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Biomedical subjects

D M Lloyd

Publications and source records attributed to D M Lloyd.

8 recordsLinked to original sources
PubMed1992

Audit of general practitioner referrals to an acute surgical unit.

One hundred and ninety referrals from general practitioners (GPs) to an acute surgical unit were audited prospectively over a 6-month period. A total of 78 admissions were considered inappropriate of whom 23 patients were thought to have needed neither surgical admission nor opinion. The estimated expenditure resulting from admissions deemed inappropriate was 25,000 pounds. The daytime commitments of more senior staff on routine emergency duty days meant they were not easily available to deal with calls concerning acute GP referrals. These admissions reduce the efficiency of the service; this may be improved by a senior member of the team accepting and screening GP calls.

Acute Disease↗
PubMed1992

Role of sequential leucocyte counts and C-reactive protein measurements in acute appendicitis.

The accurate clinical diagnosis of acute appendicitis is difficult, and many techniques have been suggested to improve diagnostic accuracy such as laparoscopy, ultrasonography and barium enema examination. In this study serial total leucocyte counts and serial C-reactive protein (CRP) concentrations in acute appendicitis were measured. The sensitivity and specificity of serial leucocyte counts in acute appendicitis were 92 and 100 per cent, and for CRP concentrations 69 and 75 per cent, respectively. The sensitivity and specificity of serial total leucocyte counts fulfilled the criteria for a diagnostic test. It is suggested that in patients with equivocal clinical findings, clinical observation combined with serial leucocyte counts may improve decision making.

Acute Disease↗
PubMed1991

Passive smoking and the risk of heart attack or coronary death.

OBJECTIVES: To estimate the prevalence of passive smoking in an Australian population, the magnitude of risk of myocardial infarction or coronary death associated with passive smoking and the extent to which fibrinogen concentrations might be affected by passive smoking. DESIGN: A population-based case-control study of myocardial infarction or coronary death and passive smoking, and measurement of fibrinogen in a random sample from the same population. SETTING AND PARTICIPANTS: Residents of the Lower Hunter Region of New South Wales aged 35-69 years in 1988-1989. Case subjects were all those who suffered myocardial infarction or coronary death. Control subjects were participants in a risk factor prevalence survey. OUTCOME MEASURES: Myocardial infarction or coronary death, defined by criteria of the WHO MONICA Project, and fibrinogen concentration (measured in controls only). RESULTS: Prevalence of passive smoking at home was 20% for male case subjects, 13% for male control subjects, 29% for female case subjects and 19% for female control subjects. The corresponding prevalence rates for passive smoking at work were 40%, 44%, 41% and 37%. Odds ratios of myocardial infarction or coronary death for active smokers compared with non-smokers were 4.70 (95% confidence interval [CI], 3.35-6.58) in women and 2.71 (95% CI, 2.07-3.53) in men. For women the odds ratios of myocardial infarction or coronary death for those exposed to passive smoking at home were 2.46 (95% CI, 1.47-4.13) among non-smokers and 1.48 (95% CI, 0.67-3.30) among ex-smokers. For men the odds ratios for passive smoking at home were 0.97 (95% CI, 0.50-1.86) for non-smokers and 1.78 (95% CI, 1.13-2.79) for ex-smokers. The odds ratios for passive smoking at work did not suggest increased risk. Fibrinogen concentrations were generally higher among people exposed to passive smoking at home or work compared with those not exposed but were not as high as concentrations in active smokers. CONCLUSIONS: Passive smoking increases the risk of coronary heart disease and increased fibrinogen concentration provides a marker of its effect.

Adult↗
PubMed1991

How soon after quitting smoking does risk of heart attack decline?

A population-based case-control study (involving 1282 cases and 2068 controls) was conducted to examine the risk of myocardial infarction or coronary death after cigarette smokers quit smoking. The odds ratios for current smokers were significantly elevated compared to non-smokers (OR = 2.7 for men and OR = 4.7 for women). For ex-smokers odds ratios declined rapidly after quitting and after about 3 years they were not significantly different from unity. Fibrinogen concentrations measured in the controls only were higher in current smokers and ex-smokers up to 2 years after quitting than in non-smokers and after that time were similar to levels in non-smokers; however, most of the differences among categories of smokers were not statistically significant. These results support the hypothesis that risk of a coronary event in ex-smokers declines rapidly after quitting and within 2-3 years is similar to the risk for non-smokers.

Adult↗
PubMed1976

Studies on oxidative phosphorylation and steroidogenesis by ovarian mitochondria after gonadotropic stimulation.

No differences in oxidative phosphorylation or in the per cent of [4-14C]progesterone were found in ovarian mitochondria of immature rats after treatment with 20 IU of pregnant mare serum gonadotropin (PMSG) iv 30 min before killing. However, treatment of immature rats with 20 IU of PMSG sc 54 h prior to killing decreased the ADP:O ratio and increased the per cent of [4-14C]cholesterol conversion. Electron microscopic studies showed that mitochondria with lamellar cristae were prominent in ovaries of untreated rats, while large pleomorphic mitochondria and mitochondria with tubulovesicular cristae dominated in ovaries of PMSG-treated rats. Ovarian homogenates separated by zonal centrifugation showed three peaks od cytochrome oxidase activity which shifted to the heavier end of the gradient after PMSG treatment. These studies suggest that PMSG treatment influences ovarian mitochondria, possibly by stimulating the synthesis of additional functional components and/or the biogenesis of new mitochondria. Aminoglutethimide addition to bovine luteal mitochondria decreased steroidogenesis by 60% when succinate was used as substrate. However, there was a 16% increase in the ADP:O ratio, apparently due to a decrease in oxygen utilization. When oligomycin was added to luteal mitochondria, there was a 30% decrease in the ACP:O ratio but a 300% increase in [4-14C]cholesterol conversion. Dinitrophenol also decreased mitochondrial steroidogenesis. These results suggest that energy obtained from succinate oxidation can be diverted from phosphorylation to support steroidogenesis.

Age Factors↗