984 resultados para Neuronal death


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Suicide-related behavior (SRB) among heroin users is a complex and multifaceted continuum, including such fringe areas as indifference and "risky" behavior. The article investigates the nuances and intersections of SRB, using qualitative semi-structured interviews with 60 regular heroin users recruited primarily from syringe programs in Geelong, Australia. Twenty-eight percent of interviewees reported a previous suicide attempt and 45% reported serious consideration of it. Types of SRB reported included: Suicide attempts, instrumental suicide-related behaviors, suicidal ideation, indifference and risk-taking thoughts and behaviors. Heroin users engage in much behavior which inhabits a grey area of SRB. The use of a nomenclature which addresses the elements of lethality and intent improves the ability of research to properly define and categorize SRB in drug-using populations. But the categories should not be overinclusive; indifferent attitudes towards death and risk-taking behaviors can sometimes be a functional response to the risk environment of heroin users.

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The thesis investigated ambivalent attitudes towards death in injecting drug users, factors that may lead to such ambivalent attitudes and implications for health promotion campaigns. It was found that this relationship with death was principally attributable to government drug policy in Australia.

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This thesis examines representations of death in a selection of contemporary texts for Australian adolescent audiences. It demonstrates that, although death is a complex subject, a characteristically Australian 'way of death' is identifiable in these fictions and it is invariably associated with issues of sexuality, gender and power.

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Death determines distinctly different, almost inverse, responses and outcomes for Emily Dickinson and Emily Brontë. Death is an imaginative poetic solution for Dickinson, demonstrating her belief that art is the only way to transcend death. But death is the ultimate solution for Brontë, for whom freedom of the imagination leads to mystical unity and continuity.

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Health promotion strategies ultimately rely on people perceiving the consequences of their behaviour as negative. If someone is indifferent towards death, it would logically follow that health promotion messages such as safe using messages would have little resonance. This study aimed to investigate attitudes towards death in a group of injecting drug users (IDUs) and how such attitudes may impact upon the efficacy/relevance of 'safe using' (health promotion) messages.

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Panic disorder can serve as a clinical model for testing whether mental stress can cause heart disease. Potential neural mechanisms of cardiac risk are the sympathetic activation during panic attacks, continuing release of adrenaline as a co-transmitter in the cardiac sympathetic nerves, and impairment of noradrenaline neuronal reuptake, augmenting sympathetic neural respnses.

The phenotype of impaired neuronal reuptake of noradrenaline: an epigenetic mechanism? We suspect that this phenotype, in sensitizing people to heart symptom development, is a cause of panic disorder, and by magnifying the sympathetic neural signal in the heart, underlies increased cardiac risk. No loss of function mutations of the coding region of the norepinephrine transporter (NET) are evident, but we do detect hypermethylation of CpG islands in the NET gene promoter region. Chromatin immunoprecipitation methodology demonstrates binding of the inhibitory transcription factor, MeCP2, to promoter region DNA in panic disorder patients.

Cardiovascular illnesses co-morbid with panic disorder. Panic disorder commonly coexists with essential hypertension and the postural tachycardia syndrome. In both of these cardiovascular disorders the impaired neuronal noradrenaline reuptake phenotype is also present and, as with panic disorder, is associated with NET gene promoter region DNA hypermethylation. An epigenetic ‘co-morbidity’ perhaps underlies the clinical concordance.

Brain neurotransmitters. Using internal jugular venous sampling, in the absence of a panic attack we find normal norepinephrine turnover, but based on measurements of the overflow of the serotonin metabolite, 5HIAA, a marked increase (six to sevenfold) in brain serotonin turnover in patients with panic disorder. This appears to represent the underlying neurotransmitter substrate for the disorder. Whether this brain serotonergic activation is a prime mover, or consequential on other primary causes of panic disorder, including cardiac sensitization by faulty neuronal noradrenaline reuptake leading to cardiac symptoms and the enhanced vigilance which accompanies them, is unclear at present.

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Explores how affluence and the development of new technologies has come at a huge, and potentially devastating, cost - an epidemic of obesity and a world clogged by waste.

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We generated a mouse line with a missense mutation (S248F) in the gene (CHRNA4) encoding the α4 subunit of neuronal nicotinic acetylcholine receptor (nAChR). Mutant mice demonstrate brief nicotine induced dystonia that resembles the clinical events seen in patients with the same mutation. Drug-induced dystonia is more pronounced in female mice, thus our aim was to determine if the S248F mutation changed the properties of fast- and slow-twitch muscle fibres from female mutant mice. Reverse transcriptase-PCR confirmed CHRNA4 gene expression in the brain but not skeletal muscles in normal and mutant mice. Ca2+ and Sr2+ force activation curves were obtained using skinned muscle fibres prepared from slow-twitch (soleus) and fast-twitch (EDL) muscles. Two significant results were found: (1) the (pCa50 - pSr50) value from EDL fibres was smaller in mutant mice than in wild type (1.01 vs. 1.30), (2) the percentage force produced at pSr 5.5 was larger in mutants than in wild type (5.76 vs. 0.24%). Both results indicate a shift to slow-twitch characteristics in the mutant. This conclusion is supported by the identification of the myosin heavy chain (MHC) isoforms. Mutant EDL fibres expressed MHC I (usually only found in slow-twitch fibres) as well as MHC IIa. Despite the lack of spontaneous dystonic events, our findings suggest that mutant mice may be having subclinical events or the mutation results in a chronic alteration to muscle neural input.

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