Base de dados : MedCarib
Pesquisa : D01.625.050 [Categoria DeCS]
Referências encontradas : 32 [refinar]
Mostrando: 1 .. 10   no formato [Longo]

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  1 / 32 MedCarib  
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Fotocópia
Id: 15650
Autor: Waterlow, John C.
Título: The partition of nitrogen in the urine of malnourished Jamaican infants
Fonte: Am J Clin Nutr;12(3):235-40, March, 1963.
Idioma: En.
Resumo: Twenty-four-hour urine specimens were collected from Jamaican infants immediately after admission to the hospital, and at various stages of recovery. Measurements were made of urea, ammonia, creatinine and "residual nitrogen," which includes creatine, uric acid, amino acids and undetermined nitrogen. The partition of urinary nitrogen agreed with Folin's concept of 1905; the proportion of urea nitrogen depended only on the amount of total nitrogen present. The absolute amounts of ammonia nitrogen and residual nitrogen were relatively constant and no higher during malnutrition than after recovery. The urea nitrogen expressed as a percentage of the total nitrogen (i.e., the "urea index") may be useful for the assessment of protein intake.(AU)
Responsável: JM3.1 - Médical Library
JM3.1; RC620.A1A4


  2 / 32 MedCarib  
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Fotocópia
Id: 14822
Autor: Alleyne, George A. O; Roobol, Anne.
Título: Renal metabolic processes and acid-base changes
Fonte: Med Clin North Am;59(3):781-95, May 1975.
Idioma: En.
Responsável: JM3.1 - Médical Library
JM3.1; R11.M525


  3 / 32 MedCarib  
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Fotocópia
Id: 14819
Autor: Alleyne, George A. O; Roobol, Anne.
Título: Regulation of renal cortex ammoniagenesis. I. Stimulation of renal cortex ammoniagenesis in vitro by plasma isolated from acutely acidotic rats
Fonte: J Clin Invest;53(1):117-21, Jan. 1974.
Idioma: En.
Resumo: We studied the acute renal metabolic response in rats made acidotic by a single oral dose of ammonium chloride. Cortical slices from acutely (2-h) acidotic rats utilized more glutamine and produced more ammonia and glucose from glutamine than slices from normal animals. When cortical slices from normal rats were pretreated in vitro with plasma isolated from acutely acidotic rats, they achieved similar increases in glutamine utilization, ammonia formation, and gluconeogensis from glutamine. We did not observe such stimulation in normal cortical slices pretreated in a low pH-low bicarbonate medium. Our data show that a non-dialysable factor is present plasma from acutely acidotic rats that may be responsible for the early increase in the urinary ammonia observed in such animals (AU)
Responsável: JM3.1 - Médical Library
JM3.1; R11.J67


  4 / 32 MedCarib  
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Fotocópia
Id: 14631
Autor: Klahr, Saulo; Alleyne, George A. O.
Título: Effects of chronic protein-calorie malnutrition on the kidney
Fonte: Kidney Int;3:129-141, 1973.
Idioma: En.
Responsável: JM3.1 - Médical Library
JM3.1; Reprint collection


  5 / 32 MedCarib  
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Fotocópia
Id: 14592
Autor: Alleyne, George A. O; Besterman, H. S; Flores, Hernando.
Título: The effect of phenyl ethyl biguanide in vivo and in vitro on gluconeogenesis and ammonia production in rats
Fonte: Clin Sci;40(2):107-15, 1971.
Idioma: En.
Resumo: The drug phenyl ethyl biguanide (PEBG) was used in vivo and in vitro to study further the relationship between renal gluconeogenesis and ammonia production in the rat. When PEBG was injected intraperitoneally into the rats, it caused a decrease in urinary ammonia in spite of a greater degree of systemic acidosis. PEBG injections also blocked the increase in glucose and ammonia production by renal cortical slices from rats which had been made acidotic by oral administration of ammonium chloride 2h previously. With increasing concentrations of PEBG in vitro, there was inhibition of gluconeogenesis and ammonia production from glutamine and glutamate as substrates. The two processes were equally inhibited when glutamate was used as substrate but with glutamine, gluconeogenesis was more inhiblted than ammonia production. The inhibition of renal gluconeogenesis by PEBG in vitro was similar when succinate, oxaloacetate, fructose, glutamine and glutamate were used as substrates. The results show that PEBG does not inhibit gluconeogenesis by blocking a specific site in the gluconeogenic pathway. In addition, further proof is provided of the physiological interrelationship of renal ammonia production and gluconeogenesis (Summary)
Responsável: JM3.1 - Médical Library
JM3.1; R31.C56


