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Biomedical subjects

A Mas

Publications and source records attributed to A Mas.

At least 163 records · Page 9Linked to original sources
PubMed1988

Post-transfusional vs. sporadic non-A, non-B chronic hepatitis. A clinico-pathological and evolutive study.

The clinical, morphological and evolutive features of 60 patients with chronic hepatitis, presumably caused by non-A, non-B virus infection, have been retrospectively analyzed. In all the cases the disease began as an acute episode of viral hepatitis that was followed by persistently abnormal liver function tests. No patient had evidence of current or past hepatitis B virus infection and other known causes of chronic liver disease were excluded. Thirty patients had received blood transfusions in the recent past, five were drug addicts and the source of the infection was not identified in the remaining 25, in whom the disease was considered to be sporadic. Clinical or biochemical differences between patients with post-transfusional and sporadic non-A, non-B chronic hepatitis were not observed, but liver histology showed a higher proportion of patients with chronic persistent hepatitis in the sporadic (72%) than in the transfusional group (53%). On follow-up, sustained normalization of liver function tests was observed in 46% of the cases with sporadic hepatitis but only in 13% of the cases with post-transfusion hepatitis. These observations suggest that non-A, non-B chronic hepatitis is more severe in patients with transfusion-related infection than in sporadic cases.

Adult↗
PubMed1987

Recombinant alpha 2c-interferon therapy in fulminant viral hepatitis.

Recombinant alpha 2c-interferon was administered to 12 consecutive patients with fulminant viral hepatitis. The disease was caused by coinfection by HBV and HDV in seven patients, by HDV superinfection of a chronic HBV carrier in two, by HBV alone in two and by HAV in one. Eight patients were drug addicts. Interferon administration was initiated shortly after the onset of hepatic encephalopathy and no patient was in grade IV coma at the beginning of therapy. Ten patients died and only two survived. One of the survivors was an asymptomatic HBV carrier superinfected by HDV in whom treatment with interferon for 3 months did not prevent the development of chronic delta infection and liver cirrhosis. These results show that alpha 2c-interferon does not have significant therapeutic value in fulminant viral hepatitis, particularly if it is caused by HDV.

Adolescent↗
PubMed1986

Influence of HBV replication and delta agent superinfection on T cell subsets and killer (Leu 7+) in chronic hepatitis B virus infection.

Peripheral blood T-lymphocyte subsets and cells reacting for Leu 7 antigen, which identifies a subset of killer and natural killer cells, have been examined in 32 patients chronically infected by the hepatitis B or D viruses (HBV, HDV) and in 28 normal subjects. The T8+ lymphocytes were increased and the T4/T8 ratio was decreased in patients with HBV replication (identified by the presence of HBcAg in liver and HBV-DNA in serum) and in patients with HDV infection (HDAg in liver). These patients had more active liver disease than patients without evidence of viral replication, B or D, who showed normal lymphocyte counts. Leu 7+ lymphocytes were also increased in patients with viral replication and active disease and correlated positively with alaninaminotransferase serum levels. These observations suggest the participation of both T8+ and Leu7+ cells in the pathogenesis of liver cell injury in HBsAg-positive chronic liver disease.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1986

Distribution and kinetics of injected nickel in the pregnant rat.

Radioactive nickel (Ni) was injected intraperitoneally both carrier-free and in 4 mg/kg body weight of Ni as NiCl2 doses in control and pregnant rats on days 12 and 19 after impregnation. The time-course of disappearance of radioactivity from the tissues and blood of the rat was determined, as well as the degree of incorporation of radioactivity from the injected doses. The maximal uptake of the metal 15 min after injection corresponded to kidney uptake, followed by pancreas, blood plasma and then all other target organs studied. The presence of cold nickel resulted in higher uptake of the metal without much change in the proportion of distribution between tissues. The kinetics of disappearance was similar in all tissues and was little affected by pregnancy, with mean half-lives of about 3-5 h irrespective of doses.

Animals↗
PubMed1986

Effects of a nickel load upon the concentration of plasma metabolites in pregnant rats.

The effects of an intraperitoneal nickel load upon plasma glucose, urea, amino acids, lactate and glucagon, as well as upon liver glycogen have been determined in 12-and 19-day pregnant rats compared with controls. Nickel induced considerable increases in both glucose and glucagon levels, delayed in 19-day pregnant rats with respect to controls, and deep and permanent decreases in glycogen and amino acids in pregnant rats. The effects of glucagon are related to the insulin resistance of pregnant rats and a relationship between nickel toxicity and the lacking capacity to recover the basal values of some parameters is suggested.

Amino Acids↗
PubMed1986

Nickel fixation by rat plasma and 21-day placental homogenates.

