Association of the NQO1 C609T polymorphism with Alzheimer's disease in Chinese populations: a meta-analysis.

Several molecular genetics studies have investigated the association of NQO1 C609T polymorphism with Alzheimer's disease (AD) susceptibility in Chinese populations; however, the findings are inconclusive. To investigate the association, we performed the present meta-analysis of 5 case-control studies (including 735 AD cases and 828 controls). We searched literature from PubMed, Embase, HuGNet and CNKI databases for eligible articles that evaluated the association between NQO1 C609T polymorphism and AD risk. We used odds ratios (ORs) with 95% confidence intervals (CIs) to evaluate the strength of the association. Overall, C609T polymorphism was significantly associated with an increased AD risk (homozygote: OR = 1.87, 95% CI = 1.39-2.51, P = 0.000; heterozygote: OR = 1.93, 95% CI = 1.22-3.06, P = 0.019; dominant: OR = 1.97, 95% CI = 1.25-3.12, P = 0.004). When stratified by source of control, significant results were observed in subjects of population-based (PB), whereas no increased risk was observed among the hospital-based (HB). When stratified by APOEϵ4 carrier status, no effect of the NQO1 C609T polymorphism was seen in subjects of APOEϵ4 carriers and APOEϵ4 non-carriers. In conclusion, our results showed that NQO1 C609T polymorphism increases the risk of AD in Chinese populations. Larger studies with different ethnic populations are required to validate our findings.

A comparison study between two analyzers for determining serum ferritin.

BACKGROUND: The measurement of serum ferritin (SF) is generally considered to be a reliable indicator of iron status in vivo. The accurate assessment of SF concentration promoted us to evaluate the analytical performance of two automated immunoassays. METHODS: A total of 125 different concentrations of clinical samples were routinely collected and determined by two analytical systems: the Architect i2000 system from Abbott Laboratories and the Cobas E601 from Roche Diagnostics. We evaluated the analytical performance of the two systems and compared the measurements of SF results, which covered the whole analytical range. RESULTS: The analytical performance and accuracy of the two systems were fairly good, and a satisfactory correlation was achieved between the two methods (r = 0.99), but Bland-Altman analysis suggested that the Cobas E601 was, on average, 60.6 ng/mL higher than the i2000, with wide limits of agreement (95% limits of agreement: -78.3 to 199.5 ng/mL). CONCLUSIONS: These findings suggested that the two methods had good correlation but were not interchangeable. Patients should always be monitored for SF with the same method and it should be indicated in the report.

Association between statin use and colorectal cancer risk: a meta-analysis of 42 studies.

PURPOSE: There is a long-standing debate about whether statins have chemopreventive properties against colorectal cancer (CRC), but the results remain inconclusive. We therefore present a meta-analysis to investigate the association between statin use and risk of CRC. METHODS: A comprehensive literature search was undertaken through July 2013 looking for eligible studies. Pooled relative risk (RR) estimates and 95 % confidence intervals (CIs) were used to calculate estimated effect. RESULTS: Forty-two studies [18 case-control studies, 13 cohort studies, and 11 randomized controlled trials (RCTs)] were included in this analysis. Overall, statin use was associated with a modest reduction in the risk of CRC (RR = 0.90, 95 % CI 0.86-0.95). When the analyses were stratified into subgroups, a significant decreased association of CRC risk was observed in observational studies (RR = 0.89, 95 % CI 0.84-0.95), rectal cancer (RR = 0.81, 95 % CI 0.66-0.99), and lipophilic statin (RR = 0.88, 95 % CI 0.85-0.93), but not in RCTs (RR = 0.96, 95 % CI 0.85-1.08), colon cancer, and hydrophilic statin. However, long-term statin use (≥5 years) did not significantly affect the risk of CRC (RR = 0.96, 95 % CI 0.90-1.03). Cumulative meta-analysis showed that statin use significantly reduces the risk of CRC, which has been available between 2007 and 2013. CONCLUSIONS: Our results suggest that statin use is associated with a modest reduced risk of CRC; apparent associations were found for lipophilic statin use. However, long-term statin use did not appear to significantly affect the risk of CRC.

