[Retracted] miR­639 is associated with advanced cancer stages and promotes proliferation and migration of nasopharyngeal carcinoma.

[This retracts the article DOI: 10.3892/ol.2018.9512.].

Dynamic observation on collateral circulation construction of patient with vertebral artery restenosis after stenting: case report.

Purpose/aim of the study: Posterior circulation stroke (PCS) accounts for 20% of ischemic stroke, and vertebrobasilar stenosis is an important cause of PCS. Notably, not all patients with artery stenosis progress to ischemic stroke, and one of the important reason is that collateral circulation construction plays important protection role in this process.Clinical presentation: Here, we present the case of a 71-year-old male who presented with lightheadedness and three episodes of loss of consciousness after bilateral subclavian artery stenting. Digital subtraction angiography (DSA) demonstrated severe stenosis of the left vertebral artery, and the bilateral subclavian artery was kept open. The patient was then given the left vertebral artery stenting in an effort to resolve the vascular stenosis. As expected, he achieved a complete remission after stenting. However, 6 months later the patient suffered from loss of consciousness again. Repeat DSA confirmed restenosis of the left vertebral artery, and revealed a collateral flow to the left vertebral artery which fed by external carotid collateral branches. Then DSA was performed after 12 months, and another collateral circulation involving thyrocervical trunk was also found supplying flow to the left vertebral artery. In this process, the frequency of loss of consciousness gradually decreased as the collateral circulation construction. Conclusion: Through this case, we observe the whole process of the collateral circulation construction. Moreover, this case serves as a testament to the variability and complexity of vertebrobasilar arteriopathies, suggesting promotion of collateral flow offers the opportunity for outcome improvement.

Interleukin-6 gene -572 G > C polymorphism and myocardial infarction risk.

INTRODUCTION: The association between interleukin-6 (IL-6) gene -572 G^C polymorphism and myocardial infarction (MI) risk has not been established. We adopted this meta-analysis for further insight into the case-control studies. MATERIALS AND METHODS: To investigate the genetic association, we searched multiple databases, including Web of Science, EMbase, CBM disc, PubMed and CNKI. Also, we manually identified the searched references. All the statistical analyses were conducted using Stata 11.0. RESULTS: A total of five studies were identified, involving 2,526 MI cases and 3,027 controls. The results revealed a significant association between IL-6 gene -572 G^C polymorphism and MI, implying that the IL-6 gene -572 C allele may be a protective factor for MI (for C allele vs K allele: OR = 0.85, 95% CI = 0.73-0.99, p = 0.041; for C/C vs G/G: OR = 0.55, 95% CI = 0.31-0.98, p = 0.044; for C/C vs G/C + G/G: OR = 0.60, 95% CI = 0.41-0.89, p = 0.011). However, in the subgroup analysis with regard to ethnicity, no significant correlation was identified between IL-6 gene -572 G^C polymorphism and MI among Europeans. CONCLUSION: The IL-6 gene -572 C allele may be a protective factor for MI. Future studies involving larger sample bases are still recommended.

Significance of hemodynamic assessment by pressure wire for endovascular therapy of subclavian steal syndrome.

OBJECTIVE: Subclavian steal syndrome results from hemodynamic impairment due to stenosis or occlusion of subclavian artery. Therefore, it is important for subclavian steal syndrome patients to assess hemodynamic status during endovascular therapy. METHODS: Eleven subclavian steal syndrome patients undergoing endovascular therapy attended this study. Pressure wire was used to measure trans-stenosis pressure difference (ΔP). Digital subtraction angiography, Transcranial Doppler and Electronic sphygmomanometer were introduced to assess stenotic rate, steal grade and inter-arm systolic pressure difference, respectively. Clinical symptoms and restenosis were followed up after endovascular therapy. The associations of ΔP with stenotic rate, inter-arm pressure difference, steal degree, clinic symptoms and restenosis were analyzed in this paper. RESULTS: Prior to the therapy, ΔP moderately correlated with stenotic rate (r = 0.757, p = 0.007) and inter-arm pressure difference (r = 0.701, p = 0.016). ΔP was ≥6 mmHg in all patients, and 6-9 mmHg for grade 1 steal and ≥10 mmHg for grade 2 and 3 steals. After the therapy, all patients had technique success, and 10 patients had clinic success, and 1 patient appeared restenosis. ΔP was ≤3 mmHg and steal disappeared in the patients with clinical success. ΔP was 18 mmHg and grade 3 steal still existed in one patient without clinical success. One patient with 1 mmHg of ΔP after therapy appeared restenosis in the follow-up. CONCLUSION: The trans-stenosis pressure difference is closely related to steal degree and clinical symptoms. The measurement of hemodynamic status by pressure wire is very useful to guide endovascular therapy in subclavian steal syndrome patients. However, the restenosis may still occur, even though the hemodynamic impairment is improved.

miR-639 is associated with advanced cancer stages and promotes proliferation and migration of nasopharyngeal carcinoma.

