171 resultados para Substance abuse
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A competitive RT-PCR assay was used to quantify the expression of the GABA(A) receptor beta(1), beta(2) and beta(3) isoform mRNA transcripts in the superior frontal cortex and motor cortex of 21 control and 22 alcoholic cases. A single set of primers was designed that permitted amplification of all three transcripts and the internal standard simultaneously; differentiation of the individual transcripts was achieved by restriction enzyme digestion. Construction of a standard curve, using the internal standard and a concentration range of beta(2) cRNA-enabled quantitation of mRNA expression levels. No significant difference in mRNA expression was found between the control and alcoholic case groups in either the superior frontal or motor cortex for the beta(2) or beta(3) isoforms. A significant interaction was found between isoform and area, although, the two case groups did not partition on this measure. The interaction was due to a significant difference between superior frontal and motor cortex for the beta(3) isoform; this regional comparison was not significant for beta(2) mRNA. Age at death and post-mortem delay (PMD) had no significant effect on beta mRNA expression in either case group in either region. A beta(1) signal could not be detected in the RT-PCR assay. (C) 2004 Elsevier Ltd. All rights reserved.
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The purpose of this analysis is threefold: first, to extract from the literature, current levels of GP detection of at-risk drinking by their patients, rates at which general practitioners (GPs) offer an intervention; and the effectiveness of these interventions; secondly, to develop a model based on this literature to be used in conjunction with scenario analysis; and thirdly, to consider the cost implications of current efforts and various scenarios. This study deals specifically with Australian general practice. A two-step procedure is used in the scenario analysis, which involves identifying opportunities for detection, intervention, effectiveness and assigning probabilities to outcomes. The results suggest that increasing rates of GP intervention achieves greatest benefit and return on resource use. For every 5% point increase in the rate of GP intervention, an additional 26 754 at-risk drinkers modify their drinking behaviour at a cost of $231.45 per patient. This compares with a cost per patient modifying drinking behaviour of $232.60 and $208.31 for every 5% point increase in the rates of detection and effectiveness, respectively. The knowledge, skill and attitude of practitioners toward drinking are significant, and they can be the prime motivators in persuading their patients to modify drinking behaviour.
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This study investigated smoking behaviour among Indigenous youth. A sample of schools (n = 12) in north Queensland with large proportions of Indigenous students was selected. Details about the prevalence of smoking behaviour in both Indigenous and non-Indigenous students ( n = 883) were gathered. Data were also collected on the cultural, social, and psychological factors associated with cigarette smoking for Indigenous and non-Indigenous students. This survey indicated smoking rates for Indigenous and non-Indigenous students were 24% and 30%, respectively. The study found similarities between both groups regarding where they obtained their cigarettes ( friends) and their reasons for not smoking ( their parents and health). Results of this survey challenge the belief that Indigenous youth are significantly different in their smoking patterns and behaviours compared to non-Indigenous secondary school students in rural regions. It indicated the potential importance of school communities in promoting non-smoking behaviours among Indigenous students even in the face of strong normative pressures from elsewhere in the community. This survey can be used to monitor smoking prevalence among Indigenous secondary students in north Queensland, help guide the development of culturally appropriate school curriculum resources and contribute to the overall evaluation of smoking prevention and smoking cessation programs which are developed for Indigenous secondary school students.
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Alcohol dependence may result from neuroadaptation involving alteration of gene expression after long-term alcohol exposure. The systematic study of gene expression profiles of the human alcoholic brain was initiated using the method of polymerase chain reaction (PCR)-differential display and was followed by DNA microarray. To date, more than 100 alcohol-responsive genes have been identified from the frontal cortex, motor cortex and nucleus accumbens of the human brain. These genes have a wide range of functions in the brain and indicate diverse actions of alcohol on neuronal function. This review discusses the current information on the genetic basis of alcoholism and the induction and characterization of these alcohol-responsive genes.
