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Background: The provision of graded supervision affording progressive autonomy is fundamental to the progression of a medical learner toward competency for independent practice; the decision of how much supervision versus autonomy to provide a trainee in the execution of clinical care constitutes an entrustment decision. Despite entrustment decision making occurring both daily in practice and summatively at points of matriculation through stages of medical training, the factors influencing entrustment decisions remain poorly understood across clinical contexts. Objective: This study was designed to explore the central research question: How are entrustment decisions made in the medical intensive care unit (ICU)? Methods: This qualitative case study used semistructured interviews with attending pulmonary and critical care physicians in the medical ICU at a major midwestern medical center to explore the entrustment decision-making process as it was enacted in the clinical environment. Results: Five major themes emerged from the data: 1) task, circumstance, and trainee factors contribute to entrustment decision making; 2) ad hoc entrustment decisions are enacted by supervisors with a consideration of the care team as a unit, not only an individual; 3) autonomy does not only arise out of entrustment, but outcomes of prior autonomous actions by the trainee inform the intention to entrust; 4) entrustment decision making includes a social process of back-and-forth akin to negotiation; and 5) entrustment is a learned skill. Conclusion: The process of entrustment decision making in the ICU is more complex than prior frameworks have captured; a model with more complete incorporation of the factors that influence entrustment in the ICU is presented. It is not clear how often ad hoc entrustment decisions in clinical practice are primarily driven by factors pertaining directly to trainee competence, which carries implications in the use of entrustment for assessment. [ABSTRACT FROM AUTHOR]

Introduction: The 21-point Brain Care Score (BCS) was developed through a modified Delphi process in partnership with practitioners and patients to promote behavior changes and lifestyle choices in order to sustainably reduce the risk of dementia and stroke. We aimed to assess the associations of the BCS with risk of incident dementia and stroke. Methods: The BCS was derived from the United Kingdom Biobank (UKB) baseline evaluation for participants aged 40–69  years, recruited between 2006–2010. Associations of BCS and risk of subsequent incident dementia and stroke were estimated using Cox proportional hazard regressions, adjusted for sex assigned at birth and stratified by age groups at baseline. Results: The BCS (median: 12; IQR:11–14) was derived for 398,990 UKB participants (mean age: 57; females: 54%). There were 5,354 incident cases of dementia and 7,259 incident cases of stroke recorded during a median follow-up of 12.5  years. A five-point higher BCS at baseline was associated with a 59% (95%CI: 40-72%) lower risk of dementia among participants aged <50. Among those aged 50– 59, the figure was 32% (95%CI: 20-42%) and 8% (95%CI: 2-14%) for those aged >59  years. A five-point higher BCS was associated with a 48% (95%CI: 39-56%) lower risk of stroke among participants aged <50, 52% (95%CI, 47-56%) among those aged 50–59, and 33% (95%CI, 29-37%) among those aged >59. Discussion: The BCS has clinically relevant and statistically significant associations with risk of dementia and stroke in approximately 0.4 million UK people. Future research includes investigating the feasibility, adaptability and implementation of the BCS for patients and providers worldwide. [ABSTRACT FROM AUTHOR]

UK Biobank is an intensively characterised prospective cohort of 500,000 adults aged 40-69 years when recruited between 2006 and 2010. The study was established to enable researchersworldwide to undertake health-related research in the public interest. The existence of such a large, detailed prospective cohort with a high degree of participant engagement enabled its rapid repurposing for coronavirus disease-2019 (COVID-19) research. In response to the pandemic, the frequency of updates on hospitalisations and deaths among participants was immediately increased, and new data linkages were established to national severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) testing and primary care health records to facilitate research into the determinants of severe COVID-19. UK Biobank also instigated several sub-studies on COVID-19. In 2020, monthly blood samples were collected from approximately 20,000 individuals to investigate the distribution and determinants of SARS-CoV-2 infection, and to assess the persistence of antibodies following infection with another blood sample collected after 12 months. UK Biobank also performed repeat imaging of approximately 2,000 participants (half of whom had evidence of previous SARS-CoV-2 infection and half did not) to investigate the impact of the virus on changes in measures of internal organ structure and function. In addition, approximately 200,000 UK Biobank participants took part in a self-test SARS-CoV-2 antibody sub-study (between February and November 2021) to collect objective data on previous SARS-CoV-2 infection. These studies are enabling unique research into the genetic, lifestyle and environmental determinants of SARSCoV-2 infection and severe COVID-19, as well as their long-term health effects. UK Biobank's contribution to the national and international response to the pandemic represents a case study for its broader value, now and in the future, to precision medicine research. [ABSTRACT FROM AUTHOR]

Salmonella enterica serovar Typhimurium uses two-component regulatory systems (TCRSs) to respond to environmental stimuli. Upon infection, the TCRSs PhoP-PhoQ (PhoPQ) and PmrA-PmrB (PmrAB) are activated by environmental signals detected in the lumen of the intestine and within host cells. TCRS-mediated gene expression leads to upregulation of genes involved in lipopolysaccharide (LPS) modification and cationic antimicrobial peptide (CAMP) resistance. This research expands on previous studies which have shown that CAMPs can activate Salmonella TCRSs in vitro. The focus of this work was to determine if CAMPs can act as environmental signals for PhoPQ- and PmrAB-mediated gene expression in vitro, during infection of macrophages and in a mouse model of infection. Monitoring of PhoPQ and PmrAB activation using recombinase-based in vivo expression technology (RIVET), alkaline phosphtase and β-galactosidase reporter fusion constructs demonstrated that S. Typhimurium PhoQ can sense CAMPs in vitro. In mouse macrophages, the cathelecidin CRAMP does not activate the PhoPQ regulon. Acidification of the Salmonella-containing vacuole activates PhoP- and PmrA-regulated loci but blocking acidification still does not reveal a role for CRAMP in TCRS activation in mouse macrophages. However, assays performed in susceptible wild type (WT), CRAMP knockout (KO), and matrilysin (a metalloproteinase necessary for activating murine α-defensins) KO mice suggest CRAMP, but not α-defensins, serve as a putative direct TCRS activation signal in the mouse intestine. These studies provide a better understanding of the in vivo environments that result in activation of these virulence-associated TCRSs. [ABSTRACT FROM AUTHOR]