The aim of the present study was to investigate the role of plasmacytoma variant translocation gene 1 (PVT1) in the occurrence and development of sepsis-induced inflammation and cardiac dysfunction and its underlying mechanism. A sepsis rat model was first established by cecal ligation and puncture. The mRNA levels of PVT1 and microRNA-143 in the myocardial tissues of rats were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis. Cardiac function, levels of myocardial injury markers and inflammatory indicators were detected following PVT1 knockdown. The regulatory effect of microRNA-143 on PVT1 was assessed using a luciferase reporter gene assay and RT-qPCR analysis. The specific role of PVT1 in regulating the mitogen-activated protein kinase (MAPK)/nuclear factor (NF)-κB pathway was detected using western blot analysis. PVT1 was downregulated and microRNA-143 was upregulated in the myocardial tissues of sepsis rats. The left ventricular peak pressure was markedly decreased in the sepsis rats. By contrast, the left ventricular end diastolic pressure, levels of inflammatory indicators, myocardial injury markers and complement proteins of C5 and C5a were increased in the sepsis rats. The above changes were reversed by PVT1 knockdown or the upregulation of microRNA-143. MicroRNA-143 was confirmed as being bound to PVT1 using the luciferase reporter gene assay and RT-qPCR analysis. Upregulated PVT1 was capable of activating the MAPK/NF-κB pathway. Taken together, PVT1 was upregulated in the myocardial tissues of sepsis rats, which inhibited cardiac function and promoted the secretion of inflammatory factors; and the mechanism was associated with the MAPK/NF-κB pathway.
Acute kidney injury (AKI) is a complex syndrome with a variety of possible etiologies and symptoms. It is characterized by high mortality and poor recovery of renal function. The incidence and mortality rates of patients with AKI in intensive care units are extremely high. It is generally accepted that early identification and prompt treatment of AKI are essential to improve outcomes. This study aimed to develop a model based on risk stratification to identify and diagnose early stage AKI for improved prognosis in critically ill patients.This was a single-center, retrospective, observational study. Based on relevant literature, we selected 13 risk factors (age, sex, hypertension, diabetes, coronary heart disease, chronic kidney disease, total bilirubin, emergency surgery, mechanical ventilation, sepsis, heart failure, cancer, and hypoalbuminemia) for AKI assessment using the Kidney Disease Improving Global Outcomes (KDIGO) diagnostic criteria. Univariate and multivariate analyses were used to determine risk factors for eventual entry into the predictive model. The AKI predictive model was established using binary logistic regression, and the area under the receiver operating characteristic curve (AUROC or AUC) was used to evaluate the predictive ability of the model and to determine critical values.The AKI predictive model was established using binary logistic regression. The AUROC of the predictive model was 0.81, with a sensitivity of 69.8%, specificity of 83.4%, and positive likelihood ratio of 4.2.A predictive model for AKI in critically ill patients was established using 5 related risk factors: heart failure, chronic kidney disease, emergency surgery, sepsis, and total bilirubin; however, the predictive ability requires validation.
Background: To explore the potential role of the platelet/lymphocyte ratio (PLR) as a prognostic marker in septic patients with acute kidney injury (AKI) and to provide theoretical evidence for the epidemiological study of the prognosis of patients with septic AKI in its early stage. Methods: A pilot study was conducted. A logistic regression analysis was conducted to screen the risk factors, and the selected factors were performed using multiple logistic regression analysis; a Receiver Operating Characteristic curve was used to determine the optimal cutoff value of the PLR and then to calculate the sensitivity and specificity of the PLR ratio. Results: Mechanical ventilation, platelet count, PLR, and arterial blood lactate concentration have a correlation with sepsis ( p < 0.05). An elevated PLR is significantly associated with a worse prognosis of sepsis-induced AKI (higher mortality). Conclusion: The PLR might be an effective factor in predicting a worse prognosis of septic AKI patients.
The objective of this study was to investigate the efficacy of vitamin C in patients experiencing sepsis and septic shock. The PubMed, Embase and Cochrane Library databases were searched for randomized controlled trials (RCTs) about vitamin C treatments for critically ill patients suffering from sepsis and septic shock from inception until December 31, 2019. The primary outcome was mortality, and the secondary outcomes were the ICU length of stay and the dose of vasopressors. A meta-analysis of nine RCTs with a total of 584 patients (301 in the intervention group and 283 in the control group) was conducted. There were significant differences between the vitamin C group and the control group in 28-day mortality (fixed effects OR = 0.60 95% CI [0.42, 0.85], p = 0.004) and in the dose of vasopressors (SMD = −0.88 95% CI [−1.48, −0.29], p = 0.003); however, the ICU length of stay was the same between the two groups (SMD = −0.33 95% CI [−0.87, 0.20] p = 0.23). This meta-analysis demonstrated that the use of vitamin C (compared with placebo) led to a reduction in ICU mortality and a reduction in the dose of vasopressors in patients with septic shock. However, the ICU length of stay was not significantly different between the two groups. Therefore, multicentre and high-quality RCTs are needed to further clarify the safety and effectiveness of vitamin C among patients with sepsis and septic shock.
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