Citations

Abstract Introduction The Geriatric Emergency Care Applied Research Network 2.0‐Advancing Dementia Care (GEAR 2.0‐ADC) aims to advance research efforts to improve the emergency care of persons living with dementia (PLWDs). Objective To support this objective, GEAR 2.0‐ADC convened a virtual consensus conference to prioritize emergency care research opportunities for PLWDs inclusive of perspectives of PLWDs to ensure identification of research gaps in response to their experiences and priorities. Inclusion of PLWDs as research partners is increasingly recognized as a best practice, however, approaches to facilitating consensus participation are lacking. Methods Best practices for supporting the engagement of PLWDs in a consensus conference, applied across its three phases (pre‐conference, during the conference, and post‐conference), include: establishing a learning environment focused on research priorities before the event, presenting information in ways that align with participants' learning preferences while accommodating cognitive impairments, and providing multiple opportunities and methods for gathering post‐conference feedback from PLWDs. Results These strategies were identified by PLWDs and care partners (CPs) through semi‐structured interviews, who were involved in the convening process, aimed at exploring ways to enhance facilitation techniques for participants. Conclusion Additionally, these summarized insights aim to encourage the use of community‐engaged approaches in discussions and consensus‐building around research priorities in emergency care, particularly for PLWDs and their CPs.

AbstractOuter hair cell (OHC) metabolism is blocked by cisplatin. Concurrent changes in the renal handling of magnesium occur because of the damage cisplatin causes to the renal proximal tubule cells within the thick ascending loop of Henle. Although there is no evidence of cisplatin within the OHCs, there are significant levels of intracellular calcium, the antagonist to magnesium at the cell membrane. The OHC motile response is dependent on intracellular calcium. When the calcium current is suppressed by an antagonist, the extracellular OHC microphonic potential decreases. Magnesium deficiency is known to produce hyperexcitabililty within the central nervous system, including fatal audiogenic seizures. In addition, increases in the amplitude of the auditory brainstem response wave V occur with aminoglycoside therapy and magnesium deficiency. This paper illustrates the amplitude growth of distortion product otoacoustic emissions in two patients treated with cisplatin and explores the possible underlying reasons why this may be related to magnesium metabolism. Abbreviations: DPOAEs = distortion product otoacoustic emissions, OAEs = otoacoustic emissions, OHC = outer hair cell, TEOAEs = transient otoacoustic emissions