Impact of the COVID-19 Pandemic on Orthopedic Surgery Residency Training.

This study sought to investigate the impact of the coronavirus disease 2019 (COVID-19) pandemic on orthopedic surgery residency training across the United States. A 26-question online survey was created and sent to all orthopedic surgery residency programs across the United States. Areas of emphasis in the survey included the pandemic's effect on work hours, operative experience, didactics, and medical student recruitment. There were 142 respondents to the survey. One hundred seventeen (82.4%) respondents stated that their residency changed to an alternative/surge schedule during the pandemic. Regarding the degree to which the pandemic affected their training, 77 (54.2%) respondents gave a rating of 8 to 10 on a scale of 0 to 10. Similarly, 94 (66.2%) residents indicated that their operative experience had decreased significantly. Twenty-two (15.5%) residents expected that their next year clinical abilities would not be affected. One hundred thirty-seven (96.5%) residents stated their program transitioned to online didactics. Responses regarding the effectiveness of online didactics were mixed. One hundred twenty-six (88.7%) respondents stated the pandemic would negatively affect the 2021 National Residency Matching Program match. This study demonstrated that the COVID-19 pandemic greatly affected orthopedic surgery residency training in the United States. Resident operative experience decreased significantly, and most respondents indicated a switch to online didactics. Effects were also felt to extend to fourth-year scheduling and the 2021 National Residency Matching Program match. [Orthopedics. 2023;46(5):315-319.].

Mechanosensitive TRPV4 channels stabilize VE-cadherin junctions to regulate tumor vascular integrity and metastasis.

The transient receptor potential vanilloid 4 (TRPV4) channel is a mechanosensor in endothelial cells (EC) that regulates cyclic strain-induced reorientation and flow-mediated nitric oxide production. We have recently demonstrated that TRPV4 expression is reduced in tumor EC and tumors grown in TRPV4KO mice exhibited enhanced growth and immature leaky vessels. However, the mechanism by which TRPV4 regulates tumor vascular integrity and metastasis is not known. Here, we demonstrate that VE-cadherin expression at the cell-cell contacts is significantly reduced in TRPV4-deficient tumor EC and TRPV4KO EC. In vivo angiogenesis assays with Matrigel of varying stiffness (700-900 Pa) revealed a significant stiffness-dependent reduction in VE-cadherin-positive vessels in Matrigel plugs from TRPV4KO mice compared with WT mice, despite an increase in vessel growth. Further, syngeneic Lewis Lung Carcinomatumor experiments demonstrated a significant decrease in VE-cadherin positive vessels in TRPV4KO tumors compared with WT. Functionally, enhanced tumor cell metastasis to the lung was observed in TRPV4KO mice. Our findings demonstrate that TRPV4 channels regulate tumor vessel integrity by maintaining VE-cadherin expression at cell-cell contacts and identifies TRPV4 as a novel target for metastasis.