie intake; however, a persistent muscle potassium depletion is also consistent with a reduction of cell "capacity' for potassium, possibly due to muscle protein catabolism, although muscle cell protein values do not show a significant reduction.

Acid-Base Equilibrium↗
PubMed1981

Increased erythrocyte lithium--sodium countertransport in essential hypertension: its relationship to family history of hypertension.

1. Erythrocyte lithium--sodium countertransport was measured in 46 normotensive healthy controls without family history of hypertension, 15 subjects with essential hypertension, but without evidence of family history of high blood pressure, and 43 subjects with essential hypertension and at least one hypertensive first-degree relative. 2. Mean values (mmol h-1 l-1 of erythrocytes) were 0.248 +/- 0.092 in controls, 0.258 +/- 0.087 in hypertensive subjects without family history (not significant vs controls), 0.360 +/- 0.115 in hypertensive subjects with family history of hypertension (P less than 0.001 vs controls), 0.334 +/- 0.117 in all hypertensive subjects, both with and without family history (P less than 0.001 vs controls). 3. Our data confirm the finding of an increased erythrocyte lithium--sodium countertransport, but with a significant overlap between essential hypertension and control values. Lithium--sodium countertransport is higher only in hypertensive subjects with at least one hypertensive first-degree relative. 4. We suggest that the increase of lithium--sodium countertransport in erythrocytes is not a consistent marker of essential hypertension. It seems to be associated with the family prevalence and/or the hereditability of hypertension, rather than with high blood pressure per se.

Adult↗
PubMed1980

[Na/K transport in red blood cells from normal subjects: methodological problems (author's transl)].

In this work we present a method which evaluates the facility of applying and reproducing ion fluxes in human cells using radioactive 22Na as a tracer. Intracellular sodium concentration, rate constants for total (oKNa TOT), ouabain-sensitive (oKNa OUABs) and ouabain-insensitive (oKNa OUABins), sodium efflux and relative effluxes obtained by multiplying the rate constant by the sodium concentration were measured in the red cells of 20 normal subjects. Our results have been shown to be comparable with those obtained in other reports and show a statistically significant relationship between intracellular sodium concentration and the rate constant for active sodium efflux: one would conclude that the intracellular sodium constant probably depends on the activity of the sodium pump genetically determined in each individual. Since such a method is precise can be exactly reproduced, it can be applied to the study of cellular metabolism of different clinical disorders characterized by significant fluid and electrolyte imbalances.

Adult↗
PubMed1980

[Na/K transport in red blood cells from severely burned patients (author's transl)].

The working of the Na/K pump in the red cells of 6 patients with extensive burns was analyzed using radioactive substances with the aim of comparing their red cells with those of 20 normal subjects. In the red cells of patients with extensive burns was found that the intracellular sodium concentration was clearly increased, that the rate constant of ouabain-sensitive efflux diminished, and that the total sodium efflux was augmented by the increase of the ouabain-insensitive part. It is likely that the intra and extra-cellular transportation defects produce an accumulation of sodium inside the cell which succeeds in stimulating the activity of the pump. Although this pump is impaired, the high sodium concentration obtains a new steady state characterized by apparently normal ouabain-sensitive sodium efflux and by an increased ouabain insensitive efflux. The pathogenesis of these defects of cellular homeostasis which are linked to the presence of various complex mechanisms (shock, calorie balance, fluid and electrolyte imbalances, the circulation of "toxic substances" etc), in cases of extensive burns, has not been completely elucidated.

Adult↗
PubMed1978

Studies on bicarbonate reabsorption in chronic renal failure.

The role of nephron loss, extracellular fluid volume (ECFV) expansion and body potassium stores on bicarbonate reabsorption in chronic renal failure (CRF) was evaluated. In 17 CRF and 3 control subjects, tubular HCO3 reabsorption was studied by HCO3 1M titration technique; ECFV (22Na space at 4th hour) and cell K content (muscle biopsy) were also determined. Nephron loss per se does not cause any change of HCO3 reabsorption rate per unit GFR. With ECFV expansion induced by HCO3 infusion, a Tm HCO3 is rapidly reached only in controls and in CRF patients showing a significant basal ECFV expansion. In these subjects reabsorbed HCO3/Na ratio is constant, suggesting that under these conditions, HCO3 reabsorption depends on the same mechanisms that control Na reabsorption. In cell K depleted CRF patients, HCO3 reabsorption rises more than in controls and no Tm HCO3 is detected, at least within the limits of isotonic ECFV expansion induced by titration; in these subjects HCO3 reabsorption does not appear to be limited by natriuretic factors. In CRF subjects with normal ECFV and cell K, there is a greater HCO3 tolerance to ECFV expansion induced by titration technique than in controls.

Absorption↗