Background The aim of this study was to assess the prognostic significance of preoperative systemic inflammation score (SIS) on patients with esophageal squamous cell carcinoma (ESCC). Methods A total of 357 ESCC patients who accepted radical esophagectomy between January 2008 and December 2009 at our institution were recruited in the analysis. The cut-off finder application was used to calculate the optimal cutoff values. The Chi-squared test or Fisher’s exact test were used to analyze categorical variables. Overall survival (OS) was calculated using the Kaplan-Meier method and the log-rank test. Multivariate analysis was calculated using Cox regression analysis model. A model combining SIS was created and its performance was evaluated using the Akaike information criterion (AIC) and concordance index (C-index). Results The median follow-up time was 58 months (range, 1–84 months). The 5-year OS rate was 50% (95% CI, 49.94–50.06%). The optimal cut-off values for preoperative neutrophil to lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR) and serum albumin (Alb) were 2.27, 3.79 and 36.55, respectively. Univariate analyses revealed that gender ( P = 0.047), T stage ( P < 0.001), N stage ( P < 0.001), vascular invasion ( P < 0.001), tumor location ( P = 0.018), tumor length( P < 0.001), NLR ( P = 0.006), LMR ( P = 0.007), serum Alb ( P = 0.001), and SIS ( P < 0.001) were significantly associated with OS. Independent prognostic factors for OS were T stage, N stage, tumor location, tumor length, and SIS. However, NLR was not an independent prognostic factor in multivariate analysis. The model combining SIS had smaller AIC and higher C-index compared to the model without SIS, which suggesting that the adding the SIS to the multivariate model increasing the predictive accuracy of the OS in the ESCC patients treated with radical esophagectomy and 3-field lymphadenectomy (3-FL). Conclusions SIS may treat as a novel prognostic factor than NLR for ESCC patients who underwent radical esophagectomy and 3-FL. However, Larger-scale studies are needed to validate these findings. Electronic supplementary material The online version of this article (10.1186/s12885-019-5940-6) contains supplementary material, which is available to authorized users.

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Sepsis-induced cardiac dysfunction remains a major cause of morbidity and mortality in patients suffered from severe trauma. Mesenchymal stem cells (MSCs) -based treatment has been verified as a promising approach to mitigate the sepsis-induced cardiac dysfunction, but the mechanism is still ambiguous. Thus, our study was designed to explore the potential role of MSCs in sepsis-induced cardiac dysfunction. In vivo bioluminescence imaging revealed 80% acute donor cell death of bone marrow-derived MSCs (BM-MSCs) within 3 days after transplantation. However, echocardiography demonstrated that systolic function in wild-type mice group were reduced after sepsis, while the cardiac function was relatively well persevered in cardiac-conditional deletion of Raptor (component of mTORC1 complex) mice group. Raptor KO group treated with BM-MSCs appeared better cardiac function than other groups (P<0.05). In vitro cell study revealed that co-culture of H9C2 (Raptor-Knock down) and BM-MSC could attenuate the level of proinflammatory cytokines and promote the expression of anti-inflammatory cytokine accompanied by mTORC2-Akt activation (P<0.05). In contrast, co-culture H9C2 (Raptor-O.E) and BM-MSC could aggravate the inflammatory response accompanied by the activation of mTORC1-p70S6K and inhibition of mTORC2-Akt (P<0.05). The immunomodulatory property of MSC is related to the inhibition of mTORC1-p70S6K and activation of mTORC2-Akt signaling pathway. mTORC1-p70S6K and mTORC2-Akt pathways were involved in the therapeutic adjuncts of MSC. The possible mechanism due to MSC`s immunomodulatory property through activation of mTORC2-Akt and inhibition of mTORC1-p70S6K signal pathways which may lead to modulate the expression of inflammation cytokines.

Low dose decitabine combined with taxol and platinum was well-tolerated and suitable for treating refractory/refractory ovarian cancer. The change in CA125 levels might be a potential predictor for patient clinical response. The efficacy of low dose decitabine for treatment of ovarian cancer requires more volunteers for further investigation.