Coffee consumption and prostate cancer risk: an updated meta-analysis.

PURPOSE: Many epidemiological studies have been conducted to explore the association between coffee consumption and prostate cancer. However, the results remain inconsistent. We performed a large meta-analysis of relevant studies to derive a more precise estimation of this relationship. METHODS: Systematic searches of PubMed and several other databases up to June 2013 were retrieved. All epidemiologic studies regarding coffee consumption and prostate cancer risk were included, and odds ratios (ORs) with 95 % confidence intervals (CIs) were calculated to estimate the strength of the association. RESULTS: Twelve case-control studies involving 7,909 prostate cancer cases and 9,461 controls and nine cohort studies involving 455,123 subjects were included in our analysis. Compared with the lowest category, the unstratified highest category of coffee consumption showed a significance reduction in prostate cancer risk of a fixed-effects model (OR 0.91, CI 0.86-0.97). A borderline significant influence was also found when the stratified highest category (US ≥ 4, Europe ≥ 5) of coffee consumption was compared with the reference category (OR 0.96, CI 0.92-1.00), but no relationships were observed for the other two categories. In another analysis conducted by coffee consumption and prostate cancer stage and Gleason grade, our results showed a significant inverse association in all categories of prostate cancer except Gleason <7 grade in a fixed-effects model; the results remained the same, except for advanced prostate cancer, in a random-effects model. CONCLUSIONS: Our meta-analysis suggests that high (e.g., highest ≥ 4 or 5 cups/day) coffee consumption may not only be associated with a reduced risk of overall prostate cancer, but also inversely associated with fatal and high-grade prostate cancer.

The role of retinoic acid receptors in the signal pathway of all-trans retinoic acid-induced differentiation in adriamycin-induced podocyte injury.

All-trans retinoic acid (ATRA) plays an essential role in cell survival and differentiation by binding to retinoic acid receptors (RARs), including RAR-α, RAR-ß, and RAR-γ. Injury to podocytes is the most frequent cause of glomerulosclerosis (GS). This study was performed to investigate which of the RAR subtypes is involved in the signal pathway of ATRA-induced differentiation of injured podocytes. ATRA (0.1 µM) was administered to Adriamycin (ADR)-induced, injured podocytes, in vitro. Morphological changes were observed. The protein/mRNA expression of podocin, nephrin, transforming growth factor ß1(TGF-ß1), and the RARs (RAR-α,ß,γ) was measured by RT-PCR and Western blotting. ATRA treatment ameliorated cell hypertrophy and reduced the shedding of the cytoplasm which was observed under light microscope and the extension of the foot processes was observed under scan electron microscope. Compared with the injured podocytes, ATRA exposure significantly increased the protein/mRNA expression of nephrin and podocin and it markedly reduced TGF-ß1 (all p < 0.05). Compared with the injured podocytes, the protein/mRNA expression of RAR-α and RAR-γ was significantly increased after ATRA exposure; however, the expression level of RAR-ß was not significantly different. The RAR-α/γ protein expression level was positively correlated with nephrin and podocin (-α, r = 0.637, 0.663; -γ, r = 0.882, 0.878; all p < 0.05), and negatively correlated with TGF-ß1 (-α, r = -0.650; -γ, r = -0.739; all p < 0.05). The RAR-ß protein expression level was not correlated with nephrin, podocin and TGF-ß1 (r = -0.312, 0.079, -0.279; all p > 0.05). In conclusion, RAR-α/γ (and RAR-ß to a lesser degree) may be involved in the signal pathway of ATRA-induced differentiation in injured podocytes.

C-reactive protein genetic polymorphisms increase susceptibility to HBV-related hepatocellular carcinoma in a Chinese population.