Early detection of nasopharyngeal carcinoma (NPC) is of vital importance for improving prognosis and survival rates. MicroRNA (miRNA) are a class of short and non-coding RNA molecules that are capable of inhibiting the translation of mRNA of target genes. Previous studies have revealed that miRNA are involved in tumorigenesis and cancer development. The RNase-resistance of circulating miRNA have made them valuable non-invasive biomarkers, and has therefore drawn particular attention to their therapeutic potential. The aim of the present study was to investigate the expression of the previously uncharacterized miR-639 in NPC. In a study population of 139 patients, higher expression of miR-639 was associated with metastasis, more advanced cancer stages, and lower disease-free survival rates. In vitro experiments involving transfection of human NPC C666-1 and NPC/HK1 cell lines with miR-639 mimics and antagomir indicated that overexpressing miR-639 promoted cell proliferation and migration, suppression of miR-639 inhibited proliferation and migration. The present study provides evidence that miR-639 is differentially expressed in NPC tissues of varying cancer stages, and suggests that quantifying circulating miR-639 may be of importance for non-invasive diagnosis and prognostic evaluation, and may have potential therapeutic utility.

Multiple Silent Brain Infarcts Are Associated with Severer Stroke in Patients with First-Ever Ischemic Stroke without Advanced Leukoaraiosis.

BACKGROUND: Silent brain infarct (SBI) is associated with symptomatic stroke, but the association between SBI and acute ischemic stroke severity is uncertain. We aimed at investigating the association between SBI number and stroke severity in patients with first-ever ischemic stroke without advanced leukoaraiosis. METHODS: This study included 115 patients with first-ever ischemic stroke without advanced leukoaraiosis. National Institutes of Health Stroke Scale (NIHSS) scores were measured. Magnetic resonance imaging (MRI) was performed to detect the acute ischemic infarct and SBI. The location of infarct was divided into anterior and posterior circulations. The size of infarct was divided into large (≥15 mm) and small (<15 mm) infarctions. The number of SBIs was divided into single and multiple (r2) subgroups. The association between SBI and the NIHSS score was analyzed by stratification of stroke locations. The associations between SBI and the NIHSS score and the size of the acute ischemic infarct were analyzed by logistic regression. RESULTS: Of the 74 patients with SBI, single SBI was 30 (40.5%) and multiple SBIs were 44 (59.5%). Age (odds ratio [OR] = 1.125, P < .001) and hypertension (OR = 3.562, P < .05) were independent risk factors for SBI. When adjusted for all the other vascular risk factors, multiple SBIs had a higher percentage of more than 3 NIHSS scores (OR = 3.59, 95% confidence interval [CI]: 1.00-12.99, P = .048) and a large acute ischemic infarct (OR = 3.71, 95% CI: 1.23-11.22, P = .020) than no SBI. CONCLUSION: Multiple SBIs have severer neurological deficits and larger infarcts for ischemic stroke than no SBI, which may suggest the large-artery or cardiovascular vasculopathy evolution and poor collateral circulation in patients with multiple SBIs.

PPARγ Inhibits VSMC Proliferation and Migration via Attenuating Oxidative Stress through Upregulating UCP2.

