Search

IntroductionSeveral published results have established variations in respect to plasma/serum macrophage migration inhibitory factor (MIF) levels and gene polymorphisms with systemic lupus erythematosus (SLE). This study gave a more concise estimation on the MIF levels for SLE patients and established the association between MIF polymorphisms and SLE.Material and methodsAll articles were searched from PubMed, Embase, Web of Science, Wan-Fang, Chinese Biological Medical Literature, and China National Knowledge Infrastructure up to 6th October 2017, with no language restriction. Pooled standard mean difference with 95% confidence interval was evaluated using random effect model. Thirteen articles were used for this meta-analysis, with 620 SLE patients and 779 healthy controls assessed for MIF levels, and 2,159 SLE patients and 2,574 healthy controls considered for MIF-173 C/G and MIF-794 CATT polymorphisms.ResultsThere was a significant higher MIF levels in SLE patients than in healthy controls (p = 0.004). The subgroup analysis showed Asians and ages < 30 had higher MIF levels in SLE patients than in healthy controls. It was evident that patients with systemic lupus erythematosus diseases activity index scores < 8 and ≥ 8, and disease duration for both year < 5 and ≥ 5 of SLE had higher MIF levels when compared to healthy controls. We found a significant association between SLE and MIF-173 C/G, but not MIF-794 CATT.ConclusionsThis study provided evidence of significant higher MIF levels in SLE patients and supported the association of MIF-173 C/G and SLE. However, we were not able to establish an association between MIF-794 CATT and SLE.

This study was aimed at investigating the time course changes in left ventricular myocardial deformation using layer-specific strain echocardiography, which might provide insights into the cardiac pathophysiology of diabetes mellitus. A total of 36 New Zealand white rabbits were randomly divided into control (n = 18) and diabetes mellitus (DM, n = 18) groups. DM was induced in the DM group by intravenous injection of alloxan (ALX). Echocardiography was performed at 3, 6 and 9 mo to evaluate myocardial deformation. Layer-specific longitudinal and circumferential strains were assessed from the endocardium, mid-myocardium and epicardium by 2-D speckle-tracking echocardiography (STE). Three-layer longitudinal strain (LS) was calculated in the apical three-chamber view, and three-layer circumferential strain (CS) was observed in the short-axis view at the level of the papillary muscle. All rabbits were euthanized after echocardiography, and Masson staining was performed. Compared with the control group, LS and CS decreased gradually from the endocardium to the mid-myocardium to the epicardium. At 3 mo, no significant difference was observed between three-layer LS and three-layer CS (p > 0.05). At 6 mo, the LS of the endocardium (LSendo) and CS of the endocardium (CSendo) were lower in the DM group than in the control group (p > 0.05), whereas at 9 mo, all parameters, except LSendo and CSendo, had significantly decreased (p

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with complex genetic predisposing factors involved. PU.1 is an important member of the ETS transcription factors family which has diverse functions such as regulating the proliferation, differentiation of immune cells and multiple inflammatory cytokines. Previous studies preliminary explored the relation between PU.1 and SLE. To further explain the potential role of PU.1 in the pathogenesis of SLE, 40 SLE patients and 20 age-sex matched healthy controls (HC) were recruited in this study. Flow cytometry was used to test the percentages of CD4+PU.1+T cells in peripheral blood mononuclear cells (PBMCs) from patients with SLE and HC. Expression levels of PU.1 mRNA in CD4+T cells from SLE patients and HC were analyzed by real-time transcription-polymerase chain reaction. Expression levels of plasma IL-1β, IL-9, IL-18, IL-6, IFN-α, TNF-α, IL-10 and TGF-β1 were measured by enzyme-linked immunosorbent assay. The percentage of CD4+PU.1+T cells in PBMCs from patients with SLE was significantly higher than that from HC (P 0.05). Associations of PU.1 mRNA expression in CD4+T cells with major clinical and laboratory parameters of SLE patients were also analyzed, but no significant correlations were found. Consistent with previous studies, SLE patients had increased IL-1β, IL-18, IL-6, IFN-α, TNF-α and IL-10 plasma concentrations than HC (P

Background CCN1 plays a crucial role in the modulation of cardiovascular diseases. However, whether CCN1 genetic variants are involved in the susceptibility of ACS remains unknown. Hence, the present study investigates the association between CCN1 polymorphisms and ACS among Han and Uygur populations in Xinjiang, China. Results In this case-control study, 1234 Han (547 ACS patients and 687 controls) and 932 Uygur (471 ACS patients and 461 controls) were genotyped using SNPscanTM for three single-nucleotide polymorphisms (SNPs, rs6576776, rs954353, and rs3753794) of the human CCN1 gene. In the Uygur population, we found that the detected frequencies of the C allele (25.3% vs. 18.3%, PP=0.001) of rs6576776 were significantly higher in the ACS patients than in the control participants. Differences in rs6576776 regarding the dominant model (CC+CG vs. GG, 44.2% vs. 55.8%, P=0.001) and the recessive model (CC vs. CG+GG, 6.4% vs. 93.6%, P=0.016) were observed between the two groups. The frequencies of the GGC and AGC haplotypes in those with ACS were significantly higher than those in the control group (all PP=0.003). In Han population, neither the distribution of genotypes and alleles of the CCN1 gene three SNPs nor the distribution of haplotypes constructed with the three SNPs exhibited a significant difference between the ACS patients and control participants. Conclusions Our study document that the CCN1 gene rs6576776 C allele is associated with higher susceptibility of ACS and that the frequencies of GGC and AGC haplotypes are higher among the Uygur ACS patients.

Dyslipidemia is one of the main risk factors for coronary heart disease (CHD). The E3 ubiquitin ligase which is encoded by the ring finger protein 145 (RNF145) gene is very important in the mediation of cholesterol synthesis and effectively treats hypercholesterolemia. Thus, the purpose of the present research is to investigate the connection between the polymorphism of the RNF145 gene and cholesterol levels in the populations in Xinjiang, China. A total of 1396 participants (Male: 628, Female: 768) were included in this study for genetic analysis of RNF145 gene, and we used the modified multiple connection detection response (iMLDR) technology to label two SNPs (rs17056583, rs12188266) of RNF145 genotyping. The relationship between the genotypes and the lipid profiles was analyzed with general linear model analysis after adjusting confounding variables. Through the analysis of the two SNPs in RNF145 gene, we discovered that both rs17056583 and rs12188266 were related to total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) concentrations (All P