Chronic inflammation has been implicated in the etiology of hepatocellular carcinoma (HCC). The C-reactive protein (CRP) genetic polymorphisms affected serum CRP concentrations and elevation of CRP has been considered as the hallmark of acute and chronic inflammation. In this study, we investigated the association between CRP genetic polymorphisms and HBV-related HCC risk in a Chinese population. Two polymorphisms in the CRP gene (rs3093059 and rs2794521) were examined in 192 HBV-related HCC patients, 277 non-HCC patients with HBV infection, and 192 healthy controls using polymerase chain reaction-restriction fragment length polymorphism method. DNA direct sequencing was performed to validate the results of genotyping. We found that there were significant differences in the genotype and allele frequencies of the CRP gene rs3093059 polymorphism between the HBV-related HCC patients and the non-HCC patients with HBV infection. The rs3093059 TC genotype was associated with a significant increased HCC risk as compared with the TT genotype (odds ratio (OR) = 1.98, 95 % confidence interval (CI) 1.32-2.95, P = 0.001). The rs3093059 C allele was correlated with a significant increased HCC risk as compared with the T allele (OR = 1.65, 95 % CI 1.16-2.30, P = 0.005). Furthermore, the rs3093059 TC combined with CC genotypes were found to correlate with a significant increased HCC risk compared with the TT genotype in dominant model (OR = 1.92, 95 % CI 1.29-2.82, P = 0.001). However, we did not find any significant effect of CRP rs2794521 polymorphism on HCC risk in this population. In haplotype analysis between HBV-related HCC patients and non-HCC patients with HBV infection, the TC haplotype was found correlated with a significant increased HCC risk (OR = 1.750, 95 % CI 1.234-2.480, P = 0.001). The results suggested that the CRP rs3093059 polymorphism may contribute to increased HCC risk in HBV-infected patients in the Chinese population. Further large and well-designed studies in diverse ethnic populations are needed to confirm our results.

Low circulating adiponectin levels in women with polycystic ovary syndrome: an updated meta-analysis.

Adiponectin, as an important adipocytokine, plays a pivotal role in the regulation of insulin sensitivity and metabolism. It has been reported that circulating adiponectin levels were decreased in women with polycystic ovary syndrome (PCOS). However, the results remained inconsistent. In order to derive a more precise estimation of this relationship, a large meta-analysis was performed in this study. A comprehensive systematic electronic search was conducted in electronic databases PubMed, EMBASE, and Web of Science up to November 30, 2013. Pooled weighted mean differences (WMDs) with 95% confidence intervals (CIs) were calculated to estimate the strength of the association. A meta-analysis technique was used to study 38 trials involving 1,944 PCOS women and 1,654 healthy controls. Overall pooled adiponectin levels in women with PCOS were significantly reduced compared with healthy controls (WMD -2.67, 95% CI -3.22 to -2.13; P = 0.000), yet with significant heterogeneity across studies (I(2) = 95.9%, P = 0.000). In subgroup analysis by HOMA-IR ratio and total testosterone ratio, inconsistent results were presented. No single study was found to affect the overall results by sensitivity testing. Meta-regression suggested that BMI might contribute little to the heterogeneity between including studies. Cumulative meta-analysis demonstrated the reliability and stability of the meta-analysis results. No evidence of publication bias was observed. Our meta-analysis suggested that circulating adiponectin levels in women with PCOS were significantly lower than those in healthy controls, which indicated that circulating adiponectin might play a role in the development of PCOS.

DNA repair gene XRCC3 polymorphisms and bladder cancer risk: a meta-analysis.