  6 / 32 MedCarib  
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Fotocópia
Id: 14497
Autor: Golden, Michael H. N; Jackson, Alan A.
Título: "Metabolic pool" and the use of 15N-labelled amino acids [letter] Authors' reply
Fonte: Clin Sci;61(3):349-51, Sept. 1981.
Idioma: En.
Responsável: JM3.1 - Médical Library
JM3.1; R31.C56


  7 / 32 MedCarib  
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Fotocópia
Id: 13785
Autor: Bennett, Franklyn I.
Título: The effect of acidosis on the renal metabolism of glutamine in the rat.
Fonte: Kingston; ; Apr. 1977. 227 p. tab.
Idioma: En.
Tese: Apresentada a University of the West Indies (Mona) para obtenção do grau de Doctor of Philosophy (Biochemistry).
Resumo: Glutamine is the major source of urinary ammonia and this study examines the metabolism of that amino acid in rats under varying acid-base conditions. Other workers have shown that in acidosis there is enhanced renal oxidation of glutamine, which requires increased amounts of acetyl CoA. The present study has shown that during acidosis there was no change in the activity of oxaloacetate decarboxylase and malic enzyme, two enzymes capable of increasing the formation of acetyl CoA. This study also showed that 3-mercaptopicolinic acid inhibited PEPCK - the rate limiting enzyme of gluconeogenesis - and thereby inhibited ammoniagenesis from glutamine mainly by inhibiting deamination. Metabolic acidosis was induced with NH4C1 or HC1. In rats given NH4C1 there was an immediate increase in blood ammonia levels and urinary excretion of ammonia, but this did not occur with rats fed HC1 which showed no change in urinary ammonia but a decrease in urea excretion. Rats fed either NH4C1 or HC1 had similar increases in the plasma concentrations of glutamine, renal PEPCK activity, ammonia and glucose production by renal cortical slices. The time course of changes in metabolic intermediates was measured in rats given NH4C1 or HC1. NH4C1 caused a striking decrease in renal levels of malate, 2-oxoglutarate and phosphoenol pyruvate. Similar changes were observed with HC1, but in addition the levels of glucose and glucose-6-phosphate were elevated. The results of the studies with 3-mercaptopicolinic acid and the metabolite profile in response to acidosis are both constant with the theory that displacement of the glutamic dehydrogenase equilibrium is an important mechanism in the control of glutamine utilisation and the ammoniagenic response to acidosis (AU)
Responsável: JM23.1 - Main Library
JM23.1; U Thesis


  8 / 32 MedCarib  
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Fotocópia
Id: 13672
Autor: Persaud, Chandarika.
Título: Studies of 15N-alanine metabolism in man: estimation of whole body protein turnover rates, alanine flux, de novo synthesis of alanine contribution to urinary ammonia.
Fonte: Kingston; s.n; Nov. 1983. viii,63 p. ills, tab.
Idioma: En.
Tese: Apresentada a University of the West Indies (Mona) para obtenção do grau de Masters of Science in Nutrition.
Resumo: A primed intermittent oral dose and a primed continuous intravenous infusion of 15N-alanine was administered to healthy males to determine the rates of protein turnover, synthesis and breakdown. The subjects were fed an adequate intake throughout the day. Urine and blood samples were collected. Mean rate of protein flux as measured by the enrichment of urinary ammonia and urea were found to be 2.25±.21 and 3.00±.42 g. protein/kg./day respectively during the total administration. The values obtained from the intravenous study were 1.87 g. protein/kg./day with ammonia and 4.57 g. protein/kg./day with urea. When each end product and the respective technique was considered the mean rate obtained using 15N-alanine was lower than that reported using 15N-glycine. However, the rank order of the values for the different methods was similar to those with 15N-glycine. Mean plasma alanine flux after the oral and intravenous studies were 548 ±128 and 281 µmol/kg./hr. respectively. Red cells alanine flux was different and higher than plasma flux in each study. During the studies a considerable amount of label was transferred to urinary ammonia and urea while glutamate and alanine had low enrichments. In the fed state, after the oral dose, de novo alanine synthesis was calculated to be 457.4 µmol/kg./hr. This accounted for eighty-three percent of plasma alanine flux, thus seventeen percent of alanine moving through the venous plasma compartment originated from performed alanine. Up to sixteen to twenty-two percent of urinary ammonia was derived from alanine (Summary)
Responsável: JM23.1 - Main Library
JM23.1; U Thesis


