THERAPEUTIC MOLECULES

The present invention relates generally to a ligand for a protein associated with modulating obesity, diabetes and metabolic energy levels in animals including humans. More particularly, the present invention provides a ligand of the protein, Beacon, and its homologs. The identification of a Beacon ligand permits the identification of agents which agonize or antagonize the Beacon-ligand interaction and, hence, the development of therapeutic molecules useful in modulating obesity, diabetes and/or energy imbalance.

THERAPEUTIC MOLECULES

The present invention relates generally to a ligand for a protein associated with modulating obesity, diabetes and metabolic energy levels in animals including humans. More particularly, the present invention provides a ligand of the protein, Beacon, and its homologs. The identification of a Beacon ligand permits the identification of agents which agonize or antagonize the Beacon-ligand interaction and, hence, the development of therapeutic molecules useful in modulating obesity, diabetes and/or energy imbalance.

Therapeutic molecules

The present invention relates generally to a ligand for a protein associated with modulating obesity, diabetes and metabolic energy levels in animals including humans. More particularly, the present invention provides a ligand of the protein, Beacon, and its homologs. The identification of a Beacon ligand permits the identification of agents which agonize or antagonize the Beacon-ligand interaction and, hence, the development of therapeutic molecules useful in modulating obesity, diabetes and/or energy imbalance.

THERAPEUTIC MOLECULES

The present invention relates generally to a ligand for a protein associated with modulating obesity, diabetes and metabolic energy levels in animals including humans. More particularly, the present invention provides a ligand of the protein, Beacon, and its homologs. The identification of a Beacon ligand permits the identification of agents which agonize or antagonize the Beacon-ligand interaction and, hence, the development of therapeutic molecules useful in modulating obesity, diabetes and/or energy imbalance.

Captured by the game : might a focus on the ‘therapeutic relationship’ diminish the attention we give to the client’s intimate network?

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

Assessing the therapeutic climate of prisons

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.

The neuroprogressive nature of major depressive disorder: pathways to disease evolution and resistance, and therapeutic implications

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.

Early events of HIV-1 infection : can signalling be the next therapeutic target?

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.

Targeting cyclooxygenase-2 in depression is not a viable therapeutic approach and may even aggravate the pathophysiology underpinning depression

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.

Therapeutic equivalence and the generic competition paradox

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.

Collaborative care skills training workshops : helping carers cope with eating disorders from the UK to Australia

Purpose

The Collaborative Care Skills Training workshops, developed by Treasure and associates aim to improve the well-being, coping strategies and problem-solving skills of carers of someone with an eating disorder. Evidence has demonstrated the effectiveness of the workshops in the UK where it was developed. The aim of this pilot study was to examine whether conducting the workshops in different contexts by facilitators trained in its delivery could lead to similar impact.
Methods

The workshops were conducted with 15 carers in VIC, Australia and delivered by experienced health professionals trained in its content and delivery. A non-experimental research design with repeated measures was implemented. Quantitative data were collected at pre-and post-intervention and 8 weeks after completion of the workshops.
Results

Participation led to significant reductions in carers’ reported expressed emotion, dysfunctional coping, distress, burden and accommodation and enabling of the eating disorder behaviour, which were maintained at the 8-week follow-up.
Conclusion

Results suggest the workshops are effective in reducing carer distress and burden as well as modifying unhelpful emotional interactional styles when caring for family members with an eating disorder. The content of the workshops and its delivery, once experienced facilitators have received training, are transferable to other contexts.