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UAB AMC School of Medicine grew by $100 million in National Institutes of Health funding and moved up 10 spots in ranking. In 2018, UAB Hospital had 10 specialties ranked by U.S. News & World Report, 7 more than in 2013. This article outlines the approach taken and provides a conceptual framework for other AMCs eager to transform their structure and culture and position themselves for growth.

To investigate the current state and quality of compassion education interventions offered to health care providers during training or practice, determine how the components of each education intervention map onto the domains of an empirically based clinical model of compassion, and identify the most common approaches to compassion education.

The MEDLINE, Embase, CINAHL Plus with Full Text, Sociological Abstracts, Web of Science, ERIC, and Education Research Complete databases were searched from inception to March 2020 in this systematic review. Studies that evaluated a compassion education intervention for health care providers or those in training to enhance compassion toward patients and/or families were included. A narrative synthesis of the included studies was performed. The components of each intervention were mapped onto the domains of compassion described in the Patient Compassion Model.

One hundred eight peer-reviewed publications describing 103 interventions were included. Modalities ranged fg over time; and incorporate patient, preceptor, and peer evaluations.

Most interventions were limited as they focused on a single domain of compassion; did not adequately define compassion; were assessed exclusively by self-report; were devoid of a comparator/control group; and did not evaluate retention, sustainability, and translation to clinical practice over time. The authors suggest that compassion education interventions be grounded in an empirically based definition of compassion; use a competency-based approach; employ multimodal teaching methods that address the requisite attitudes, skills, behaviors, and knowledge within the multiple domains of compassion; evaluate learning over time; and incorporate patient, preceptor, and peer evaluations.

For more than 20 years, hip fracture 1-year mortality has remained around 20%. An elevation of the postoperative troponin peak within 72 hours (myocardial injury after noncardiac surgery [MINS]) is associated with a greater risk of short-term mortality in the general population. However, there seem to be conflicting results in the specific population who undergo hip fracture surgery, with some studies finding an association between troponin and mortality and some not. The objective of the present study was to investigate the association of MINS and the short- (before 28th day), intermediate- (before 180th day), and long-term (before 365th day) mortality after hip fracture surgery.

We conducted a single-center retrospective cohort of patients undergoing hip fracture surgery from November 2013 to December 2015. MINS was defined as postoperative troponin peak within the 72 hours >5 ng/L. Four MINS subgroups were defined according to the value of troponin peak (ie, ≥5-<20, ≥20-<65, ≥65-<1000, and fore and after exclusion of patients presenting an ACS. HR and aHR for each subgroup of troponin level were significantly associated with an increased probability of survival, except for the 5 to 20 ng/L group for which aHR was not significant (1.75, 95% CI, 0.82-3.74). In the landmark analysis, there was still an association between survival at the 365th day and troponin peak after the short- and intermediate-term truncated mortality.

MINS is associated with short-, intermediate-, and long-term mortality after hip fracture surgery. Peptide 17 cell line This could be a valuable indicator to determine the population at high risk of mortality that could benefit from targeted prevention and possible intervention.

MINS is associated with short-, intermediate-, and long-term mortality after hip fracture surgery. This could be a valuable indicator to determine the population at high risk of mortality that could benefit from targeted prevention and possible intervention.BACKGROUNDRecent studies have reported T cell immunity to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in unexposed donors, possibly due to crossrecognition by T cells specific for common cold coronaviruses (CCCs). True T cell crossreactivity, defined as the recognition by a single TCR of more than one distinct peptide-MHC ligand, has never been shown in the context of SARS-CoV-2.METHODSWe used the viral functional expansion of specific T cells (ViraFEST) platform to identify T cell responses crossreactive for the spike (S) glycoproteins of SARS-CoV-2 and CCCs at the T cell receptor (TCR) clonotype level in convalescent COVID-19 patients (CCPs) and SARS-CoV-2-unexposed donors. Confirmation of SARS-CoV-2/CCC crossreactivity and assessments of functional avidity were performed using a TCR cloning and transfection system.RESULTSMemory CD4+ T cell clonotypes that crossrecognized the S proteins of SARS-CoV-2 and at least one other CCC were detected in 65% of CCPs and unexposed donors. Several otute of Biomedical Imaging and Bioengineering. The Bloomberg~Kimmel Institute for Cancer Immunotherapy, The Johns Hopkins University Provost, and The Bill and Melinda Gates Foundation provided funding for this study.One of the primary mechanisms of tumor cell immune evasion is the loss of antigenicity, which arises due to lack of immunogenic tumor antigens as well as dysregulation of the antigen processing machinery. In a screen for small-molecule compounds from herbal medicine that potentiate T cell-mediated cytotoxicity, we identified atractylenolide I (ATT-I), which substantially promotes tumor antigen presentation of both human and mouse colorectal cancer (CRC) cells and thereby enhances the cytotoxic response of CD8+ T cells. Cellular thermal shift assay (CETSA) with multiplexed quantitative mass spectrometry identified the proteasome 26S subunit non-ATPase 4 (PSMD4), an essential component of the immunoproteasome complex, as a primary target protein of ATT-I. Binding of ATT-I with PSMD4 augments the antigen-processing activity of immunoproteasome, leading to enhanced MHC-I-mediated antigen presentation on cancer cells. In syngeneic mouse CRC models and human patient-derived CRC organoid models, ATT-I treatment promotes the cytotoxicity of CD8+ T cells and thus profoundly enhances the efficacy of immune checkpoint blockade therapy.