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Objective: The soluble cluster of differentiation 14 subtype (sCD14-ST) or presepsin has recently been identified as a promising biomarker in sepsis. The present meta-analysis is performed to assess the prognostic value of presepsin in septic patients. Further, we compare the prognostic performance between presepsin and procalcitonin (PCT) in predicting all-cause mortality in these patients. Methods: A systemic and comprehensive search was conducted in PubMed, Embase and Cochrane databases by using Exploded Medical Subject Headings and appropriate corresponding keywords. Studies were eligible if they assessed the prognostic value of presepsin in sepsis and provided sufficient information to construct a 2×2 contingency table. A bivariate meta-analysis model was used to calculate the pooled sensitivity, specificity, positive/negative likelihood ratios and diagnostic odds ratio. The Chi-square and I 2 index were used to assess the heterogeneity and inconsistency. The Deek’s funnel plot asymmetry test was used to assess the likelihood of publication bias. Results: Nine publications, comprising 1,561 patients, were included in this study. The overall area under the receiver operating characteristic curve (AUROC) of presepsin was 0.77 (95% CI, 0.73–0.81) with a pooled prognostic sensitivity (SEN) and specificity (SPE) of 0.83 (95% CI, 0.72–0.90) and 0.69 (95% CI, 0.63–0.74), respectively. Additionally, the PLR, NLR and DOR of presepsin were 2.6 (95% CI, 2.1–3.3), 0.25 (95% CI, 0.15–0.44) and 10 (95% CI, 5–22), respectively. The AUROC of PCT was 0.81 (95% CI, 0.78–0.84) with a pooled SEN of 0.76 (95% CI, 0.55–0.89) and SPE of 0.74 (95% CI, 0.33–0.94). There is no statistically significant difference in the performance of pooled SEN and SPE between presepsin and PCT, with a p value of 0.39 and 0.71, respectively. Conclusions: Based on the results of this meta-analysis, both presepsin and PCT are promising biomarkers for the prognosis of mortality in sepsis.

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BackgroundDiabetic cardiomyopathy (DCM) is a common but underestimated cause of heart failure in patients with diabetes. This study investigated the myocardial-protective effects of nicorandil (Nic) on rats with DCM.Material/MethodsA total of forty-seven 180–220 g male Wistar rats were randomly divided into 4 groups: a control group (control, n=8), a DCM group (DCM, n=13), a nicorandil-pretreated DCM group (Nic1, n=13), and a nicorandil-treated DCM group (Nic2, n=13). A rat model of type 2 diabetes was induced by high-fat and high-sugar diet and intraperitoneal injection of streptozotocin (STZ). Nicorandil (3 mg/kg/d) was orally administrated to rats in the Nic1 group starting at week 4. Nicorandil (3 mg/kg/d) was orally administrated only after the induction of diabetes in the Nic2 group. The serum lipoids, plasma glucose, insulin levels, heart weight index, serum creatine kinase (CK), lactate dehydrogenase (LDH) levels, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) were analyzed in all groups.ResultsThe DCM group showed increased heart weight index, serum LDH, CK, and MDA content and decreased serum SOD activity, as compared with the control group (P<0.05). The DCM-induced increases in heart weight index, serum LDH, CK, and MDA content and decrease in serum SOD activity were attenuated in both Nic1 and Nic2 groups (P<0.05). However, there was no significant difference between Nic1 and Nic2 groups (P>0.05).ConclusionsNicorandil has protective effects on cardiac hypertrophy in DCM rats through increased SOD activity and decreased MDA content. Therefore, nicorandil may be a therapeutic method for diabetic patients with DCM.