Background Sepsis is a common critical condition caused by the body’s overwhelming response to certain infective agents. Many biomarkers, including the serum lactate level, have been used for sepsis diagnosis and guiding treatment. Recently, the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) recommended the Sequential Organ Failure Assessment (SOFA) and the quick SOFA (qSOFA) rather than lactate for screening sepsis and assess prognosis. Here, we aim to explore and compare the prognostic accuracy of the lactate level, the SOFA score and the qSOFA score for mortality in septic patients using the public Medical Information Mart for Intensive Care III database (MIMIC III). Methods The baseline characteristics, laboratory test results and outcomes for sepsis patients were retrieved from MIMIC III. Survival was analysed by the Kaplan-Meier method. Univariate and multivariate analysis was performed to identify predictors of prognosis. Receiver operating characteristic curve (ROC) analysis was conducted to compare lactate with SOFA and qSOFA scores. Results A total of 3713 cases were initially identified. The analysis cohort included 1865 patients. The 24-h average lactate levels and the worst scores during the first 24 h of ICU admission were collected. Patients in the higher lactate group had higher mortality than those in the lower lactate group. Lactate was an independent predictor of sepsis prognosis. The AUROC of lactate (AUROC, 0.664 [95% CI, 0.639–0.689]) was significantly higher than that of qSOFA (AUROC, 0.547 [95% CI, 0.521–0.574]), and it was similar to the AUROC of SOFA (AUROC, 0.686 [95% CI, 0.661–0.710]). But the timing of lactate relative to SOFA and qSOFA scores was inconsistent. Conclusion Lactate is an independent prognostic predictor of mortality for patients with sepsis. It has superior discriminative power to qSOFA, and shows discriminative ability similar to that of SOFA. Electronic supplementary material The online version of this article (10.1186/s13049-019-0609-3) contains supplementary material, which is available to authorized users.
1.1. Objective: Qianliexin Capsule (QLX), a traditional Chinese medicine, has been widely used to treat Chronic Nonbacterial Prostatitis (CNP) in China. Here, metabolic profiling was utilized to clarify the bio-targets of QLX in CNP treatment. Methods:An estradiol-induced prostatitis rat model was used to mimic the hormonal imbalance-induced CNP. The urine and serum were collected to analyze metabolic profiles by ultra-high-performance liquid chromatography-mass spectrometry (UPLC-MS). Results:An anti-inflammatory role for QLX was seen in the estradiol-induced prostatitis rats, and the Lower Urinary Tract Symptoms (LUTS) were relieved by QLX. The unique metabolic profiling in CNP was significantly changed by addition of QLX. Thirty-nine metabolites identified in serum and urine, that are involved in multiply pathways, were significantly reversed by QLX in the CNP rats. Among them, glycerophospholipid metabolism, sphingolipid metabolism and fructose and mannose metabolic pathways were the most significantly influenced by QLX and were closely associated with the anti-inflammatory role of QLX in CNP. Conclusion: The changed metabolic profile after QLX addition may be associated with the pharmacologic function of QLX in CNP.
BackgroundRecent studies have reported that Integrin alpha 2 (ITGA2) plays an essential role in tumor cell proliferation, invasion, metastasis, and angiogenesis. An abnormally expressed ITGA2 correlates with unfavorable prognoses in multiple types of cancer. However, the specific mechanism of how ITGA2 contributes to tumorigenesis remains unclear.MethodsThe GEPIA web tool was used to find the clinical relevance of ITGA2 in cancer, and this significance was verified using Western blotting analysis of paired patient tissues and immunohistochemistry of the pancreatic cancer tissue. Functional assays, such as the MTS assay, colony formation assay, and transwell assay, were used to determine the biological role of ITGA2 in human cancer. The relationship between ITGA2 and programmed death-ligand 1 (PD-L1) was examined using Western blot analysis, RT-qPCR assay, and immunohistochemistry. The protein-protein interaction between ITGA2 and STAT3 was detected via co-immunoprecipitation.ResultsOur study showed that ITGA2 was markedly overexpressed in several malignant tumor cells and clinical tissues. Blocking ITGA2 inhibited the proliferation and invasion ability of cancer cells significantly, whereas overexpressed ITGA2 increased the degree of those processes considerably. Additionally, the RNA-seq assay indicated that ITGA2 transcriptionally regulated the expression of PD-L1 in pancreatic cancer. We also demonstrated that ITGA2 interacted with STAT3 and up-regulated the phosphorylation of STAT3; this interaction might involve the mechanism of ITGA2 inducing PD-L1 expression in cancer cells. Our results suggest that ITGA2 plays a critical role in cancer cell progression and the regulation of PD-L1 by activating the STAT3 pathway.ConclusionsWe identified a novel mechanism by which ITGA2 plays a critical role in modulating cancer immune response by transcriptionally increasing the expression of PD-L1 in cancer cells. Thus, targeting ITGA2 is an effective method to enhance the efficacy of checkpoint immunotherapy against cancer.
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