59 resultados para Crumpton, H. J. (Hezekiah John), b. 1828.
em University of Queensland eSpace - Australia
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Regional and national surveys provide a broadscale description of the koala's present distribution in Australia. A detailed understanding of its distribution is precluded, however, by past and continuing land clearing across large parts of the koala's range. Koala population density increased in some regions during the late 1800s and then declined dramatically in the early 1900s. The decline was associated with habitat loss, hunting, disease, fire, and drought. Declines are continuing in Queensland and New South Wales. In contrast, dense koala populations in habitat isolates in Victoria and South Australia are managed to reduce population size and browse damage. Current understanding of koala distribution and abundance suggests that the species does not meet Australian criteria as endangered or vulnerable fauna. Its conservation status needs to be reviewed, however, in light of the extensive land clearing in New South Wales and Queensland since the last (1980s) broadscale surveys. Consequently, we recommend that broadacre clearing by curtailed in New South Wales and Queensland and that regular, comprehensive, standardized, national koala surveys be undertaken. Given the fragmentation of koala habitat and regional differences in the status of the koala, we recommended that studies on regional variation in the koala be intensified and that koala ecology in fragmented and naturally restricted habitats be developed. More generally, the National Koala Conservation Strategy should be implemented.
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Birthweight affects neonatal mortality and morbidity and has been used as a marker of foetal undernutrition in studies of prenatal effects on adult characteristics. It is potentially influenced by genetic and environmental influences on the mother, and effects of foetal genotype, which is partially derived from the maternal genotype. Interpretations of variation in birthweight and associated characteristics as being due to prenatal environment ignore other possible modes of materno-foetal transmission. Subjects were adult twins recruited through the Australian Twin Registry, aged 17 to 87 years, and the sample comprised 1820 men and 4048 women. Twins reported their own birthweight as part of a health questionnaire. Body Mass Index (BMI) was calculated from self-reports of height and weight. Correlations between co-twins' birthweights were high for both monozygotic (r = 0.77) and dizygotic (r = 0.67) pairs, leading to substantial estimates of shared environmental effects (56% of variance) with significant additive genetic (23%) and non-shared environmental (21%) components. Adult BMI was mainly influenced by genetic factors, both additive (36% of variance) and nonadditive (35%). The correlation between birthweight and BMI was positive, in that heavier babies became on average more obese adults. A bivariate model of birthweight and adult BMI showed significant positive genetic (rg = 0.16, p = 0.005) and environmental (re = 0.08, p = 0.000011) correlations. Intra-uterine environmental or perinatal influences shared by cotwins exercise a strong influence on birthweight, but the factors which affect both birthweight and adult BMI are partly genetic and partly non-shared environmental.
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Variation in the personality trait of neuroticism is known to be affected by genetic influences, but despite a number of association studies, the genes involved have not yet been characterized. In a recent study of platelet monoamine oxidase in 1,551 twin subjects, we found a significant association between monoamine oxidase activity and scores on the Eysenck Personality Questionnaire neuroticism scale. Further analyses presented here indicate that both neuroticism and monoamine oxidase activity are associated with variation in smoking habits, and that adjusting for the effect of smoking strengthens the association between MAO and neuroticism. Analysis of the genetic and environmental sources of covariation between neuroticism, smoking, and monoamine oxidase activity show that approximately 8% of the genetic variance in neuroticism is due to the same additive genetic effects that contribute to variation in monoamine oxidase activity, suggesting that variation in neuroticism is associated in part with aspects of serotonin metabolism. (C) 2001 Wiley-Liss, Inc.
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Background: Alcohol increases body iron stores. Alcohol and iron may increase oxidative stress and the risk of alcohol-related liver disease. The relationship between low or safe levels of alcohol use and indices of body iron stores, and the factors that affect the alcohol-iron relationship, have not been fully characterized. Other aspects of the biological response to alcohol use have been reported to depend on iron status. Methods: We have measured serum iron, transferrin, and ferritin as indices of iron stores in 3375 adult twin subjects recruited through the Australian Twin Registry. Information on alcohol use and dependence and smoking was obtained from questionnaires and interviews. Results: Serum iron and ferritin increased progressively across classes of alcohol intake. The effects of beer consumption were greater than those of wine or spirits. Ferritin concentration was significantly higher in subjects who had ever been alcohol dependent. There was no evidence of interactions between HFE genotype or body mass index and alcohol. Alcohol intake-adjusted carbohydrate-deficient transferrin was increased in women in the lowest quartile of ferritin results, whereas adjusted gamma -glutamyltransferase, aspartate aminotransferase, and alanine aminotransferase values were increased in subjects with high ferritin. Conclusions: Alcohol intake at low level increases ferritin and, by inference, body iron stores. This may be either beneficial or harmful, depending on circumstances. The response of biological markers of alcohol intake can be affected by body iron stores; this has implications for test sensitivity and specificity and for variation in biological responses to alcohol use.
