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Biomedical subjects

P W Colley

Publications and source records attributed to P W Colley.

8 recordsLinked to original sources
PubMed1996

Cystic fibrosis carrier screening in two New South Wales country towns.

OBJECTIVE: To assess the feasibility of offering community testing for carrier status of delta F508, a gene mutation associated with cystic fibrosis (CF). DESIGN: Prospective pilot survey. SETTING: General practice, the two main high schools and workplaces in the country towns of Young and Harden (combined population, 14,940; with 7707 people aged 16-55 years) in New South Wales (NSW). PARTICIPANTS: Individuals aged 16 years and over. MAIN OUTCOME MEASURES: Number of delta F508 carriers, test uptake rates, mode of learning about the testing, motivation for testing, retention of knowledge about CF, and test results and emotional effects of knowledge about carrier status. RESULTS: We tested 610 people (8% of the population aged 16-55 years) and identified 47 carriers (20% of the expected number in the 7707 people aged 16-55 years). Testing in schools had the highest uptake. Retention of knowledge was high; all delta F508-positive individuals recalled their carrier status accurately. Anxiety was transient among carriers; over 90% of all respondents felt they had made the right decision to be tested. CONCLUSIONS: We recommend community testing for carrier detection and suggest targeting those with a family history of CF and girls aged over 16 in high schools.

Adolescent↗
PubMed1994

Clinical and linkage study of a large family with simple ectopia lentis linked to FBN1.

Simple ectopia lentis (EL) was studied in a large family, by clinical examination and analysis of linkage to markers in the region of FBN1, the gene for fibrillin which causes Marfan syndrome on chromosome 15. No patient had clinical or echocardiographic evidence of Marfan syndrome, although there was a trend towards relatively longer measurements of height; lower segment; arm span; middle finger, hand, and foot length in the affected members of the family, compared with unaffected sibs of the same sex. Analysis of linkage to intragenic FBN1 markers was inconclusive because they were relatively uniformative. Construction of a multipoint background map from the CEPH reference families identified microsatellite markers linked closely to FBN1 which could demonstrate linkage of EL in this family to the FBN1 region. LINKMAP analysis detected a multipoint lod score of 5.68 at D15S119, a marker approximately 6 cM distal to FBN1, and a multipoint lod score of 5.04 at FBN1. The EL gene in this family is likely to be allelic to Marfan syndrome, and molecular characterization of the FBN1 mutation should now be possible.

Adolescent↗
PubMed1988

Chronic ethanol administration depresses fatty acid synthesis in rat adipose tissue.

Administration of ethanol as part of a nutritionally adequate liquid diet to female Wistar rats was found to depress markedly incorporation of labelled glucose into adipose-tissue acylglycerol fatty acids. Similar results with labelled pyruvate and acetate suggested inhibition of the fatty-acid-synthesis pathway at, or distal to, the acetyl-CoA carboxylase step. Activities of acetyl-CoA carboxylase and fatty acid synthetase were markedly lower in ethanol-fed animals. The activity of another lipogenic enzyme, phosphatidate phosphohydrolase, was not affected by chronic ethanol feeding. These findings suggest that chronic ethanol administration has marked effects on adipose-tissue lipogenesis.

Acetates↗
PubMed1986

Decrease in lipogenesis and glucose oxidation of rat adipose tissue after chronic ethanol feeding.

This investigation was performed to determine whether chronic ethanol feeding affects adipose tissue lipogenesis and glucose metabolism. Female Wistar rats were pair-fed nutritionally adequate liquid diets containing ethanol as 36% of energy or an isocaloric amount of carbohydrate for 3 weeks. Chronic ethanol feeding resulted in a depression of adipose tissue lipogenesis as assessed by labeled glucose incorporation into glyceride glycerol and glyceride fatty acids. Glucose oxidation was also impaired after chronic ethanol feeding. Such changes may contribute to the postprandial hypertriacyglyceridemia observed in alcoholics.

Adipose Tissue↗
PubMed1983

Increased phospholipid synthesis in the stimulated rat and human pancreas.

Stimulation of the exocrine pancreas is associated with marked changes in pancreatic phospholipid metabolism. It has been previously established that de novo synthesis of phospholipids constitutes part of this "phospholipid effect". This study has demonstrated that in vitro stimulation of the rat pancreas utilising bethanecol and pancreozymin results in increased incorporation of labelled glucose into phosphatidyl inositol and, to a lesser extent, other phospholipids, suggesting increased de novo synthesis of these compounds. However, secretin which is believed to act via a different intracellular pathway, did not exert such an effect. The relevance of this animal model is indicated by the demonstration of increased incorporation of labelled glucose into phospholipids of human pancreas stimulated in vitro by bethanecol or sincalide (the active carboxy terminal octapeptide of pancreozymin).

Animals↗
PubMed1982

Alcohol causes a fatty pancreas. A rat model of ethanol-induced pancreatic steatosis.

To develop an animal mode of alcoholic pancreatic steatosis, female Wistar rats were pair fed liquid diets, containing ethanol as 36% of calories or an isocaloric amount of carbohydrate for 3 weeks. Electron microscopic examination showed lipid vesicles localized principally at the bases of pancreatic acinar cells in the ethanol-fed rats. Ethanol feeding significantly increased pancreatic content of cholesteryl ester without changing levels of other lipids. Ethanol feeding enhanced labeled acetate, palmitate, oleate, and linoleate incorporation into cholesteryl ester. Therefore, increased esterification of cholesterol may, in part, explain the observed accumulation of cholesteryl ester.

Alcoholism↗
PubMed1981

Ethanol-induced changes in cardiac lipid metabolism.

The influence of ethanol on cardiac lipid metabolism has been investigated in the rat. Acute in vitro ethanol significantly stimulated the incorporation of 14C-1-acetate but not 14C-U-glucose into cardiac lipid in rats fed a diet free of ethanol for 3 weeks. Stimulation of incorporation was not uniform but was confined to the diglyceride and triglyceride fractions. This response of cardiac tissue lipid metabolism to acute ethanol was not observed in rats pair fed an isocaloric diet containing 36% of calories as ethanol. Chronic ethanol feeding significantly increased cardiac triglyceride content when compared with pair-fed controls. It also stimulated oxidation of labeled palmitate, but did not affect in vitro lipogenesis.

Animals↗