Myocardial infarction (MI), the leading cause of mortality and disability worldwide, is a disease in which multiple environmental and genetic factors are involved. Recently, researches suggested that insertion/deletion (ins/del) variation of NFKB1 gene rs28362491 is a functional polymorphism. In the present study, we aimed to explore the relation between variation of NFKB1 gene rs28362491 and MI by polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP) in 359 MI patients and 1085 control participants. Gensini score was used to evaluate the degree of coronary artery stenosis in MI patients. The plasma levels of interleukin-6 (IL-6), IL-8, malonaldehyde (MDA) and superoxide dismutase (SOD) were randomly measured by ELISA both in MI patients and control participants. We found that the detected frequencies of D allele (41.2% vs. 36.4%, P = 0.021) and DD genotype (17.5% vs. 12.0%, P = 0.022) were significantly higher in MI patients than in control participants. Compared with II or ID genotype carriers, the Gensini score in MI patients with DD genotype was 32–43% higher (both P P = 0.001 vs. II or ID genotype). Of note, IL-6 levels in MI patients carrying DD genotype were significantly higher than that in control participants and other genotype carriers in MI patients (both P NFKB1 gene rs28362491 DD genotype was associated with a higher risk of MI and more severe coronary artery lesion, which also had a potential influence on the level of inflammatory cytokine IL-6.

Background Molecular subtyping of triple-negative breast cancers (TNBCs) via gene expression profiling is essential for understanding the molecular essence of this heterogeneous disease and for guiding individualized treatment. We aim to devise a clinically practical method based on immunohistochemistry (IHC) for the molecular subtyping of TNBCs. Materials and methods By analyzing the RNA sequencing data on TNBCs from Fudan University Shanghai Cancer Center (FUSCC) (n = 360) and The Cancer Genome Atlas data set (n = 158), we determined markers that can identify specific molecular subtypes. We performed immunohistochemical staining on tumor sections of 210 TNBCs from FUSCC, established an IHC-based classifier, and applied it to another two cohorts (n = 183 and 214). Results We selected androgen receptor (AR), CD8, FOXC1, and DCLK1 as immunohistochemical markers and classified TNBCs into five subtypes based on the staining results: (a) IHC-based luminal androgen receptor (IHC-LAR; AR-positive [+]), (b) IHC-based immunomodulatory (IHC-IM; AR-negative [-], CD8+), (c) IHC-based basal-like immune-suppressed (IHC-BLIS; AR-, CD8-, FOXC1+), (d) IHC-based mesenchymal (IHC-MES; AR-, CD8-, FOXC1-, DCLK1+), and (e) IHC-based unclassifiable (AR-, CD8-, FOXC1-, DCLK1-). The κ statistic indicated substantial agreement between the IHC-based classification and mRNA-based classification. Multivariate survival analysis suggested that our IHC-based classification was an independent prognostic factor for relapse-free survival. Transcriptomic data and pathological observations implied potential treatment strategies for different subtypes. The IHC-LAR subtype showed relative activation of HER2 pathway. The IHC-IM subtype tended to exhibit an immune-inflamed phenotype characterized by the infiltration of CD8+ T cells into tumor parenchyma. The IHC-BLIS subtype showed high expression of a VEGF signature. The IHC-MES subtype displayed activation of JAK/STAT3 signaling pathway. Conclusion We developed an IHC-based approach to classify TNBCs into molecular subtypes. This IHC-based classification can provide additional information for prognostic evaluation. It allows for subgrouping of TNBC patients in clinical trials and evaluating the efficacy of targeted therapies within certain subtypes. Implications for practice An immunohistochemistry (IHC)-based classification approach was developed for triple-negative breast cancer (TNBC), which exhibited substantial agreement with the mRNA expression-based classification. This IHC-based classification (a) allows for subgrouping of TNBC patients in large clinical trials and evaluating the efficacy of targeted therapies within certain subtypes, (b) will contribute to the practical application of subtype-specific treatment for patients with TNBC, and (c) can provide additional information beyond traditional prognostic factors in relapse prediction.

Primary Sjögren's syndrome (pSS) has been related to a higher risk of comorbidities, but studies examining comorbidities among patients with and without extraglandular manifestations are limited. The objectives of this study were to assess the prevalence of comorbidities in Chinese pSS patients and to determine the relationship between comorbidities and extraglandular manifestations.This cross-sectional study was based on the multicenter pSS registry established by the Chinese Rheumatism Data Center. Patients fulfilling the 2002 American-European criteria or the 2016 classification criteria for pSS were enrolled from May 2016 to December 2018. Demographic data, disease characteristics, comorbidities (cardiovascular disease, thyroid disorder, malignancy, and fragility fracture), and extraglandular manifestations were collected. Multivariate analyses were used to assess the relationships between comorbidities and extraglandular manifestations.A total of 4087 pSS patients were included (95.7% female and mean age of 51.2 ± 13.1 years). The baseline prevalence of comorbidities was 3.8% for cardiovascular diseases, 12.1% for thyroid disorders, 1.8% for malignancies, and 1.7% for fragility fractures. The presence of extraglandular manifestations was associated with more comorbidities. Patients with more than one extraglandular manifestation had a higher prevalence of cardiovascular disease (adjusted odds ratio [aOR] 2.004, 95% confidence interval [CI] 1.221-3.288), thyroid disorder (aOR 1.380, 95% CI 1.022-1.863), and fragility fracture (aOR 2.684, 95% CI 1.505-4.786) after adjustment for age, sex, disease duration, and the significant variables in the univariate analysis.The presence of extraglandular manifestations in pSS was associated with an increased comorbidity burden, especially cardiovascular disease, thyroid disorder, and fragility fracture. Key Points • This is the first study assessing the association between extraglandular manifestations and comorbidity burden based on the largest pSS registry in China. • Patients with multiple extraglandular manifestations tend to have increased comorbid cardiovascular disease, thyroid disorder, and fragility fracture.

Published studies have shown contradictory results in the association of serum/plasma levels of homocysteine (HCY) with systemic lupus erythematosus (SLE). This study is to systematically evaluate the association of serum/plasma HCY levels in SLE. A search was done using PubMed, Embase, Web of Science, and ScienceDirect databases up to 7 April 2019. Thirty-six articles including 2919 SLE patients and 3120 healthy controls were finally included in this meta-analysis. The HCY levels were significantly higher in SLE patients than in healthy controls (P 0.001). The subgroup analysis revealed that Asian, African, Arab, Mixed, White and others as well as ages ( 35 and ≥ 35) had significant higher HCY levels in SLE patients than in the healthy controls. The study indicated that patients with disease activity index scores 8 (P 0.001) and ≥ 8 (P = 0.003) of SLE had significant higher HCY levels as compared with the healthy controls. It was also revealed that disease duration in SLE patients for 10 and ≥ 10 years (P 0.001) had significant higher HCY levels as compared with the healthy controls. A significant higher HCY level for body mass index ( 23 and ≥ 23) was found as well as measurement type in SLE patients than healthy controls. This meta-analysis demonstrated higher HCY levels in patients with SLE than healthy controls, suggesting a possible role of HCY in the disease.Key Points• Homocysteine (HCY) is closely related to the mechanisms of systemic lupus erythematosus (SLE).• This study reveals a significant correlation between HCY levels and the various indexes of disease activity.• This study reveals that medication may influence HCY levels in SLE.• This study also discovers that the subgroup analysis of all the factors influences the HCY levels in SLE patients.

