Background There are limited data on the characteristics of 30‐day readmission after hospitalization with coronavirus disease 2019 (COVID‐19). Objectives To examine the rate, timing, causes, predictors and outcomes of 30‐day readmission after COVID‐19 hospitalization. Methods From 13 March to 9 April 2020, all patients hospitalized with COVID‐19 and discharged alive were included in this retrospective observational study. Multivariable logistic regression was used to identify the predictors of 30‐day readmission, and a restricted cubic spline function was utilized to assess the linearity of the association between continuous predictors and 30‐day readmission. Results A total of 1062 patients were included in the analysis, with a median follow‐up time of 62 days. The mean age of patients was 56.5 years, and 40.5% were women. At the end of the study, a total of 48 (4.5%) patients were readmitted within 30 days of discharge, and a median time to readmission was 5 days. The most common primary diagnosis of 30‐day readmission was a hypoxic respiratory failure (68.8%) followed by thromboembolism (12.5%) and sepsis (6.3%). The patients with a peak serum creatinine level of ≥1.29 mg/dL during the index hospitalization, compared to those with a creatinine of <1.29 mg/dL, had 2.4 times increased risk of 30‐day readmission (adjusted odds ratio: 2.41; 95% CI: 1.23–4.74). The mortality rate during the readmission was 22.9%. Conclusion With 4.5% of the thirty‐day readmission rate, COVID‐19 survivors were readmitted early after hospital discharge, mainly due to morbidities of COVID‐19. One in five readmitted COVID‐19 survivors died during their readmission.

Hydrogen peroxide (HO) increases paracellular permeability of Madin-Darby canine kidney (MDCK) cells, but the mechanism mediating this effect remains unclear. Treatment of MDCK cells with HO activated ERK 1/2. Inhibition of ERK 1/2 activation blocked the ability of HO to increase paracellular permeability. Knockdown of zonula occludens-1 (ZO-1) protein but not occludin eliminated the ability of HO to increase paracellular permeability. HO treatment did not, however, affect the total cell content or contents of the Triton X-100-soluble and -insoluble fractions for occludin, ZO-1, or ZO-2. HO treatment decreased the number of F-actin stress fibers in the basal portion of the cells. Similar to wild-type MDCK cells, HO increased ERK 1/2 activation in ZO-1 knockdown and occludin knockdown cells. Inhibition of ERK 1/2 activation blocked the increase in paracellular permeability in occludin knockdown cells. ZO-1 knockdown cell paracellular permeability was regulated by PP1, an src inhibitor, indicating that the loss of response to HO was not a general loss of the ability to regulate the paracellular barrier. Inhibition of myosin ATPase activity with blebbistatin increased paracellular permeability in ZO-1 knockdown cells but not in wild-type MDCK cells. HO treatment sensitized wild-type MDCK cells to inhibition of myosin ATPase. Knockdown of TOCA-1 protein, which promotes formation of local branched actin networks, reproduced the effects of ZO-1 protein knockdown. These results demonstrate that HO increases MDCK cell paracellular permeability through activation of ERK 1/2. This HO action requires ZO-1 protein and TOCA-1 protein, suggesting involvement of the actin cytoskeleton.

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The purpose of our study was to evaluate the rate of ventral hernia repair (VHR) after open abdominal aortic anneurysm in New York State compared with the rate of VHR after open abdominal aortic bypass procedures. The Statewide Planning and Research Cooperative System database was queried for all abdominal aortic aneurysm (AAA) and bypass procedures performed between 2000 and 2010. Social security death index was used to identify patients who died. The cause-specific Cox proportional hazard model was applied to compare the risk of having follow-up VHR between patients with AAA and bypass with death as a competing risk event. A multivariable model was used to explore independent relationship with the risk of having follow-up ventral hernia after adjusting for other factors. There were 9314 patients who underwent open AAA repair, 739 (7.93%) of which had subsequent VHR. Comparatively, 8280 patients underwent aortofemoral or aortoiliac bypass procedures, with 480 (5.8%) undergoing subsequent VHR. The observed one-year, five-year, and 10-year VHR rates for AAA versus bypass were 2.8 versus 1.8 per cent, 10.0 versus 8.0 per cent, 10.7 versus 9.38 per cent, respectively. After controlling for all other factors, patients undergoing AAA repair were more likely and elderly patients were less likely to undergo VHR (P < 0.0001). Patients with serious comorbid conditions such as valvular disease, diabetes mellitus, and neurologic disorders were less likely to undergo subsequent VHR controlling for other factors. VHR after AAA procedures is more common compared with bypass procedures for occlusive disease. Because this patient population has significant comorbidity, prophylactic mesh placement may play a role in preventing necessity for future procedures.

Background Sarcomas are a rare and heterogeneous group of tumors originating from mesenchymal or connective tissue. They represent less than 1% of all adult cancers. The etiology and epidemiology of sarcomas remain understudied and poorly understood. The main objective of our study was to systematically assess the association between various occupational exposures and risk of sarcomas. Methods We performed a systematic literature search using the PubMed, Scopus, EMBASE and Cochrane databases to identify relevant cohort and case–control studies. A meta-analysis method was applied on the incidence and mortality outcomes where the estimate with 95% confidence interval (CI) was obtained. Results We included a total of 50 publications in our systematic review and 35 in meta-analysis. For exposures to phenoxy herbicides and chlorophenols, the pooled odds ratio (OR) for sarcoma was 1.85 (95% CI: 1.22, 2.82), based on 16 studies with 2254 participants, while the pooled standardized mortality ratio was 40.93 (95% CI 2.19, 765.90), based on 4 cohort studies with 59,289 participants. For exposure to vinyl chloride monomers the pooled risk ratios for angiosarcoma of the liver and other STS were 19.23 (95% CI 2.03, 182.46) and 2.23 (95 CI 1.55, 3.22) respectively based on 3 cohort studies with 12,816 participants. Exposure to dioxins was associated with an increased STS mortality; the pooled standardized mortality ratio was 2.56 (95% CI 1.60, 4.10) based on 4 cohort studies with 30,797 participants. Finally, woodworking occupation was associated with an increased risk of STS with the pooled OR of 2.16 (95% CI 1.39, 3.36). Conclusions Our findings suggest a positive association between higher exposure to dioxins and increased mortality from STS, between cumulative exposure to vinyl chloride monomers and increased mortality from angiosarcoma of the liver and STS, and between woodworking occupation and STS incidence. These findings were all statistically significant.