991 resultados para Therapeutic alliance rupture


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A recent project sought to clarify how psychotherapists and mental health workers understand psychosocial health and pathology. In this enquiry, I paid particular attention to the client’s interpersonal networks: did the professionals actively consider, and if so to what extent, ‘intimate social and family relationships’ in constructing their understanding of the presenting problem and in the process they used for goal setting. Twenty-two semi-structured interviews were undertaken, eleven with psychotherapists and eleven with mental health workers. Across both groups, interviewees tended not to see their clients as embedded, relational entities, but primarily, often quite exclusively, as autonomous beings. Second, interviewees accorded a high value to the importance of ‘the therapeutic relationship’. Is it possible that the emphasis practitioners place on ‘the therapeutic relationship’ has the effect of marginalising the attention that is given to the client’s significant-other network

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This study examined perceptions of the prison social climate in two Australian prisons from the perspective of both prison staff and prisoners. Ratings of social climate were compared between a specialist treatment prison that provides intensive rehabilitation programs to violent, sexual, and substance-using offenders and a mainstream prison that does not specialize in offender rehabilitation. The results suggested that staff and prisoners at the specialist treatment prison rated the social climate as more conducive to rehabilitation, although the differences were less pronounced for prisoners. These findings are discussed in relation to the development of specialist therapeutic prisons and how assessments of social climate might inform assessments of their success.

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In some patients with major depressive disorder (MDD), individual illness characteristics appear consistent with those of a neuroprogressive illness. Features of neuroprogression include poorer symptomatic, treatment and functional outcomes in patients with earlier disease onset and increased number and length of depressive episodes. In such patients, longer and more frequent depressive episodes appear to increase vulnerability for further episodes, precipitating an accelerating and progressive illness course leading to functional decline. Evidence from clinical, biochemical and neuroimaging studies appear to support this model and are informing novel therapeutic approaches. This paper reviews current knowledge of the neuroprogressive processes that may occur in MDD, including structural brain consequences and potential molecular mechanisms including the role of neurotransmitter systems, inflammatory, oxidative and nitrosative stress pathways, neurotrophins and regulation of neurogenesis, cortisol and the hypothalamic–pituitary–adrenal axis modulation, mitochondrial dysfunction and epigenetic and dietary influences. Evidence-based novel treatments informed by this knowledge are discussed.

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Intracellular signaling events are signposts of biological processes, which govern the direction and action of biological activities. Through millions of years of evolution, pathogens, such as viruses, have evolved to hijack host cell machinery to infect their targets and are therefore dependent on host cell signaling for replication. This review will detail our current understanding of the signaling events that are important for the early steps of HIV-1 replication. More specifically, the therapeutic potential of signaling events associated with chemokine coreceptors, virus entry, viral synapses, and post-entry processes will be discussed. We argue that these pathways may represent novel targets for antiviral therapy.

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Depression is a complex progressive disorder accompanied by activation of inflammatory and Th-1 driven pathways, oxidative and nitrosative stress (O&NS), lowered antioxidant levels, mitochondrial dysfunctions, neuroprogression and increased bacterial translocation. In depression, activation of immuno-inflammatory pathways is associated with an increased risk for cardio-vascular disorder (CVD). Because of the inflammatory component, the use of cyclooxygenase 2 (COX-2) inhibitors, such as celecoxib, has been advocated to treat depression. Electronic databases, i.e. PUBMED, Scopus and Google Scholar were used as sources for this selective review on the effects of COX-2 inhibitors aggravating the abovementioned pathways. COX-2 inhibitors may induce neuroinflammation, exacerbate Th1 driven responses, increase lipid peroxidation, decrease the levels of key antioxidants, damage mitochondria and aggravate neuroprogression. COX-2 inhibitors may aggravate bacterial translocation and CVD through Th1-driven mechanisms. COX-2 inhibitors may aggravate the pathophysiology of depression. Since Th1 and O&NS pathways are risk factors for CVD, the use of COX-2 inhibitors may further aggravate the increased risk for CVD in depression. Selectively targeting COX-2 may not be a viable therapeutic approach to treat depression. Multi-targeting of the different pathways that play a role in depression is more likely to yield good treatment results.