We investigated whether increased expression of activated mitogen-activated protein kinase (MAPK) kinases 1 (MEK1) restores ischemic post-conditioning (IPostC) protection in hypertrophic myocardium following ischemia/reperfusion (I/R) injury. C57Bl/6 mice received recombinant adeno-associated virus type 9 (rAAV9)-mediated activated MEK1 gene delivery systemically, then following the induction of cardiac hypertrophy via transverse aortic constriction for 4 weeks. In a Langendorff model, hypertrophic hearts were subjected to 40 min/60 min I/R or with IPostC intervention consisting of 6 cycles of 10 s reperfusion and 10 s no-flow before a 60-min reperfusion. Hemodynamics, infarct size (IS), myocyte apoptosis and changes in expression of reperfusion injury salvage kinase (RISK) pathway were examined. rAAV9-MEK1 gene delivery led to a 4.3-fold and 2.7-fold increase in MEK1 mRNA and protein expression in the heart versus their control values. I/R resulted in a larger IS in hypertrophic than in non-hypertrophic hearts (52.3 ± 4.7% vs. 40.0 ± 2.5%, P

Macrophage migration inhibitory factor (MIF) has been recognized as a major player in the pathogenesis of atherosclerosis. This study determined the association between polymorphisms of MIF gene and acute coronary syndrome (ACS). The polymorphism of MIF gene (rs755622, rs1007888 and rs2096525) was analyzed in 1153 healthy controls and 699 ACS cases in Chinese Han population. Plasma MIF level was also measured in part of ACS patients (139/19.9%) and healthy controls (129/11.2%) randomly. Most participants including healthy controls and ACS patients carried rs755622 GG (63.1% vs. 56.7%) and CG genotypes (33.1% vs. 38.9%) and G allele of rs755622 (79.6% vs. 76.1%, respectively), while CC genotype (3.8% vs. 4.4%) and C allele (20.4% vs. 23.9%) carriers were the lowest. Multivariate logistic regression analysis showed that carriers with rs755622 C allele had a higher risk of ACS compared to other genotypes (AOR = 1.278, 95% CI: 1.042–1.567). In addition, CC genotype carriers had the highest plasma levels of MIF than other genotype carriers. The MIF level in ACS patients with CC genotype was significantly higher than ACS patients carrying GG genotype and healthy controls carrying 3 different genotypes of MIF gene rs755622. Our findings indicate that MIF gene rs755622 variant C allele is associated with increased risk of ACS. Identification of this MIF gene polymorphism may help for predicting the risk of ACS.

Background This study was designed to investigate whether differential DNA methylationin of cholesterol absorption candidate genes can function as a biomarker for patients with coronary heart disease (CHD). Methods DNA methylation levels of the candidate genes FLOT1, FLOT2 and SOAT1 were measured in peripheral blood leukocytes (PBLs) from 99 patients diagnosed with CHD and 89 control subjects without CHD. A total of 110 CPG sites around promoter regions of them were examined. Results Compared with groups without CHD, patients with CHD had lower methylation levels of SOAT1 (PP = 0.005). After adjustment of other confounders, methylation levels of SOAT1 were still associated with CHD (P = 0.001, OR = 0.290, 95% CI: 0.150–0.561). Conclusions SOAT1 methylation may be associated with development of CHD. Patients with lower methylation levels in SOAT1 may have increased risks for CHD. Further studies on the specific mechanisms of this relationship are necessary.

Abnormal vitamin D metabolism is involved in the pathogenesis of rheumatoid arthritis (RA). In this study, we evaluated the association of single nucleotide polymorphisms (SNPs) and methylation levels in vitamin D metabolic pathway genes with RA susceptibility. Ten SNPs in vitamin D metabolic pathway genes (CYP2R1, CYP24A1, VDR, CYP27B1) were genotyped in 477 RA patients and 496 controls by improved multiple ligase detection reaction (iMLDR). The methylation levels of the promoter regions of these genes were detected in 122 RA patients and 123 controls using Illumina Hiseq platform. We found that the CYP2R1 rs1993116 GA genotype, CYP27B1 rs4646536 GA genotype, rs4646536 A allele frequencies were significantly increased in RA patients when compared to controls. The decreased risk of rs1993116, rs4646536 was found under the dominant mode in RA patients. However, no significant association was found between CYP2R1 rs7936142, rs12794714, CYP24A1 rs2762934, rs6068816, rs2296239, rs2296241, VDR rs11574129, rs3847987 polymorphism, and RA susceptibility. The VDR, CYP27B1 methylation levels in RA patients were significantly lower than those in controls, while CYP2R1, CYP24A1 methylation levels were not associated with RA. There were no statistical associations between CYP2R1, CYP24A1, VDR, CYP27B1 methylation levels and their respective genotype in RA patients. In addition, plasma 25OHD level in RA patients was significantly lower than that in healthy controls. In summary, our results showed that CYP2R1, CYP27B1 genetic variations were associated with the genetic background of RA, while altered VDR, CYP27B1 methylation levels were related to the risk of RA.

Background FBXW7 gene expression is positively correlated with glycolipid metabolism and is associated with diabetes in animal models. In the current study, we focused on exploring whether genetic variants of the FBXW7 gene were associated with type 2 diabetes (T2DM) and the risk factors for T2DM in Uygur people in Xinjiang, China. Methods A total of 2164 Chinese Uygur subjects (673 T2DM patients and 1491 controls) were recruited for our case–control study, and four SNPs (rs10033601, rs2255137, rs2292743 and rs35311955) of the FBXW7 gene were genotyped using the improved multiplex ligation detection reaction (iMLDR) technique. Results Our study showed that the genotypes using the overdominant model (GA vs AA + GG) of rs10033601 and using the overdominant model (TA vs TT + AA) of rs2292743 were significantly different between T2DM patients and the controls (P = 0.005 and P = 0.012, respectively). After multivariate adjustments for confounders, the rs10033601 and rs2292743 SNPs were still independent risk factors for T2DM [GA vs AA + GG: odds ratio = 1.35, 95% confidence interval (CI) = 1.12–1.64, P = 0.002; TA vs TT + AA: OR = 1.28, 95% CI = 1.06–1.55, P = 0.011]. Participants within the Chinese Uygur populations and who with the GA genotype of rs10033601 and the TA genotype of rs2292743 were associated with significantly elevated glucose levels. Conclusions Our study revealed that both rs10033601 and rs2292743 of the FBXW7 gene were associated with T2DM in the Uygur populations in Xinjiang.