Increasing evidence showed that abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are common event in the pathophysiology of many vascular diseases, including atherosclerosis and restenosis after angioplasty. Among the underlying mechanisms, oxidative stress is one of the principal contributors to the proliferation and migration of VSMCs. Oxidative stress occurs as a result of persistent production of reactive oxygen species (ROS). Recently, the protective effects of peroxisome proliferator-activated receptor γ (PPARγ) against oxidative stress/ROS in other cell types provide new insights to inhibit the suggests that PPARγ may regulate VSMCs function. However, it remains unclear whether activation of PPARγ can attenuate oxidative stress and further inhibit VSMC proliferation and migration. In this study, we therefore investigated the effect of PPARγ on inhibiting VSMC oxidative stress and the capability of proliferation and migration, and the potential role of mitochondrial uncoupling protein 2 (UCP2) in oxidative stress. It was found that platelet derived growth factor-BB (PDGF-BB) induced VSMC proliferation and migration as well as ROS production; PPARγ inhibited PDGF-BB-induced VSMC proliferation, migration and oxidative stress; PPARγ activation upregulated UCP2 expression in VSMCs; PPARγ inhibited PDGF-BB-induced ROS in VSMCs by upregulating UCP2 expression; PPARγ ameliorated injury-induced oxidative stress and intimal hyperplasia (IH) in UCP2-dependent manner. In conclusion, our study provides evidence that activation of PPARγ can attenuate ROS and VSMC proliferation and migration by upregulating UCP2 expression, and thus inhibit IH following carotid injury. These findings suggest PPARγ may represent a prospective target for the prevention and treatment of IH-associated vascular diseases.

The Histone Acetyltransferase GCN5 Expression Is Elevated and Regulated by c-Myc and E2F1 Transcription Factors in Human Colon Cancer.

The histone acetyltransferase GCN5 has been suggested to be involved in promoting cancer cell growth. But its role in human colon cancer development remains unknown. Herein we discovered that GCN5 expression is significantly upregulated in human colon adenocarcinoma tissues. We further demonstrate that GCN5 is upregulated in human colon cancer at the mRNA level. Surprisingly, two transcription factors, the oncogenic c-Myc and the proapoptotic E2F1, are responsible for GCN5 mRNA transcription. Knockdown of c-Myc inhibited colon cancer cell proliferation largely through downregulating GCN5 transcription, which can be fully rescued by the ectopic GCN5 expression. In contrast, E2F1 expression induced human colon cancer cell death, and suppression of GCN5 expression in cells with E2F1 overexpression further facilitated cell apoptosis, suggesting that GCN5 expression is induced by E2F1 as a possible negative feedback in suppressing E2F1-mediated cell apoptosis. In addition, suppression of GCN5 with its specific inhibitor CPTH2 inhibited human colon cancer cell growth. Our studies reveal that GCN5 plays a positive role in human colon cancer development, and its suppression holds a great therapeutic potential in antitumor therapy.

Genetic polymorphisms of interleukin-6 gene and susceptibility to coronary artery disease in Chinese population: Evidence based on 4582 subjects.

The aim of this study was to explore whether interleukin-6 (IL-6) gene (-174 G/C and -572 C/G) polymorphisms are associated with susceptibility to coronary artery disease (CAD) risk in Chinese population. All the statistical tests were performed using Stata version 11.0. Twelve articles involving 16 studies were included in this meta-analysis, covering a total of 2309 CAD cases and 2273 controls. For IL-6 gene -572 C/G polymorphism, the results showed evidence for significant association between IL-6 gene -572 C/G polymorphism and CAD risk (for G allele vs. C allele: OR=1.48, 95% CI=1.26-1.74, p<0.001; for G/G vs. C/C: OR=2.60, 95% CI=1.54-4.39, p<0.001; for G/G vs. G/C+C/C: OR=2.15, 95% CI=1.35-3.42, p=0.001; for G/G+G/C vs. C/C: OR=1.55, 95% CI=1.29-1.85, p<0.001). However, for IL-6 gene -174 G/C polymorphism, no significant association was found between this variation and CAD risk. In summary, our meta-analysis showed evidence that IL-6 gene -572 C/G polymorphism may be a risk factor for CAD susceptibility. For IL-6 gene -174 G/C polymorphism, no significant association was found between this variation and CAD risk.

Genetic polymorphism of the estrogen receptor alpha gene and susceptibility to osteoarthritis: evidence based on 15,022 subjects.

