52 resultados para mechanisms of influence

em Deakin Research Online - Australia


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INTRODUCTION AND AIMS: Industry groups with vested interests in policy regularly work to protect their profits via the endorsement of ineffective voluntary regulation and interventions, extensive lobbying activity and minimising the health impact of consumption behaviours. This study aims to examine all alcohol industry submissions to the Australian House of Representatives Standing Committee on Social Policy and Legal Affairs into Fetal Alcohol Spectrum Disorders (FASD), to assist in understanding how those with vested interests contribute to policy development. The analysis aims to document the strategies and arguments used by alcohol industry bodies in their submissions and to compare these with known strategies of vested-interest groups. DESIGN AND METHODS: All 92 submissions to the Inquiry were screened to include only those submitted by alcohol industry bodies (five submissions). Content domains were derived based on the major themes emerging from the industry submissions and on common vested-interest behaviours identified in previous literature. RESULTS: The following content categories were identified: Concerns about FASD; Current industry activities and FASD prevention; Value of mandatory warning labels; and Credibility of independent public health researchers and organisations. DISCUSSION AND CONCLUSIONS: Alcohol industry submissions sought to undermine community concern, debate the evidence, promote ineffective measure which are no threat to the profit margins and attack independent health professionals and researchers. In doing so, their behaviour is entirely consistent with their responses to other issues, such as violence and chronic health, and copies the tactics employed by the tobacco industry.

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This article uses panel data from 1976 to 2003 to investigate the ways in which banking and stock markets influence economic growth in situations of high and low country risk. The mean and Standard Deviation (SD) of country risk are adopted to classify 28 countries into Low Risk Low Volatility (LRLV) and High Risk High Volatility (HRHV) subgroups. Through the technique of error correction-based panel co-integration developed by Westerlund (2007), several results are obtained. First, LRLV countries can expand the capitalization of stock market to enhance long-term economic growth. Second, HRHV countries, on the other hand, use two distinct strategies to promote long-term economic growth. Initially they develop their equity markets, which promote economic growth directly. Strengthened equity markets, in turn, aid in the development of credit markets, which subsequently brings an economic boom. Finally, regardless of selected subgroups, the contribution of stock market capitalization to economic growth appears to be substantially larger than that of bank credit, highlighting the importance of stock markets.

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Development of the methodology for creating reliable digital material representation (DMR) models of dual-phase steels and investigation of influence of the martensite volume fraction on fracture behavior under tensile load are the main goals of the paper. First, an approach based on image processing algorithms for creating a DMR is described. Then, obtained digital microstructures are used as input for the numerical model of deformation, which takes into account mechanisms of ductile fracture. Ferrite and martensite material model parameters are evaluated on the basis of micropillar compression tests. Finally, the model is used to investigate the impact of the martensite volume fraction on the DP steel behavior under plastic deformation. Results of calculations are presented and discussed in the paper.

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OBJECTIVES: It is well accepted that diet quality has an important role in the prevention and treatment of several physical diseases. However, its influence on mental health has received far less attention, although there is increasing evidence to support a relationship with depression. In this narrative review, investigations into the relationship between diet and bipolar disorder are examined and the potential implications in the management and treatment of bipolar disorder are reviewed. METHODS: The authors provide a narrative review of the relevant information. RESULTS: Research is limited, although there are preliminary findings to suggest a relationship between diet and bipolar disorder. Findings from cross-sectional research suggest that people with bipolar disorder consume an unhealthier dietary pattern. This has significant treatment implications as bipolar disorder has a high comorbidity with several physical diseases. In addition, diet also influences several biological processes that are dysregulated in bipolar disorder, namely monoaminergic activity, immune/inflammatory processes, oxidative stress, mitochondrial activity, and neuroprogression. CONCLUSIONS: The role of diet in bipolar disorder requires further attention in research as it presents as a factor that may contribute to the worsening course of this condition and may potentially enhance current treatment outcomes.

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The ability of mammals to tightly regulate systemic copper levels is vital for
health as demonstrated by the severity of the genetic copper deficiency and copper toxicity disorders, Menkes disease and Wilson disease, respectively. Analysis of these genetic disorders has led to a substantial increase in the understanding of the role of copper in health and disease. The isolation of the genes involved in these diseases and use of yeast mutants with altered copper and iron homeostasis has revealed a range of molecular mechanisms governing copper homeostasis. These mechanisms include regulation of cellular copper uptake and efflux and involve the use of chaperones for safe intracellular copper distribution. Here we provide an overview of the physiological role of copper and the molecular mechanisms
regulating systemic and cellular copper levels in mammals. Furthermore, we discuss the pathophysiological mechanisms and consequences of copper deficiency/overload in relation to disease.

