Background The effect of concurrent diabetes on the outcome of sepsis is not conclusively known. A meta-analysis published in 2017 indicated that diabetes did not influence the mortality of patients with sepsis but increased the risk of acute renal injury. In view of publication of several new studies in recent years, there is a need for updated evidence. Methods A systematic search was conducted using the PubMed, Scopus, Embase, and Google Scholar databases. Studies that were done in patients with sepsis, were observational in design- either cohort or case–control or analysed retrospective data were considered for inclusion. Statistical analysis was performed using STATA software. Results A total of 21 studies were included. The risk of in-hospital mortality (RR 0.98, 95% CI 0.93, 1.04) and mortality at latest follow up i.e., within 90 days of discharge (RR 0.94, 95% CI 0.86, 1.04) among diabetic and non-diabetic subjects was statistically similar. There was an increased risk of in-hospital mortality among those with high blood glucose level at admission (RR 1.45, 95% CI 1.01, 2.09). Among those who were diabetic, the risk of acute renal failure (RR 1.54, 95% CI 1.34, 1.78) was higher than non-diabetics. The risk of respiratory failure, adverse cardiac events, need for additional hospitalization post-discharge and length of hospital stay was similar among diabetics and non-diabetics. Conclusions Diabetes is not associated with poor survival outcomes in patients with sepsis but is associated with increased risk of acute renal failure. High blood glucose levels, irrespective of the diabetes status, are associated with increased risk of in-hospital mortality. Findings underscore the need for better evaluation of renal function in diabetic patients with concurrent sepsis.

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Modern electronic devices are highly demanded for high-performance piezoelectric materials. Herein, Pb(Ni, Nb)O3-Pb(Lu, Nb)O3-PbTiO3 piezoelectric ceramics are investigated, among which 0.52PNN-0.16PLN-0.32PT ceramic shows the best performance (d33 = 850 pC/N,...

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Long noncoding RNAs (lncRNAs) have been widely proven to be involved in liver lipid homeostasis. Herein, we identify an upregulated lncRNA named lncRP11-675F6.3 in response to rapamycin treatment using a microarray in HepG2 cells. Knockdown of lncRP11-675F6 . 3 leads to a significant reduction in apolipoprotein 100 (ApoB100), microsomal triglyceride transfer protein (MTTP), ApoE and ApoC3 with increased cellular triglyceride level and autophagy. Furthermore, we find that ApoB100 is obviously colocalized with GFP-LC3 in autophagosomes when lncRP11-675F6 . 3 is knocked down, indicating that elevated triglyceride accumulation likely related to autophagy induces the degradation of ApoB100 and impairs very low-density lipoprotein (VLDL) assembly. We then identify and validate that hexokinase 1 (HK1) acts as the binding protein of lncRP11-675F6.3 and mediates triglyceride regulation and cell autophagy. More importantly, we find that lncRP11-675F6.3 and HK1 attenuate high fat diet induced nonalcoholic fatty liver disease (NAFLD) by regulating VLDL-related proteins and autophagy. In conclusion, this study reveals that lncRP11-675F6.3 is potentially involved in the downstream of mTOR signaling pathway and the regulatory network of hepatic triglyceride metabolism in cooperation with its interacting protein HK1, which may provide a new target for fatty liver disorder treatment.