Association Between Aspirin Use and Risk of Aneurysmal Subarachnoid Hemorrhage: A Meta-analysis.

OBJECTIVE: To assess the association between aspirin use and risk of aneurysmal subarachnoid hemorrhage (aSAH). METHODS: A systematic search was performed in various databases updated on October 22, 2019. The heterogeneity test was performed for each outcome variable. Random-effect model and fixed-effect model were respectively conducted according to the heterogeneity statistics. Trial sequential analysis was used to control random errors. RESULTS: Ten studies involving 1,107,616 patients were involved in this meta-analysis. No significant association was shown between aspirin users and non-aspirin users regarding the risk of aSAH (odds ratio [OR]: 0.981, 95% confidential interval [CI]: 0.773-1.312, P = 0.897]. The results of subgroup analyses indicated that the risk of aSAH was notably associated with a short-term use of aspirin (<3 months) (OR: 1.697, 95% CI: 1.175-2.452, P = 0.005), but not aspirin use for 3-12 months (OR: 1.026, 95% CI: 0.609-1.730, P = 0.922), 1-3 years (OR: 0.942, 95% CI: 0.660-1.346, P = 0.744), >3 years (OR: 0.892, 95% CI: 0.573-1.389, P = 0.612), ≤2 times per week (OR: 0.857, 95% CI: 0.560-1.313, P = 0.479), ≥3 times per week (OR: 1.104, 95% CI: 0.555-2.193, P = 0.778) and former use (OR: 1.029, 95% CI: 0.482-2.196, P = 0.941). CONCLUSIONS: A short-term use of aspirin (<3 months) is associated with an elevated risk of aSAH, whereas the role of its long-term use in either decreasing or increasing the risk of aSAH still requires well-designed, large-scale randomized control trials for verification.

Association between common polymorphisms in ERCC gene and glioma risk: A meta-analysis of 15 studies.

BACKGROUND: A number of studies have investigated the roles of excision repair cross complementation group 1 (ERCC1), ERCC2, and ERCC5 genes polymorphisms in the development of glioma; however, the results were inconsistent. Here, we performed a meta-analysis to investigate the association between 6 polymorphisms in the ERCC genes (rs3212986, rs11615, rs13181, rs1799793, rs238406, rs17655) and glioma risk. METHODS: The PubMed, Embase, and Web of science were searched up to September 6, 2016, for studies on the association between ERCC polymorphisms and glioma risk. A fixed-effects or random-effects model was used to calculate the pooled odds ratios based on the results from the heterogeneity tests. Sensitivity and cumulative meta-analyses were also performed. RESULTS: A total of 15 studies were eligible for the pooled analysis, conducted in 2 populations of ethnic descent: 8 Europeans and 7 Asians. The results showed that ERCC1 rs3212986 polymorphism was positively associated with glioma [AA vs CC: odds ratio (OR) = 1.298, 95% confidence interval (95% CI) = 1.043-1.230, P = .025]. Association of the ERCC2 rs13181 and rs1799793 polymorphisms was only observed in Asians (CC vs AA for rs13181: OR = 1.539, 95% CI = 1.122-2.109, P = .007; AA vs GG for rs1799793: OR = 1.474, 95% CI = 1.090-1.994, P = .012). However, no association was observed between glioma risk and ERCC1 rs11615, ERCC2 rs238406, and ERCC5 rs17655 polymorphisms. Moreover, sensitivity and cumulative meta-analyses confirmed the stability of the results. CONCLUSIONS: Our meta-analysis indicated that the ERCC1 rs3212986 polymorphism and 2 polymorphisms in ERCC2 gene (rs13181 and rs1799793) contributed to the susceptibility of glioma.

Expression of indoleamine 2,3-dioxygenase in nasopharyngeal carcinoma impairs the cytolytic function of peripheral blood lymphocytes.

BACKGROUND: Tumor-specific cytotoxic T cells and infiltrating lymphocytes are frequently found in tumor tissues in patients with nasopharyngeal carcinoma (NPC). Most patients with NPC, however, especially those with advanced stages, have a poor clinical prognosis despite conventional immunotherapy. The aim of this work was to examine the effect of indoleamine 2,3-dioxygenase (IDO), an immunosuppressive enzyme, on the lymphocyte function in NPC. METHODS: The NPC cell line CNE2 was treated by interferon-gamma (IFNgamma) and the levels of IDO expression was analyzed by Western blotting and reverse phase high-performance liquid chromatography (HPLC). Lymphocytes from health human exposed to the milieu created by IDO-positive CNE2 cells and the lymphocyte cytotoxicity to target tumor cells was analyzed by standard lactate dehydrogenase (LDH) release assay. Additionally, expression of IDO was determined by Immunohistochemical assay in the tumor tissues form clinically evaluated NPC. RESULTS: IDO expression was acutely induced in the NPC cell line CNE2 by low dose interferon-gamma (IFNgamma) or by co-incubation with activated lymphocytes. Exposure to the milieu created by IDO-positive CNE2 cells did not promote lymphocyte death, but lymphocyte cytotoxicity against target tumor cells was impaired. The suppression of lymphocyte cytotoxic function was fully restored when the conditioned medium was replaced by fresh medium for 24 h. In additionally, the IDO-positive cells were found scattered in the tumor tissues from patients with NPC. CONCLUSION: Altogether, these findings suggest that IDO-mediated immunosuppression may be involved in the tumor immune evasion, and that blocking IDO activity in tumor cells may help to re-establish an effective anti-tumor T cell response in NPC.