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Following the passage of the Waxman-Hatch Act (1984), FDA approval for a generic drug requires the establishment of bio-equivalence between the generic drug and an FDA approved branded drug. However, a large body of evidence in the medical community suggests that bio-equivalence does not guarantee therapeutic equivalence; in some instances the lack of therapeutic equivalence can lead to fatal consequences for patients switching to generic products. In this paper, we construct a simple model to analyze the implications of therapeutic non-equivalence between branded and generic drugs. We show, theoretically and empirically, that this distinction can provide a plausible explanation of the generic competition paradox.

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Autism is a complex developmental disorder with an unknown etiology and without any curative treatment. The mitochondrial electron transfer chains play a major role in the production of ATP, and the generation and management of reactive oxidative stress (ROS). This paper is a systematic review of the role of the mitochondrial electron transport chain in autism, and a consequent hypothesis for treating autism is synthesized.

An electronic search with pre-specified inclusion criteria was conducted in order to retrieve all the published articles about the mitochondrial electron transport chain in autism. The two databases of PUBMED and Google Scholar were searched.


From one hundred twenty five retrieved titles, 12 (three case control study and 9 case reports) articles met inclusion criteria. All of the included studies indicated dysfunction of electron transport chain in autism.

The mitochondrial electron transfer chain seems impaired in some children with autism and ROS production is additionally enhanced. It is hypothesized that interventions involving alternative electron shuttling may improve autism through lowering the production of ROS. In addition, it is expected that this alternative electron shuttling to cytochrome c might enhance the production of ATP which is impaired in the disorder.

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This paper is concerned with the ethics of relationships in doctoral supervision. We give an overview of four paradigms of doctoral supervision that have endured over the past 25 years and elucidate some of their strengths and limitations, contextualise them historically and consider their implications for doctoral supervision in the contemporary university. Two common threads across the four paradigms are a view of doctoral supervision as pedagogical practice and that supervisors have primary responsibility for the supervision of doctoral students. We challenge these assumptions. In their place, we propose that the goal of doctoral supervision is praxis and that this involves a learning alliance between multiple institutional agents grounded in a relational ethics of mutual responsibility.

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Therapeutic online games are potentially a valuable way of improving the mental health of young people. The purpose of this paper is to discuss the qualitative component of a formal evaluation conducted on Reach Out Central (ROC), an online game for 16-25 year olds which aims to improve mental health. Participants completing a post-program survey from the evaluation (n=154) were required to respond to two open-ended questions; what they liked most, and least, about ROC. Responses indicate that online games can be a successful way of educating, as well as attracting and engaging, young people. Suggestions are made regarding issues future developers should take into consideration when developing programs of a similar nature.

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This article explores the development of a food policy body called the Food Alliance and the role of the organization in encouraging the development of food policy that integrates health and ecological issues. The Food Alliance is located within the Australian state of Victoria. A policy triangle is used as a framework to describe and analyse the work of the Food Alliance. Lessons are drawn about effective strategies for influencing integrated food policy. This occurs in a context where food policy typically favours powerful industry and agricultural interests and where relationships between the health and environmental sectors are in their infancy. The implications for planning and organizing a state-wide food policy are explored from the perspective of policy and the ways in which this can be influenced through working with key stakeholders.

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There is compelling evidence to support an aetiological role for inflammation, oxidative and nitrosative stress (O&NS), and mitochondrial dysfunction in the pathophysiology of major neuropsychiatric disorders, including depression, schizophrenia, bipolar disorder, and Alzheimer's disease (AD). These may represent new pathways for therapy. Aspirin is a non-steroidal anti-inflammatory drug that is an irreversible inhibitor of both cyclooxygenase (COX)-1 and COX-2, It stimulates endogenous production of anti-inflammatory regulatory 'braking signals', including lipoxins, which dampen the inflammatory response and reduce levels of inflammatory biomarkers, including C-reactive protein, tumor necrosis factor- and interleukin (IL)--6 , but not negative immunoregulatory cytokines, such as IL-4 and IL-10. Aspirin can reduce oxidative stress and protect against oxidative damage. Early evidence suggests there are beneficial effects of aspirin in preclinical and clinical studies in mood disorders and schizophrenia, and epidemiological data suggests that high-dose aspirin is associated with a reduced risk of AD. Aspirin, one of the oldest agents in medicine, is a potential new therapy for a range of neuropsychiatric disorders, and may provide proof-of-principle support for the role of inflammation and O&NS in the pathophysiology of this diverse group of disorders.