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A high degradation extent of benzo[a]pyrene (BaP) should not be considered as the sole desirable criterion for the bioremediation of BaP-contaminated soils because some of its accumulated metabolites still have severe health risks to human. Two main metabolites of BaP, benzo[a]pyrene-1,6-quinone (BP1,6-quinone) and 3-hydroxybenzo[a]pyrene (3-OHBP) were identified by high performance liquid chromatography (HPLC) with standards. This study was the first time that degradation of both BaP and the two metabolites was carried out by chemical oxidation and biodegradation. Three main phases during the whole degradation process were proposed.

Hydrogen peroxide–zinc (H2O2–Zn), the fungus – Aspergillus niger and the bacteria – Zoogloea sp. played an important role in the different phases. The degradation parameters of the system were also optimized, and the results showed that the effect of degradation was the best when fungus–bacteria combined with H2O2–Zn, the concentration range of BaP in the cultures was 30–120 mg/l, the initial pH of the cultures was 6.0. However, as co-metabolites, phenanthrene significant inhibited the degradation of BaP. This combined degradation system compared with the conventional method of degradation by domestic fungus only, enhanced the degradation extent of BaP by more than 20% on the 12 d. The highest accumulation of BP1,6-quinone and 3-OHBP were reduced by nearly 10% in the degradation experiments, which further proved that the combined degradation system was more effective as far as joint toxicity of BaP and its metabolites are concerned.

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This study investigated vasodilator mechanisms in the dorsal aorta of the elephant fish, Callorhinchus milii, using anatomical and physiological approaches. Nitric oxide synthase could only be located in the perivascular nerve fibres and not the endothelium of the dorsal aorta, using NADPH histochemistry and immunohistochemistry. In vitro organ bath experiments demonstrated that a NO/soluble guanylyl cyclase (GC) system appeared to be absent in the vascular smooth muscle, since the NO donors SNP (10−4 mol l−1) and SIN-1 (10−5 mol l−1) were without effect. Nicotine (3 × 10−4 mol l−1) mediated a vasodilation that was not affected by ODQ (10−5 mol l−1), l-NNA (10−4 mol l−1), indomethacin (10−5 mol l−1), or removal of the endothelium. In contrast, the voltage-gated sodium channel inhibitor, tetrodotoxin (10−5 mol l−1), significantly decreased the dilation induced by nicotine, suggesting that it contained a neural component. Pre-incubation of the dorsal aorta with the calcitonin gene-related peptide (CGRP) receptor antagonist, CGRP8–37 (10−6 mol l1) also caused a significant decrease in the nicotine-induced dilation. We propose that nicotine is mediating a neurally-derived vasodilation in the dorsal aorta that is independent of NO, prostaglandins and the endothelium, and partly mediated by CGRP.

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The study examined the role of defense mechanisms in homophobic attitudes of older male adolescents aged 17e18 years. A cross-sectional survey collected data from final year high school students (N ¼ 86) attending an all male school in a regional centre in Victoria, Australia. The school was identified by teachers as having a problematic culture of homophobic intolerance. Participants were divided into homophobic and non-homophobic groups based on their scores on the Homophobia Scale Questionnaire. Discriminant analysis was conducted to identify the predictors that would best categorise students into those two groups on the basis of defense styles derived from the Defense Style Questionnaire-40 (DSQ-40). The strongest predictors of homophobia amongst defense styles were idealisation, denial, somatisation and devaluation accounting for 18.31%, 17.64%, 13.10% and 11.35% of the variance, respectively. Results generally supported the larger contribution of more immature defenses to higher levels of homophobia.

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We have developed hematopoietic cells resistant to the cytotoxic effects of oxysterols. Oxysterol-resistant HL60 cells were generated by continuous exposure to three different oxysterols—25-hydroxycholesterol (25-OHC), 7-beta-hydroxycholesterol (7β-OHC) and 7-keto-cholesterol (7κ-C). We investigated the effects of 25-OHC, 7β-OHC, 7κ-C and the apoptotic agent staurosporine on these cells. The effect of the calcium channel blocker nifedipine on oxysterol cytotoxicity was also investigated. Differential display and real-time PCR were used to quantitate gene expression of oxysterol-sensitive and -resistant cells. Our results demonstrate that resistance to the cytotoxic effects of oxysterols is relatively specific to the type of oxysterol, and that the cytotoxicity of 25-OHC but not that of 7β-OHC and 7κ-C, appears to occur by a calcium dependent mechanism. Oxysterol-resistant cells demonstrated no significant difference in the expression of several genes previously implicated in oxysterol resistance, but expressed the bcl-2 gene at significantly lower levels than those observed in control cells. We identified three novel genes differentially expressed in resistant cells when compared to HL60 control cells. Taken together, the results of this study reveal potentially novel mechanisms of oxysterol cytotoxicity and resistance, and indicate that cytotoxicity of 25-OHC, 7β-OHC and 7κ-C occur by independent, yet overlapping mechanisms.