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Biomedical subjects

D Clark

Publications and source records attributed to D Clark.

At least 325 records · Page 18Linked to original sources
PubMed1982

The epidemiology of indoor nitrogen dioxide in the U.K.

The results of three studies on the effect of gas cooking on the lung function of children are reported. The studies which have been carried out in England and Scotland with children aged 6-11, 6-7 and 5-6 years, respectively, show that there is only a weak association between indoor levels of NO2 and respiratory illness. Nevertheless, the consistency of the difference in the rate of respiratory diseases in children from homes with electric and gas cookers suggest there is some hazard to the use of unflued gas appliances which may warrant further epidemiological investigation.

Child↗
PubMed1981

Isolation of cytomegalovirus from the amniotic fluid during the third trimester.

A case is presented in which cytomegalovirus was isolated from the amniotic fluid at 36 weeks' gestation in a pregnancy complicated by cytomegalovirus hepatitis at 10 weeks of gestation. Abnormalities noted in the newborn infant included an undescended testis, right equinovarus, and hypotonia. All cultures revealed cytomegalovirus. Subsequent immunoglobulin studies, chest x-ray film, and bone films were all normal.

Adolescent↗
PubMed1981

Relation between high density lipoprotein cholesterol and coronary artery disease in asymptomatic men.

The well established inverse relation of high density lipoprotein cholesterol (HDL) and the risk of coronary artery disease was tested in a cross-sectional group of 572 asymptomatic aircrew members who were being screened for risk of coronary artery disease. A battery of tests was performed, including determinations of fasting serum cholesterol, HDL cholesterol and triglycerides and performance of a maximal symptom-limited exercise tolerance test. Of the 572 patients, 132 also had an abnormal S-T segment response to exercise testing or were otherwise believed to have an increased risk of organic heart disease and subsequently underwent coronary angiography. Significant coronary artery disease was found in 16 men and minimal or subcritical coronary disease in 14; coronary angiograms were normal in the remaining 102 men. The remaining 440 men, who were believed to have a 1 percent chance of having coronary artery disease by sequential testing of risk factors and treadmill testing, had a mean cholesterol level of 213 mg/100 ml, a mean HDL cholesterol of 51 mg/100 ml and a mean cholesterol/HDL ratio of 4.4. The mean values of cholesterol, HDL cholesterol and cholesterol/HDL cholesterol did not differ significantly in men with normal angiographic finding and those with subcritical coronary disease. However, 14 of 16 men with coronary artery disease had a cholesterol/HDL ratio of 6.0 or more whereas only 4 men with normal coronary arteries had a ratio of 6.0 or more. Of the classical coronary risk factors evaluated, the cholesterol/HDL ratio of 6.0 or more had the highest odds ratio (172:1). It appears that determination of HDL cholesterol level helps to identify asymptomatic persons with a greater risk of having coronary artery disease.

Adult↗
PubMed1981

Permeability and susceptibility of Escherichia coli to beta-lactam compounds.

In general, the susceptibility of envelope mutants of Escherichia coli to beta-lactam compounds correlates well with the permeability of these antibiotics through the outer membrane. However, several mutants were isolated which, although apparently freely permeable to penicillins, showed only marginal increases in susceptibility to these agents.

Anti-Bacterial Agents↗
PubMed1981

Regulation of fatty acid degradation in Escherichia coli: analysis by operon fusion.

Fusion of the lacZ gene coding for beta-galactosidase to the fadA,B and fadE operons was accomplished by using the phage Mu d (Apr lac). In such fusion strains, beta-galactosidase was induced by long-chain fatty acids and repressed by glucose, as is the normal pattern of control for the enzymes of the fad regulon. The level of induction seen was approximately 10-fold for both the fadA and fadE operons. These results demonstrate that the previously observed regulation of both the fadA and fadE operons is at the transcriptional level. When an insertion mutation in the fadR (repressor) gene was introduced into the fusion strains, beta-galactosidase was produced constitutively. A series of fatty acids of different chain lengths were tested as inducers. Acids of chain lengths of 10 carbon atoms or less failed to induce, those of 12 carbon atoms induced partly, and those of 14 or more carbon atoms induced fully. Imidazole was found to counteract the glucose repression of the fadA operon as recently demonstrated for the ara operon.

