138 resultados para Nicotine addiction


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Background: Exposure to other people’s cigarette smoke (environmental tobacco smoke, or ETS) is an important child health issue.
Objectives: To determine the effectiveness of interventions aiming to reduce exposure of children to ETS.
Search strategy: The Tobacco Addiction Group register of studies was searched.MEDLINE, EMBASE and four other health and psychology databases were searched electronically, bibliographies of retrieved primary studies were checked and specialists in the area consulted.
Selection criteria:
Controlled trials with or without random allocation were included in this review if they addressed participants (parents and other family members, child care workers and teachers) involved with the care and education of infants and young children (aged 0-12 years). All mechanisms for reduction of children’s environmental tobacco smoke exposure, and smoking prevention, cessation, and control programmes targeting these participants are included. These include smoke free policies and legislation, health promotion, social behavioural therapies, technology, education and clinical interventions.
Data collection and analysis: Two reviewers independently assessed studies and extracted data. Due to heterogeneity of methodologies and outcomes, no summary measures were possible and results were synthesised using narrative summaries.
Main results:
Nineteen studies met the inclusion criteria, one of which was subsequently excluded. Three interventions were targeted at populations or community settings, seven studies were conducted in the well child health care setting and eight in the ill child health care setting. Twelve of these studies are from North America. In 12 of the 18 studies there was reduction of ETS exposure for children in both intervention and comparison groups. In only four of the 18 studies was there a statistically significant intervention effect. Three of these successful studies employed intensive counselling interventions targeted to smoking parents. There is little difference between the well infant, child respiratory illness and other child illness settings as contexts for parental smoking cessation interventions. The fourth successful intervention was in the school setting targeting the ETS exposure of children from smoking fathers.
Authors’ conclusions: Brief counselling interventions, successful in the adult health setting when coming from physicians, cannot be extrapolated to adults in the setting of child health. There is limited support for more intensive counselling interventions. There is no clear evidence for differences between the respiratory, non-respiratory ill child, well child and peripartum settings as contexts for reduction of children’s ETS exposure.

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The key definitional elements of the concept of craving remain highly contentious amongst addiction researchers. We argue that attempts to operationalize the craving construct may benefit from the conceptual and methodological advances that have occurred in the field of consciousness studies. Specifically, it is contended that the concept of craving cannot be fully articulated in the absence of a consideration of Husserl's notion of the intentional structure of human consciousness and related concepts such as phenomenology, discrete states of consciousness and altered states of consciousness. Extrapolating from the consciousness studies literature, we formulate numerous suggestions for future research intended to facilitate the operationalization of craving experiences.

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Cancer pain is estimated to occur in 30% to 70% of patients with early-stage cancer and 60% to 95% with advanced cancer. Current research shows that cancer pain continues to be undertreated despite the availability of analgesics and established guidelines to maximize their effectiveness. The purpose of this study was to describe oncology patients' pain experience during an episode of hospitalization with particular emphasis on exploring the relationship between oncology patients' beliefs about pain and the treatment they received. Consecutive patients (n = 126) were interviewed 48 hours after admission to an urban and a regional hospital in Australia; 47.6% of patients had experienced moderate to severe pain in the previous 24 hours but had only received 40.4% of available analgesic. Patients held varying beliefs about pain and pain treatments in particular, 41% held strong beliefs about the potential for addiction to narcotics. Patients who held this belief reported higher current pain, worst pain intensity, and higher average pain intensity in the previous 24 hours. Effective pain management in the inpatient oncology setting continues to be an important clinical issue, and patients do not receive all available pain treatment. There may be an important association between patients' beliefs about pain and pain management and the pain management they receive.