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The Alcohol Use Disorders Identification Test (AUDIT) has been used widely and is reported to be superior to conventional questionnaires in detection of current hazardous and harmful alcohol use. We assessed the validity of an Australian modification of the AUDIT (the AusAUDIT), which has been employed widely in Australian and New Zealand early intervention programmes. We used a cross-sectional study of 370 subjects from the follow-up phase of a randomized controlled trial of early intervention to reduce hazardous alcohol consumption. Scores on the AusAUDIT were compared against 12-month ICD-10 diagnoses of harmful alcohol use and dependence, as determined by the Composite International Diagnostic Interview, and against self-report of alcohol consumption exceeding Australian National Health and Medical Research Council (NH&MRC) recommended limits. AusAUDIT had good internal consistency and discriminated significantly between persons meeting criteria for ICD-10 alcohol use disorders, and drinkers who did not. At currently recommended cut-off scores, AusAUDIT detected more than 85% of people meeting criteria for ICD-10 alcohol use disorders, or drinking over NH&MRC recommended limits, but its specificity was limited (29% in men, and 58% in women for drinking over NH&MRC limits). No subset of questions performed as well as the full AusAUDIT in detection of drinking problems, but the alcohol consumption items provided a reasonable screen for drinking over NH&MRC limits. We conclude that AusAUDIT is effective in detecting problematic drinking, but positive cases should be confirmed by clinical assessment. The findings illustrate the need for validation of questionnaire modifications, and the difficulty in increasing test sensitivity without reducing specificity.
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Background: Several studies have shown that variation in serum gamma-glutamyltransferase (GGT) in the population is associated with risk of death or development of cardiovascular disease, type 2 diabetes, stroke, or hypertension. This association is only partly explained by associations between GGT and recognized risk factors. Our aim was to estimate the relative importance of genetic and environmental sources of variation in GGT as well as genetic and environmental sources of covariation between GGT and other liver enzymes and markers of cardiovascular risk in adult twin pairs. Methods: We recruited 1134 men and 2241 women through the Australian Twin Registry. Data were collected through mailed questionnaires, telephone interviews, and by analysis of blood samples. Sources of variation in GGT, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) and of covariation between GGT and cardiovascular risk factors were assessed by maximum-likelihood model-fitting. Results: Serum GGT, ALT, and AST were affected by additive genetic and nonshared environmental factors, with heritabilities estimated at 0.52, 0.48, and 0.32, respectively. One-half of the genetic variance in GGT was shared with ALT, AST, or both. There were highly significant correlations between GGT and body mass index; serum lipids, lipoproteins, glucose, and insulin; and blood pressure. These correlations were more attributable to genes that affect both GGT and known cardiovascular risk factors than to environmental factors. Conclusions: Variation in serum enzymes that reflect liver function showed significant genetic effects, and there was evidence that both genetic and environmental factors that affect these enzymes can also affect cardiovascular risk. (C) 2002 American Association for Clinical Chemistry.
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This study investigated the influence of genes and environment on the variation of apolipoprotein and lipid levels, which are important intermediate phenotypes in the pathways toward cardiovascular disease. Heritability estimates are presented, including those for apolipoprotein E and All levels which have rarely been reported before. We studied twin samples from the Netherlands (two cohorts; n = 160 pairs, aged 13-22 and n = 204 pairs, aged 34-62), Australia (n = 1362 pairs, aged 28-92) and Sweden (n = 302 pairs, aged 42-88). The variation of apolipoprotein and lipid levels depended largely on the influences of additive genetic factors in each twin sample. There was no significant evidence for the influence of common environment. No sex differences in heritability estimates for any phenotype in any of the samples were observed. Heritabilities ranged from 0.48-0.87, with most heritabilities exceeding 0.60. The heritability estimates in the Dutch samples were significantly higher than in the Australian sample. The heritabilities for the Swedish were intermediate to the Dutch and the Australian samples and not significantly different from the heritabilities in these other two samples. Although sample specific effects are present, we have shown that genes play a major role in determining the variance of apolipoprotein and lipid levels in four independent twin samples from three different countries.
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Previous studies have shown a significant effect of insulin administration on serum dehydroepiandrosterone sulfate (DHEA-S) concentration and its metabolic rate, with evidence for the effect in men, but not in women. This could lead to differences in the sources of variation in serum DHEA-S between men and women and in its covariation with insulin concentration. This study aimed to test whether these hypotheses were supported in a sample of healthy adult twins. Serum DHEA-S (n=2287) and plasma insulin (n=2436) were measured in samples from adult male and female twins recruited through the Australian Twin Registry. Models of genetic and environmental sources of variation and covariation were tested against the data. DHEA-S showed substantial genetic effects in both men and women after adjustment for covariates, including sex, age, body mass index, and time since the last meal. There was no significant phenotypic or genetic correlation between DHEA-S and insulin in either men or women. Despite the experimental evidence for insulin infusion producing a reduction in serum DHEA-S and some effect of meals on the observed DHEA-S concentration, there were no associations between insulin and DHEA-S at the population level. Variations in DHEA-S are due to age, sex, obesity, and substantial polygenic genetic influences.
