Co-design of youth appropriate services for young people with rheumatic fever/rheumatic heart disease in Counties Manukau District.

AIM: To co-design a rheumatic fever service model which enables young people with acute rheumatic fever/rheumatic heart disease (ARF/RHD) and their families to access the health and wellbeing services they need. METHOD: Co-design, a collaborative and participatory approach, was used to gather experiences and ideas from 21 consumers and 30 health professionals. Thematic analysis was undertaken. RESULTS: Maori and Pacific patients and their whanau/aiga identified the importance of whanau/aiga support and involvement throughout their ARF/RHD journey. They described that the way care was delivered was often frustrating, fragmented and lacked effective communication. Participants expressed the need for information to improve their understanding of ARF/RHD. Health professionals identified the need for better continuity of care and felt that they were currently working siloed from other professionals with little visibility of other roles or opportunity for collaboration. The ideas for improvement were grouped into themes and resulted in development and prototyping of peer support groups, patient and staff education resources, clinical dashboard and pathway development, and an enhanced model of care for delivery to patients receiving penicillin prophylaxis. CONCLUSION: The co-design process enabled consumers and staff of ARF/RHD services to share experiences, identify ideas for improvement, co-design prototypes and test initiatives to better support the needs of those delivering and receiving ARF/RHD services.

Measuring health consumers' engagement at the governance level: development and validation of the Middlemore Consumer Engagement Questionnaire.

AIM: To develop and validate a questionnaire to measure health CE at governance level. METHOD: This study used qualitative and quantitative methods (including focus groups, cognitive interviews and an international survey), and consisted of two phases. In Phase 1, an initial list of items was generated and refined with feedback from health consumer representatives. In Phase 2, a draft survey was distributed to n=227 consumers from New Zealand, Australia and Canada. The benefit and relevance of using the questionnaire was explored through face-to-face interviews with five CE leaders from New Zealand healthcare organisations. RESULTS: The proposed questionnaire comprises 25 statements relating to CE. Respondents indicate their level of agreement with the statements on a five-point Likert-type scale. Focus group and cognitive interview participants found the questionnaire relevant and easy to understand. The questionnaire scores correlated with the PPEET, another instrument measuring consumer engagement, and showed excellent internal consistency (Cronbach's alpha=0.97), unidimensionality and test-retest reliability (r=0.84). CONCLUSION: The proposed questionnaire measures CE at governance level and can be used for international comparisons and benchmarking. It showed sound psychometric properties and its value and relevance was recognised by health consumer representatives and leaders with CE roles in New Zealand healthcare organisations.

Ezh2 does not mediate retinal ganglion cell homeostasis or their susceptibility to injury.

Epigenetic predisposition is thought to critically contribute to adult-onset disorders, such as retinal neurodegeneration. The histone methyltransferase, enhancer of zeste homolog 2 (Ezh2), is transiently expressed in the perinatal retina, particularly enriched in retinal ganglion cells (RGCs). We previously showed that embryonic deletion of Ezh2 from retinal progenitors led to progressive photoreceptor degeneration throughout life, demonstrating a role for embryonic predisposition of Ezh2-mediated repressive mark in maintaining the survival and function of photoreceptors in the adult. Enrichment of Ezh2 in RGCs leads to the question if Ezh2 also mediates gene expression and function in postnatal RGCs, and if its deficiency changes RGC susceptibility to cell death under injury or disease in the adult. To test this, we generated mice carrying targeted deletion of Ezh2 from RGC progenitors driven by Math5-Cre (mKO). mKO mice showed no detectable defect in RGC development, survival, or cell homeostasis as determined by physiological analysis, live imaging, histology, and immunohistochemistry. Moreover, RGCs of Ezh2 deficient mice revealed similar susceptibility against glaucomatous and acute optic nerve trauma-induced neurodegeneration compared to littermate floxed or wild-type control mice. In agreement with the above findings, analysis of RNA sequencing of RGCs purified from Ezh2 deficient mice revealed few gene changes that were related to RGC development, survival and function. These results, together with our previous report, support a cell lineage-specific mechanism of Ezh2-mediated gene repression, especially those critically involved in cellular function and homeostasis.