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Biomedical subjects

M M Thaler

Publications and source records attributed to M M Thaler.

At least 55 records · Page 3Linked to original sources
PubMed1979

Cholestyramine treatment of chronic diarrhea associated with immune deficiency syndrome.

A 5-year-old boy with known severe combined immunodeficiency disease presented with chronic diarrhea, malabsorption and retarded growth. Candida albicans was found in distal duodenal fluid, and invading the intestinal mucosa. Chronic diarrhea persisted after antimycotic therapy, but responded to treatment with cholestyramine. Repeated courses of cholestyramine resin over a 6-month period were required for complete resolution of the gastrointestinal symptomatology.

Candidiasis↗
PubMed1979

Shwachman-Diamond sydnrome and chronic liver disease.

Clinically inapparent persistent chronic liver disease in a 15-month-old male patient with Shwachman-Diamond syndrome is presented. Cryptic hepatic involvement may be an unrecognized feature of the syndrome and should be evaluated in all cases.

Chronic Disease↗
PubMed1979

Suppression of tumor-associated hyperfibrinogenemia and free fatty acidemia with p-phenoxybenzalbutyrate (clofibrate).

Previous work in our laboratory has indicated that free fatty acids stimulate synthesis of fibrinogen by the liver. The effect of the hypolipidemic agent clofibrate on hyperfibrinogenemia associated with tumors was evaluated by monitoring clofibrate-induced changes in plasma fibrinogen concentration and biosynthesis of the protein in Buffalo rats implanted with a localized, nonmetastasizing neoplasm derived from a tumorigenic hepatoma cell line (HTC4). In tumor-bearing animals not treated with clofibrate, cancer growth was associated with elevated rates of fibrinogen synthesis and a doubling of plasma fibrinogen concentrations. Plasma free fatty acid concentrations and serum free fatty acid/albumin molar ratios were also increased in tumor-bearing rats. Treatment with clofibrate in doses which normalized the plasma free fatty acid/albumin ratio also prevented the tumor-associated rise in plasma fibrinogen. Rates of fibrinogen synthesis were lowered significantly in clofibrate-treated animals. Tumor growth was not affected by clofibrate. These results indicate that hyperfibrinogenemia associated with nonmetastasizing tumors may reflect changes in lipid metabolism which are neutralized by clofibrate. Thus, treatment with clofibrate or other hypolipidemic agents should be evaluated in cancer patients with elevated plasma fibrinogen levels and their attendant complications.

Animals↗
PubMed1978

Surface analysis and depth profiles of calcium in hepatoma cells during pyruvate-induced DNA synthesis.

Induction of DNA synthesis is associated with increased uptake of calcium in cultured cells. Calcium distribution within the plasma membrane and adjacent cytoplasmic layers of hepatoma cells was investigated with X-ray photoelectron spectroscopy and oxygen plasma etching. Cells in minimal growth medium initiate active DNA synthesis 16 h after addition of sodium pyruvate. Cells stimulated with pyruvate and pyruvate-free controls were analysed by X-ray photoelectron spectroscopy--oxygen plasma etching at 0--40 A (layer I), 0--450 A (layer II) and 0--4000 A (layer III from the outer cell surface. Calcium concentrations were elevated in induced cells compared with controls: +20% in layer I, +60% in layer II, and +300% in layer III. As the plasma membrane is 90--120 A thick, these results indicate that pyruvate-induced DNA synthesis is preceded by an increase in calcium, most marked in the cytoplasm subjacent to the plasma membrane, moderate at its inner surface, and minimal at its outer surface.

Animals↗
PubMed1977

Reye syndrome without initial hepatic involvement.

We report Reye syndrome in an 11-year-old boy whose first symptoms were generalized convulsions and coma without clinical or laboratory evidence of liver disease. Serum glutamic oxaloacetic transaminase and lactate dehydrogenase (LDH) values increased strikingly on the third day after the onset of coma. These enzymatic changes were associated with prolongation of prothrombin time. A rise in blood ammonia concentrations began on the fourth day of coma. The diagnosis of Reye syndrome was confirmed by a liver biopsy and at autopsy. This case demonstrates that encephalopathy in Reye syndrome can develop prior to detectable hepatic involvement, and suggests that factors unrelated to generalized liver damage may occasionally play a role in the pathogenesis of this obscure disorder.

Child↗
PubMed1977

Influence of intravenous nutrients on bilirubin transport. I. Amino acid solutions.

The effects of synthetic amino acids on bilirubin transport were investigated with competitive binding assays, peroxidase assays, isotopic studies of bilirubin uptake by red cells, and difference spectroscopy. Results indicated that amino acids had no significant effect on the distribution of bilirubin at pigment to albumin molar ratios likely to be encountered in clinical situations.

Albumins↗
PubMed1977

Influence of intravenous nutrients on bilirubin transport. II. Emulsified lipid solutions.

The effects of an emulsified intravenous fat preparation (Intralipid) on bilirubin transport were analyzed by cholestyramine extraction, spectrophotometric analysis, Sephadex gel filtration, peroxidase assay, bilirubin uptake by red blood cells, and by toxicity in tissue culture (L-929) cells. Intralipid is capable of binding bilirubin, but does not compete effectively with bilirubin bound to high affinity sites on albumin. The emulsified fat appears to have a higher affinity for bilirubin than for cell membranes. Red blood cells become coated with Intralipid, resulting in an increased association of bilirubin with the cell surface, but a decrease in pigment actually incorporated into the red cell membrane. In tissue culture experiments, Intralipid protected the cells from bilirubin toxicity. It is concluded that Intralipid may enhance the carrying capacity of serum for bilirubin, and thus exert a protective effect on tissues.

Albumins↗
PubMed1977

Influence of intravenous nutrients on bilirubin transport. III. Emulsified fat infusion.

Infusions and injections of Intralipid were administered to congenitally jaundiced rats (Gunn) in whom the total body bilirubin pool was uniformly labeled with radioactive bilirubin. These isotopic studies indicated that Intralipid treatment had no effect on the kinetics of bilirubin formation, transport, tissue distribution, and clearance. There were no significant differences between control and fat emulsion-treated animals in the total bilirubin pool, plasma bilirubin pool, biologic half-life of bilirubin, fractional turnover, and exponential decline in plasma bilirubin specific activity at steady state. Bilirubin concentrations in blood, plasma, liver, kidneys, brain, adipose tissue, and muscle were unaltered during the course of continuous infusions (up to 24 hr) of Intralipid. These results indicate that Intralipid administered in clinically applicable doses and regimens has no discernible effects on bilirubin metabolism in jaundiced rats.

Animals↗
PubMed1977

Stimulation of bilirubin formation in liver of newborn rats by fasting and glucagon.

Fasting in newborn Gunn rats caused an increase in serum bilirubin concentration and in liver bilirubin concentration and specific activity, and a significant stimulation of the heme catabolic enzyme, heme oxygenase, in liver. Treatment with glucagon enhanced conversion of newly formed endogenously prelabeled hepatic heme to bilirubin, with subsequent transfer of pigment to the circulation. Activity of heme oxygenase was increased in liver of hormone-treated newborns. These findings suggest that degradation of hemes from nonerythroid sources may play a role in hyperbilirubinemia association of hemes from nonerythroid sources may play a role in hyperbilirubinemia assiciated with hypoglycemia and caloric deficiency in newborn infants, and may contribute to elevated serum bilirubin levels in fasting adults.

Aminolevulinic Acid↗