LinkedIn Usage Trends Among Surgeons at a Large Academic Institute.

INTRODUCTION: Social networking platforms have evolved into a self-promotional space. The LinkedIn platform allows users to share knowledge, research accomplishments, and network in an academic setting. Our objective was to determine LinkedIn usage trends among surgeons at a large academic institution. METHODS: A list of surgeons within the department of surgery at a large academic institute was compiled. All publicly available profiles were analyzed for their LinkedIn activity and followership. Active accounts were defined as users who have posted or interacted with any posts within the last year. Comparisons of LinkedIn usage grouped by gender, surgery division, and rank were analyzed. RESULTS: A total of 133 surgeons were included. Among these surgeons, 88 had a LinkedIn profile (66.2%); however, only 43 surgeons had active usage on this platform (32.3%). The median number of followers among surgeons with a profile was 110 (IQR [24-427]). Male surgeons had a higher median of followers (167 IQR [38-502]) compared to female (54 IQR [21-209]). A greater percentage of male surgeons had a profile compared to female surgeons (68.5% M versus 61.0% F, P = 0.12). The transplant surgery division had the highest percentage of LinkedIn accounts (90.9%) followed by surgical oncology (87.5%). However, active usage was led by the pediatric surgery division (80.0%), followed by the plastic surgery division (71.4%). Instructors, assistant professors, associate professors, and professors all had LinkedIn accounts; however, instructors were the least active users with 33.3% being active on their LinkedIn. The lowest percentage of those with LinkedIn accounts were instructors (50%). Professors were found to be the most active users at 57.1%. CONCLUSIONS: Social media use is on the rise in academic surgery. Within a department of surgery at a large academic institution, only 32.3% were active users of LinkedIn, suggesting that there is room for improvement in utilizing this resource as a tool for mentorship, professional development, and networking.

Altered sphingolipid pathway in SARS-CoV-2 infected human lung tissue.

Introduction: The SARS-CoV-2 mediated COVID-19 pandemic has impacted millions worldwide. Hyper-inflammatory processes, including cytokine storm, contribute to long-standing tissue injury and damage in COVID-19. The metabolism of sphingolipids as regulators of cell survival, differentiation, and proliferation has been implicated in inflammatory signaling and cytokine responses. Sphingosine-kinase-1 (SK1) and ceramide-synthase-2 (CERS2) generate metabolites that regulate the anti- and pro-apoptotic processes, respectively. Alterations in SK1 and CERS2 expression may contribute to the inflammation and tissue damage during COVID-19. The central objective of this study is to evaluate structural changes in the lung post-SARS-CoV-2 infection and to investigate whether the sphingolipid rheostat is altered in response to SARS-CoV-2 infection. Methods: Central and peripheral lung tissues from COVID-19+ or control autopsies and resected lung tissue from COVID-19 convalescents were subjected to histologic evaluation of airspace and collagen deposisiton, and immunohistochemical evaluation of SK1 and CERS2. Results: Here, we report significant reduction in air space and increase in collagen deposition in lung autopsy tissues from patients who died from COVID-19 (COVID-19+) and COVID-19 convalescent individuals. SK1 expression increased in the lungs of COVID-19+ autopsies and COVID-19 convalescent lung tissue compared to controls and was mostly associated with Type II pneumocytes and alveolar macrophages. No significant difference in CERS2 expression was noted. SARS-CoV-2 infection upregulates SK1 and increases the ratio of SK1 to CERS2 expression in lung tissues of COVID-19 autopsies and COVID-19 convalescents. Discussion: These data suggest an alteration in the sphingolipid rheostat in lung tissue during COVID-19, suggesting a potential contribution to the inflammation and tissue damage associated with viral infection.

Local SARS-CoV-2 Peptide-Specific Immune Responses in Lungs of Convalescent and Uninfected Human Subjects.

Multi-specific and long-lasting T cell immunity have been recognized as indicators for long term protection against pathogens including the novel coronavirus SARS-CoV-2, the causative agent of the COVID-19 pandemic. Functional significance of peripheral memory T cells in individuals recovering from COVID-19 (COVID-19 + ) are beginning to be appreciated; but little is known about lung resident memory T cells (lung TRM) in SARS-CoV-2 infection. Here, we utilize a perfused three dimensional (3D) human lung tissue model and identify pre-existing local T cell immunity against SARS-CoV-2 proteins in lung tissues. We report ex vivo maintenance of functional multi-specific IFN-γ secreting lung TRM in COVID-19 + and their induction in lung tissues of vaccinated COVID-19 + . Importantly, we identify SARS-CoV-2 peptide-responding B cells and IgA + plasma cells in lung tissues of COVID-19 + in ex vivo 3D-tissue models. Our study highlights the importance of balanced and local anti-viral immune response in the lung with persistent induction of TRM and IgA + plasma cells for future protection against SARS-CoV-2 infection. Further, our data suggest that inclusion of multiple viral antigens in vaccine approaches may broaden the functional profile of memory T cells to combat the severity of coronavirus infection.