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BackgroundRunt-related transcription factor 3 (RUNX3) is a member of the runt-domain family of transcription factors and has been reported to be a candidate tumor suppressor in gastric cancer. However, the association between RUNX3 promoter methylation and gastric cancer remains unclear.MethodsWe systematically reviewed studies of RUNX3 promoter methylation and gastric cancer published in English or Chinese from January 2000 to January 2011, and quantified the association between RUNX3 promoter methylation and gastric cancer using meta-analysis methods.ResultsA total of 1740 samples in 974 participants from seventeen studies were included in the meta-analysis. A significant association was observed between RUNX3 promoter methylation and gastric cancer, with an aggregated odds ratio (OR) of 5.63 (95%CI 3.15, 10.07). There was obvious heterogeneity among studies. Subgroup analyses (including by tissue origin, country and age), meta-regression were performed to determine the source of the heterogeneity. Meta-regression showed that the trend in ORs was inversely correlated with age. No publication bias was detected. The ORs for RUNX3 methylation in well-differentiated vs undifferentiated gastric cancers, and in intestinal-type vs diffuse-type carcinomas were 0.59 (95%CI: 0.30, 1.16) and 2.62 (95%CI: 1.33, 5.14), respectively. There were no significant differences in RUNX3 methylation in cancer tissues in relation to age, gender, TNM stage, invasion of tumors into blood vessel or lymphatic ducts, or tumor stage.ConclusionsThis meta-analysis identified a strong association between methylation of the RUNX3 promoter and gastric cancer, confirming the role of RUNX3 as a tumor suppressor gene.

BackgroundMetabolic syndrome (MetS) is associated with carotid intima-media thickness (CIMT), which is a good predictor of cardiovascular disease (CVD). However, among individuals with MetS, direct comparative data regarding the utility of the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio to diagnose carotid atherosclerosis are scarce, particularly in Chinese populations. We aimed to determine the relationship between the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio and carotid atherosclerosis among Chinese individuals with MetS.MethodsWe performed a retrospective study of 5822 Chinese participants who underwent a routine health screening examination. Lipid profiles, fasting glucose, fasting insulin, CRP, apoB, apoAΙ and CIMT were measured.ResultsWe observed that among Chinese individuals with MetS, men (53.95 ± 0.58 ys) developed carotid atherosclerosis at a younger age than women (58.47 ± 1.17 ys) (P < 0.001). Both the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio positively correlated with carotid atherosclerosis among Chinese individuals with MetS, particularly among women. Meanwhile, CIMT increased progressively across the quartiles of the non-HDL-C/HDL-C ratio (P for trend, < 0.05). Receiver Operating Characteristic (ROC) analysis indicated that the AUC of the apoB/apoAΙ ratio (0.561) was higher than that of the non-HDL-C/HDL-C ratio (0.522) in men (P < 0.05) and the AUC of the apoB/apoAΙ ratio (0.640) was lower than that of the non-HDL-C/HDL-C ratio (0.695) in women (P < 0.05). Among Chinese individuals with MetS, the AUC of the non-HDL-C/HDL-C ratio was more prominent among women compared with men (P < 0.05).ConclusionOur findings indicate that among individuals with MetS, Chinese men develop carotid atherosclerosis at a much younger age than women. There were no significant differences between the apoB/apoAΙ ratio and the non-HDL-C/HDL-C ratio for the prediction of carotid atherosclerosis among Chinese individuals with MetS. Among Chinese individuals with MetS, the utility of the non-HDL-C/HDL-C ratio was found to be greater among women than among men.

The aim of the present study was to investigate the effect of cantharidin (CTD) on human gastric cancer cells and to explore the underlying mechanisms of these effects. The human gastric cancer SGC-7901 and BGC-823 cell lines were treated with CTD. MTS assays were then employed to examine cellular proliferation, flow cytometry was used to analyze the cell cycle and apoptosis, and western blot analysis was used to determine protein expression levels. It was found that CTD inhibited the proliferation of the human gastric cancer SGC-7901 and BGC-823 cells in a dose- and time-dependent manner in vitro. CTD also induced G2/M phase arrest and cellular apoptosis in a dose-dependent manner. In addition, CTD increased the levels of p21, caspase-7, -8 and -9, activated caspase-3, poly ADP ribose polymerase and Bad, but decreased the levels of cyclin-dependent kinase 1, cyclin A and B, B-cell lymphoma-2 (Bcl-2) and Bid. The present results suggested that CTD may inhibit the proliferation of human gastric cancer SGC-7901 and BGC-823 cells in vitro by inducing G2/M phase arrest and cell apoptosis. CTD may induce cellular G2/M phase arrest by regulating cycle-associated proteins and induce apoptosis by activating a caspase cascade or regulating the Bcl-2 family proteins.

Recent studies have demonstrated that the central dopaminergic system is implicated in the mechanism underlying general anesthesia. Here, we investigated whether dopaminergic ventral tegmental area (VTA) neurons participate in general anesthesia. Dopaminergic VTA neurons were selectively ablated from male Sprague Dawley rats via the bilateral infusion of 6-hydroxydopamine (6-OHDA) into the VTA. Two weeks after infusion, the number of dopaminergic neurons in the bilateral VTA was markedly reduced in the 6-OHDA-treated rats compared with the vehicle-treated rats. These bilateral VTA lesions significantly prolonged the recovery time for propofol but did not significantly alter its onset time or 50% effective dose (ED50) value. In addition, the anesthetic responses to isoflurane and ketamine were unaffected by the VTA lesions. Our findings suggested that dopaminergic VTA neurons might be involved in the emergence from propofol anesthesia.