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Biomedical subjects

M E May

Publications and source records attributed to M E May.

At least 37 records · Page 2Linked to original sources
PubMed1987

Evidence for activation of a respiratory burst in the interaction of human neutrophils with Mycobacterium tuberculosis.

We examined the capacity of human neutrophils to develop a respiratory burst, as monitored by superoxide release, in response to interaction with Mycobacterium tuberculosis. Serum-opsonized, heat-killed mycobacteria induced significant release of superoxide from neutrophils after 30 min of exposure, with a maximum release of 34 +/- 1.7 nmol/30 min per 5 X 10(6) neutrophils occurring with a mycobacterium/neutrophil ratio of 40:1. Similar levels of superoxide release were induced by live mycobacteria. Neutrophil superoxide production was reduced significantly with exposure to unopsonized organisms or by substitution of heat-inactivated serum for opsonization. Mycobacterial components including culture filtrate, purified protein derivative, and the cell wall polysaccharide arabinogalactan failed to induce significant release of superoxide from neutrophils. Transmission electron microscopy demonstrated that more than 90% of the neutrophils had ingested heat-killed mycobacteria concomitant with the development of respiratory burst activity. These data suggest that the presumed failure of neutrophil killing of mycobacteria cannot be attributed to a lack of phagocytosis or respiratory burst activation.

Humans↗
PubMed1985

Rapid adrenocorticotropic hormone test in practice. Retrospective review.

Retrospective analysis of the rapid adrenocorticotropic hormone (ACTH) test in a large adult population shows a marked interdependence of the basal cortisol concentration, peak cortisol concentration, and increase in cortisol concentration. Repetition of the rapid ACTH test in the same patient does not improve diagnostic accuracy. A significant number of falsely abnormal rapid ACTH test results were observed (in comparison to continuous ACTH infusion as a reference test). This supports the use of the rapid ACTH test as a screening test, but not as a diagnostic test for adrenocortical failure. It is proposed that a peak cortisol level greater than or equal to 20 micrograms/dl (550 nmol/liter) is a sufficient single criterion for normal adrenal function as assessed by the rapid ACTH test.

Adrenal Cortex Function Tests↗
PubMed1985

Hyporeninemic hypoaldosteronism. New associations.

Hyporeninemic hypoaldosteronism occurred in a 49-year-old man with chronic endocrine and exocrine pancreatic insufficiency secondary to pancreatectomy and in a 64-year-old man with recurrent pancreatitis, exocrine pancreatic insufficiency, and prolonged magnesium deficiency. Hyporeninemic hypoaldosteronism has never, to our knowledge, been reported in these clinical settings before and may be masked by the malabsorption of pancreatic insufficiency.

Aldosterone↗
PubMed1984

Basophils in peripheral blood and bone marrow. A retrospective review.

The records on 375 consecutive bone marrow aspirations were reviewed to establish the incidence and association of peripheral and bone marrow basophilia. Seventeen cases of peripheral basophilia were identified (4.5 percent incidence) and were associated with iron deficiency (five cases), lung carcinoma (four cases), anemia of undetermined cause (four cases), and chronic myelogenous leukemia, myelodysplasia, chronic renal failure, and acute myelogenous leukemia (one case each). There were six cases of marrow basophilia, including iron-deficiency anemia (two cases), sideroblastic anemia with myelodysplasia, mild dyspoiesis, anemia of chronic disease, and acute erythroleukemia. Marrow basophilia was significantly associated with myelodysplasia and sideroblastic anemia, but was not found in 37 patients with lymphoproliferative disorders. There were no instances of simultaneous marrow and peripheral basophilia. These data support the concept that marrow basophilia is a specific, although not sensitive, marker of disruption of the normal marrow maturation controls.

Basophils↗
PubMed1984

Pleural mesothelial sequestration of iron in the rat.

Examination of morphology and iron deposition in pulmonary tissue from rats loaded with parenteral iron demonstrated a significant increase (compared to controls) of iron in pleural lining cells. No significant differences were noted in iron deposition in macrophages or in lung parenchyma. These results suggest that the pleural surface may represent an unrecognized target tissue in hemochromatosis.

Animals↗
PubMed1983

Renal impairment in experimental hemochromatosis in rats.

Parenteral administration of iron as the complex with nitrilotriacetate resulted in moderate iron deposition in the renal cortex along with heavy deposition of iron in liver, heart, and exocrine pancreas. Iron treated rats exhibited slight but significant changes in serum chemistries consistent with mild renal insufficiency: increased chloride and creatinine and decreased sodium, calcium and CO2 content as a group with isolated increases in urea nitrogen (2/9) and phosphorus (3/9). Serum albumin was decreased and the normal correlation of serum calcium with serum albumin was abolished by iron overload. Although food intake/g body weight was similar in the two groups, both water intake and urine output relative to solute load were increased in iron-overloaded rats. We conclude that the renal insufficiency occasionally reported in human hemochromatosis may reflect a direct nephrotoxic action of iron.

Animals↗
PubMed1983

Plasmapheresis in thyroxine overdose: a case report.

Thyrotoxicosis from an overdose of medicinal thyroid is a condition which may be associated with a significant delay in onset of toxicity. We report a case treated with plasmapheresis, and conclude that the amount of thyroid hormone removed was insignificant compared to the total ingestion. We also note that the plasma half-life of thyroxine is apparently reduced in an acute massive ingestion.

Adult↗
PubMed1982

Developmental changes in rat liver branched-chain 2-oxo acid dehydrogenase.

