Biomedical subjects

D Kerr

Publications and source records attributed to D Kerr.

At least 55 records · Page 3Linked to original sources

PubMed1985

Fluid replacement during hypothermia.

Hypothermia produces acidosis, depressed cardiac function, hypovolemia and hypotension. This study was designed to examine the cardiovascular dynamics involved with restoration of the hypovolemia before rewarming. Mixed breed splenectomized adult dogs (n = 16) were anesthetized with pentobarbital and cooled to a right atrial temperature of 25 degrees C at a rate of 3 degrees C X h-1. The animals were maintained at 25 degrees C for 6 h and rewarmed at 3 degrees C X h-1. Group 1 was given no fluid, Group 2 was given saline (20% of plasma volume infused in 10 min). 2 h after reaching 25 degrees C and Group 3 received saline just prior to rewarming. The hematocrit was elevated in all groups (p less than 0.05) upon cooling, but did not differ between groups even after saline was given. Cardiac output (Co) at 25 degrees C was 35% of precooled values. Group 2 increased their Q by 15% with fluid and this Q was maintained at higher levels than Groups 1 or 3 for the next 4 h. Plasma volume, heart rate, and cardiac contractility returned to control levels upon rewarming, but Q remained low (less than 10%). The level of Q at the start of rewarming did not affect the final level of Q.

Acid-Base Equilibrium↗

PubMed1984

Deficiency of the iron-sulfur clusters of mitochondrial reduced nicotinamide-adenine dinucleotide-ubiquinone oxidoreductase (complex I) in an infant with congenital lactic acidosis.

We report the case of an infant with hypoglycemia, progressive lactic acidosis, an increased serum lactate/pyruvate ratio, and elevated plasma alanine, who had a moderate to profound decrease in the ability of mitochondria from four organs to oxidize pyruvate, malate plus glutamate, citrate, and other NAD+-linked respiratory substrates. The capacity to oxidize the flavin adenine dinucleotide-linked substrate, succinate, was normal. The most pronounced deficiency was in skeletal muscle, the least in kidney mitochondria. Enzymatic assays on isolated mitochondria ruled out defects in complexes II, III, and IV of the respiratory chain. Further studies showed that the defect was localized in the inner membrane mitochondrial NADH-ubiquinone oxidoreductase (complex I). When ferricyanide was used as an artificial electron acceptor, complex I activity was normal, indicating that electrons from NADH could reduce the flavin mononucleotide cofactor. However, electron paramagnetic resonance spectroscopy performed on liver submitochondrial particles showed an almost total loss of the iron-sulfur clusters characteristic of complex I, whereas normal signals were noted for other mitochondrial iron-sulfur clusters. This infant is presented as the first reported case of congenital lactic acidosis caused by a deficiency of the iron-sulfur clusters of complex I of the mitochondrial electron transport chain.

Acidosis↗

PubMed1984

Human leukocyte (alpha) interferon in metastatic malignant melanoma: the American Cancer Society phase II trial.

Forty-four evaluable patients with metastatic malignant melanoma confined to the skin, subcutaneous tissues, lymph nodes, and/or lung were randomly assigned to receive either 1 X 10(6), 3 X 10(6), or 9 X 10(6) units of partially purified human leukocyte (alpha) interferon by daily im injection for 42 days. One patient achieved a partial response, two had minor responses, and three others had mixed responses. The only partial response was observed at the lowest dose of interferon. Toxicity increased in frequency and intensity with increasing interferon dose. This preparation of interferon at the doses, route, and schedule used appears to have little efficacy in metastatic malignant melanoma.

Adolescent↗

PubMed1983

Thiamin inadequacy in infants: lack of evidence of amprolium in egg yolk.

This study investigated the hypothesis that the consumption of egg yolks might lead to thiamin inadequacy in infants because of the possible contamination of the egg yolks with amprolium. Earlier workers showed that the presence of amprolium in the diet inhibits the absorption of thiamin. Amprolium is added to some poultry feeds to control coccidiosis: it is readily incorporated in the egg yolk and egg yolk is one of the solid foods offered to infants at weaning. We found that under current commercial poultry feeding practices in WA it is extremely unlikely that any amprolium would be present in commercial eggs or poultry. Amprolium was undetectable in eggs purchased at several retail outlets. Thus there is no evidence that consumption of egg yolk contributes to thiamin inadequacy in infants.

Amprolium↗

PubMed1982

Treatment of inborn errors of urea synthesis: activation of alternative pathways of waste nitrogen synthesis and excretion.

Children with inborn errors of urea synthesis accumulate ammonium and other nitrogenous precursors of urea, leading to episodic coma and a high mortality rate. We used alternative pathways for the excretion of waste nitrogen as substitutes for the defective ureagenic pathways in 26 infants. These pathways involve synthesis and excretion of hippurate after sodium benzoate administration, and of citrulline and argininosuccinate after arginine supplementation. The children were treated for seven to 62 months; 22 survived. The mean plasma level of ammonium ( +/- S.E.) was 36 +/- 2 mumol per liter, and that of benzoate was 1.5 +/- 1.0 mg per deciliter. Alternative pathways accounted for between 28 and 59 per cent of the total "effective" excretion of waste nitrogen. Nineteen infants had normal height, weight, and head circumference, and 13 had normal intellectual development. Activation of alternative pathways of waste nitrogen excretion can prolong survival and improve clinical outcome in children with inborn errors of urea synthesis.

Amino Acid Metabolism, Inborn Errors↗

PubMed1982

Decreased essential amino acid requirements without catabolism in phenylketonuria and maple syrup urine disease.

The normal infant requirement for essential amino acids includes requirements for growth, obligatory catabolism, and other minor losses. The fraction required for obligatory catabolism was estimated by the difference between the normal requirement and the dietary tolerance of infants lacking the enzymes needed for catabolism of phenylalanine and leucine. The average dietary tolerance for phenylalanine in infants with classical phenylketonuria is approximately 42, 31, and 23 mg/100 kcal at 0 to 4, 4 to 12, and 12 to 24 months, respectively. This is equivalent to 68, 58, and 50% of the estimated normal requirement for phenylalanine at these ages. The average leucine tolerance of two infants with classical maple syrup urine disease was approximately 80, 50, and 38 mg/100 kcal at the same ages, corresponding to 53, 38, and 33% of the estimated normal requirement for leucine. The decrease in relative requirements for these amino acids with increasing age can be accounted for by decreased body protein accretion. The difference from the normal requirement is proportional to previous estimates of obligatory protein catabolism. Four infants with variant milder forms of phenylketonuria and one with maple syrup urine disease were found to tolerate amino acid intakes which were substantially greater than the tolerance of infants with the classical disorders, in some cases exceeding the normal requirements. These differences in tolerance, which may reflect partial enzyme activity, were not predictable in individual cases.

Amino Acids↗

PubMed1981