Background: Obesity is an independent risk factor for cardiovascular disease. We investigated whether and to what extent visceral obesity-related indices were associated with coronary collateralization (CC) in chronic total occlusion (CTO) patients.Methods: This retrospective cohort study involved 1,008 consecutive patients with CTO who underwent CTO-percutaneous coronary artery intervention (PCI). CC was graded according to the Rentrop scoring system. Data on demographic and clinical characteristics were collected by cardiovascular doctors. Logistic regression, receiver operating characteristic (ROC) curve and Kaplan-Meier analyses were performed to assess the predictive value of visceral obesity-related indices for CC.Results: Overall, 1,008 inpatients were assigned to the poor CC group (n = 592) and good CC group (n = 416). In multivariate-adjusted logistic regression analyses, all visceral obesity-related indices (P-value < 0.001) were significantly associated with CC. After ROC analysis and the Delong test, the Chinese visceral adiposity index (CVAI) had the largest area under the curve (AUC) of 0.741 (0.711–0.771). Further analysis revealed that CVAI quartile remained a risk factor for poor CC in all groups, CVAI was associated with a 1.018-fold higher risk of poor CC (OR = 1.018, 95% CI: 1.014–1.021, P < 0.001). Individuals in the top CVAI quartile group had the highest risk of poor CC (OR = 10.657, 95% CI: 6.492–17.493, P < 0.001). Subgroup analyses showed similar results, and CVAI quartile remained a risk factor for poor CC. Moreover, increased CVAI predicted poor prognosis in CTO patients.Conclusion: In summary, this study indicated that all the increased visceral obesity-related indices were significantly associated with increased poor CC risk. After adjusting for potential risks, CVAI had the best performance for estimating CC and predicting prognosis in CTO patients.

Aims A number of studies have attempted to demonstrate the benefits associated with personalized antiplatelet therapy guided by platelet function testing, which has led to disappointing findings. In this study, we used a new platelet function test to guide antiplatelet therapy in stable coronary artery disease (CAD) patients after percutaneous coronary intervention (PCI). Methods and results In the present randomized controlled trial, a total of 2237 patients with stable CAD undergoing PCI were randomly chosen to be administered personalized antiplatelet therapy (personalized group; n = 1123) or standard antiplatelet treatment (standard group; n = 1114). The patients in the standard therapy group, without detecting the platelet aggregation rate, were administered a 75 mg/day clopidogrel maintenance dosage plus 100 mg/day of aspirin for at least 6 months after the procedure. For the patients in the personalized therapy group, the antiplatelet strategy was performed according to the maximum aggregation rate (MAR), determined using a novel platelet analyser, PL-12. If MAR > 55%, 90 mg ticagrelor was administered twice daily plus 100 mg/day of aspirin after PCI. If MAR ≤55%, 75 mg/day clopidogrel plus 100 mg/day of aspirin was administered after PCI. The primary endpoint was net clinical adverse events, which were a composite of cardiac death, myocardial infarction, stroke, stent thrombosis, urgent revascularization, and bleeding [Bleeding Academic Research Consortium (BARC) definitions, Type 2, 3, or 5], in the 180-day period after randomization. The primary endpoint was reached in 58 patients in the personalized group, compared with 85 patients in the standard group [5.1% vs. 7.5%, hazard ratio (HR) 0.678, 95% confidence interval (CI) 0.486–0.947, P = 0.023], on intention-to-treat analysis. We also found that the net clinical adverse events (including ischaemic and bleeding events) were significantly reduced in the personalized group at 30 days after PCI compared to the standard group (1.5% vs. 3.0%, HR 0.510, 95% CI 0.284–0.915, P = 0.020). We did not find a significant difference in major bleeding events at either the 30-day (0.5% vs. 0.3%, P = 0.322) or the 180-day follow-up (2.1% vs. 1.6%, P = 0.364) between the two groups. Conclusion The present study suggests that personalized antiplatelet therapy according to MAR can significantly improve the net clinical benefit 180 days after PCI.

The purpose of the study was to assess the value of admission macrophage migration inhibitory factor (MIF) levels in predicting clinical outcomes in ST-elevation myocardial infarction (STEMI) patients.For this study we recruited 498 STEMI patients after they received percutaneous coronary intervention (PCI), 40 with stable angina pectoris and 137 healthy participants. Plasma MIF levels were measured at admission and after PCI. The primary end points were in-hospital mortality and major adverse cardio-and/or cerebrovascular events (MACCE) during hospitalization and 3.2-year follow-up period.Admission MIF levels were elevated in 88.4% of STEMI patients over the upper reference limit of healthy controls and it was 3- to 7-fold higher than that in stable angina pectoris and control groups (122 ± 61 vs 39 ± 19 vs 17 ± 8 ng/mL; P0.001). Admission MIF levels were significantly higher in patients who died after myocardial infarction vs survivors. For predicting in-hospital mortality using the optimal cutoff value (127.8 ng/mL) of MIF, the area under the receiver operating characteristic curve for MIF was 0.820, similar area under the receiver operating characteristic curve values for predicting short-term outcomes were observed for high-sensitivity troponin T, CK-MB, N-terminal probrain natriuretic peptide, and Global Registry of Acute Coronary Events (GRACE) score. Although peak high-sensitivity troponin T and N-terminal probrain natriuretic peptide also predicted MACCE during the follow-up period, only higher admission MIF levels predicted in-hospital mortality and MACCE during the 3.2-year follow-up. Multivariate regression analysis showed the independent predictive value of a higher admission MIF level (≥ 127.8 ng/mL) on in-hospital mortality (odds ratio, 9.1; 95% confidence interval, 1.7-47.2) and 3.2-year MACCE (hazard ratio, 2.8; 95% confidence interval, 1.5-5.6).A higher admission MIF level is an independent predictor for in-hospital mortality and long-term MACCE in STEMI patients who underwent PCI.

