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Introduction: Hip fractures often occur in medically complex patients and can be associated with high perioperative mortality. Mortality risk assessment tools that are specific to hip fracture patients have not been extensively studied. The objective of this study is to evaluate a recently published 30-day mortality risk calculator (Hip Fracture Estimator of Mortality Amsterdam [HEMA]) in a group of patients treated at a university health system., Materials & Methods: 625 patients treated surgically for hip fractures between 2015 and 2020 at our institution were retrospectively reviewed. Patients younger than age 65, periprosthetic fractures, revision procedures, and fractures treated non-operatively were excluded. Univariate and multivariate analyses were used to determine significant relationships between variables and 30-day mortality after surgery. Additional patient-specific risk factors not included in the original risk calculator were also evaluated., Results: The observed 30-day mortality was 5.6%. HEMA score was significantly associated with 30-mortality, though our cohort had significantly lower mortality rates in high-risk patients than expected based on the HEMA tool. In analyzing patient characteristics not included in HEMA score, history of dementia and elevated troponin were significantly associated with 30-day mortality., Discussion: The HEMA score reliably stratifies risk for 30-day mortality after hip fracture, though overestimates mortality in high-risk patients treated at a tertiary care center with a multidisciplinary team. The HEMA score may be enhanced by considering additional variables, including troponin level and history of dementia., Level of Evidence: IV., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier Ltd.)

Introduction: Proximal tibia fracture dislocations (PTFDs) are a subset of plateau fractures with little in the literature since description by Hohl (1967) and classification by Moore (1981). We sought to evaluate reliability in diagnosis of fracture-dislocations by traumatologists and to compare their outcomes with bicondylar tibial plateau fractures (BTPFs)., Methods: This was a retrospective cohort study at 14 level 1 trauma centers throughout North America. In all, 4771 proximal tibia fractures were reviewed by all sites and 278 possible PTFDs were identified using the Moore classification. These were reviewed by an adjudication board of three traumatologists to obtain consensus. Outcomes included inter-rater reliability of PTFD diagnosis, wound complications, malunion, range of motion (ROM), and knee pain limiting function. These were compared to BTPF data from a previous study., Results: Of 278 submitted cases, 187 were deemed PTFDs representing 4% of all proximal tibia fractures reviewed and 67% of those submitted. Inter-rater agreement by the adjudication board was good (83%). Sixty-one PTFDs (33%) were unicondylar. Eleven (6%) had ligamentous repair and 72 (39%) had meniscal repair. Two required vascular repair. Infection was more common among PTFDs than BTPFs (14% vs 9%, p = 0.038). Malunion occurred in 25% of PTFDs. ROM was worse among PTFDs, although likely not clinically significant. Knee pain limited function at final follow-up in 24% of both cohorts., Conclusions: PTFDs represent 4% of proximal tibia fractures. They are often unicondylar and may go unrecognized. Malunion is common, and PTFD outcomes may be worse than bicondylar fractures., Competing Interests: Declarations of Competing Interest None, (Copyright © 2021 Elsevier Ltd. All rights reserved.)

After acute infection Epstein-Barr virus (EBV)-specific memory CD8+ T cells exit cell cycle, and a proportion of these antigen-experienced cells re-express CD45RA (CD45 which predominantly express exon A). However, the signals involved are not known. We investigated the roles of interleukin 15 (IL-15) and interferon-alpha/beta (IFN-I) in these processes, since these mediators have a crucial but undefined role in the maintenance of CD8+ T-cell memory. We show that IFN-I (but not IL-15) allows activated EBV-specific CD8+ T cells to leave cell cycle without entering apoptosis. This was associated with up-regulation of the cyclin inhibitor p27, but not of CD45RA. In contrast, IL-15 (but not IFN-I) induced "homeostatic" proliferation and CD45RA re-expression by these cells in vitro. Different signals, therefore, induce quiescence and CD45RA re-expression in activated EBV-specific CD8+ T cells. After T-cell receptor (TCR) activation freshly isolated CD45RA+ antigen-experienced CD8+ T cells show poor proliferative activity but are highly cytotoxic and secrete IFN-gamma efficiently. This suggests functional reprogramming toward effector function but away from proliferation. The induction of quiescence and the generation of proliferation-independent effector CD8+ T cells that re-express CD45RA may minimize the impact of replicative senescence in virus-specific populations that would otherwise occur during decades of persistent infection.

During acute infection, latent and lytic Epstein-Barr virus (EBV) epitope-specific CD8(+) T cells have a CD45RO(+) CD45RA(-) phenotype. However, after resolution of the infection, a large proportion of these cells, particularly those specific for lytic viral epitopes, re-express the CD45RA molecule. The role of CD8(+) CD45RA(+) T cells in ongoing immunity to EBV and other viruses is unknown. We now demonstrate that, relative to their CD45RO(+) counterparts, the EBV-specific CD8(+) T cells that revert to CD45RA expression after acute infectious mononucleosis are not in cell cycle, have longer telomeres, and are more resistant to apoptosis partly because of increased Bcl-2 expression. However, the EBV-specific CD8(+) CD45RA(+) T cells have shorter telomeres than the total CD8(+) CD45RA(+) T-cell pool and predominantly express low levels of the CCR7 chemokine receptor, indicating that they are not naive cells. In addition, EBV-specific CD8(+) CD45RA(+) T cells can be induced to proliferate and exhibit potent cytotoxic activity against target cells loaded with specific peptide. Our results strongly suggest, therefore, that EBV-specific CD8(+) CD45RA(+) T cells represent a stabilized virus-specific memory pool and not terminally differentiated effector cells. The identification of mechanisms that enable stable virus-specific CD8(+) T cells to persist after acute infection may lead to the enhancement of antiviral immunity in immunocompromised and elderly persons.