PubMed Health⌕ Search

Biomedical subjects

L Zieve

Publications and source records attributed to L Zieve.

At least 55 records · Page 3Linked to original sources
PubMed1980

Zinc deficiency: a complication of Crohn's disease.

Twenty-one of 52 patients with regional enteritis had low serum zinc concentrations on initial testing. Fourteen of 31 patients followed longitudinally had low serum zinc concentrations. Two patients are presented as case reports who developed acrodermatitis skin lesions that responded to zinc therapy. Hypogonadism, growth retardation, and abnormalities in taste were frequent complications in Crohn's patients with low serum zinc levels. Certain complications of regional enteritis may be due, in part, to zinc deficiency.

Adult↗
PubMed1980

Psychomotor performance defects in cirrhotic patients without overt encephalopathy.

Psychometric tests were administered to 36 alcoholic patients with cirrhosis without overt portal systemic encephalopathy and to 32 alcoholics without liver diseases. Verbal ability was preserved in both groups. The cirrhotic patients scored worse than the alcoholics without liver disease on most of the tests of psychomotor performance. Based on the three most discriminative tests, 50% of the cirrhotic patients had one or more scores that were more abnormal than those of any member of the alcoholic group. Significant correlations were found between the severity of liver disease and most tests of performance in the cirrhotic group, due primarily to the influence of serum albumin as a component of the severity index. We conclude that psychomotor tests are sensitive tools for the detection of latent encephalopathy, and that nutritional status probably plays a role in determining test performance.

Adult↗
PubMed1979

Reversal of ammonia coma in rats by L-dopa: a peripheral effect.

Ammonia coma was produced in rats within 10 to 15 minutes of an intraperitonealinjection of 1.7 mmol NH4CL. This coma was prevented with 1.68 mmol L-dopa given by gastric intubation 15 minutes before the ammonium salt injection. The effect of L-dopa was correlated with a decrease in blood and brain ammonia, an increase in brain dopamine, and an increase in renal excretion of ammonia and urea. Intraventricular infusion of dopamine sufficient to raise the brain dopamine to the same extent did not prevent the ammonia coma nor affect the blood and brain ammonia concentrations. Bilateral nephrectomy eliminated the beneficial effect of L-dopa on blood and brain ammonia and the ammonia coma was not prevented. Thus, the reduction in blood and brain ammonia and the prevention of ammonia coma after L-dopa, can be accounted for by the peripheral effect of dopamine on renal function rather than its central action. These results provide a reasonable explanation for the beneficial effects observed in some encephalopathic patients receiving L-dopa.

Ammonia↗
PubMed1978

Splenic protein synthesis in magnesium deficiency: mechanism of the inhibition.

To investigate the basis for the depressed protein synthesis in vivo in magnesium deficient spleens, the activities of splenic subcellular fractions in polypeptide synthesis were studied in vitro. Splenic ribosomes from Mg deficient animals were normal structurally and functionally. In contrast, supernatant fractions from the deficient spleens had a reduced ability to incorporate labeled amino acids into protein, both in the presence of endogenous mRNA and in the presence of added polyuridylic acid. The specific defects observed in the Mg deficient supernatants were twofold: There was a modest reduction in the rate of acylation of tRNA and a more marked reduction in the activity of the elongation factors, EF-I and EF-II. The reduction in elongation factor activity was quantitatively sufficient to account for the inhibition of protein synthesis in vivo.

Amino Acyl-tRNA Synthetases↗
PubMed1978

Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss.

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.

Animals↗
PubMed1977

Effects of magnesium deficiency on protein and nucleic acid synthesis in vivo.

The effects of magnesium deficiency on the in vivo incorporation of labeled precursors into tissue macromolecules were studied. In severe Mg deficiency developing over 4 months, total protein synthesis in spleen and thymus was depressed by 40% to 50%, while DNA synthesis was increased by as much as 350%. RNA synthesis was not significantly altered. Protein synthesis in kidney was also reduced. In the intact liver, DNA synthesis was increased and RNA synthesis reduced, but protein synthesis was unchanged. The regeneration of the liver after partial hepatectomy was impaired, however, which suggested that the capacity of the liver protein synthetic system was reduced. The effects of magnesium deficiency were unaltered by the ingestion of ethanol that comprised approximately 25% of total energy. Each of the organs enlarged in Mg deficiency, and the spleen was strikingly hyperplastic. The increase in splenic DNA synthesis in the presence of depressed protein synthesis may be an early stage in a lymphoproliferative process leading ultimately to neoplasia.

Animals↗
PubMed1977

Can hepatic coma be caused by a reduction of brain noradrenaline or dopamine?