BACKGROUND: Early myocardial reperfusion therapy (< 12 h) in patients with acute myocardial infarction (AMI) can significantly improve their prognosis. However, the effect of late reperfusion (> 12 h) remains controversial. In this study, the effects of late reperfusion versus standard drug therapy on the outcomes of patients with AMI were evaluated by systematic review and meta-analysis. METHODS: PubMed, Embase, Medline, Cochrane, Wanfang, and CNKI databases were searched for eligible studies for the present study. Meta-analysis was performed using RevMan 5.3.3 software. Relative risk (RR) and the 95% confidence interval (CI) were used to compare the outcomes between the two groups. The main outcome measures were major adverse cardiac events (MACEs), all-cause mortality, recurrent myocardial infarction (MI), and heart failure. RESULTS: Eighteen studies were identified including 14,677 patients, of whom 5157 received late reperfusion with percutaneous coronary intervention (PCI) and 9520 received medication therapy (MT). Compared to MT, late PCI was associated with decreased all-cause mortality (RR 0.60, 95% CI 0.44–0.83; p = 0.002), MACEs (RR 0.67; 95% CI 0.50–0.89; p < 0.001), and heart failure (RR 0.76; 95% CI 0.60–0.97; p = 0.03), while there was also a trend toward decreased recurrent MI (RR 0.70; 95% CI 0.47–1.05; p = 0.08). However, subgroup analysis according to time to PCI showed that the clinical benefit was only from PCI after 12 h but not from 2 to 60 days of the onset of symptoms. CONCLUSIONS: The present meta-analysis suggested that PCI performed > 12 h but not 2–60 days after AMI is associated with significant improvement in clinical outcomes. However, these results need further rigorously designed large sample size clinical trials to be validated.

Aim: To understand age- and gender-related differences and secular trends in coronary artery disease (CAD) lipid profiles and the characteristic of dyslipidemia in western China. Methods: An age-matched case-control study, including 2400 patients and 1200 controls was performed. All blood lipid tests evaluated from January 2012 to January 2015 at First Affiliated Hospital of Xinjiang Medical University were analyzed. Details of the gender and age of the patients were available. Trends were calculated using linear regression and Mantel-Haenszel X2 analyses. Results: We determined the associations among total cholesterol (TC), triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A-1 (apoA-1), apolipoprotein B (apoB), nonhigh-density lipoprotein cholesterol (non-HDL-C), and high-density lipoprotein cholesterol (HDL-C) with CAD for different ages and gender. Except for patients who were

Background. Gamma-glutamyl transferase (GGT) has been detected in coronary plaques. However, the association between serum GGT levels and coronary atherosclerotic plaque vulnerability in patients with coronary artery disease (CAD) as detected by optical coherence tomography (OCT) has not been investigated.Methods. We performed a retrospective study of consecutively enrolled CAD patients undergoing preintervention OCT examination during coronary angiography. Plaque vulnerability was defined as the presence of ruptured plaques or thin-cap fibroatheroma (TCFA) upon OCT. The association between serum GGT levels and coronary plaque vulnerability was evaluated using multivariate logistic regression analysis.Results. A total of 142 patients were included in our analysis. OCT examination detected ruptured plaques in 16 patients, nonruptured plaques with TCFA in 17 patients, and nonruptured plaques and non-TCFA in 109 patients. Univariate analyses showed that gender, diabetes, Apolipoprotein A1 (ApoA1) and high-density lipoprotein cholesterol (HDL-c), and diagnosis of acute coronary syndrome (ACS) were associated with plaque vulnerability (P all < 0.05). Patients grouped according to serum GGT tertiles did not differ statistically in baseline characteristics or OCT findings. Results of multivariate logistic analyses showed that diabetes and diagnosis of ACS were associated with plaque rupture and TCFA (P < 0.05).Conclusions. GGT serum levels were not associated with OCT detected coronary vulnerability in our cohort of CAD patient.

BACKGROUND Prolactin (PRL), an inflammatory hormone with cytokine properties, has long been proposed to play a crucial role in the pathogenesis of autoimmune disorders, including rheumatoid arthritis (RA). However, the circulating levels of PRL in RA were discordant among published studies. METHODS PubMed, Embase, and The Cochrane Library database were systematically searched from inception up to 30 June 2018. The available studies were obtained from the initial search in accordance with the rigorous inclusion and exclusion criteria. Relevant data from the included literatures were extracted. Methodological quality was evaluated in order to refine the final search results. All statistical analyses were conducted using software STATA version 12.0. RESULTS Of 698 articles were yielded for eligibility, a finally analysis involving 628 RA cases and 430 controls from 14 published studies were included. When compared to healthy controls, there was a significantly higher level of circulating PRL in patients with RA with a pooled SMD of 1.08 (95% CI = 0.41 to 1.74, P

The aim of this study was to investigate the B cell-associated transcription factors, Ets-1 and microRNA, miR-326 in systemic lupus erythematosus (SLE) patients, and their correlation with the pathogenesis of SLE. A total of 44 SLE patients and 20 healthy controls were enrolled in this research, all patients fulfilled the American College of Rheumatology classification criteria for SLE. The mRNA expression of Ets-1 and miR-326 in CD19+B cells from SLE patients were examined by qRT-PCR. The percentages of CD19+CD138+plasma cells were analyzed by Flow cytometry. We found decreased expression of Ets-1 mRNA in SLE patients compared with the healthy controls ([0.228 (0.145, 0.507)] vs [0.583 (0.452, 0.763)], p = 0.001),while increased expression of miR-326 mRNA in CD19+B cells SLE patients compared with the healthy controls([1.092 (0.457, 2.855)] vs [0.685 (0.274, 0.819)], p = 0.008). The percentage of CD19+CD138+plasma cells in SLE patients was higher than that of healthy controls (0.55 ± 0.21% vs 0.36 ± 0.21%, p = 0.002). Moreover, a negative correlation between expression of Ets-1 mRNA and miR-326 mRNA in CD19+B cells was detected (r = − 0.334, p = 0.027). A significant association between the occurrences of CD19+CD138+plasma cells and the levels of Ets-1 mRNA and miR-326 mRNA was observed (r = − 0.417, p = 0.005 and r = 0.482, p = 0.001, respectively). Our results suggest that miR-326 might promote B cells differentiation by targeting Ets-1, a negative regulator of B cells differentiation and therefore participate in the pathogenesis of SLE.

Background: Coronary artery disease (CAD) is the most common cause of left ventricular dysfunction (LVD). Confl icting evidence exists with regards to available treatments and patient prognosis. Revascularization may improve ventricular function while coronary artery bypass surgery (CABG) has signifi cantly improved survival. The effectiveness of percutaneous coronary intervention (PCI) has also not been thoroughly investigated to date.

