Formulating policies and procedures for managing diving related deaths: a whole of state engagement from frontline and hospital services in Tasmania.

Introduction: Tasmania is a small island state off the southern edge of Australia where a comparatively high proportion of the 558,000 population partake in recreational or occupational diving. While diving is a relatively safe sport and occupation, Tasmania has a significantly higher diving death rate per head of population than other States in Australia (four times the national diving mortality rate). Methods: Three compressed gas diving deaths occurred in seven months between 2021-2022 prompting a review of the statewide approach for the immediate response of personnel to diving-related deaths. The review engaged first responders including the Police Marine and Rescue Service, hospital-based departments including the Department of Hyperbaric and Diving Medicine, and the mortuary and coroner's office. Results: An aide-mémoire for all craft groups, digitalised checklists for first responders (irrespective of diving knowledge), and a single-paged algorithm to highlight inter-agency communication pathways in the event of a diving death were designed to enhance current practices and collaboration. Conclusions: If used, these aids for managing diving related deaths should ensure that time-critical information is appropriately captured and stored to optimise information provided for the coronial investigation.

Sialic acid is a critical fetal defense against maternal complement attack.

The negatively charged sugar sialic acid (Sia) occupies the outermost position in the bulk of cell surface glycans. Lack of sialylated glycans due to genetic ablation of the Sia-activating enzyme CMP-sialic acid synthase (CMAS) resulted in embryonic lethality around day 9.5 post coitum (E9.5) in mice. Developmental failure was caused by complement activation on trophoblasts in Cmas-/- implants and was accompanied by infiltration of maternal neutrophils at the fetal-maternal interface, intrauterine growth restriction, impaired placental development, and a thickened Reichert's membrane. This phenotype, which shared features with complement receptor 1-related protein Y (Crry) depletion, was rescued in E8.5 Cmas-/- mice upon injection of cobra venom factor, resulting in exhaustion of the maternal complement component C3. Here we show that Sia is dispensable for early development of the embryo proper but pivotal for fetal-maternal immune homeostasis during pregnancy, i.e., for protecting the allograft implant against attack by the maternal innate immune system. Finally, embryos devoid of cell surface sialylation suffered from malnutrition due to inadequate placentation as a secondary effect.