Acyl-CoA Dehydrogenase↗
PubMed1981

Amelioration of the pulmonary effects of massive autotransfusion with corticosteroids in the dog.

In this study, pulmonary changes were investigated following massive autotransfusion with local anticoagulation as well as whether or not corticosteroids would provide a protective effect. Twenty mongrel dogs were bled into the peritoneal cavity and autotransfused with the Sorenson system for a total of twice their blood volume. Blood was reinfused by means of 40 micron effective filters. Ten dogs were given 30 milligrams per kilogram of methylprednisolone sodium succinate at the time that autotransfusion was begun. Dogs of the control group had a decrease in cardiac output and oxygen delivery. Steroid-treated dogs had insignificant hemodynamic changes. Both groups showed a slight rise in pulmonary vascular resistance, but the arterial pO2 and pCO2 were unaltered. Two independent pathologists, in a blind study, examined the upper lobe of the left lung for hemorrhage, congestion, edema and fibrin thrombi. Nine of ten dogs in the control study had marked changes. A similar degree of alteration was recorded in only five of ten dogs in the steroid treated group. Corticosteroids mitigated the deleterious effects of massive autotransfusion in a canine model, and this may indicate their use in the critically injured patients undergoing this procedure.

Adrenal Cortex Hormones↗
PubMed1980

Regulation of phospholipid biosynthesis in Escherichia coli. Cloning of the structural gene for the biosynthetic sn-glycerol-3-phosphate dehydrogenase.

The structural gene for the Escherichia coli biosynthetic sn-glycerol-3-phosphate (glycerol-P) dehydrogenase gpsA, was transferred from a defective transducing phage (lambda dcysE, gpsA) into the Eco RI site of plasmid pMB9 by recombinant DNA techniques. The recombinant plasmids suppressed the glycerol-P requirement of gpsA- mutants and strains bearing one such plasmid, pDC2, overproduced the glycerol-P dehydrogenase about 60-fold. The glycerol-P dehydrogenase from a strain bearing the pDC2 was purified 200-fold to homogeneity. This is contrasted to the 12,000-fold purification required to purify the enzyme from a wild type strain (Edgar, J. R., and Bell, R. M. (1978) J. Biol. Chem. 253, 6348-6353). The homogeneous enzyme purified from a strain bearing the pDC2 plasmide was strongly inhibited by glycerol-P (Ki of 2.5 microM). The introduction of the pDC2 plasmid into glycerol-P auxotrophs containing a Km-defective glycerol-P acyltranferase, defined by the plsB locus, caused a 60-fold overproduction of the glycerol-P requirement. This strongly suggests that the intracellular level of glycerol-P is stringently regulated in vivo by a mechanism involving feedback inhibition of the glycerol-P dehydrogenase by glycerol-P.

Cloning, Molecular↗
PubMed1980

Escherichia coli mutants with altered control of alcohol dehydrogenase and nitrate reductase.

Mutants of Escherichia coli which overproduce alcohol dehydrogenase were obtained by selection for the ability to use ethanol as an acetate source in a strain auxotrophic for acetate. A mutant having a 20-fold overproduction of alcohol dehydrogenase was able to use ethanol only to fulfill its acetate requirement, whereas two mutants with a 60-fold overproduction were able to use ethanol as a sole carbon source. The latter two mutants produced only 25% of the wild-type level of nitrate reductase, when grown under anaerobic conditions. Alcohol dehydrogenase production was largely unaffected by catabolite repression but was repressed by nitrate under both aerobic and anaerobic conditions. The genetic locus responsible for alcohol dehydrogenase overproduction was located at min 27 on the E. coli genetic map; the gene order, as determined by transduction, was trp tonB adh chlC hemA. The possible relationship of alcohol dehydrogenase to anaerobic redox systems such as formate-nitrate reductase is discussed.

Alcohol Oxidoreductases↗