Dataset Information

Correlations of MCP-1 -2518A>G polymorphism and serum levels with cerebral infarction risk: a meta-analysis.

ABSTRACT: This meta-analysis was performed to evaluate the relationships between the monocyte chemoattractant protein-1 (MCP-1) -2518A>G (rs1024611 A>G) polymorphism and its serum levels, and the risk of cerebral infarction. The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched for relevant articles published before October 1st, 2013 without language restrictions. Meta-analysis was conducted using the STATA 12.0 software. Crude odds ratios (ORs) or standardized mean difference (SMD) with their 95% confidence intervals (95% CIs) were calculated. Twelve case-control studies that met all the inclusion criteria were included in this meta-analysis. A total of 1272 patients with cerebral infarction and 1210 healthy control subjects were involved in this meta-analysis. Our meta-analysis results reveal that the MCP-1 -2518A>G polymorphism might increase the risk of cerebral infarction (A allele vs. G allele: OR=1.37, 95% CI: 1.18-1.60, p<0.001; GA+AA vs. GG: OR=1.33, 95% CI: 1.09-1.62, p=0.005; respectively). Furthermore, cerebral infarction patients had higher levels of serum MCP-1 than did healthy control subjects (SMD=2.96, 95% CI: 2.00-3.92, p<0.001). Statistical analysis revealed no evidence of publication bias in this meta-analysis (all p>0.05). Our findings indicate that the MCP-1 -2518A>G polymorphism and serum MCP-1 levels may contribute to the development of cerebral infarction. Thus, the MCP-1 -2518A>G polymorphism and serum MCP-1 levels could be potential biomarkers for the early detection of cerebral infarction.

SUBMITTER: Gao HH

PROVIDER: S-EPMC4117263 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature

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Correlations of MCP-1 -2518A>G polymorphism and serum levels with cerebral infarction risk: a meta-analysis.

Gao Hong-Hua HH Gao Lian-Bo LB Wen Jia-Mei JM

DNA and cell biology 20140410 8

This meta-analysis was performed to evaluate the relationships between the monocyte chemoattractant protein-1 (MCP-1) -2518A>G (rs1024611 A>G) polymorphism and its serum levels, and the risk of cerebral infarction. The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched for relevant articles published before October 1st, 2013 without language restrictions. Meta-analysis was conducted using the STATA 12.0 software. Crude odds ratios (OR ...[more]

PMID: 24720638

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Project description:Studies of key metabolite variations and their biological mechanisms in cerebral infarction (CI) have increased our understanding of the pathophysiology of the disease. However, how metabolite variations in different periods of CI influence these biological processes and whether key metabolites from different periods may better predict disease progression are still unknown. We performed a systematic investigation using the metabonomics method. Various metabolites in different pathways were investigated by serum metabolic profiling of 143 patients diagnosed with CI and 59 healthy controls. Phe-Phe, carnitine C18:1, palmitic acid, cis-8,11,14-eicosatrienoic acid, palmitoleic acid, 1-linoleoyl-rac-glycerol, MAG 18:1, MAG 20:3, phosphoric acid, 5α-dihydrotestosterone, Ca, K, and GGT were the major components in the early period of CI. GCDCA, glycocholate, PC 36:5, LPC 18:2, and PA showed obvious changes in the intermediate time. In contrast, trans-vaccenic acid, linolenic acid, linoleic acid, all-cis-4,7,10,13,16-docosapentaenoic acid, arachidonic acid, DHA, FFA 18:1, FFA 18:2, FFA 18:3, FFA 20:4, FFA 22:6, PC 34:1, PC 36:3, PC 38:4, ALP, and Crea displayed changes in the later time. More importantly, we found that phenylalanine metabolism, medium-chain acylcarnitines, long-chain acylcarnitines, choline, DHEA, LPC 18:0, LPC 18:1, FFA 18:0, FFA 22:4, TG, ALB, IDBIL, and DBIL played vital roles in the development of different periods of CI. Increased phenylacetyl-L-glutamine was detected and may be a biomarker for CI. It was of great significance that we identified key metabolic pathways and risk metabolites in different periods of CI different from those previously reported. Specific data are detailed in the Conclusion section. In addition, we also explored metabolite differences of CI patients complicated with high blood glucose compared with healthy controls. Further work in this area may inform personalized treatment approaches in clinical practice for CI by experimentally elucidating the pathophysiological mechanisms.

Project description:AimTo investigate the associations of interleukin-17 (IL-17) genetic polymorphisms and serum levels with ulcerative colitis (UC) risk.MethodsRelevant articles were identified through a search of the following electronic databases, excluding language restriction: (1) the Cochrane Library Database (Issue 12, 2013); (2) Web of Science (1945-2013); (3) PubMed (1966-2013); (4) CINAHL (1982-2013); (5) EMBASE (1980-2013); and (6) the Chinese Biomedical Database (1982-2013). Meta-analysis was conducted using STATA 12.0 software. Crude odds ratios and standardized mean differences (SMDs) with corresponding 95% confidence intervals (CIs) were calculated. All of the included studies met all of the following five criteria: (1) the study design must be a clinical cohort or a case-control study; (2) the study must relate to the relationship between IL-17A/F genetic polymorphisms or serum IL-17 levels and the risk of UC; (3) all patients must meet the diagnostic criteria for UC; (4) the study must provide sufficient information about single nucleotide polymorphism frequencies or serum IL-17 levels; and (5) the genotype distribution of healthy controls must conform to the Hardy-Weinberg equilibrium (HWE). The Newcastle-Ottawa Scale (NOS) criteria were used to assess the methodological quality of the studies. The NOS criteria included three aspects: (1) subject selection: 0-4; (2) comparability of subjects: 0-2; and (3) clinical outcome: 0-3. NOS scores ranged from 0 to 9, with a score ≥ 7 indicating good quality.ResultsOf the initial 177 articles, only 16 case-control studies met all of the inclusion criteria. A total of 1614 UC patients and 2863 healthy controls were included in this study. Fourteen studies were performed on Asian populations, and two studies on Caucasian populations. Results of the meta-analysis revealed that IL-17A and IL-17F genetic polymorphisms potentially increased UC risk under both allele and dominant models (P < 0.001 for all). The results also showed that UC patients had higher serum IL-17 levels than healthy controls (SMD = 5.95, 95%CI: 4.25-7.65, P < 0.001). Furthermore, serum IL-17 levels significantly correlated with the severity of UC (moderate vs mild: SMD = 2.59, 95%CI: 0.03-5.16, P < 0.05; severe vs mild: SMD = 7.09, 95%CI: 3.96-10.23, P < 0.001; severe vs moderate: SMD = 5.84, 95%CI: 5.09-6.59, P < 0.001). The NOS score was ≥ 5 for all of the included studies. Based on the sensitivity analysis, no single study influenced the overall pooled estimates. Neither the Begger's funnel plots nor Egger's test displayed strong statistical evidence for publication bias (IL-17A/F genetic polymorphisms: t = -2.60, P = 0.019; serum IL-17 levels: t = -1.54, P = 0.141).ConclusionThe findings strongly suggest that IL-17A/F genetic polymorphisms and serum IL-17 levels contribute to the development and progression of UC.

Dataset Information

Correlations of MCP-1 -2518A>G polymorphism and serum levels with cerebral infarction risk: a meta-analysis.

Publications

Correlations of MCP-1 -2518A>G polymorphism and serum levels with cerebral infarction risk: a meta-analysis.

Similar Datasets

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