Intraventricular infusions of octopamine which raised brain octopamine concentrations more than 20 000-fold resulted in reductions in brain noradrenaline and dopamine by as much as 90% without affecting the alertness or activity of normal rats. As this reduction of brain catecholamines is much greater than any reported in hepatic coma, we do not believe that values observed in experimental hepatic failure have aetiological significance for the encephalopathy that ensues.

Animals↗
PubMed1977

An improved method for measuring blood mercaptans.

An improved method for measuring MT in the blood is described which uses zinc as a reducing agent and utilizes a more sensitive gas chromatograph. The method measures covalently bound MT that was not previously detected and permits determinations in patients for the first time. The average normal whole blood MT in rat blood was 200 +/- 42 pmol/ml and in human blood 229 +/- 29 pmol/ml. Eleven rats in experimental hepatic coma following acute massive hepatic necrosis had blood levels four to 18 times the average normal, and seven cirrhotic patients with hepatic encephalopathy or coma had blood levels four to five times the average normal.

Animals↗
PubMed1976

Intracellular distribution of phosphate in the underfed rat developing weakness and coma following total parenteral nutrition.

Underfed rats infused intravenously with a glucose-amino acid solution at the rate of 390 kcal/kg/day developed a syndrome of muscular weakness, neuropathy, lethargy and precoma or coma associated with severe hypophosphatemia. The movement of phosphate into the cells was studied to determine where it went and into which organic compounds it was incorporated. All but 8% of the labeled phosphate was found in liver, muscle, bone, and carcass residue. Liver cells took up as much phosphate as bone and twice as much as muscle, on weight basis. About 90% of the labeled phosphate entering liver was found in the acid-soluble fraction. The specific activity of liver phosphate increased in the infused underfed rats compared to uninfused underfed rats. Infusion of the underfed rat until signs of the syndrome appeared was associated with a 2.7- to 5-fold increase over the correspondingly infused normal rat in the labeling of glucose-6-phosphate, glucose-1-phosphate, and 6-phosphogluconate. No increase over the infused normal rat was observed in most of the other sugar phosphate compounds nor in the non-sugar phosphate compounds such as phospholipids, nucleic acids or proteins. he changes in sugar phosphates observed in the underfed rats probably reflect the enzymatic atrophy associated with underfeeding and the consequent inability to respond to the huge glucose load.

Animals↗
PubMed1976

Effect of fatty acids on the disposition of ammonia.

Subcoma doses of fatty acids and ammonium salts injected intraperitoneally at the same time into rats or cats act synergistically to produce coma. Under these circumstances, the blood ammonia, is more than double that when the NH4+ is given alone. After these observations a rat liver homogenate system was utilized to study the effect of fatty acids on ammonia utilization in urea, glutamate and glutamine synthesis in vitro. Acetylglutamate-catalyzed urea synthesis was completely inhibited by 45 mM octanoate and was depressed 46% by 9.5 mM octanoate. Citrulline synthesis was similarly inhibited 86 and 28%, respectively. The concentration of liver octanoate at the moment of occurrence of coma after an in vivo injection was approximately 10 mM. The inhibitory effect of fatty acids on the utilization of NH4+ in the urea cycle was greater the longer the fatty acid chain. The critical step in this interference with ammonia metabolism was the inhibition of carbamyl phosphate synthetase. Argininosuccinate synthetase activity was also inhibited to a lesser degree, but ornithine transcarbamylase, argininosuccinate lyase and arginase were unaffected. Glutamate dehydrogenase was likewise inhibited in liver (83%) and brain (43%) by 13 mM octanoate, whereas glutamine synthetase was unaffected. Thus, the two main processes whereby ammonia is metabolized were inhibited by fatty acids at concentrations that exist pathologically, which accounts, at least in part, for the rise in blood ammonia in vivo.

Ammonia↗
PubMed1976

Alterations in volatile free fatty acids of blood after hepatectomy.

Volatile free fatty acids (VFA) in blood increased approximately twofold in dogs subjected to total hepatectomy. The average total plasma VFA preoperatively was 1,585 mug percent and shortly before death, postoperatively, was 2,798 mug percent. The corresponding red cell concentrations were essentially the same. Acetic acid was 81 percent of the total VFA, propionic acid 7 percent, isobutyric acid 4 percent, butyric acid one percent, and isovaleric acid 5 percent. There was little or no isovalerate in red cells. The increments in the individual fatty acids after hepatectomy were highly variable, but the average increase with time was almost linear. The increase in VFA probably reflects an increased utilization of the branched-chain aminoacids by extrahepatic tissues.

Acetates↗