Long-term carbon black inhalation induced the inflammation and autophagy of cerebellum in rats.

Carbon black (CB) has been demonstrated to have adverse effects on the lung tissue. Few studies explored the effects of CB on the cerebellum, widely recognized to contribute to gait and balance coordination and timing in the motor domain. Some studies have reported that inflammatory response and damaged autophagy are important mechanisms of CB toxicity and can be repaired after the recovery. The present study aimed to determine whether long-term CB exposure could induce the inflammation and damaged autophagy of the cerebellum. The rats were randomly divided into four groups. The control group received the filtered air for 90 days; the carbon black (CB) group received CB particles for 90 days; the recovery (R) group received CB for 90 days and recovered for another 14 days; the recovery control (RC) group received filtered air for 104 days. The purpose of the R group was to test whether neuroinflammation and autophagy could be repaired after short-term recovery. The western blot and immunohistochemistry revealed that long-term CB exposure induced augmented level of pro-inflammatory cytokines (Interleukin-1ß, IL-1ß; Interleukin-6, IL-6; and Tumor Necrosis Factor-α, TNF-α) and anti-inflammatory cytokine (Interleukin-10, IL-10). The autophagic markers (Beclin1 and LC3) were increased in both CB group and R group. These findings clearly demonstrated that long-term CB exposure induced inflammation and autophagy in the cerebellum, which were not obviously improved after short-term recovery.

Additional lymphadenectomy might not improve survival of patients with resectable metastatic colorectal adenocarcinoma of T4 stage, proximal location, poor/undifferentiation, or N3/N4 stages: a large population-based study.

This study was performed to evaluate the prognostic effect of lymphadenectomy on outcomes in patients with resectable metastatic colorectal adenocarcinoma (mCRC). We selected patients with mCRC from 2004 to 2013 from Surveillance, Epidemiology, and End Results Program (SEER) database. Kaplan-Meier analysis, univariate Cox regression and multivariate Cox regression analysis were performed to assess the clinical value of lymphadenectomy on overall survival (OS) and cause-specific survival (CSS) of patients with resectable mCRC. A total 24178 eligible patients were included, 23056 (95.36%) of which received lymphadenectomy. Results showed that lymphadenectomy was an independent protective factor for survival of patients with mCRC overall [OS (HR: 0.86, 95%CI: 0.79-0.93, P=0.002) and CSS (HR: 0.85, 95%CI: 0.78-0.93, P<0.001)]. Further analysis showed that lymphadenectomy improved survival of patients with T1 stage [OS (HR: 0.51, 95%CI: 0.39-0.66, P<0.001); CSS (HR: 0.48, 95%CI: 0.36-0.65, P<0.001)], distal [OS (HR: 0.65, 95%CI: 0.56-0.75, P<0.001); CSS (HR: 0.65, 95%CI: 0.65-0.75, P<0.001)], rectal [OS (HR: 0.60, 95%CI: 0.52-0.70, P<0.001); CSS (HR: 0.59, 95%CI: 0.51-0.69, P<0.001)] , well/moderately differentiated [OS (HR: 0.62, 95%CI: 0.56-0.70, P<0.001); CSS (HR: 0.62, 95%CI: 0.55-0.69, P<0.001)], N1 stage [OS (HR: 0.76, 95%CI: 0.67-0.85, P<0.001); CSS (HR: 0.74, 95%CI: 0.65-0.84, P<0.001)] and N2 stage [OS (HR: 0.63, 95%CI: 0.54-0.74, P<0.001; CSS (HR: 0.65, 95%CI: 0.55-0.77, P<0.001)) mCRC. While lymphadenectomy might not improve survival of patients with T4 stage, proximal, poor or undifferentiated, N3 and N4 stage mCRC. In general, Additional lymphadenectomy was suggested for patients with mCRC overall. However, lymphadenectomy might not improve survival of patients with mCRC of higher malignancy tendency, such as T4 stage, proximal location, poor or undifferentiation, N3 and N4 stages.

Combination of TNM staging and pathway based risk score models in patients with gastric cancer.

Due to the complexity and heterogeneity of gastric cancer (GC) in individual patient, current staging system is inadequate for predicting outcome of GC. Comprehensive computational and bioinformatics approach may triumph for the prediction. In this study, GC patients were devided according to stage and treatment: curative surgery plus chemoradiotherapy in stage II, curative surgery plus chemoradiotherapy in stages III, and IV, unresectable metastatic gastric cancer. The training sets were downloaded from GEO datasets (GSE26253 and GSE14208). Gene set enrichment analysis (GSEA) was performed to explore enriched difference between recurrence and nonrecurrence. The core enrichment genes of enriched pathways significantly associated with recurrence or progression were identified using Cox proportional hazards analysis. Thereafter, the risk score models were externally validated in independent datasets-GSE15081 and The Cancer Genome Atlas (TCGA). We generated respective risk score models of patients in different stages and treatment. A five-gene signature comprising FARP1, SGCE, SGCA, LAMA4, and COL9A2 was strongly associated with recurrence of patients with curative surgery plus chemoradiotherapy in stage II. A six-gene signature consisting of SHH, NF1, AP4B1, COMP, MATN3, and CCL8 was correlated with recurrence of patients with curative surgery plus chemoradiotherapy in stages III and IV. And a four-gene signature composing of ABCC2, AHNAK2, RNF43, and GSPT2 was highly related to progression of patients with unresectable metastatic GC. Taking into consideration TNM stage and gene signature reflecting recurrence or progression, the risk score models significantly improved the accuracy in predicting outcome of GC.