The X-ray repair cross-complementing group 3 (XRCC3) in homologous recombination repair (HRR) pathway plays a vital role in DNA double-strand break repair (DSBR). Variants in the XRCC3 gene might result in altered protein structure or function which may influence DSBR efficiency and lead to cancer. Numerous epidemiological studies have been conducted to evaluate the association between XRCC3 polymorphisms and bladder cancer risk. However, the results of these previous studies have been inconsistent. To derive a more precise estimation of the association, we performed a meta-analysis of all available studies relating XRCC3 polymorphisms and bladder cancer. All studies published up to April 2013 on the association between XRCC3 polymorphisms and bladder cancer risk were identified by searching electronic databases PubMed, EMBASE, and Chinese Biomedical Literature databases. The association between the XRCC3 polymorphisms and bladder cancer risk was assessed by odds ratios (ORs) together with their 95% confidence intervals (CIs). A total of 16 case-control studies met the inclusion criteria and were selected. With respect to C18067T polymorphism, significant increased bladder cancer risk was found when all eligible studies were pooled into the meta-analysis (TT vs. CC: OR = 1.174, 95%CI = 1.033-1.335, P = 0.014 and recessive model TT vs. TC + CC: OR = 1.147, 95%CI = 1.020-1.290, P = 0.022, respectively). The results were still significant after excluding the Hardy-Weinberg equilibrium violation studies (TT vs. CC: OR = 1.178, 95%CI = 1.036-1.339, P = 0.013 and recessive model TT vs. TC + CC: OR = 1.144, 95%CI = 1.017-1.287, P = 0.025, respectively). In subgroup analysis by ethnicity, significant elevated risk was found among Asians (dominant model TT + TC vs. CC: OR = 1.285, 95%CI = 1.012-1.631). In the subgroup analyses according to smoking status, no significant association was detected in all genetic comparison models. With respect to A17893G and A4541G polymorphisms, no significant association with bladder cancer risk was observed in the overall and subgroup analyses. This meta-analysis suggests that the XRCC3 C18067T polymorphism was associated with increased bladder cancer risk especially among Asians. However, the XRCC3 A17893G and A4541G polymorphisms may not play important roles in bladder carcinogenesis. Further studies with larger sample sizes are needed to validate our finds.

Prognostic significance of dickkopf-1 overexpression in solid tumors: a meta-analysis.

The prognostic significance of dickkopf-1 (DKK1) overexpression in solid tumors remains inconclusive. We performed a meta-analysis to evaluate the impact of DKK1 overexpression in solid tumors on patients' overall survival (OS) and disease-free survival (DFS). The pooled hazard ratio (HR) with 95 % confidence interval (CI) was used to estimate the effects. Thirteen studies were included for meta-analysis; four that evaluated hepatocellular carcinoma (HCC), two each that evaluated ovarian carcinoma, esophageal carcinoma, and lung cancer, and one each that evaluated other cancers, namely gastric cancer, breast cancer, urothelial carcinoma, and colorectal cancer. Twelve studies were evaluable for OS and six for DFS. Our analysis results indicated that DKK1 overexpression predicted poor OS (HR = 1.68, 95% CI 1.36-2.08; P < 0.001) and DFS (HR = 1.65, 95% CI 1.37-1.99; P < 0.001). Subgroup analyses showed that DKK1 overexpression was significantly related with poor OS in HCC patients (HR = 1.65; P < 0.001), ovarian carcinoma patients (HR = 2.63; P = 0.045), and other cancers patients (HR = 1.51; P = 0.021). Further, DKK1 overexpression was significantly related with poor DFS in HCC patients (HR = 1.53; P < 0.001) and other cancers patients (HR = 2.02; P < 0.001). This meta-analysis showed that DKK1 may be a novel prognostic marker in solid tumors in Asian patients; it could potentially help to further stratify patients for clinical treatment. More, well-designed studies from Western countries are needed to confirm this finding.

Association of p53 codon 72 polymorphism with prostate cancer: an update meta-analysis.

Many studies have been conducted to explore the association between p53 codon 72 polymorphism and prostate cancer (PCa). However, the results remain inconsistent. Therefore, we performed a large meta-analysis of relevant studies to determine a more precise estimation of this relationship. Systematic searches of the electronic databases PubMed, EMBASE, Cochrane Library, and China National Knowledge Infrastructure (CNKI) up to October 2013 were performed. Fixed or random-effects meta-analytical models were used to calculate the summary odds ratio (OR) and corresponding 95% confidence intervals (CIs). Meta-regression, Galbraith plots, subgroup analysis, and sensitivity analysis were also performed. The study included 17 case-control studies involving 2,371 PCa cases and 2,854 controls. Our results showed that the p53 codon 72 polymorphism was not associated with PCa risk in all genetic models in the overall populations. When limiting the meta-analysis to the studies conforming to Hardy-Weinberg equilibrium, the pooled analyses showed a significant association between p53 codon 72 polymorphism and PCa in a Caucasian population in co-dominant model Pro/Pro vs. Arg/Arg (OR = 1.57, 95% CI = 1.08-2.28, P = 0.017) and recessive model Pro/Pro vs. (Arg/Pro + Arg/Arg) (OR = 1.60, 95% CI = 1.12-2.27, P = 0.009). In subgroup analysis stratified by PCa stages and Gleason grades, a slight but significant association was found when advanced PCa was compared with localized PCa only in recessive model Pro/Pro vs. (Arg/Pro + Arg/Arg) (OR = 1.51, 95% CI = 1.02-2.23, P = 0.039). This meta-analysis suggested that the Pro/Pro genotype of p53 codon 72 polymorphism was associated with increased prostate cancer risk, especially among Caucasians.