OBJECTIVE: Several lines of evidence suggest that estrogen receptor alpha (ER-α) gene polymorphism may influence the development of osteoarthritis (OA). However, the results are inconsistent. The aim of this study was to explore using a meta-analysis whether rs2234693 (ER-α PvuII T/C) polymorphism confers significant susceptibility to OA. METHODS AND RESULTS: A systematic search of all relevant studies published through 17 August 2014 was conducted using the PubMed, Web of Science, Embase, Cochrane database, Current Controlled Trials, Clinicaltrials.gov, Chinese Clinical Trial Registry, CBMdisc, CNKI and Google Scholar. All statistical analyses were done with Review Manager 5.1.4. Twelve articles involving 15 studies were included in the final meta-analysis, which contained 6417 OA cases and 8605 controls. Overall, no significant association was found between the rs2234693 polymorphism and OA risk when all studies were pooled into the meta-analysis (for C allele vs. T allele: OR = 0.99, 95% CI = 0.94-1.04, p = 0.63; for C/C vs. T/T: OR = 0.97, 95% CI = 0.87-1.08, p = 0.53; for C/C vs. T/C + T/T: OR = 0.96, 95% CI = 0.88-1.06, p = 0.43; for C/C + T/C vs. T/T: OR = 1.00, 95% CI = 0.89-1.14, p = 0.94). In the subgroup analysis, significant association was found between the rs2234693 polymorphism and the OA risk in the knee osteoarthritis (KOA) group (for C/C + T/C vs. T/T: OR = 1.15, 95% CI = 1.02-1.29, p = 0.02). CONCLUSIONS: The present meta-analysis suggests that the rs2234693 polymorphism is associated with an increased KOA risk. Additional well designed genome-wide association studies are required to confirm the result.

The role of TRPV1 in improving VSMC function and attenuating hypertension.

The transient receptor potential vanilloid type 1 (TRPV1) channel, a ligand-gated cation channel of the TRP subfamily, can be activated by multiple stimuli, including capsaicin. Currently, cumulative studies have demonstrated an interesting link between TRPV1 and cardiovascular diseases, including hypertension. Additionally, the protective effect of TRPV1 against hypertension and its related disorders has been proved to be partly involved with the improved action of vascular smooth muscle cells (VSMCs). This review focuses on the current knowledge of TRPV1 in improving VSMC function and attenuating hypertension.

Toll-like receptor 4 gene Asp299Gly and Thr399Ile polymorphisms in type 2 diabetes mellitus: a meta-analysis of 15,059 subjects.

AIMS: Toll-like receptor 4 (TLR4) gene Asp299Gly and Thr399Ile polymorphisms have been reported to be associated with susceptibility to type 2 diabetes mellitus (T2DM) with inconsistent results. In an effort to clarify earlier inconclusive results, a meta-analysis evaluating the precise associations between TLR4 gene Asp299Gly and Thr399Ile polymorphisms and T2DM risk was performed. METHODS: We searched the PubMed, Embase, Web of Science, CBMdisc, CNKI, and Google Scholar until July 17, 2014. Additionally, hand searching of the references of identified articles were performed. Original observational studies dealing with the associations between TLR4 gene Asp299Gly and Thr399Ile polymorphisms and T2DM risk were selected. Heterogeneity and publication bias were determined and the meta-analysis was performed by Review Manager 5.1.4 and Stata 11.0. RESULTS: Seventeen articles involving 25 studies were included in the final meta-analysis, covering a total of 5963 T2DM cases and 9096 controls. For TLR4 gene Asp299Gly polymorphism, 17 studies were combined showing no evidence for association between TLR4 gene Asp299Gly polymorphism and T2DM risk. For TLR4 gene Thr399Ile polymorphism, eight studies were combined. There was also lack of evidence for significant association between TLR4 gene Thr399Ile polymorphism and T2DM risk. In addition, the similar results were obtained in the sensitivity analyses. CONCLUSIONS: The present meta-analysis indicates that TLR4 gene Asp299Gly and Thr399Ile polymorphisms are not associated with increased T2DM risk.

Telmisartan-induced PPARγ activity attenuates lipid accumulation in VSMCs via induction of autophagy.

