Volunteer peer support frameworks supporting older women living alone.

Volunteer peer support is an approach that enables a supportive connection between volunteers and a sub-set of community members with shared experiences or interests. To implement co-designed strategies to support older women to maintain independence and optimise wellbeing in Australia, a volunteer peer support approach was proposed. There was limited literature describing volunteer peer support frameworks to underpin interventions of this kind; and given the increasing desire for engagement of individuals and communities, articulation of the key components of such a framework is warranted. In this paper, we define volunteers and peer support, and outline existing frameworks for volunteering and peer support. We then describe the volunteer peer support framework developed for this intervention, outlining the key requirements. This information will enable others to develop an effective and sustainable structure for peer support volunteer services.

Co-designing Being Your Best program-A holistic approach to frailty in older community dwelling Australians.

Frailty is a condition characterised by increased vulnerability and decline of physical and cognitive reserves, most often affecting older people. This can lead to a cascade of repeated hospitalisations, further decline and ultimately loss of independence. Frailty and pre-frailty are modifiable; interventions such as physical exercise, cognitive training, social connection and improved nutrition, especially in a group setting, can mitigate frailty. Existing healthcare guidelines for managing frailty focus predominantly on falls, delirium, acute confusion and immobility. Uptake of referrals to services following hospital discharge is sub-optimal, indicating that a more proactive, person-centred and integrated approach to frailty is required. The aim was to co-design a program to help pre-frail and frail older people return to their homes following hospital discharge by increasing resilience and promoting independence. We engaged healthcare consumers, and healthcare professionals from three tertiary hospitals in metropolitan Melbourne (Alfred Hospital, Monash Health and Cabrini Health), and from Bolton Clarke home-based support services. Co-design is a process whereby the input of service consumers is included in the development of a program. In the healthcare sector, co-design involves discussions with healthcare consumers alongside healthcare professionals to identify issues and build knowledge to ultimately work on improving the healthcare system. From co-design sessions with 23 healthcare consumers and 17 healthcare professionals, it was apparent that frailty was perceived to affect physical and mental well-being. The co-design process resulted in refinement of the Being Your Best program to incorporate a holistic approach, addressing four domains supported by research evidence, to improve health and well-being through community- or home-based physical activity, cognitive training, social support and nutritional support. Being Your Best was developed in consultation with older people with lived experience as well as healthcare professionals and aims to mitigate the effects of frailty, and will now be tested for feasibility and acceptability.

Data on the DNA damaging and mutagenic potential of the BH3-mimetics ABT-263/Navitoclax and TW-37.

Unfortunately, the mutagenic activities of chemotherapy and radiotherapy can provoke development of therapy-induced malignancies in cancer survivors. Non-mutagenic anti-cancer therapies may be less likely to trigger subsequent malignant neoplasms. Here we present data regarding the DNA damaging and mutagenic potential of two drugs that antagonize proteins within the Bcl-2 family: ABT-263/Navitoclax and TW-37. Our data reveal that concentrations of these agents that stimulated Bax/Bak-dependent signaling provoked little DNA damage and failed to trigger mutations in surviving cells. The data supplied in this article is related to the research work entitled "Inhibition of Bcl-2 or IAP proteins does not provoke mutations in surviving cells" [1].

Inhibition of Bcl-2 or IAP proteins does not provoke mutations in surviving cells.

Chemotherapy and radiotherapy can cause permanent damage to the genomes of surviving cells, provoking severe side effects such as second malignancies in some cancer survivors. Drugs that mimic the activity of death ligands, or antagonise pro-survival proteins of the Bcl-2 or IAP families have yielded encouraging results in animal experiments and early phase clinical trials. Because these agents directly engage apoptosis pathways, rather than damaging DNA to indirectly provoke tumour cell death, we reasoned that they may offer another important advantage over conventional therapies: minimisation or elimination of side effects such as second cancers that result from mutation of surviving normal cells. Disappointingly, however, we previously found that concentrations of death receptor agonists like TRAIL that would be present in vivo in clinical settings provoked DNA damage in surviving cells. In this study, we used cell line model systems to investigate the mutagenic capacity of drugs from two other classes of direct apoptosis-inducing agents: the BH3-mimetic ABT-737 and the IAP antagonists LCL161 and AT-406. Encouragingly, our data suggest that IAP antagonists possess negligible genotoxic activity. Doses of ABT-737 that were required to damage DNA stimulated Bax/Bak-independent signalling and exceeded concentrations detected in the plasma of animals treated with this drug. These findings provide hope that cancer patients treated by BH3-mimetics or IAP antagonists may avoid mutation-related illnesses that afflict some cancer survivors treated with conventional DNA-damaging anti-cancer therapies.