The association of interleukin-16 gene polymorphisms with IL-16 serum levels and risk of nasopharyngeal carcinoma in a Chinese population.

Interleukin (IL)-16 plays a fundamental role in inflammatory diseases, as well as in the development and progression of tumors. Genetic variation in DNA sequence of IL16 gene may lead to altered cytokine production and/or activity, and this variation may modulate an individual's susceptibility to nasopharyngeal carcinoma (NPC). To test this hypothesis, we investigated the association of IL16 gene polymorphisms and serum IL-16 levels with NPC risk in a Chinese population. We analyzed IL16 gene rs11556218 T/G, rs4778889 T/C, and rs4072111 C/T polymorphisms using PCR-RFLP and DNA sequencing, and serum IL-16 levels were measured by ELISA. The IL16 rs11556218 T/G polymorphism was significantly associated with the susceptibility to NPC patients. The TG genotype was associated with a significantly higher risk of NPC as compared with the TT genotype (OR = 2.05, 95% CI 1.04-4.01; p = 0.037). Patients carrying the G allele had a significantly higher risk for developing NPC compared with individuals carrying the T allele (OR = 1.79, 95% CI 1.07-3.01; p = 0.027). The serum IL-16 levels were increased in NPC patients compared with controls (p < 0.01); the genotypes carrying the IL16 rs11556218 G variant allele were associated with increased serum IL-16 levels compared with the homozygous wild-type genotype in NPC patients (all p values <0.01). Our data suggested that IL16 rs11556218 T/G polymorphism was associated with increased susceptibility to NPC through increasing the production of serum IL-16 levels.

S-1-based therapy versus S-1 monotherapy in advanced gastric cancer: a meta-analysis.

This study aimed to derive a more precise estimate of the prognostic significance of S-1-based therapy over S-1 monotherapy in patients with advanced gastric cancer (AGC), including overall survival (OS) time, progression-free survival (PFS) time, objective response rate (ORR), and adverse events (AEs). Studies stratifying OS, PFS, ORR, and AEs in AGC patients in an S-1-based therapy versus an S-1 monotherapy setting were eligible for analysis by systematic computerized PubMed, Embase and Cochrane Library searches. Data from these studies were pooled using STATA package version 11.0. Six studies that investigated outcomes in a total of 913 AGC cases, of which 443 (48.5%) received S-1-based therapy and 470 (51.5%) received S-1 monotherapy, were included in the meta-analysis. Median OS and median PFS were significantly prolonged in AGC patients receiving S-1-based therapy compared with those receiving S-1 monotherapy (hazard ratio [HR] 0.83, 95% confidence interval [CI] 0.71-0.96, P = 0.015, and HR 0.69, 95% CI 0.60-0.80, P = 0.000, respectively). The ORR favored patients with S-1-based therapy (OR 1.65, 95% CI 1.34-2.06, P = 0.000). Higher incidence of grade 3/4 neutropenia was found in patients with S-1-based therapy (P = 0.000). For the Asian population, S-1-based therapy significantly improved OS and PFS and enhanced ORR in comparison to S-1 monotherapy. The safety profile was poorer in patients with S-1-based therapy, but could be considerable between the S-1-based therapy and S-1 monotherapy group. Our conclusion needs to be confirmed via high-quality trials and the results need to be reproduced in other regions and populations.

Glutathione S-transferase gene GSTM1, gene-gene interaction, and gastric cancer susceptibility: evidence from an updated meta-analysis.

