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Traditionally, total shoulder arthroplasty is performed using a deltopectoral approach through which the glenohumeral joint is accessed by mobilization of the subscapularis. Despite several variations on the subscapularis management techniques, postoperative complications, including subscapularis deficiency and lower functional outcomes, remain an area for improvement. The purpose of this Technical Note is to describe in detail our technique for management of the subscapularis in the setting of a stemless humeral implant through which the repair is planned and almost entirely performed at the beginning of the case, prior to the subscapularis peel. This technique aims to improve outcomes after total shoulder arthroplasty by 1) avoiding the anatomic implant with anchor drilling, 2) improving procedure efficiency, and 3) anatomically "repairing" the subscapularis prior to takedown by placing anchors exactly at the repair-tension site.

The introduction of vaccines has inspired hope in the battle against SARS-CoV-2. However, the emergence of viral variants, in the absence of potent antivirals, has left the world struggling with the uncertain nature of this disease. Antibodies currently represent the strongest correlate of immunity against SARS-CoV-2, thus we profiled the earliest humoral signatures in a large cohort of acutely ill (survivors and nonsurvivors) and mild or asymptomatic individuals with COVID-19. Although a SARS-CoV-2–specific immune response evolved rapidly in survivors of COVID-19, nonsurvivors exhibited blunted and delayed humoral immune evolution, particularly with respect to S2-specific antibodies. Given the conservation of S2 across β-coronaviruses, we found that the early development of SARS-CoV-2–specific immunity occurred in tandem with preexisting common β-coronavirus OC43 humoral immunity in survivors, which was also selectively expanded in individuals that develop a paucisymptomatic infection. These data point to the importance of cross-coronavirus immunity as a correlate of protection against COVID-19.

Three-dimensional (3D) preoperative planning software for reverse total shoulder arthroplasty (rTSA) has been implemented in recent years in order to increase accuracy, improve efficiency, and add value to the outcome. A comprehensive literature review is required to determine the utility of preoperative 3D planning software in guiding orthopedic surgeons for implant placement in rTSA. We hypothesize that implementation of 3D preoperative planning software in the setting of rTSA leads to high concordance with minimal deviation from the preoperative plan.A comprehensive and iterative literature review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) using the PubMed, Embase, OVID Medline, Scopus, Cinahl, Web of Science, and Cochrane databases for original English-language studies evaluating the impact of preoperative planning software usage on rTSA outcomes published from January 1, 2000, to present. Blinded reviewers conducted multiple screens. All included studies were graded based on level of evidence, and data concerning patient demographics and postoperative outcomes were extracted.Nine articles met inclusion criteria (1 level II, 3 level III, and 5 level IV articles), including 415 patients and 422 shoulders. Of the patients who underwent rTSA, 235 were female and 140 were male, although 3 studies (n = 40) did not report sex breakdowns for rTSA patients. The average age was 72.7 years. Four studies (79 shoulders) reported implant final position as mean deviation from planned version and planned inclination. Six studies (n = 236) reported screw angle deviation, fixation, length, and concordance. Concordance with the preoperative plan was measured in 3 studies (n = 178), resulting in complete concordance of 90% (n = 100), arthroplasty type concordance (rTSA vs. TSA) of 100% (n = 100), and glenosphere size concordance between 93% (n = 100) and 88% (n = 76). For screw length concordance, baseplate screw matched by 81% (n = 76) and 100% (n = 2), and upper (n = 35) and lower (n = 35) screw length concordance was observed as 74% and 69%, respectively. The use of preoperative planning (n = 178) was associated with low deviation from preoperative plan, more 2-screw fixations, and longer average screw length in comparison with an unplanned cohort.The use of preoperative planning software in the setting of rTSA results in minimal deviation from preoperative plan. High levels of concordance in screw angle, screw length, and glenosphere size were observed. Further prospective studies should be conducted to further substantiate these results.

Mechanisms underlying severe coronavirus disease 2019 (COVID-19) disease remain poorly understood. We analyze several thousand plasma proteins longitudinally in 306 COVID-19 patients and 78 symptomatic controls, uncovering immune and non-immune proteins linked to COVID-19. Deconvolution of our plasma proteome data using published scRNA-seq datasets reveals contributions from circulating immune and tissue cells. Sixteen percent of patients display reduced inflammation yet comparably poor outcomes. Comparison of patients who died to severely ill survivors identifies dynamic immune-cell-derived and tissue-associated proteins associated with survival, including exocrine pancreatic proteases. Using derived tissue-specific and cell-type-specific intracellular death signatures, cellular angiotensin-converting enzyme 2 (ACE2) expression, and our data, we infer whether organ damage resulted from direct or indirect effects of infection. We propose a model in which interactions among myeloid, epithelial, and T cells drive tissue damage. These datasets provide important insights and a rich resource for analysis of mechanisms of severe COVID-19 disease., Graphical abstract, Filbin et al. use plasma proteomics in 306 coronavirus disease 2019 (COVID-19) patients and 78 symptomatic controls over time to better understand the role of circulating immune cells and tissue cells in inflammation, disease severity, and survival. They propose a model in which interactions among myeloid, epithelial, and T cells drive tissue damage.