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Biomedical subjects

D Brown

Publications and source records attributed to D Brown.

At least 1,099 records · Page 61Linked to original sources
PubMed1975

The use of corticosteroids in the treatment of acute asthma.

A study of 23 patients admitted to hospital with severe acute asthma is reported in which plasma cortisol level on admission was significantly correlated with the degree of acidaemia and pulse rate. Patients who had not previously received treatment with corticosteroids responded satisfactorily to repeated daily injections of tetracosactrin depot, the rate of improvement being comparable to that observed in other patients treated with intravenous hydrocortisone hemisuccinate. A prompt and sustained rise in plasma cortisol was also seen following tetracosactrin. The total daily dose of hydrocortisone required to achieve plasma cortisol levels above 100 mug/100 ml was less when given by continuous intravenous infusion compared with intermittent injections, and a regime of 3 mg/kg body weight every six hours by infusion appeared satisfactory. Most patients reported subjective improvement by about four hours after starting treatment but objective evidence did not appear until about six hours from the start. Measurements of FEV1 and FVC proved to be the most reliable indices of the beginning of improvement although pulse rate was the first index to show maximum improvement. Previous maintenance treatment with corticosteroids in patients with asthma did not appear materially to affect the plasma half-life of intravenous hydrocortisone (4 mgm/kg body weight) when compared with healthy subjects or other patients with asthma who had not previously been treated with corticosteroids.

Acute Disease↗
PubMed1974

DNA polymerase I-dependent mutants of coliphage lambda.

Mutagenized lysates of bacteriophage lambda were screened for mutants unable to plate on DNA polymerase I-deficient (polA(-)) hosts. The mutants obtained were all recombination deficient (red(-)). These mutants, like red(-) and gam(-) mutants previously isolated by others, grow more poorly than wild-type lambda even on polA(+) hosts (burst size 14 to 30% of wild-type lambda.) In a polA(-) host, the burst size of red(-) and gam(-) mutants is reduced an additional five- to tenfold, and lysis is delayed. Wild-type lambda grows normally in polA(-) hosts. Neither lambdaN(-)nin (which doesn't express red or gam) nor lambdabio phages (from which all or part of the red-gam region is deleted) form plaques on polA(-) hosts. Apparent revertants, able to plate on polA(-) hosts, have been selected from both lambdaN(-)nin and lambdabio. Those derived from N(-)nin seem to be N(-)nin cro(-) mutants; whereas those coming from lambda bio have a new bypass mutation (pas) that lies between genes P and Q.

Chromosome Mapping↗
PubMed1974

Enhanced phagocytic capacity. The biologic basis for the elevated histochemical nitroblue tetrazolium reaction.

The biologic basis for the elevated histochemical reduction of nitroblue tetrazolium dye (NBT) in neutrophils from patients with acute bacterial infection or polycythemia vera was studied. A precipitin reaction followed mixing NBT with heparin. NBT was reduced after phagocytosis of this complex (H-NBT) by polymorphonuclear leukocytes (PMNs). Ingestion required divalent cations and was facilitated by the presence of complement. H-NBT incubated with normal but not with C2-deficient human serum converted native C3 to its inactive form. Phagocytic indices were determined in patients and controls by measuring O(2) utilization and hexose monophosphate shunt activity and by visually counting cell-associated latex particles. Significant elevations above controls were observed in phagocytes isolated from all patients with elevated histochemical NBT scores when H-NBT complex, latex, or zymosan was employed as the phagocytic particle. Increased indices were observed in the presence of fresh AB serum, heat-inactivated AB serum, or without serum. Serum from patients with elevated NBT scores did not alter phagocytosis in control phagocytes. With NADH and NADPH as substrates, total NBT diaphorase activity of sonicated leukocytes was normal in all patients. These results suggest that increased phagocytic capacity of PMNs is the primary cause of increased histochemical NBT reduction. The PMNs of patients with acute bacterial infection or polycythemia vera may have alterations in their cell membranes which lead to an enhanced rate of phagocytosis.

Animals↗