  9 / 32 MedCarib  
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Fotocópia
Id: 13645
Autor: Scott, Barbara A.
Título: Renal transport and metabolism of glutamine.
Fonte: Kingston; s.n; Dec. 1981. 127 p. tab.
Idioma: En.
Tese: Apresentada a University of the West Indies (Mona) para obtenção do grau de Master of Philosophy.
Resumo: The experiments described in this thesis were designed to investigate the mechanism of glutamine transport and the effect of acute acidosis on glutamine transport and metabolism in the rat kidney. The experiments done with kidney slices investigated the effect of several amino acids chosen from different structural groups on uptake of glutamine. Proline (an ammino acid) and glycine (at inhibitory concentrations) were found to inhibit ammonia production and glutamine uptake significantly. When a sodium free incubation buffer was used the inhibitory effect of proline and glycine on glutamine uptake disappeared, indicating that the inhibition by proline was sodium dependent. In similar experiments with isolated kidney proximal tubules in a sodium containing buffer, proline also caused a decrease in glutamine uptake and ammonia production. Intracellular/extracellular glutamine distributions ratios in tubules however, showed a marked increase in the presence of proline. The explanation for this is not that proline shares a transport site with glutamine but rather that it is metabolised to glutamate which causes an inhibition of phosphate dependent glutaminase and hence decreased glutamine utilisation. This decreased utilisation leads to an accumulation of glutamine within the renal cell and subsequently increased intracellular/extracellular glutamine distribution ratios. The inhibitory effect of proline on glutamine uptake was much less in experiments with kidney slices from chronically acidotic rats. Isolated tubules from acutely acidotic rats showed increased intracellular/extracellular glutamine distribution ratios, increased ammonia production and glutamine uptake in tubules. When tubules from normal rats were incubated in sera from acutely acidotic rats there was a similar increase in intracellular/extracellular glutamine distribution ratios, ammonia production and glutamine uptake. The effect of the serum however, was not due to the accumulation of glutamate because glutamate levels in tubules were unchanged after incubation in sera from the acutely acidotic rats (AU)
Responsável: JM23.1 - Main Library
JM23.1; U Thesis


  10 / 32 MedCarib  
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Fotocópia
Id: 13070
Autor: Badaloo, Asha V; Jackson, Alan A; Jahoor, Farook.
Título: Whole body protein turnover and resting metabolic rate in homozygous sickle cell disease
Fonte: Clin Sci;77(1):93-7, Jan. 1989.
Idioma: En.
Resumo: Whole body protein turnover and resting metabolic rate were measured in six adults with homozyguous sickle cell disease (genotype HbSS) and in six normal adults (genotype HbAA) of similar age. Turnover was measured with prime/intermittent oral doses of [15N]glycine over 18 h and resting energy expenditure was measured by indirect calorimetry. In HbSS, nitrogen flux (0.9 ± 0.08 g day-1 kg-1), protein synthesis (6.0 ± 0.5 g day-1 kg-1) and protein degradation (5.6 ± 0.5 g day-1 kg-1) were significantly increased compared with HbAA nitrogen (flux 0.5 ± 0.02g day-1 kg-1, protein synthesis 3.2 ± 0.2 g day-1 kg-1 and protein degradation 2.8 ± 0.2 g day-1 kg-1). Resting energy expenditure was significantly higher in HbSS compared with HbAA when expressed per unit of body weight (115 ± 3 and 94 ± 4 kj day-1 kg-1 respectively) or weight 0.75(317 ± 6 and 269 ± 8 kj day-1kg-0.75, respectively). The increase in protein turnover and energy expenditure suggest that patients with HbSS exist in a hypermetabolic state that requires greater dietary energy compared with HbAA. (AU)
Responsável: JM3.1 - Médical Library
JM3.1; R31.C56



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