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Background Strong evidence exists for the efficacy of screening and brief intervention for reducing hazardous drinking. However, problems have been highlighted with respect to its implementation in health-care systems, not least of which is a reluctance of some doctors to discuss alcohol proactively with their patients. Aims To determine the efficacy of a novel web-based screening and brief intervention (e-SBI) to reduce hazardous drinking. Design A double-blind randomized controlled trial. Setting A university student health service. Participants A total of 16 7 students (17-26 years) were recruited in the reception area and completed a 3-minute web-based screen including the Alcohol Use Disorder Identifiation Test (AUDIT) questionnaire. Of these, 112 tested positive, and 104 (52 females) who consented to follow-up were included in the trial. Measurements Drinking frequency, typical occasion quantity, total volume, heavy episode frequency (females > 80 g ethanol, males > 120 g ethanol), number of personal problems, an academic problems score. Intervention Participants were randomized to 10-15 minutes of web-based assessment and personalized feedback on their drinking (intervention, n = 5 1) or to a leaflet-only control group (n = 5 3). Findings Mean baseline AUDIT scores for control and intervention groups were 16.6 (SD = 6.0) and 16.6 (SD = 5.7). At 6 weeks, participants receiving e-SBI reported significantly lower total consumption (geometric mean ratio = 0.74; 9 5 % confidence interval: 0.56-0.96), lower heavy episode frequency (0.63; 0.42-0.92) and fewer personal problems (0.70; 0.54-0.91). At 6 months personal problems remained lower (0.76; 0.60-0.97), although consumption did not differ significantly. At 6 months, academic problems were lower in the intervention group relative to controls (0.72; 0.51-1.02). Conclusions e-SBI reduced hazardous drinking among university students, to an extent similar to that found for practitioner-delivered brief interventions in the general population. e-SBI offers promise as a strategy to reduce alcohol-related harm in a way that is non-intrusive, appealing to the target group, and capable of being incorporated into primary care. Research is required to replicate the findings, to determine the duration of intervention effects, and to investigate the mechanisms by which the intervention operates.
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This book is an exemplar of what the National Academy of Science does so well: to assemble a cast of very wellinformed and clever experts; to ask them to think hard and critically about an important issue over a substantial period of time; and to seek a consensus, if possible and failing that, to identify the critical issues on which wellinformed people disagree and to specify the evidence that has the greatest epistemic leverage in resolving disagreements.
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n early 2001 there was a dramatic decline in the availability of heroin in New South Wales (NSW), Australia, where previously heroin had been readily available at a low price and high purity.1 The decline was confirmed by Australia's strategic early warning system, which revealed a reduction in heroin supply across Australia and a considerable increase in price,2 particularly from January to April 2001. This "heroin shortage" provided a natural experiment in which to examine the effect of substantial changes in price and availability on injecting drug use and its associated harms in Australia's largest heroin market,2 a setting in which harm reduction strategies were widely used. Publicly funded needle and syringe programmes were introduced to Australia in 1987, and methadone maintenance programmes, which were established in the 1970s, were significantly expanded in 1985 and again in 1999.
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This paper evaluates three hypotheses about the relationship between cannabis use and psychosis in the light of recent evidence from prospective epidemiological studies. These are that: ( 1) cannabis use causes a psychotic disorder that would not have occurred in the absence of cannabis use; ( 2) that cannabis use may precipitate schizophrenia or exacerbate its symptoms; and ( 3) that cannabis use may exacerbate the symptoms of psychosis. There is limited support for the first hypothesis. As a consequence of recent prospective studies, there is now stronger support for the second hypothesis. Four recent prospective studies in three countries have found relationships between the frequency with which cannabis had been used and the risk of receiving a diagnosis of schizophrenia or of reporting psychotic symptoms. These relationships are stronger in people with a history of psychotic symptoms and they have persisted after adjustment for potentially confounding variables. The absence of any change in the incidence of schizophrenia during the three decades in which cannabis use in Australia has increased makes it unlikely that cannabis use can produce psychoses that would not have occurred in its absence. It seems more likely that cannabis use can precipitate schizophrenia in vulnerable individuals. There is also reasonable evidence for the third hypothesis that cannabis use exacerbates psychosis.
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Periodic public concern about heroin use has been a major driver of Australian drug policy in the four decades since heroin use was first reported. The number of heroin-dependent people in Australia has increased from several hundreds in the late 1960s to around 100000 by the end of the 1990s. In this paper I do the following: (1) describe collaborative research on heroin dependence that was undertaken between 1991 and 2001 by researchers at the National Drug and Alcohol Research Centre: (2) discuss the contribution that this research may have made to the formulation of policies towards the treatment of heroin dependence during a period when the policy debate crystallized around the issue of whether or not Australia should conduct a controlled trial of heroin prescription; and (3) reflect on the relationships between research and policy-making in the addictions field, specifically on the roles of investigator-initiated and commissioned research, the interface between researchers, funders and policymakers: and the need to be realistic about the likely impact of research on policy and practice.
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