BACKGROUND: The null genotype of GSTM1 have been implicated in gastric cancer risk, but numerous individual studies showed mixed, or even conflicting results. Thus, a meta-analysis was performed. RESULTS: We identified 54 individual studies involving 9,322 cases and 15,118 controls through computer-based searches of PubMed, Embase, and Cochrane Library. It was found that the null genotype of GSTM1 was associated with an increased gastric cancer risk (OR = 1.207, 95% CI: 1.106-1.317, P < 0.001), under the random-effects model (I(2) : 49.9%, PQ <0.001). From stratification analyses for ethnicity, alcohol drinking, Helicobacter pylori infection, an effect modification of gastric cancer risk was found in the subgroups of ethnicity, smoking status, Helicobacter pylori infection, whereas null result was found in the subgroups of alcohol drinking. We also undertook gene-gene interaction analysis between GSTM1 and GSTT1 genes for gastric cancer risk, and the results indicated that the dual null genotypes of GSTM1 and GSTT1 might elevate the risk of gastric cancer (OR = 1.505, 95% CI: 1.165-1.944, P = 002). CONCLUSIONS: This meta-analysis suggests that the null genotype of GSTM1 may be a important genetic risk factor for gastric cancer development.

EGF +61A/G polymorphism contributes to increased gastric cancer risk: evidence from a meta-analysis.

BACKGROUND: Epidermal growth factor (EGF) plays a pivotal role in cell proliferation, differentiation, and tumorigenesis of epithelial tissues. Variation of the EGF +61A/G (rs4444903) can lead to an alteration in EGF production and/or activity, which may result in individual susceptibility to gastric cancer. Studies investigating the association between EGF +61A/G polymorphism and gastric cancer risk produced inconsistent results. The aim of this study was to quantitatively summarize the evidence for such an association. METHODS: Eligible studies on the association between EGF +61A/G polymorphism and gastric cancer risk were identified by search of electronic databases including PubMed, EMBASE, Cochrane Library, and Chinese Biomedical Literature database (CBM). Data were extracted by two independent authors and pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association. Metaregression and subgroup analyses were performed to identify the source of heterogeneity. RESULTS: Finally, six case-control studies with 1547 gastric cancer cases and 2762 controls were eventually identified. Overall, significant increased gastric cancer risk was found when all studies were pooled in the meta-analysis (GG vs. AA: OR = 1.438, 95% CI 1.021-2.025, P = 0.038; GG + AG vs. AA: OR = 1.256, 95% CI 1.025-1.539, P = 0.028; GG vs. AG + AA: OR = 1.265, 95% CI 1.002-1.596, P = 0.048). In subgroup analysis by ethnicity, source of control, study quality, and HWE in controls, significant increased gastric cancer risk was observed in Asians, population-based studies, high quality studies, and studies consistent with HWE. In subgroup analysis according to tumor location, and histological type, significant association was observed in all subgroups. CONCLUSIONS: This meta-analysis suggested that the EGF +61A/G polymorphism contributes to increased gastric cancer risk, especially in Asian populations. Further well-designed studies based on large sample size in diverse populations are needed to confirm this association.

LAPTM4B polymorphism increases susceptibility to multiple cancers in Chinese populations: a meta-analysis.

BACKGROUND: Lysosome-associated protein transmembrane-4 beta (LAPTM4B) is a novel cancer-related gene. While recent studies have reported that the LAPTM4B polymorphism increased the susceptibility of several cancers, the results remain inconclusive. Therefore, we performed a meta-analysis to systematically summarize the possible association. RESULTS: The meta-analysis was conducted based on 17 studies in Chinese populations, including 4160 cases and 4148 controls. The relevant studies were searched through electronic databases updated in November 2013. The strength of association between the LAPTM4B polymorphism and susceptibility to multiple cancers was assessed by odds ratio (OR) and 95% confidence interval (95% CI).The meta-analysis results suggested that the LAPTM4B polymorphism was significantly associated with overall susceptibility to multiple cancers in all genetic models (*2 vs. *1, OR = 1.53, 95% CI = 1.37-1.70; *2/2 vs. *1/1, OR = 2.18, 95% CI = 1.72-2.75; *2/1 vs.*1/1, OR = 1.62, 95% CI = 1.41-1.86; *2/1 + *2/2 vs. *1/1, OR = 1.70, 95% CI = 1.47-1.97; *2/2 vs. *2/1 + *1/1, OR = 1.76, 95% CI = 1.50-2.05). Further subgroup analysis revealed a significant association between the LAPTM4B polymorphism and cancer susceptibility in the subgroups stratified by control source, cancer type, histopathologic differentiation, and TNM stage. CONCLUSIONS: This meta-analysis indicated that the LAPTM4B *2 allele was associated with increasing risk of multiple cancers, tumor initiation and development.

