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BackgroundPostoperative cognitive dysfunction (POCD) is common following cardiac and non-cardiac surgery, but the pathogenic mechanisms remain unknown. Many studies suggest that an inflammatory response is a key contributor to POCD. The current meta-analysis shows that the levels of peripheral inflammatory markers are associated with POCD.MethodsAn online search was performed to identify peer-reviewed studies without language restriction that measured peripheral inflammatory markers of patients with and without POCD, using PubMed, ScienceDirect, SinoMed and the National Knowledge Infrastructure database. Extracted data were analyzed with STATA (version 12).The standardized mean difference (SMD) and the 95% confidence interval (95%CI) were calculated for each outcome using a random effect model. Tests of heterogeneity assessment of bias, and meta-regression were performed in the meta-analysis.ResultsA total of 13 studies that measured the concentrations of peripheral inflammatory markers were included. The current meta-analysis found significantly higher concentrations of S-100β(SMD[95%CI]) (1.377 [0.423, 2.331], p-value < 0.001, N [POCD/non-POCD] =178/391, 7 studies), and interleukin(IL)-6 (SMD[95%CI]) (1.614 [0.603,2.624], p-value < 0.001, N[POCD/non-POCD] = 91/99, 5 studies), but not of neuron specific enolase, interleukin-1β, or tumor necrosis factor-α , in POCD compared with patients without POCD. In meta-regression analyses, a significant positive association was found between the SMD and the preoperative interleukin-6 peripheral blood concentration in patients with POCD (Coef.= 0.0587, p-value=0.038, 5 studies).ConclusionsThis study shows that POCD is indeed correlated with the concentrations of peripheral inflammatory markers, particularly interleukin-6 and S-100β.

The heavy tar (H-tar) of low temperature coal tar was collected from a low temperature carbonization plant in Shanbei. H-tar was extracted with petroleum ether (PE) under ultrasonic irradiation and separated into PE soluble and insoluble fractions. Then, the PE insoluble fraction was extracted in a Soxhlet extractor with PE and methanol (MeOH), respectively. PE extract, PE residue, MeOH extract, and MeOH residue were obtained. PESE (PE soluble fraction and PE extract) and MeOH extract were examined by gas chromatography-mass spectrometry (GC-MS). GC-MS analysis of PESE shows considerable alkanes and extensive series of phenols, naphthalenes, fluorenes, benz[a]anthracene, chrysene, etc. Particularly, the content of methyl phenol is about 9.0%. No GC-MS detectable species are found in MeOH extract. So, additional research will focus on PE residue. The pyrolysis behavior of PE residue was investigated by using a thermogravimetric analyzer coupled with Fourier transform infrared spectrometer (TG-FTIR). The results indicate that the release of volatiles takes place mainly between 110 and 425 °C and the maximum mass loss rate occurs at 315 °C. The main products in the whole process are CO 2 , phenols, H 2 O, saturated hydrocarbons, aromatic compounds, anhydride compounds, oxygen heterocycles, pyridines, etc. But there is no significant peak of CO. The compounds of alkanes, phenols, heterocyclic compounds, and oxygen-containing heterocyclic compounds in PE residue can be also detected. PE residue semicoke (the products of PE residue after TG) and PE residue were estimated by FTIR. PE residue is mainly composed of phenols, aliphatics, and aromatics. The analyses indicate the high degree and polycyclic aromatic structure of PE residue semicoke.

BackgroundEpithelial-mesenchymal transition (EMT) is a crucial step for solid tumor progression and plays an important role in cancer invasion and metastasis. RNF8 is an ubiquitin E3 ligase with RING domain, and plays essential roles in DNA damage response and cell cycle regulation. However the role of RNF8 in the pathogenesis of breast cancer is still unclear.MethodsThe expression of RNF8 was examined in different types of breast cell lines by Western Blotting. EMT associated markers were examined by Immunofluorescence and Western Blotting in MCF-7 when RNF8 was ectopically overexpressed, or in MDA-MB-231 when RNF8 was depleted. Transwell and wound healing assays were performed to assess the effect of RNF8 on cell mobility. The xenograft model was done with nude mice to investigate the role of RNF8 in tumor metastasis in vivo. Breast tissue arrays were used to examine the expression of RNF8 by immunohistochemistry. Kaplan-Meier survival analysis for the relationship between survival time and RNF8 signature in breast cancer was done with an online tool (http://kmplot.com/analysis/).ResultsRNF8 is overexpressed in highly metastatic breast cancer cell lines. Overexpression of RNF8 in MCF-7 significantly promoted EMT phenotypes and facilitated cell migration. On the contrary, silencing of RNF8 in MDA-MB-231 induced MET phenotypes and inhibited cell migration. Furthermore, we proved that these metastatic behavior promoting effects of RNF8 in breast cancer was associated with the inactivation of GSK-3β and activation of β-catenin signaling. With nude mice xenograft model, we found that shRNA mediated-downregulation of RNF8 reduced tumor metastasis in vivo. In addition, we found that RNF8 expression was higher in malignant breast cancer than that of the paired normal breast tissues, and was positively correlated with lymph node metastases and poor survival time.ConclusionsRNF8 induces EMT in the breast cancer cells and promotes breast cancer metastasis, suggesting that RNF8 could be used as a potential therapeutic target for the prevention and treatment of breast cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-016-0363-6) contains supplementary material, which is available to authorized users.