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Buddhism, the Thai state religion, teaches that use of intoxicants should be avoided. Nonetheless, many Thai people drink alcohol, and a proportion are alcohol-dependent or hazardous or harmful drinkers. This study examines the relationship between Buddhist upbringing and beliefs and alcohol use disorders in Thai men. Three groups, comprising 144 non/infrequent/light drinkers, 77 hazardous/harmful drinkers and 91 alcohol dependents were inter-viewed regarding their early religious life and current religious practices and beliefs. No protective association was shown between early religious life and later alcohol use disorders, indeed, having lived as a buy in a temple for a period was commoner in those with adult alcohol problems. Few subjects reported frequent involvement in current religious activities (9, 8 and 6% in the non/infrequent/light drinkers, hazardous/harmful drinkers, and alcohol dependents respectively). Hazardous/harmful drinkers [odds ratio (OR) = 0.4, 95% confidence interval (0) = 0.2-0.9] and alcohol dependents (OR = 0.5, 95% Cl = 0.2-0.9) were less likely to report being moderately to strongly religious, than were non/infrequent/light drinkers, Understanding the association between religious beliefs and drinking behaviour can potentially assist in the development of prevention and treatment programmes.
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Background: Estimates of the performance of carbohydrate deficient transferrin (CDT) and gamma glutamyltransferase (GGT) as markers of alcohol consumption have varied widely. Studies have differed in design and subject characteristics. The WHO/ISBRA Collaborative Study allows assessment and comparison of CDT, GGT, and aspartate aminotransferase (AST) as markers of drinking in a large, well-characterized, multicenter sample. Methods: A total of 1863 subjects were recruited from five countries (Australia, Brazil, Canada, Finland, and Japan). Recruitment was stratified by alcohol use, age, and sex. Demographic characteristics, alcohol consumption, and presence of ICD-10 dependence were recorded using an interview schedule based on the AUDADIS, CDT was assayed using CDTect(TM) and GGT and AST by standard methods. Statistical techniques included receiver operating characteristic (ROC) analysis. Multiple regression was used to measure the impact of factors other than alcohol on test performance. Results: CDT and GGT had comparable performance on ROC analysis, with AST performing slightly less well. CDT was a slightly but significantly better marker of high-risk consumption in men. All were more effective for detection of high-risk rather than intermediate-risk drinking. CDT and GGT levels were influenced by body mass index, sex, age, and smoking status. Conclusions: CDT was little better than GGT in detecting high- or intermediate-risk alcohol consumption in this large, multicenter, predominantly community-based sample. As the two tests are relatively independent of each other, their combination is likely to provide better performance than either test alone, Test interpretation should take account sex, age. and body mass index.
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Aims To identify influences on the development of alcohol use disorders in a Thai population, particularly parental drinking and childhood environment. Design Case-control study. Setting A university hospital, a regional hospital and a community hospital in southern Thailand. Participants Ninety-one alcohol-dependents and 177 hazardous/harmful drinkers were recruited as cases and 144 non-or infrequent drinkers as controls. Measurements Data on parental drinking, family demographic characteristics, family activities, parental disciplinary practice, early religious life and conduct disorder were obtained using a structured interview questionnaire. The main outcome measure was the subject's classification as alcohol-dependent, hazardous/harmful drinker or non-/infrequent drinker. Findings A significant relationship was found between having a drinking father and the occurrence of hazardous/harmful drinking or alcohol dependence in the subjects. Childhood factors (conduct disorder and having been a temple boy, relative probability ratios, RPRs and 95% CI: 6.39, 2.81-14.55 and 2.21, 1.19-4.08, respectively) also significantly predicted alcohol dependence, while perceived poverty and ethnic alienation was reported less frequently by hazardous/harmful drinkers and alcohol-dependents (RPRS and 95% CIs = 0.34, 0.19-0.62 and 0.59, 0.38-0.93, respectively) than the controls. The relative probability ratio for the effect of the father's infrequent drinking on the son's alcohol dependence was 2.92 (95% CI = 1.42-6.02) and for the father's heavy or dependent drinking 2.84 (95% CI=1.31-6.15). Conclusions Being exposed to a light-drinking, father increases the risk of a son's alcohol use disorders exhibited either as hazardous-harmful or dependent drinking. However, exposure to a heavy- or dependent-drinking father is associated more uniquely with an increased risk of his son being alcohol-dependent. The extent to which this is seen in other cultures is worthy of exploration.