ERCC1 expression levels predict the outcome of platinum-based chemotherapies in advanced bladder cancer: a meta-analysis.

The objective of this study was to provide a precise evaluation of whether expression levels of excision repair cross-complementation group 1 (ERCC1) are associated with objective response, overall survival (OS), and median survival in patients with advanced bladder cancer treated with platinum-based chemotherapy. Systematic computerized searches of the electronic databases PubMed, EMBASE, Ovid, ASCO, and CNKI were performed and a meta-analysis was carried out to evaluate the correlation between ERCC1 expression levels and objective response rate, OS, or progression-free survival in patients with advanced bladder cancer receiving platinum-based chemotherapy. References within the articles identified were also searched manually. STATA package version 11.0 was used for the comprehensive quantitative analyses. A total of six studies involving 356 patients, of which ERCC1 expression was high/positive in 138 (38.8%) and low/negative in 218 (61.2%), were included in the meta-analysis. The median age of the patients was 63.7 years. The objective response rate favored patients with ERCC1 low/negative expression after platinum-based chemotherapy, but showed no significant difference [odds ratio 0.86, 95% confidence interval (CI) 0.36-2.06, P=0.734]. The median OS time and the median progression-free survival time were significantly prolonged when ERCC1 low/negative expression was compared with ERCC1 high/positive expression (hazard ratio 0.69, 95% CI 0.54-0.89, P=0.004, and hazard ratio 0.76, 95% CI 0.66-0.89, P=0.000, respectively). In conclusion, low/negative expression of ERCC1 was associated with higher objective response, median progression-free survival, and median OS in patients with advanced bladder cancer treated with platinum-based chemotherapy. ERCC1 may be a suitable marker of prognosis and sensitivity to platinum-based chemotherapy in patients with advanced bladder cancer. Larger studies and further clinical trials are warranted to confirm these findings.

Association between nonsteroidal anti-inflammatory drug use and brain tumour risk: a meta-analysis.

AIMS: Several epidemiological studies have evaluated the association between nonsteroidal anti-inflammatory drugs (NSAIDs) and brain tumour risk. However, results from these studies have been inconsistent. The aim of this detailed meta-analysis is to review and summarize the evidence on this association. METHODS: A comprehensive search for articles published up to September 2013 was performed. Studies evaluating the association between exposure to NSAIDs and risk of brain tumours were included. Random-effects meta-analytical models were used to calculate the relative risk (RR) and corresponding 95% confidence intervals (CIs). Sensitivity analyses, Galbraith plots and subgroup analyses were also performed. RESULTS: Ten studies (six case-control studies, three cohort studies and one randomized controlled trial), published between 2003 and 2013, were included in this analysis. Compared with non-use, overall use of NSAIDs was not statistically significantly associated with brain tumour risk based on the random-effects models (RR = 1.01; 95% CI = 0.89, 1.15). No differences were observed when analyses were stratified by gender and brain tumour subtype. Specific analysis for aspirin and non-aspirin NSAIDs yielded similar results. However, a slightly increased risk of brain tumour in NSAID users was observed in cohort studies (RR = 1.32; 95% CI = 1.06, 1.64; P = 0.014). Furthermore, our analysis did not show a significant association between frequency and dose of aspirin use and brain tumour risk. CONCLUSIONS: Use of NSAIDs (aspirin and non-aspirin NSAIDs) does not appear to be associated with brain tumour risk, but larger studies are needed to substantiate this relationship.