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In this study, the role of nitric oxide (NO) in regulation of the pulmocutaneous vasculature of the toad, Bufo marinus was investigated. In vitro myography demonstrated the presence of a neural NO signaling mechanism in both arteries. Vasodilation induced by nicotine was inhibited by the soluble guanylyl cyclase (GC) inhibitor, 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one, and the NO synthase (NOS) inhibitor, Nω-nitro-L-arginine (L-NNA). Removal of the endothelium had no significant effect on the vasodilation. Furthermore, pretreatment with N5-(1-imino-3-butenyl)-L-ornithine (vinyl-L-NIO), a more specific inhibitor of neural NOS, caused a significant decrease in the nicotine-induced dilation. In the pulmonary artery only, a combination of L-NNA and the calcitonin gene-related peptide (CGRP) receptor antagonist, CGRP(8-37), completely blocked the nicotine-induced dilation. In both arteries, the vasodilation was also significantly decreased by glibenclamide, an ATP-sensitive K+ (K+ATP) channel inhibitor. Levcromakalim, a K+ATP channel opener, caused a dilation that was blocked by glibenclamide in both arteries. In the pulmonary artery, NO donor-mediated dilation was significantly decreased by pretreatment with glibenclamide. The physiological data were supported by NADPH-diaphorase histochemistry and immunohistochemistry, which demonstrated NOS in perivascular nerve fibers but not the endothelium of the arteries. These results indicate that the pulmonary and cutaneous arteries of B. marinus are regulated by NO from nitrergic nerves rather than NO released from the endothelium. The nitrergic vasodilation in the arteries appears to be caused, in part, via activation of K+ATP channels. Thus, NO could play an important role in determining pulmocutaneous blood flow and the magnitude of cardiac shunting.

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The presence of nitric oxide synthase (NOS) and role of nitric oxide (NO) in vascular regulation was investigated in the Australian lungfish, Neoceratodus forsteri. No evidence was found for NOS in the endothelium of large and small blood vessels following processing for NADPH-diaphorase histochemistry. However, both NADPH-diaphorase histochemistry and neural NOS immunohistochemistry demonstrated a sparse network of nitrergic nerves in the dorsal aorta, hepatic artery, and branchial arteries, but there were no nitrergic nerves in small blood vessels in tissues. In contrast, nitrergic nerves were found in non-vascular tissues of the lung, gut and kidney. Dual-wire myography was used to determine if NO signalling occurred in the branchial artery of N. forsteri. Both SNP and SIN-1 had no effect on the pre-constricted branchial artery, but the particulate guanylyl cyclase (GC) activator, C-type natriuretic peptide, always caused vasodilation. Nicotine mediated a dilation that was not inhibited by the soluble GC inhibitor, ODQ, or the NOS inhibitor, L-NNA, but was blocked by the cyclooxygenase inhibitor, indomethacin. These data suggest that NO control of the branchial artery is lacking, but that prostaglandins could be endothelial relaxing factors in the vasculature of lungfish.

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Objective: To examine the impact of smoke-free policies in Victorian gambling venues on electronic gaming machine (EGM) expenditure.

Method: Monthly EGM expenditure from July 1998 to December 2005, provided by the Victorian Commission for Gambling Regulation and the Office of the Liquor and Gambling Commissioner in South Australia, was analysed. The outcome measure was the ratio of monthly expenditure for Victoria to monthly expenditure in South Australia. Intervention analysis and autoregressive integrated moving average modelling were used to assess the impact of the smoke-free policy on expenditure.

Results: The smoke-free policy resulted in an abrupt, long-term decrease in the level of EGM expenditure. The mean level of monthly expenditure decreased by approximately 14%.

Conclusion: The smoke-free policy not only protects hospitality workers and patrons from exposure to secondhand smoke but has also had an impact on slowing gambling losses.

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Contents:  Ideas of knowledge in practice / Struan Jacobs -- Information, knowledge, and wisdom in medical practice / P. B. Greenberg -- The practice of the psychiatrist / Alex Holmes -- Social work knowledge-in-practice / Heather D'Cruz -- Disability : a personal approach / Lisa Chaffey -- Knowledge in the making : an analytical psychology perspective / Joy Norton -- Knowledge to action in the practice of nursing / Alison Hutchinson, Tracey Bucknall -- The risky business of birth / Frances Sheean and Jennifer M. Cameron -- Skills for person-centred care : health professionals supporting chronic condition prevention and self-management / Sharon Lawn and Malcolm Battersby -- Knowledge and reasoning in practice : an example from physiotherapy and occupational therapy / Megan Smith ... [et al.] -- Using knowledge in the practice of dealing with addiction : an ideal worth aiming for / Peter Miller.

