Objectives The United States has the highest number of Coronavirus Disease 2019 (COVID-19) in the world, with high variability in cases and mortality between communities. We aimed to quantify the associations between socioeconomic status and Coronavirus Disease 2019 (COVID-19) related cases and mortality in the U.S. Study Design: Nationwide COVID-19 data at the county level that was paired with the Distressed Communities Index (DCI) and its component metrics of socioeconomic status. Methods Severely distressed communities were classified by DCI>75 for univariate analyses. Adjusted rate ratios were calculated for cases and fatalities per 100,000 persons using hierarchical linear mixed models. Results This cohort included 1,089,999 cases and 62,298 deaths in 3,127 counties for a case-fatality rate of 5.7%. Severely distressed counties had significantly fewer deaths from COVID-19, but higher number of deaths/100,000. In risk-adjusted analysis, the two socioeconomic determinants of health with the strongest association with both higher cases/100,000 and higher fatalities/100,000 were percent of adults without a high school degree (cases: RR 1.10; fatalities: RR 1.08) and proportion of black residents (cases and fatalities: RR 1.03). The percentage of the population over 65 was also highly predictive for fatalities/100,000 (RR 1.07). Conclusion Lower education levels and greater percentages of black residents are strongly associated with higher rates of both COVID-19 cases and fatalities. Socioeconomic factors should be considered when implementing public health interventions in order to ameliorate the disparities in the impact of COVID-19 on distressed communities.

Among critically ill surgical patients, caloric provision across a wide acceptable range does not appear to be associated with major outcomes, including infectious complications. The optimum target for caloric provision remains elusive.

Ischemia-reperfusion (I/R) injury (IRI), which involves inflammation, vascular permeability, and edema, remains a major challenge after lung transplantation. Pannexin-1 (Panx1) channels modulate cellular ATP release during inflammation. This study tests the hypothesis that endothelial Panx1 is a key mediator of vascular inflammation and edema after I/R and that IRI can be blocked by Panx1 antagonism. A murine hilar ligation model of IRI was used whereby left lungs underwent 1 h of ischemia and 2 h of reperfusion. Treatment of wild-type mice with Panx1 inhibitors (carbenoxolone or probenecid) significantly attenuated I/R-induced pulmonary dysfunction, edema, cytokine production, and neutrophil infiltration versus vehicle-treated mice. In addition, VE-Cad-Cre/Panx1 mice (tamoxifen-inducible deletion of Panx1 in vascular endothelium) treated with tamoxifen were significantly protected from IRI (reduced dysfunction, endothelial permeability, edema, proinflammatory cytokines, and neutrophil infiltration) versus vehicle-treated mice. Furthermore, extracellular ATP levels in bronchoalveolar lavage fluid is Panx1-mediated after I/R as it was markedly attenuated by Panx1 antagonism in wild-type mice and by endothelial-specific Panx1 deficiency. Panx1 gene expression in lungs after I/R was also significantly elevated compared with sham. In vitro experiments demonstrated that TNF-α and/or hypoxia-reoxygenation induced ATP release from lung microvascular endothelial cells, which was attenuated by Panx1 inhibitors. This study is the first, to our knowledge, to demonstrate that endothelial Panx1 plays a key role in mediating vascular permeability, inflammation, edema, leukocyte infiltration, and lung dysfunction after I/R. Pharmacological antagonism of Panx1 activity may be a novel therapeutic strategy to prevent IRI and primary graft dysfunction after lung transplantation.

Background Obtaining National Institutes of Health (NIH) funding over the last 10 years has become increasingly difficult due to a decrease in the number of research grants funded and an increase in the number of NIH applications. Study Design NIH funding amounts and success rates were compared for all disciplines using data from NIH, FASEB, and Blue Ridge Medical Institute. Next, all NIH grants (2006–16) with surgeons as principal investigators were identified using NIH RePORTER and a grant impact score was calculated for each grant based on the publications’ impact factor per funding amount. Linear regression and one-way ANOVA were used for analysis. Results The number of NIH grant applications has increased by 18.7% (p=0.0009), while the number of funded grants (p < 0.0001) and R01s (p < 0.0001) across the NIH has decreased by 6.7% and 17.0%, respectively. The mean success rate of funded grants with surgeons as principal investigators (16.4%) has been significantly lower than the mean NIH funding rate (19.2%) (p = 0.011). Despite receiving only 831 R01’s during this time period, surgeon scientists were highly productive with an average grant impact score of 4.9 per $100,000, which increased over the last 10 years (0.15 ± 0.05 /year, p=0.02). Additionally, the rate of conversion of surgeon scientist mentored K awards to R01’s from 2007–12 was 46%. Conclusions Despite the declining funding over the last 10 years, surgeon scientists have demonstrated increasing productivity measured by impactful publications and higher success rates in converting early investigator awards to R01s.