Lack of association between cathepsin D C224T polymorphism and Alzheimer's disease risk: an update meta-analysis.

BACKGROUND: Cathepsin D C224T polymorphism has been reported to associate with AD susceptibility. But the results were inconsistent. This study aimed to assess the relationship between C224T polymorphism and AD risk. METHODS: The relevant studies were identified by searching PubMed, Embase, Web of Science, Google Scholar and Wan fang electronic databases updated on July 2013. The relationship between Cathepsin D C224T polymorphism and AD risk was evaluated by ORs and 95% CIs. RESULTS: A total of 25 case-control studies including 5,602 cases and 11,049 controls were included in the meta-analysis. There was no association between C224T polymorphism and AD risk with all the studies were pooled in the meta-analysis (CT vs. CC: OR = 1.125, 95% CI = 0.974-1.299, P = 0.109; CT + TT vs. CC: OR = 1.136, 95% CI = 0.978-1.320, P = 0.094). Furthermore, when stratified by ethnicity, age of onset and APOEϵ4 status, significant association did not found in all subgroups. CONCLUSION: The present meta-analysis suggested that the Cathepsin D C224T polymorphism was not associated with AD susceptibility.

Meta-analysis of randomized controlled trials on the efficacy of probiotics in Helicobacter pylori eradication therapy in children.

UNLABELLED: The efficacy of probiotics supplementation in children undergoing Helicobacter pylori (H. pylori) eradication therapy remains controversial. This study aimed to meta-analyze whether probiotics supplementation in triple therapy could improve H. pylori eradication rates and reduce therapy-related side effects in children. Electronic databases PubMed and Embase were searched to identify all randomized controlled trials in pediatric patients comparing probiotics supplementation with placebo or no extra intervention in H. pylori eradication therapy. Two authors independently extracted the data. Results were expressed as odds ratios (ORs) and accompanying 95 % confidence intervals (CIs). Stata version 12.0 was used to perform all statistical analyses. Seven studies consisting of 508 pediatric patients were included in our study. The pooled ORs (studies n = 7) of eradication rates by intention-to-treat and per-protocol analysis in the probiotics group versus the control group were 1.96 (95 % CI 1.28-3.02) and 2.25 (95 % CI 1.41-3.57), respectively. The pooled OR (studies n = 5) of incidence of total side effects was 0.32 (95 % CI 0.13-0.79), with significant heterogeneity observed (I (2) = 71.9 %). CONCLUSION: Probiotics supplementation in triple therapy for H. pylori infection may have beneficial effects on eradication and therapy-related side effects, particularly diarrhea, in children.

Reference values for serum antistreptolysin O in Chinese adult men from a Chinese male population survey.

BACKGROUND: Numerous diseases come from streptococcal infection. The antistreptolysin O (ASO) test is the most widely used serological test for streptococcal infection applied for the clinical diagnosis. The aim of this study was to establish reference values for serum ASO in Han and Zhuang Chinese from a Chinese male population survey. METHODS: A cross-sectional study in which 1,762 serum samples were collected between September 2009 and December 2009 from Chinese men aged 20 to 69 years. The reference values for serum ASO were measured with the immunonephelometric method on the Hitachi 7600 autoanalyzer. RESULTS: Serum ASO values were not normally distributed but log normally distributed. The reference value was < or = 125.00 IU/mL for serum ASO. A significant decrease with age was found, and age-dependent reference values were calculated for serum ASO levels. The Zhuang and Han groups (p < 10(-3)) exhibited differences in serum ASO. There was no significant difference according to smoking (p = 0.718) and drinking (p = 0.388) in Zhuang. However, there was a significant difference between smoking and non-smoking (p < 10(-3)) in the Han ethnic group, whereas there was no significant difference between the non-drinking and drinking groups (p = 0.245). CONCLUSIONS: The reference values for serum ASO for healthy adult men showed a huge deviation compared to the currently used reference value (200 IU/mL). Thus, the reference values for serum ASO should be established for different ethnic groups and regions.