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This qualitative study investigated personal and psychological aspects of big wave riders. A cross-sectional design with non probability purposive sampling was used to gain personal interviews with 32 elite surfers who regularly ride big, life threatening waves. Each athlete was asked three open questions: 1. What do you think are the most important qualities and attributes a surfer needs for riding big waves? 2. What type of mindset is best for riding big waves?, and 3.What motivates you to ride big waves? Content analysis of the taped interview transcripts revealed seven key qualities and attributes including having a thrill seeking, confident and goal oriented personality, a high level of mental strength and control, and an intimate relationship with the ocean. The best mindset included an individually defined arousal level, a committed attitude, and a simple, yet highly aware, focus. Motivations were primarily intrinsic, though drives indicative of a behavioral addiction to the act of riding big waves also emerged. Evidence of common developmental stages for riding big waves also arose from the interviews. Optimal mental approach and preparation techniques are discussed that will enable big wave riders, and other extreme athletes, to more safely and successfully manage extreme situations.

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Defects in fat metabolism are central to the aetiology and pathogenesis of obesity and type II diabetes. The liver plays a central role in these disease states via its regulation of glucose and fat metabolism. In addition, accumulation of fat within the liver has been associated with changes in key pathways of carbohydrate and fat metabolism. However a number of questions remain. It is hypothesised that fat accumulation within the liver is a primary defect in the aetiology and pathogenesis of obesity and type II diabetes. Fat accumulating in the liver is the result of changes in the gene expression of key enzymes and proteins involved with fat uptake, fat transport, fat oxidation, fat re-esterification or storage and export of fat from the liver and these changes are regulated by key lipid responsive transcription factors. To study these questions Psammomys obesus was utilised. This polygenic rodent model of obesity and type II diabetes develops obesity and diabetes in a similar pattern to susceptible human populations. In addition dietary and environmental changes to Psammomys obesus were employed to create different states of energy balance, which allowed the regulation of liver fat gene expression to be examined. These investigations include: 1) Measurement of fat accumulation and fatty acid binding proteins in lean, obese and diabetic Psammomys obesus. 2) Characterisation of hepatic lipid enzymes, transport protein and lipid responsive transcription factor gene expression in lean, obese and diabetic Paammomys obesus. 3) The effect of acute and chronic energy restriction on hepatic lipid metabolism in Psammomys obesus. 4) The effect of sucrose feeding on the development of obesity and type II diabetes in Psammomys obesus. 5) The effect of nicotine treatment in lean and obese Psammomys obesus, 6) The effect of high dose leptin administration on hepatic fat metabolism in Psammomys obesus. The results of these studies demonstrated that fat accumulation within the liver was not a primary defect in the aetiology and pathogenesis of obesity and type II diabetes. Fat accumulating in the liver was not the result of changes in the gene expression of key enzymes and proteins involved in hepatic fat metabolism. However changes in the mRNA level of the transcription factors PPAR∝ and SREBP-1C was associated with the development of diabetes and the gene expression of these two transcription factors was associated with changes in diabetic status.

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The β-amyloid protein (Aβ) is the major protein component of amyloid plaques found in the Alzheimer brain. Although there is a loss of acetylcholinesterase (AChE) from both cholinergic and non-cholinergic neurones in the brain of Alzheimer patients, the level of AChE is increased around amyloid plaques. Previous studies using P19 cells in culture and transgenic mice which overexpress human Aβ have suggested that this increase may be due to a direct action of Aβ on AChE expression in cells adjacent to amyloid plaques. The aim of the present study was to examine the mechanism by which Aβ increases levels of AChE in primary cortical neurones. Aβ1−42 was more potent than Aβ1−40 in its ability to increase AChE in primary cortical neurones. The increase in AChE was unrelated to the toxic effects of the Aβ peptides. The effect of Aβ1−42 on AChE was blocked by inhibitors of α7 nicotinic acetylcholine receptors (α7 nAChRs) as well as by inhibitors of L- or N-type voltage-dependent calcium channels (VDCCs), whereas agonists of α7 nAChRs (choline, nicotine) increased the level of AChE. The results demonstrate that the effect of Aβ1−42 on AChE is due to an agonist effect of Aβ1−42 on the α7 nAChR.