RESUMEN
Background: In 2020, the coronavirus disease 2019 (COVID-19) pandemic caused the cessation of nonemergent total joint arthroplasty (TJA, referring to total hip and total knee arthroplasty) operations between mid-March and April 2020. The purpose of this study is to analyze the effects and potential disparities in access to care due to the COVID-19 restrictions. Methods: A database was used to examine the demographics of patients undergoing TJA from May to December 2019 (pre-COVID-19) and from May to December 2020 (post-COVID-19 restrictions). Categorical covariates were summarized by reporting counts and percentages and compared using Fisher exact tests. Continuous covariates were summarized by reporting means and standard deviations. Two-sample t-tests were used for continuous covariates. The equality of TJA counts by year was tested using a test of proportions. Results: There were more TJA procedures performed during the post-COVID-19 period in 2020 than in the pre-COVID-19 period (1151 vs 882, P < .001). There was an increase in the relative percentage of THAs vs TKAs performed in 2020 vs 2019 (26.9% vs 18.8%, P < .001) and an increase in patients with Medicaid with a decrease in private insurance (P = .043). The average length of stay was shorter in 2020 with a greater percentage of TJAs performed outpatient (P < .001). There were no differences in patient sex, race, body mass index, smoking status, or age between the 2 periods. Conclusions: A relative increase in THA procedures, an increase in patients with Medicaid and decrease in private insurance, and a a decreased length of stay were seen after COVID-19 restrictions. These trends may reflect pandemic-related changes in insurance status as well as the growing shift to same-day discharge.
RESUMEN
The identification of specific genetic (presenilin-1 [PS1] and amyloid precursor protein [APP] mutations) and environmental factors responsible for Alzheimer's disease (AD) has revealed evidence for a shared pathway of neuronal death. Moreover, AD-specific cell defects may be observed in many other nonneuronal cells (e.g., lymphocytes). Thus, lymphocytes may serve as a cellular system in which to study risk factors of sporadic, as well as genetic AD in vivo. The aim of our present study was to clarify whether lymphocytes bearing genetic or sporadic risk factors of AD share an increased susceptibility to cell death. Additionally we examined whether a cell typespecific vulnerability pattern was present and how normal aging, the main risk factor of sporadic AD, contributes to changes in susceptibility to cell death. Here, we report that lymphocytes affected by sporadic or genetic APP and PS1 AD risk factors share an increased vulnerability to cell death and exhibit a similar cell type-specific pattern, given that enhanced vulnerability was most strongly developed in the CD4+ T-cell subtype. In this paradigm, sporadic risk factors revealed the highest impact on cell type-specific sensitivity of CD4+ T cells to apoptosis. In contrast, normal aging results in an increased susceptibility to apoptosis of both, CD4+ and CD8+ T cells.