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A Harper

Publications and source records attributed to A Harper.

At least 73 records · Page 4Linked to original sources
PubMed1987

AIDS and catatonia.

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Acquired Immunodeficiency Syndrome↗
PubMed1986

Protein metabolism in renal failure: abnormalities and possible mechanisms.

Currently, we have only fragmentary knowledge about alterations of protein metabolism in renal failure, yet several coherent strands appear to be emerging. CRF is, in part, a state of malnutrition, as evidenced by abnormalities of body composition and alterations of both plasma and intracellular amino acid patterns. Superimposed upon this baseline are abnormalities specific to renal disease, changes in the concentration of certain amino acids, and the buildup of nitrogenous wastes and potential metabolic toxins, and the interaction of these toxins with hormones or within metabolic pathways. In acute renal failure, or when intercurrent illness is added to CRF, there is an intensification of the metabolic derangements and an acceleration of the normal catabolic response. Current research is directed at improving protein anabolism by limiting total nitrogen intake, while at the same time, providing supplemental amino or keto acids to restore and maintain nutritional state. Other approaches involve the provision of alternate pathways for nitrogen disposal and by direct stimulation of nitrogen anabolism through the administration of branched-chain amino acids or their keto acid analogues. All would agree that these modifications must be performed on a background of adequate caloric intake and careful patient monitoring. Given the complex nature of the problem, careful prospective controlled studies will be necessary before any hypothesis can be accepted. It is likely that additional improvements will require both a better understanding of the underlying metabolic defects and, probably, the combined application of several of the ideas previously noted.

Adult↗
PubMed1981

The respiratory burst of phagocytic cells is associated with a rise in vacuolar pH.

Neutrophil leukocytes are the body's major defence against bacteria, which they phagocytose and kill. It has been found that phagocytosis and killing are accompanied by a dramatic rise in non-mitochondrial respiration; and that the efficiency of killing is impaired in the absence of oxygen. It is also impaired in neutrophils from patients with chronic granulomatous disease (CGD), where the respiratory burst is absent. This has been difficult to reconcile with their normal content of granule proteins that kill bacteria in vitro. Indeed, CGD cells are essentially normal both morphologically and constitutionally except that they lack a functional very low potential cytochrome b (b-245), which is a component of the oxidase system responsible for the respiratory burst of normal cells. Activation of the oxidase is associated with the generation of various reduced oxygen species which have been widely thought to be responsible for the killing of phagocytosed microorganisms either directly, or by acting as substrates for myeloperoxidase-mediated halogenation. We report here, however, that a major consequence of the defective function of this oxidase in neutrophils and monocytes from CGD patients is an absence of the normal initial rise, and an unusually rapid and extensive fall in pH which is itself associated with the impairment of the killing and digestion of intracellular staphylococci.

Granulomatous Disease, Chronic↗
PubMed1978

The effect of tobacco smoke on the metabolism and function of rat alveolar macrophages.

Alveolar macrophages harvested by bronchopulmonary lavage from rats exposed to tobacco smoke for 30 days ("smokers") showed alterations in oxidative metabolism, lactate production and phagocytosis of inert starch particles when compared with control macrophages. Phagocytosis of viable Staphylococcus aureus was unaffected by tobacco smoke. Glucose oxidation measured by conversion of glucose-1-14C to 14CO2 moderately affected while oxidation of glucose-6-14C to 14CO2 was not. Smokers routinely yielded fewer cells than controls, though these cells contained approximately 17% more protein than did controls. Opsonization of particles was not necessary for macrophages from either smoker or control animals to manifest a respiratory burst and increased superoxide and hydrogen peroxide release during phagocytosis. The glycolytic inhibitors, sodium fluoride and iodoacetamide, while effectively blocking glycolysis, did not inhibit phagocytosis by macrophages from either group. The results reported clearly distinguish alveolar macrophages from other phagocytic cells (peritoneal macrophages and polymorphonuclear leukocytes) and suggest a state of non-specific activation caused by exposure to tobacco smoke.

Animals↗