Foam cell formation is the hallmark of atherosclerosis. Both telmisartan and autophagy protect against the development of atherosclerosis. However, it has yet to be elucidated whether telmisartan prevents vascular smooth muscle cell (VSMC)-derived foam cell formation. Vascular smooth muscle cells isolated from the thoracic aorta of male C57BL/6J mice were used for this study. To induce foam cell formation, primary VSMCs were incubated in 80 µg/ml oxLDL for 24 h. LC3, beclin-1, PPARγ, AMPK, p-AMPK, mTOR and p-mTOR expression were determined via Western blot. Lipid accumulation was evaluated via oil red O staining and intracellular total cholesterol level measurement. Our study demonstrated that telmisartan dose-dependently increased the expression of beclin-1, the LC3II/LC3I ratio and the quantity of GFP-labeled autophagosomes, displaying a peak effect at 10 µM. In control siRNA-transfected VSMCs, telmisartan (10 µM) decreased lipid droplet accumulation and the total cholesterol level significantly. In contrast, in Atg7 siRNA-transfected VSMCs, telmisartan failed to attenuate lipid accumulation. In addition, telmisartan dose-dependently increased the expression of PPARγ and p-AMPK and decreased the expression of p-mTOR. GW9662 attenuated the telmisartan-induced increase in PPARγ expression, the LC3-II/LC3-I ratio and p-AMPK expression and the telmisartan-induced decrease in p-mTOR expression. Compound C restored mTOR activity and abolished the increase in the LC3-II/LC3-I ratio. Rapamycin significantly reduced p-mTOR expression and increased the LC3-II/LC3-I ratio. In conclusion, this study provides evidence that the chronic pharmacological activation of the PPARγ-mediated autophagy pathway using telmisartan may represent a promising therapeutic strategy for atherosclerosis.

Diabetes mellitus does not increase the risk of adverse long-term outcomes after intracranial stent placement.

The present study is to investigate whether diabetes mellitus (DM) increases risk of adverse long-term outcomes after intracranial stent placement. Patients receiving intracranial stenting were assigned to DM group and non-DM group according to diabetes status. The long-term follow-up endpoint was composite of any stroke and death within 30 days, any ischemic stroke beyond 30 days, and transient ischemic attack in the territory of the stented artery at any time. A total of 44 stenoses in 43 patients were retrospectively analyzed. The cumulative probability of the composite outcomes were 15.4% (95% CI 15.3-47.3%) at 1 year and 30.8% (95% CI 26.5-33.6%) at 2 years for DM group; 17.5% (95% CI 16.0-31.2%) at both 1 year and 2 years for non-DM group (log-rank test, P = 0.424). After adjusting for the confounders, the risk of DM versus non-DM for composite outcomes remained insignificant (hazard ratio: 2.84, 95% CI 0.46-17.66; P = 0.26). Our results showed that there is no significant difference between patients with DM and without DM in cumulative probability of the composite outcomes. It suggests that based on our data, there is no evidence that DM increases the risk of adverse long-term outcomes after intracranial stent placement.

The association between leukoaraiosis and carotid atherosclerosis: a systematic review and meta-analysis.

The association between large-artery atherosclerosis and leukoaraiosis (LA) has been increasingly reported with inconsistent conclusion. This systematic review examines the relationship between LA and carotid atherosclerosis, manifested as atherosclerotic stenosis, plaques and increased intima-media thickness (IMT). PubMed, Embase, and Web of Science were searched for articles published up to February 2014. Thirty-two studies that examined the relationship between LA and carotid atherosclerosis were included. All statistical analysis was conducted with Review Manager 5.2.4. Finally, 32 studies including 17,721 patients were identified. There were 7 (30%) out of 23 studies reporting significant association between LA and carotid stenosis; 11 (79%) out of 14 studies reporting significant association between LA and carotid plaque; all 9 studies reporting significant association between LA and carotid IMT; one study showing an association between LA and CAWT (similar to the role of the IMT). The quantitative meta-analysis of 10 studies showed that carotid atherosclerosis was not associated with LA (OR: 1.10; 95% CI: 0.61-1.98). A significant association was found between LA and carotid plaque (OR = 3.53; 95% CI = 1.83-6.79), and the result of IMT group showed that IMT increased risk of LA (MD = 0.11; 95% CI = 0.01-0.22). This systematic review suggested that LA has a tendency of association with carotid plaques but no association with simple carotid stenosis.

Association of rs9340799 polymorphism in estrogen receptor alpha gene with the risk of osteoarthritis: evidence based on 8,792 subjects.