Branched-chain 2-oxo acid dehydrogenase catalyses the first irreversible step in the degradation of the branched-chain amino acids leucine, isoleucine and valine. With specifically labelled 4-methyl-2-oxo[1-14C]pentanoate as substrate, the enzyme's activity was measured in rat liver homogenates. Activity (per g wet wL of liver or per mg of protein) increased most rapidly during the perinatal period (2 days before to 1 day after birth), reaching approximately adult values by the time of weaning. The apparent Vmax, of the enzyme increased with age, but its Km appeared unchanged. The data suggest that hepatic branched-chain 2-oxo acid dehydrogenase is induced or activated during the perinatal period. The enzyme's activity at birth was unaffected by maternal diabetes, or by treating the mother with pharmacological doses of corticosterone or 3,3',5-tri-iodothyronine, during the last 5 days of pregnancy.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1982

Reversed-phase high-performance liquid chromatography analysis of 6-thioguanine applicable to pharmacologic studies in humans.

6-thioguanine (6TG) and its metabolites were analyzed in human plasma with a reversed-phase high-performance liquid chromatographic methods. 6TG and related compounds were extracted from plasma with an equal volume of 2 N perchloric acid at a 50-100% recovery efficiency. The neutralized extracts were chromatographed on a muBondapak C18 column by two separate isocratic conditions. 6TG, 6-thiouric acid, 6-thioxanthine, 6-thioguanosine, and 6-methylthiouric acid were analyzed with 0.01 M sodium acetate, pH 3.5-10% methanol as the mobile phase and 340 nm for detection. 6-Methylthioguanine and three unknown metabolites were separated with acetate-25% methanol and 310 nm detection. One of the unknowns was identified as 6-methylthioguanosine. External standard calibration was used for quantitation. The 6TG detection limit was 0.8 nmol/ml in plasma.

Chromatography, High Pressure Liquid↗
PubMed1980

Mechanism of the stimulation of branched chain oxoacid oxidation in liver by carnitine.

The oxidation of 4-methyl-2-oxopentanoate (alpha-ketoisocaproate) by rat liver mitochondria was shown to be independent of exogenous coenzyme A and exogenous NAD+. Carnitine stimulated the oxidation of 4-methyl-2-oxopentanoate in rat liver homogenates and mitochondria; octanoate, DL-octanoylcarnitine, 4-pentenoate, and 3-methylbutyrate (isovalerate) were inhibitory, and 2-bromopalmitate had no effect. Addition of carnitine was found to increase the export from the mitochondria of acylcarnitines derived from 4-methyl-2-oxopentanoate in the presence of absence of 4-pentenoate but not in the presence of octanoylcarnitine. It is concluded that the branched chain oxoacid dehydrogenase is localized on the inner surface of the inner mitochondrial membrane and that it is regulated in part by the intramitochondrial levels of branched chain fatty acyl-CoA esters and/or free CoA.

Animals↗
PubMed1980

A caution in the use of tritiated substrates for monoamine oxidase assays.

A monoamine oxidase assay utilizing generally labeled [3H]serotonin as substrate became nonlinear after only approximately 5% conversion of initial c.p.m. to product. Subsequent analysis showed that a significant proportion of the tritium label was readily exchangeable into water and that monoamine oxidase activity increased release of label as water. The use of generally labeled substrates for oxidase activities is not recommended.

Animals↗
PubMed1980

Effects of diabetes on oxidative decarboxylation of branched-chain keto acids.

Oxidative decarboxylation is the first irreversible step in the degradation of leucine. The effect of streptozotocin diabetes on this reaction was studied in cell-free rat liver preparations, using [1-14C]alpha-ketoisocaproate as substrate. Diabetes increased the branched-chain ketoacid dehydrogenase (BCKD) activity (per g liver or per mg protein) of homogenates, but the ratios of homogenate BCKD activity to other mitochondrial markers remained unchanged. A cytosolic branched-chain ketoacid decarboxylase activity (15-22% of homogenate activity), which did not require NAD, CoA, or NADP, was also increased in diabetics. Insulin treatment of diabetics normalized enzyme activity in all fractions. The apparent Km of BCKD in homogenates was 43-45 microM; diabetes increased the apparent Vmax from 165 nmol x min-1 x g tissue-1 to 260 nmol x min-1 x g-1. In contrast, the Km for cytosolic alpha-ketoisocaproate decarboxylation was 270 microM in controls, and diabetes resulted in both a lower Km (210 microM) and a higher Vmax. Adrenalectomy did not affect activity in homogenates from controls, but partially reversed the diabetes-associated increase. Glucagon pretreatment of controls did not affect activity. In summary, distinct mitochondrial and cytosolic enzymes decarboxylate alpha-ketoisocaproate in liver. The increased hepatic capacity of diabetic rats to degrade the carbon skeleton of leucine is attributed mainly to a relative increase in mitochondrial mass.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1980

Iron nitrilotriacetate--induced experimental diabetes in rats.

The etiology of diabetes in some conditions of iron overload is not known. We studied growth, glucose tolerance, and pancreatic islet cell morphology and cytochemistry in rats administered parenteral FeNTA. These rats developed glucosuria, slowing of growth with eventual weight loss, polyuria, polydipsia, and death. They had normal fasting plasma glucose levels but decreased glucose tolerance and insulin response to glucose. Although no Prussian blue staining of iron was observed in pancreatic islets by light microscopy, at the ultrastructural level insulin-secreting beta-cells showed ferrin iron deposits localized to the plasmalemma and the cytoplasmic surface of secretory granule membranes. Prussian blue staining was also observed in parenchymal cells of the liver, heart, and kidney, in order of decreasing intensity. Animals treated with an equivalent dose of NTA, saline, or iron-dextran in saline had normal growth and response to glucose and did not exhibit pancreatic iron deposits at the light or ultrastructural level. These results support the hypothesis that iron affects pancreatic islet cell function and may be an etiologic agent of diabetes mellitus in hemochromatosis.

Acetates↗