Publications by authors named "C F RYDER"
Objective: This paper investigates Burn First Aid Treatment (BFAT) provided to Aboriginal and Torres Strait Islander children in Australia at the scene of injury using data from a population-based cohort study.
Study Design: The participants were 208 Aboriginal and Torres Strait Islander children aged < 16 years who sustained a burns injury between 2015-2018, and their carers. The primary outcome measure was gold standard BFAT, (defined as at least 20 min of cool, running water within 3 h of the injury); additional measures included type of first aid, length of first aid provided, and carer's knowledge of first aid.
Objectives: Research characterizing work-related injuries and illnesses (WRII) has predominantly focused on inpatients and deaths, despite evidence that 4% of WRII are admitted as inpatients and deaths are less than 0.2% of acute WRII. Our aim is to determine the usefulness of incorporating emergency department (ED) hospital data into current occupational health surveillance systems.
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- - The study highlights the significant issue of type 2 diabetes in Aboriginal communities, particularly focusing on Ngarrindjeri Country in South Australia, and criticizes the prevalent Western biomedical frameworks that overlook local contexts and strengths.
- - Utilizing a combination of Aboriginal and Western research methods, the study collected qualitative data from 15 participants through yarning sessions, identifying barriers rooted in the impacts of colonization, as well as community strengths that support diabetes care.
- - The findings suggest that despite facing numerous challenges, Aboriginal people in the area possess unique resources and capabilities to combat diabetes, emphasizing the need for health initiatives that respect local knowledge and prioritize community-led, holistic approaches over traditional medical models.
This work identifies MALAT1 as a requisite downstream effector of oncogenic feedforward inflammatory circuits necessary for the development of TET2-mutated CH and fulminant myeloid malignancy. We elucidate a novel mechanism by which MALAT1 "shields" p65 from dephosphorylation to potentiate this circuit and nominate MALAT1 inhibition as a future therapeutic strategy.
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