Our aim was to assess the association between obesity and the risk of unfavourable outcomes (composite of severe disease and mortality) in inpatients with COVID-19. We conducted a systematic search of databases between December 2019 and 28th June 2020. Studies were included if they reported or allowed estimation of an odds ratio (OR) for unfavourable outcome in obese compared to non-obese patients hospitalised for COVID-19. Twenty cohort studies of 28 355 hospitalised patients with COVID-19 infection were included. Meta-analysis estimated a pooled OR of 2.02 (1.41–2.89, p<0.001) for an unfavourable outcome in obese versus non-obese patients when adjusted for age, sex and co-morbidities. When unadjusted for confounders, the OR for unfavourable outcomes was 1.25 (CI 1.07–1.45, p=0.005). An increased adjusted OR was also seen for death (OR 1.51; CI 1.13–2.21, p=0.006) and severe illness (OR 2.26; CI 1.47–3.48, p<0.001). Compared to a normal BMI, the risk of an unfavourable outcome was increased even in overweight patients, with severe obesity having an escalated risk.Obesity is independently associated with an unfavourable outcome of COVID-19 illness, with obese patients having twice the risk of a composite outcome of severe disease or mortality, and a 50% increased risk of death.

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Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), resulted in an unprecedented global crisis. Although primarily a respiratory illness, dysregulated immune responses may lead to multi-organ dysfunction. Prior data showed that the resident microbial communities of gastrointestinal and respiratory tracts act as modulators of local and systemic inflammatory activity (the gut–lung axis). Evolving evidence now signals an alteration in the gut microbiome, brought upon either by cytokines from the infected respiratory tract or from direct infection of the gut, or both. Dysbiosis leads to a “leaky gut”. The intestinal permeability then allows access to bacterial products and toxins into the circulatory system and further exacerbates the systemic inflammatory response. In this review, we discuss the available data related to the role of the gut microbiome in the development and progression of COVID-19. We provide mechanistic insights into early data with a focus on immunological crosstalk and the microbiome’s potential as a biomarker and therapeutic target.

Background: Endogenous endophthalmitis (EE) is a devastating complication that develops as a metastatic infection in patients with Klebsiella pneumoniae pyogenic liver abscess (KPPLA). The existing data are heterogeneous and the actual disease burden and risk factors for the development of EE among patients with KPPLA have not been systematically examined. We performed a systematic review and meta-analysis to examine the incidence of EE, temporal trend of EE, and risk factors for EE in patients with KPPLA. Methodology: The MEDLINE, EMBASE, Web of Science, and Cochrane Library databases were searched for articles published from inception to 2020 that evaluated the incidence of EE among patients with KPPLA. By a random-effects method, a pooled estimate of its incidence with 95% confidence intervals was estimated along with examination of its temporal and geographic variations. Pooled odds ratios were calculated for risk factors. Results: Fifteen retrospective studies reporting data on 11889 patients with KPPLA met the inclusion criteria and were analyzed. With 217 patients developing EE, the pooled incidence of EE was 4.5% (95% confidence interval 2.4% to 8.2%). The heterogeneity was considerable and significant (Cochran's Q 243.5, p < 0.001, I 2 = 94.2%). Conclusion:This meta-analysis estimates the actual incidence of EE among patients with KPPLA, where EE is reported in about 1 of 22 patients with KPPLA. Infection caused by K1 capsular serotype was an independent risk factor.

Polyethylene‐b‐poly(methyl methacrylate) (PE‐b‐PMMA) diblock copolymer has important interfacial applications. Hence, a PE‐b‐isotactic PMMA diblock copolymer was synthesized using SiMe2(Ind)2ZrMe2 and MAO cocatalyst. The polymerization mechanism and the origin of PMMA isotacticity were duly explained. An appropriate nonisothermal Avrami‐Erofeev crystallization model was developed to compare the crystallization kinetics of the above copolymer with that of a PE homopolymer. For both polymers, the model well matched the entire differential scanning calorimeter crystallinity profile, notably for a single Avrami‐Erofeev index, and predicted cylindrical crystal growth. This model particularly overcomes the limitations of the published nonisothermal crystallization models, and provides interesting insight into PE crystallization. The PMMA block significantly decreased the heats of crystallization and fusion, % crystallinity, and the relative crystallization function; increased the nonisothermal crystallization rate constant; and introduced minimal dilution effect whereas the PE block formed a continuous or percolated phase. This study correlates catalyst structure, copolymer block tacticity, and PE nonisothermal crystallization and melting behavior. © 2012 American Institute of Chemical Engineers AIChE J, 59: 200–214, 2013