Osteoarthritis (OA) is one of the most common skeletal disease, which seriously affects the quality of life of patients, particularly in the middle-aged and elderly individuals. We aimed to explore whether rs9340799 [estrogen receptor alpha (ER-α) XbaI A/G] polymorphism was associated with OA using a meta-analysis. A literature search for eligible studies published before March 28, 2014 was conducted in the PubMed, Web of Science, Embase, Cochrane database, Current Controlled Trials, Clinicaltrials.gov, Chinese Clinical Trial Registry, CBMdisc, CNKI, Google Scholar and Baidu Library. The association between the rs9340799 polymorphism and OA risk was assessed by odds ratios (ORs) together with their 95 % confidence intervals (CIs). A total of 663 articles were found. After article review and quality assessment, 10 articles involving 2,924 OA cases and 5,868 controls were included in the final meta-analysis. The combined evidence suggested that rs9340799 polymorphism contributed significantly to an increased risk of OA (for G allele vs. A allele: OR = 1.21, 95 % CI 1.03-1.43, p = 0.02; for G/G vs. A/A: OR = 1.30, 95 % CI 1.07-1.57, p = 0.009). In the subgroup analyses, significant associations were found between the rs9340799 polymorphism and the OA risk in the European group, Asian group, and knee osteoarthritis group, respectively. These results suggested that the rs9340799 polymorphism might be associated with the risk of OA. However, the results should be interpreted with caution because of the publication bias.

Association between intercellular adhesion molecule-1 gene K469E polymorphism and the risk of stroke in a Chinese population: a meta-analysis.

Several epidemiologic studies have evaluated the association between intercellular adhesion molecule-1 (ICAM-1) gene K469E polymorphism and stroke, but the results were inconsistent. The present meta-analysis was performed to investigate the relationship between K469E polymorphism and stroke in the Chinese population. A comprehensive search for related studies from the electronic databases of PubMed, Embase, Web of Science, CBMdisc and CNKI as well as a manual search of the references of identified articles was performed. Data were extracted to calculate for allelic, additive, dominant and recessive models using pooled odds ratios (ORs) along with 95% confidence intervals (CIs) by Review Manager 5.0 and Stata 11.0. Different effect models, subgroup analysis, sensitivity analysis, publication bias and power calculations were used to improve the comprehensive analysis. Finally, a total of 12 studies containing 1593 cases and 1555 controls were included in the final meta-analysis. No evidence of significant association between ICAM-1 gene K469E polymorphism and stroke was found in all four models (allelic model: OR = 1.07, 95%CI = 0.78-1.47; additive model: OR = 1.21, 95% CI = 0.67-2.16 (EE vs. KK); OR = 1.04, 95%CI = 0.75-1.45 (EK vs. KK); dominant model: OR = 1.07, 95% CI = 0.73-1.56; and recessive model: OR = 1.18, 95% CI = 0.77-1.83, respectively) based on the overall population, as well as subgroup analysis and sensitivity analysis. In conclusion, the present meta-analysis showed no evidence of significant association between ICAM-1 gene K469E polymorphism and stroke in the Chinese population. Nonetheless, this conclusion should be interpreted cautiously due to the low statistical power and considerable heterogeneity. Therefore, larger sample-size studies with homogeneous cases and well-matched controls are needed to further address this correlation.

ATP-binding cassette transporter 1 C69T and V825I polymorphisms in the development of atherosclerosis: a meta-analysis of 18,320 subjects.

INTRODUCTION: ATP-binding cassette transporter 1 (ABCA1), a member of the ATP-binding cassette family, plays a critical role in the development of atherosclerosis (AS). This meta-analysis was performed to assess the associations of ABCA1 C69T and V825I polymorphisms with AS susceptibility. MATERIALS AND METHODS: A comprehensive search was conducted to identify all eligible studies from PubMed, Embase, Web of Science, Cochrane database, CBMdisc, CNKI and Google Scholar. Additionally, hand searching of the references of identified articles was performed. All statistical analyses were done with Review Manager 5.1.4 and Stata 11.0. RESULTS: Eleven articles involving 14 studies were included in the final meta-analysis. For the ABCA1 C69T polymorphism, six studies involving 1854 AS cases and 5744 controls were combined showing significant association between this variant and AS risk (for T allele vs. C allele: OR =1.44, 95% CI =1.04-1.24, p =0.005; for T/T vs. C/C: OR =1.39, 95% CI =1.12-1.73, p =0.003; for T/T vs. C/T+C/C: OR =1.34, 95% CI =1.09-1.65, p =0.006; for T/T+C/T vs. C/C: OR =1.13, 95% CI =1.01-1.27, p =0.040). For the ABCA1 V825I polymorphism, eight studies involving 2026 AS cases and 8696 controls were combined. There was no significant association between the variant and AS risk (for I allele vs. V allele: OR =1.18, 95% CI =0.90-1.53, p =0.230; for I/I vs. V/V: OR =1.29, 95% CI =0.75-2.23, p =0.360; for I/I vs. V/I+V/V: OR =1.40, 95% CI =0.87-2.26, p =0.160; for I/I+V/I vs. V/V: OR =1.15, 95% CI =1.00-1.33, p =0.060). CONCLUSIONS: This meta-analysis suggested that the ABCA1 C69T polymorphism was associated with an increased AS risk. Furthermore, there was no significant association between the ABCA1 V825I polymorphism and AS risk.