Macrophage migration inhibitory factor (MIF) is an essential mediator of atherosclerotic plaque progression and instability leading to intracoronary thrombosis, therefore contributing to coronary artery disease (CAD). In this study, we investigated the relationship between MIF gene polymorphism and CAD in Chinese Han population. Three single nucleotide polymorphisms (SNP, rs755622, rs1007888 and rs2096525) of MIF gene were genotyped by TaqMan genotyping assay in 1120 control participants and 1176 CAD patients. Coronary angiography was performed in all CAD patients and Gensini score was used to assess the severity of coronary artery lesions. The plasma levels of MIF and other inflammatory mediators were measured by ELISA. The CAD patients had a higher frequency of CC genotype and C allele of rs755622 compared with that in control subjects (CC genotype: 6.5% vs. 3.9%, P = 0.008, C allele: 24.0% vs. 20.6%, P = 0.005). The rs755622 CC genotype was associated with an increased risk of CAD (OR: 1.804, 95%CI: 1.221–2.664, P = 0.003). CAD patients with a variation of rs755622 CC genotype had significantly higher Gensini score compared with patients with GG or CG genotype (all P P MIF gene rs755622 variation and CAD in Chinese Han population. Individuals who carrying MIF gene rs755622 CC genotype were more susceptible to CAD and had more severe coronary artery lesion. This variation also had a potential influence in circulating MIF levels.

BACKGROUND: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been recognized as a major player in the pathogenesis of coronary artery disease (CAD). The aim of the study was to determine the association between polymorphisms of the MALAT1 gene and acute coronary syndrome (ACS) in a Chinese population in Xinjiang. METHODS: In the case-control study, we genotyped three nucleotide polymorphisms (rs3200401, rs4102217, rs600231) of the MALAT1 gene using SNPscan(TM) typing assays (1,053 controls and 929 ACS patients). Furthermore, we explored a predictive model using MALAT1 rs600231 and clinical variables to predict the risk of ACS. Finally, the relative expression of long noncoding RNA (lncRNA) MALAT1 was also measured in 92 ACS patients and 92 controls using quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: The prevalence of the GG genotype of rs600231 in ACS group was higher than that in control group (15.7% vs. 14.7%, P=0.048). The dominant model differed (AG + GG vs. AA) and the G allele of rs600231 in ACS group was higher than that in control group (for dominant model: 66.2% vs. 60.9%, P=0.014; for allele: 41.0% vs. 37.8%, P=0.042). Multivariate logistic regression analysis and the predictive nomogram model showed that the dominant model of rs600231 remained an independent risk factor for ACS [odds ratio (OR) =1.32, 95% confidence interval (CI): 1.07–1.63, P=0.009]. The area under the receiver operating characteristic (ROC) curve (AUC) for the nomogram model for the prediction of ACS was 0.738 (95% CI: 0.716–0.761). In addition, in the AG and GG phenotypes, the relative expression of lncRNA MALAT1 was significantly higher in ACS patients than in controls with the same phenotypes (P

Background Coronary artery disease (CAD) is the leading cause of death worldwide. In this study, we aimed to explore whether some genetic variants of the human IDOL gene were associated with CAD among Chinese population in Xinjiang. Methods We designed two independent case–control studies. The first one included in the Han population (448 CAD patients and 343 controls), and the second one is the Uygur population (304 CAD patients and 318 controls). We genotyped three SNPs (rs2072783, rs2205796, and rs909562) of the IDOL gene. Results Our results revealed that, in the Han female subjects, for rs2205796, the distribution of alleles, dominant model (TT vs. GG + GT) and the additive model (GG + TT vs. GT) showed significant differences between CAD patients and the control subjects (P = 0.048, P = 0.014, and P = 0.032, respectively). Conclusions The rs2205796 polymorphism of the IDOL gene is associated with CAD in the Chinese Han female population in Xinjiang, China.

Objective To evaluate the efficacy and safety of SHR4640, a highly selective urate transporter 1 inhibitor, in Chinese subjects with hyperuricaemia. Methods This was a randomized double-blind dose-ranging phase II study. Subjects whose serum uric acid (sUA) levels were ≥480 µmol/l with gout, ≥480 µmol/l without gout but with comorbidities, or ≥540 µmol/l were enrolled. Subjects were randomly assigned (1:1:1:1:1) to receive once daily 2.5 mg, 5 mg, 10 mg of SHR4640, 50 mg of benzbromarone or placebo, respectively. The primary end point was the proportion of subjects who achieved target sUA level of ≤360 µmol/l at week 5. Results 99.5% of subjects (n = 197) were male and 95.9% of subjects had gout history. The proportions of subjects who achieved target sUA at week 5 were 32.5%, 72.5% and 61.5% in the 5 mg, 10 mg SHR4640 and benzbromarone groups, respectively, significantly higher than the placebo group (0%; P Conclusions The present study indicated a superior sUA-lowering effect and well tolerated safety profile after 5-week treatment with once-daily 5 mg/10 mg of SHR4640 as compared with placebo in Chinese subjects with hyperuricaemia. Trial registration ClinicalTrials.gov number, NCT03185793

Background HMGCR, SCAP, SREBF1, SREBF2 and TBL2 are well-known genes that are involved in the process of lipid metabolism. However, it is not known whether epigenetic changes of these genes are associated with lipid metabolism. In this study, the methylation levels of the HMGCR, SCAP, SREBF1, SREBF2 and TBL2 genes were analyzed between samples from a hyper-low-density lipoprotein cholesterolemia (hyper-LDL) group and a control group to examine the association between the methylation levels of these genes and the risk of hyper-LDL. Methods In this study, a case-control approach was used to explore the association between DNA methylation and hyper-LDL. The DNA methylation levels of HMGCR, SCAP, SREBF1, SREBF2 and TBL2 genes and 231 CpG sites in the promoter regions of these genes were measured in 98 hyper-LDL participants and 89 participants without hypo-LDL. Results Compared with participants without hyper-LDL, patients with hyper-LDL TBL2 gene had lower methylation levels (11.93 vs. 12.02, P = 0.004). The methylation haplotypes with significant abundance in the TBL2 gene are tcttttttttt (P = 0.034), ctttttttcct (P = 0.025), ctctttctttt (P = 0.040), ccttttttttt (P = 0.028), and tctttttttttttttt. Conclusion The study demonstrates that participants with hyper-LDL have lower methylation of TBL2. The results suggest that DNA methylation of TBL2 can decrease the risk for hyper-LDL in humans.

