Background:Published studies about passive smoking and cervical cancer have found inconsistent results. Hence, the present meta-analysis was performed to assess this association.Methods:A systematical search was performed to identify eligible cohort and case–control studies in PubMed, Scopus, Elsevier ScienceDirect, and Web of Science databases (up to March, 2018). The quality of included studies was assessed by the Newcastle–Ottawa quality scale (NOS). The random effects model (REM) was used to calculate the pooled odds ratio (ORs). Subgroup and sensitivity analyses were performed. Publication bias was assessed by funnel plot, using Begg's test and Egger's test.Results:Around 14 eligible studies were included for analysis, which included a total of 384,995 participants. The pooled ORs of passive smoking with cervical cancer risk was 1.70 (95% CI: 1.40–2.07, I2 = 64.3%). Subgroups stratified by continent, study design, quality score, and cervical cancer types/phases suggested that the result was robust. For instance, the pooled ORs for the cohort and case–control studies was 1.37 (95% CI: 1.16–1.62, I2 = 0%) and 2.09 (95% CI: 1.52–2.89, I2 = 76.6%), respectively. The pooled ORs ranged from 1.61 (95%CI: 1.34–1.92) to 1.77 (95%CI: 1.44–2.16) after one study was removed each time in the sensitivity analyses, indicating that the result was stable. Publication bias was detected by funnel plot and Egger's tests. The recalculated ORs were 1.33 (95% CI: 1.21–1.47).Conclusions:This meta-analysis provides evidence that passive smoking is associated with an increased risk of cervical cancer.

The aim of this study was to evaluate the global scientific output of neurotoxicity of nanoparticles (NPs) and explore their hot spots and research trends. Articles about the neurotoxicity of NPs between 2008 and 2017 were taken from the Web of Science Core Collection database. The VOSviewer was used to analyze annual publications, countries/institutions, funding agencies, research objects, major journals, and international cooperation. The reference co-citation map and keywords were used to analyze the mechanisms of neurotoxicity of NPs. Six hundred and forty-one eligible studies were included for analysis, and the annual publications increased with time in the past decade. Based on the bibliometric analysis, China and the United States were the main countries in this field. Metals and metal oxides were the main types of NPs. Cell, rat, and mouse were the primary research objects of NPs. The main research hot spots might focus on the pathogenesis of NPs, such as oxidative stress and apoptosis. This study will help researchers understand the research status, hot spots, and trends of neurotoxicity of NPs.

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Breast cancer is the primary problem threatening women’s health. The combined application of valproic acid (VPA) and hydroxyurea (HU) has a synergistic effect on killing breast cancer cells, but the molecular mechanism remains elusive. Replication protein A2 phosphorylation (pRPA2), is essential for homologous recombination (HR) repair and cell cycle. Here we showed that in response to HU, the VPA significantly decreased the tumor cells survival, and promoted S-phase slippage, which was associated with the decrease of pCHK1 and WEE1/pCDK1-mediated checkpoint kinases phosphorylation pathway and inhibited pRPA2/Rad51-mediated HR repair pathway; the mutation of pRPA2 significantly diminished the above effect, indicating that VPA-caused HU sensitization was pRPA2 dependent. It was further found that VPA and HU combination treatment also resulted in the decrease of endonuclease MUS81. After MUS81 elimination, not only the level of pRPA2 was abolished in response to HU treatment, but also VPA-caused HU sensitization was significantly down-regulated through pRPA2-mediated checkpoint kinases phosphorylation and HR repair pathways. In addition, the VPA altered the tumor microenvironment and reduced tumor burden by recruiting macrophages to tumor sites; the Kaplan-Meier analysis showed that patients with high pRPA2 expression had significantly worse survival. Overall, our findings demonstrated that VPA influences HR repair and cell cycle through down-regulating MUS81-pRPA2 pathway in response to HU treatment.

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