A meta-analysis of the relationship between MTHFR gene A1298C polymorphism and the risk of adult stroke.

BACKGROUND: The association between methylenetetrahydrofolate reductase (MTHFR) gene A1298C polymorphism and adult stroke remains controversial. The present article was designed to clarify this relationship through pooled analysis of the numerous epidemiological studies focusing on this association. METHODS: We comprehensively searched all published papers in electronic database including PubMed, Embase, Web of Science, Chinese Biomedical Literature on disc (CBMdisc) and China National Knowledge Infrastructure (CNKI) up to 2013. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) for allelic (C allele vs. A allele), additive (CC vs. AA), dominant (CC+AC vs. AA), and recessive (CC vs. AA+AC) models were calculated. Subgroup and sensitivity analyses were performed to detect the heterogeneity and examine the reliability of results, respectively. Begg's funnel plots and Egger's regression test were used to assess the potential publication bias. RESULTS: A total of fifteen studies containing 2,361 cases and 2,653 controls were included in the final meta-analysis. The combined results of overall analysis showed that there was significant association between MTHFR gene A1298C polymorphism and adult stroke (allelic model: OR=1.36, 95% CI=1.11-1.67; additive model: OR=1.88, 95% CI=1.12-3.18; dominant model: OR=1.33, 95% CI=1.08-1.65 and recessive model: OR=1.77, 95% CI=1.07-2.94, respectively). On subgroup analysis by ethnicity of study population, significant association was shown in meta-analysis based on Asian population (allelic model: OR=1.40, 95% CI=1.19-1.65; additive model: OR=2.58, 95% CI=1.34-4.96; dominant model: OR=1.44, 95% CI=1.20-1.73 and recessive model: OR=2.12, 95% CI=1.20-3.76, respectively), but not in Caucasian population (allelic model: OR=1.30, 95% CI=0.93-1.82; additive model: OR=1.65, 95% CI=0.81-3.33; dominant model: OR=1.17, 95% CI=0.86-1.61 and recessive model: OR=1.70, 95% CI=0.83-3.50, respectively). In addition, the heterogeneity was effectively removed or decreased by limiting the included studies with population of Asian ethnicity. Furthermore, the corresponding pooled ORs were not materially changed in all genetic models of meta-analysis after limiting the included studies with population-based controls. However, except the recessive model, publication bias presented in the allelic, additive, dominant models identified by the Begg's funnel plots and Egger's regression test. CONCLUSIONS: In conclusion, the overall analysis suggests that MTHFR gene A1298C polymorphism plays an important role in the development of adult stroke. Genotype CC of MTHFR-1298A/C could increase the risk of stroke and may act as a predictor for clinical evaluation, especially in the Asian population. More studies with large-scale and different ethnicities are required to further confirm our findings.

Interleukin-10 gene -1082 G/A polymorphism in cervical cancer and cervical intraepithelial neoplasia: meta-analysis.

OBJECTIVES: To assess the association between polymorphism in the interleukin (IL)-10 promoter region of 1082 G/A and the risk of cervical cancer and/or cervical intraepithelial neoplasia (CIN), using meta-analysis. METHODS: The electronic literature databases PubMed®, Embase®, Web of Science, CBMdisc and CNKI were searched for relevant studies. The strength of association between IL-10 gene -1082 G/A polymorphism and cervical cancer and/or CIN was measured using pooled odds ratios with 95% confidence intervals in four genetic models: allelic model (A allele versus G allele); additive model (A/A versus G/G); recessive model (A/A versus G/A+G/G); dominant model (A/A+G/A versus G/G). RESULTS: Eight studies involving 1983 cases and 1618 controls were identified and included in the meta-analysis. No significant associations were found between IL-10 gene -1082 G/A polymorphism and cervical cancer and/or CIN in any of the genetic models. CONCLUSIONS: IL-10 gene -1082 G/A polymorphism does not appear to be associated with the risk of cervical cancer and/or CIN.