Hyperlipidemia is one of the main risk factors for coronary artery disease (CAD). In the present study, we aimed to explore whether the single-nucleotide polymorphisms (SNPs) in amyloid precursor-like protein (APLP) 2 (APLP2) gene were associated with high lipid levels in Chinese population in Xinjiang, China. We recruited 1738 subjects (1187 men, 551 women) from the First Affiliated Hospital of Xinjiang Medical University, and genotyped three SNPs (rs2054247, rs3740881 and rs747180) of APLP2 gene in all subjects by using the improved multiplex ligation detection reaction (iMLDR) method. Our study revealed that the rs2054247 SNP was associated with serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) levels, and high-density lipoprotein cholesterol (HDL-C) in additive model (all P

Background Coronary artery disease (CAD) remains one of the major causes of death in humans. Genetic testing may allow early detection and prevention of this disease. This study aimed to investigate the association between the macrophage migration inhibitory factor (MIF) -173G/C (rs755622) polymorphism and susceptibility to CAD based on a meta-analysis. Methods We searched several databases to identify observational case-control studies investigating the association between the MIF -173G > C (rs755622) polymorphism and CAD risk published before July 30, 2019. Data were analyzed using the STATA software. Results Six studies, comprising a total of 1172 CAD cases and 1564 controls evaluated for MIF polymorphisms, were included. The occurrence of CAD was found to be associated with the C allele of the MIF rs755622 SNP in the total population (C/G, OR = 1.489, 95% CI = 1.223–1.813). Further, MIF –173G/C polymorphism was significantly associated with CAD under the allelic model in the Asian (C/G, OR = 1.775, 95% CI = 1.365–2.309) and Caucasian (C/G, OR = 1.288, 95% CI 1.003–1.654) subgroups. The data showed that the risk of CAD was higher in the population carrying the C allele. Conclusions We found evidence of associations between MIF -173C/G and CAD susceptibility in the Asian and Caucasian populations.

ObjectivesA combined equation based on white cell count (WCC) and total bilirubin (TB) was assessed for its ability to predict adverse clinical outcomes in patients with acute ST-segment elevation myocardial infarction (STEMI) with primary percutaneous coronary intervention (PCI).DesignA single-centre, prospective cohort study.SettingThe First Affiliated Hospital of Xinjiang Medical University.MethodA total of 615 patients with STEMI postprimary PCI were enrolled. WCC and TB were collected at admission. Logistic regression was used to determine the combined equation. The primary endpoints were in-hospital mortality and major adverse cardiovascular events (MACE), which composed of cardiac death, cardiac shock, malignant arrhythmia (ventricular tachycardia, ventricular fibrillation), severe cardiac insufficiency, non-fatal myocardial infarction, angina pectoris readmission, severe cardiac insufficiency (cardiac III–IV level), stent restenosis and target vessels revascularisation during the hospitalisation and 36 months follow-up period.Result77 patients occurred in MACE during the hospitalisation (17 in-hospital mortality). WCC and TB were taken as an independent variables to make a category of logistic regression analysis of in-hospital MACE, the logistic regression model was: logit (P)=−8.00+0.265 WCC+0.077 TB, the combination of WCC and TB was more valuable on evaluating the in-hospital mortality (area under the curve 0.804, 95% CI 0.678 to 0.929, pConclusionThe combination of WCC and TB is an independent predictor for in-hospital outcomes in patients with STEMI than single detection.

Background: Biological agents are commonly used for the treatment of ulcerative colitis (UC). As new treatments, tofacitinib, and fecal microbiota transplantation (FMT) have demonstrated efficacy in treating UC. This network meta-analysis aims to determine the efficacy and safety of biological agents, tofacitinib, and FMT. Methods: A network meta-analysis was conducted by systematically searching the PubMed, Embase, and Cochrane Libraries. According to strict inclusion and exclusion criteria, we included randomized controlled trials (RCTs) of biological agents, tofacitinib, and FMT in UC. A random-effect model was chosen by the network meta-analysis and sensitivity analysis. Heterogeneity test and publication bias test were performed to determine the efficacy of treatments. Results: Data were extracted from 16 RCTs and we found that all treatments were more effective than the placebos. A total of 21 comparisons were made to determine efficiency. We found that infliximab, vedolizumab, and FMT performed better curative effect in terms of absolute effects and relative ranks. Furthermore, there was no statistical difference in the efficacy of biological agents, tofacitinib, and FMT. Moreover, no treatments were found to increase the occurrence of adverse events when compared with placebos, except infliximab. However, vedolizumab seemed to reduce the occurrence of adverse events compared with infliximab. Conclusion: Of the biological agents, vedolizumab and infliximab were the most effective, suggesting that biological agents are still a better choice. Nevertheless, tofacitinib and FMT may be promising alternatives with high efficacies. However, more safety and maintenance studies need to be conducted in future for the acquisition of more accurate results. Abbreviations: FMT: Fecal microbiota transplantation; UC: Ulcerative colitis; RCTs: Randomized controlled trials; IBD: Inflammatory bowel disease; CD: Crohn’s disease; IBS: Irritable bowel syndrome; CDI: Clostridium difficile infections; ITT: Intention-to-treat; RR: Relative risk; CI: Confidence interval; CrI: Credible intervals; IFX: Infliximab; ADA: Adalimumab; TFB: Tofacitinib; GLM: Golimumab; VDZ: Vedolizumab; PBO: Placebo; wk: week; F: Female; M: Male; AEs: Adverse events; SAEs: Serious adverse events; anti-TNF: Anti-tumor necrosis factors

Objective. Recent studies have focused on the special roles of NADPH-oxidase in multiple autoimmune diseases. Nevertheless, the association of genetic variation in NADPH-oxidase genes with rheumatoid arthritis (RA) was not extensively studied in a Chinese population. We performed this study to examine the association of NCF2, NCF4, and CYBA gene polymorphisms with RA susceptibility in a Chinese population. Methods. Six single nucleotide polymorphisms (SNPs) (NCF2 rs10911363, NCF4 rs1883112, rs4821544, rs729749, CYBA rs3794624, and rs4673) were genotyped in a cohort composed of 593 RA patients and 596 normal controls. Improved multiple ligase detection reaction (iMLDR) was used for genotyping. Results. We observed that NCF4 rs4821544 CT genotype and C allele frequencies in RA patients were significantly decreased when compared to controls (CT vs. TT: P = 0.043 ; C vs. T: P = 0.031 ), and rs4821544 polymorphism was significantly associated with an increased RA risk under the dominant model (TT vs. CT+CC: P = 0.031 ). Our results also indicated that rs729749 CT genotype frequency was significantly lower in RA patients than that in controls (CT vs. CC: P = 0.033 ). Moreover, the rs729749 CT genotype frequency was also significantly decreased in RA patients in males (CT vs. CC: P = 0.024 ). No significant association between NCF2 and CYBA gene polymorphisms and RA susceptibility was observed. There were significant associations between rs4821544 TT genotype and T allele frequencies and anti-CCP in male RA patients. Conclusions. In summary, NCF4 rs4821544 and rs729749 polymorphisms might contribute to RA susceptibility, while NCF2 and CYBA gene polymorphisms were not associated with RA susceptibility.