The effectiveness of 19-day placenta homogenates in the binding and retention of nickel was compared with that of rat plasma in a simple dialysis system. The energy of activation of both placenta and plasma were of the same range (-5 kJ/mol). The specificity of the nickel binding system was considerable, as the presence of concentrations of zinc, iron or copper five orders of magnitude larger resulted only in the loss of a maximum of 10% of the pre-bound nickel in 24 h at 20 degrees C. This strong fixation of nickel seems to be specific and is probably the same in placenta and in plasma.

Animals↗
PubMed1986

Effect of an acute injection of nickel upon essential metal homeostasis in the rat. Influence of sex and pregnancy.

The content of calcium, copper, iron, magnesium and zinc in the plasma, liver and kidney of control female and male, as well as pregnant rats on days 12 and 19 after a i.p. injection of 4 mg/kg of nickel was studied. The content of 19-day conceptuses was also measured. The injection of nickel provoked significant alterations in the essential metal homeostasis, more marked in the case of pregnant rats, with additional differences between male and female animals. In general, nickel provoked increases in metal concentrations in tissues, with diverse changes in plasma. In a number of tissues and metals, the effects lasted up to 48 hours after the single injections, long after the nickel being washed off the animal. The results suggest some sort of long-lasting nickel effect upon metal homeostasis, which is postulated not to be directly related to acute effects and which is enhanced by pregnancy.

Animals↗
PubMed1985

The acute toxicity and teratogenicity of nickel in pregnant rats.

The increase susceptibility of the pregnant rat to intraperitoneally administered nickel (Ni) is apparent at 12 and 19 days of pregnancy and cannot be due, therefore, to the increase in total body weight. Teratogenic malformations occur when Ni is administered during organogenesis and are maximal at dose levels that are toxic for the dam. The yolk sac and chorioallantoic placentas accumulate Ni, but this does not prevent the transport of the metal to the embryo or foetus. The Ni concentrations in the conceptuses decrease more slowly with time than those in the maternal organs. In the foetuses, the decrease in concentration is due to the increase in weight, since the content of Ni increases between 4 h and 24 h. Foetal uptake of [14C]thymidine, [3H]leucine and 65Zn is unaffected at 3 h after the injection of the dam with 4 mg Ni/kg body wt. Incorporation of [3H]leucine into foetal protein, but not the incorporation of [14C]-thymidine into DNA, is decreased at this time. A major effect of treatment with this teratogenic dose is an increase in the maternal plasma glucose concentration which, in turn, alters the supply of the sugar to the foetus. The possible relevance of temporary foetal hyperglycaemia to teratogenesis is discussed.

Abnormalities, Drug-Induced↗
PubMed1985

Cadmium and lead toxicity effects on zinc, copper, nickel and iron distribution in the developing chick embryo.

The teratologic effects on chicken embryos induced by the load of 100 micrograms of cadmium or lead nitrate salts injected into the yolk on day 5 of incubation as well as their effects upon zinc, copper, nickel and iron distribution were studied. Despite a significant teratologic influence of lead, cadmium administration did not induce significant effects. A week after injections, embryo lead content, but not cadmium concentration, increased; this differential action suggested an active uptake of lead by the embryo, not observed for cadmium. Both cadmium and lead affected significantly the iron, copper and zinc homeostasis in the egg. Cadmium induced these changes probably through alterations in the metallic ion transport processes towards the embryo.

Animals↗
PubMed1985

Effects of an acute administration of nickel upon blood glucose compartmentation in pregnant rats.

The effects of a nickel injection i.p. to male, female virgin and 12- and 19-day pregnant rats upon plasma glucose concentration as well as blood cell free glucose content have been determined. The hyperglycaemic response to nickel of female rats was more marked than that of males, with an increase in intracellular glucose, more marked during pregnancy, which even surpassed the plasma concentration of glucose. Twelve-day pregnant rats maintained huge intracellular glucose concentrations even after the beginning of the decline in plasma levels, whereas this was not observed in 19-day pregnant rats. The possible rôle of the conceptuses in the removal of excess circulating glucose at this age is discussed.

Animals↗
PubMed1982

Acute thallium poisoning: an evaluation of different forms of treatment.

Hemodialysis, forced potassium diuresis, chelating agents per os, and Dithiocarb given intravenously during short periods of time were used for the treatment of acute thallium poisoning (ingestion of 750 mg of thallium sulfate), and the effectiveness of these different therapeutic procedures was analyzed. Chelating agents per os (Prussian blue, Dithiocarb, and Dithiozone) were ineffective in our patient, since fecal excretion of thallium was very low and unmodified by them. Forced potassium diuresis and hemodialysis were very useful therapeutic measures, especially in the first 12 days following ingestion. Dithiocarb perfusion seems to be the most effective method for enhancing urinary thallium excretion. This method might be most useful in the treatment of thallium poisoning if its deleterious effects could be eliminated.

Acute Disease↗