Achieving Equity in EMS Care and Patient Outcomes through Quality Management Systems: A Position Statement.

Improving health and safety in our communities requires deliberate focus and commitment to equity. Inequities are differences in access, treatment, and outcomes between individuals and across populations that are systemic, avoidable, and unjust. Within health care in general, and Emergency Medical Services (EMS) in particular, there are demonstrated inequities in the quality of care provided to patients based on a number of characteristics linked to discrimination, exclusion, or bias. Given the critical role that EMS plays within the health care system, it is imperative that EMS systems reduce inequities by delivering evidence-based, high-quality care for the communities and patients we serve.To achieve equity in EMS care delivery and patient outcomes, the National Association of EMS Physicians recommends that EMS systems and agencies:make health equity a strategic priority and commit to improving equity at all levels.assess and monitor clinical and safety quality measures through the lens of inequities as an integrated part of the quality management process.ensure that data elements are structured to enable equity analysis at every level and routinely evaluate data for limitations hindering equity analysis and improvement.involve patients and community stakeholders in determining data ownership and stewardship to ensure its ongoing evolution and fitness for use for measuring care inequities.address biases as they translate into the quality of care and standards of respect for patients.pursue equity through a framework rooted in the principles of improvement science.

Polydnaviral ankyrin proteins aid parasitic wasp survival by coordinate and selective inhibition of hematopoietic and immune NF-kappa B signaling in insect hosts.

Polydnaviruses are mutualists of their parasitoid wasps and express genes in immune cells of their Lepidopteran hosts. Polydnaviral genomes carry multiple copies of viral ankyrins or vankyrins. Vankyrin proteins are homologous to IκB proteins, but lack sequences for regulated degradation. We tested if Ichnoviral Vankyrins differentially impede Toll-NF-κB-dependent hematopoietic and immune signaling in a heterologous in vivo Drosophila, system. We first show that hematopoiesis and the cellular encapsulation response against parasitoid wasps are tightly-linked via NF-κB signaling. The niche, which neighbors the larval hematopoietic progenitors, responds to parasite infection. Drosophila NF-κB proteins are expressed in the niche, and non cell-autonomously influence fate choice in basal and parasite-activated hematopoiesis. These effects are blocked by the Vankyrin I²-vank-3, but not by P-vank-1, as is the expression of a NF-κB target transgene. I²-vank-3 and P-vank-1 differentially obstruct cellular and humoral inflammation. Additionally, their maternal expression weakens ventral embryonic patterning. We propose that selective perturbation of NF-κB-IκB interactions in natural hosts of parasitic wasps negatively impacts the outcome of hematopoietic and immune signaling and this immune deficit contributes to parasite survival and species success in nature.