The aim of this investigation is to investigate the long noncoding ribonucleic acid and mRNA expression profiles of acute myocardial infarction patients and matched healthy controls particularly the higher-ranked long noncoding ribonucleic acid ENST00000581794.1 in co-expression. This study group found that ENST00000581794.1 was up-regulated in acute myocardial infarction patients in pre-experiment. It is suggested that ENST00000581794.1 may be a potential biomarker of acute myocardial infarction. Fifty eight patients with acute myocardial infarction and 58 healthy controls were included in this study from September 2017 to February 2018. Venous blood samples were collected from patients within 6 h from the onset of chest pain and RT-qPCR measured the expression levels of long noncoding ribonucleic acid in peripheral blood mononuclear cells. All patients were followed for 12±1 mo. The expression levels of ENST00000581794.1 were significantly different between the two groups. The receiver operating characteristic curve showed that long noncoding ribonucleic acid ENST00000581794.1 (area under the curve = 0.744, 95 % confidence interval: 0.61~0.88, p=0.004) had a predictive effect on major adverse cardiovascular events. Survival curve analysis demonstrated that the incidence of major adverse cardiovascular events became significantly higher in patients with high expression of ENST00000581794.1 as the observation time increased. Multivariate regression analysis indicated that ENST00000581794.1 was an independent predictor of major adverse cardiovascular events in patients with acute myocardial infarction (hazard ratio: 1.17, 95 % confidence interval: 1.00~1.37, p=0.048). Highly expressed ENST00000581794.1 in peripheral blood mononuclear cells may be used as a biomarker for diagnosis and prognosis of acute myocardial infarction.

Currently published data regarding the potential role of osteoprotegerin (OPG), osteocalcin (OCN) and osteopontin (OPN) for the discrimination between rheumatoid arthritis (RA) and osteoarthritis (OA) are contradictory. To derive a more precise evaluation, a meta-analysis was performed.Published literatures comparing plasma/serum OPG, OCN and OPN levels between RA group and OA controls were searched in PubMed, Embase and the Cochrane Library. The Newcastle-Ottawa Scale was used to assess the study quality. Pooled standard mean difference (SMD) with 95% confidence interval (CI) was calculated by random-effect model analysis. Heterogeneity test was performed by the Q statistic and quantified using INine studies including 438 RA patients and 255 OA patients were finally incorporated in the meta-analysis after examining title, type, abstracts and full text. The results showed that RA patients had higher plasma/serum OPN (pooled SMD = -2.57, 95% CI = -4.72 to -0.41) levels when compared to OA patients. No significant difference in plasma/serum OPG (pooled SMD = -0.29, 95% CI = -1.07‒0.49) and OCN (pooled SMD = -0.09, 95% CI = -0.48‒0.31) levels were found between RA patients and OA patients. Subgroup analysis indicated that plasma/serum OPG levels had no significant differences between RA patients and OA patients in Europe and Asian.Overall, there is no significant difference in circulating OPG and OCN levels between RA patients and OA patients. However, plasma/serum OPN level is significantly higher in RA patients compared with OA patients.

The relationship between living conditions in urban and rural areas during childhood and subsequent inflammatory bowel disease (IBD) remains controversial.To explore the association between environmental exposures early in life and the subsequent risk of IBD.Literature searches were conducted in the following databases: PubMed, EMBASE, and Conference Proceedings Citation Index. Studies were analyzed separately using rate ratios (RRs) or odds ratios (ORs) with 95% confidence intervals.The search strategy identified 15 studies. Of these, 9 studies explored the association between urban exposure during childhood and ulcerative colitis (UC), and 12 and 4 studies explored this relationship with Crohn's disease (CD) and IBD, respectively. A meta-analysis showed that the pooled ORs estimated for the case-control studies of UC, CD, and IBD were 1.16 (0.83, 1.61), 1.45 (1.45, 1.85), and 1.34 (1.11, 1.62), respectively. The pooled RR estimated for the cohort studies of CD and IBD was 1.48 (1.17, 1.87). The stratified analysis and meta-regression showed significant relationships between CD and living conditions in case-control studies published during 2010-2017 and in non-European countries (P 0.05).Living conditions during childhood are positively associated with the subsequent development of IBD. Urban living environment is more common among those with CD than UC.

Currently, many studies have focused on the possibility of using mean platelet volume (MPV) as a biomarker for disease activity in patients with systemic lupus erythematosus (SLE). To derive a more accurate estimation, a meta-analysis was conducted. Embase, PubMed, The Cochrane Library database and several Chinese databases (up to Nov 1 2017) were used to acquire published literatures on association of MPV levels with disease activity in SLE patients. Fixed-effects or random-effect model analysis was performed to calculate pooled standard mean difference (SMD) with 95% confidence interval (CI). Heterogeneity test was tested by the Q statistic and quantified using I2. A funnel plot and Egger’s linear regression test were used to evaluate the potential publication bias. A total of 618 articles were identified, nine studies with 376 active SLE patients and 270 inactive SLE patients were finally included. No significant difference in MPV level was found between active SLE patients and inactive SLE patients (SMD = − 0.05, 95% CI: − 0.83, 0.73). Subgroup analyses stratified by age or region also demonstrated consistent results. No significant publication bias was observed (P > 0.05). The sensitivity analysis showed no significant change when any one study was excluded. In summary, our meta-analysis does not support the use of MPV as an indicator for monitoring disease activity in SLE patients. Further longitudinal studies with larger sample size are warranted to unveil the possibility of using MPV as a biomarker of disease activity.

The goal of this study was to investigate platelet parameters in populations with hypertension subtypes among the Han, Uygur, and Kazakh ethnic groups and their associated risk factors in Xinjiang, northwestern China. In total, 9816 adult participants were recruited from a multiethnic, cross-sectional cardiovascular risk survey. Our results indicated that the platelet counts in Han, Uygur, and Kazakh participants with isolated systolic hypertension (ISH), isolated diastolic hypertension (IDH), and systolic diastolic hypertension (SDH) varied significantly (P

The objective of this study is to analyze clinical manifestations, features of imaging, and laboratory assessment of patients with neuropsychiatric SLE (NPSLE) for better diagnosis and outcome prediction. One hundred eighteen NPSLE patients admitted to the Anhui Provincial Hospital in Hefei, China, between January 2006 and December 2016 were enrolled and analyzed retrospectively. All patients fulfilled the American College of Rheumatology revised classification criteria for SLE. Patients with NPSLE fulfilled the American College of Rheumatology (ACR) nomenclature and case definitions. All NPSLE patients underwent neurological investigations including MRI of nervous system, electroencephalograms, or CSF examination as part of the diagnostic evaluation of nervous system involvement. All statistical analyses were performed. According to different types of data, different statistical methods were used to determine factors associated with abnormal MRI among NPSLE patients. Statistical significance was defined as P value

The aim of the present study was to investigate the predictive value of the plasma matrix metalloproteinase-9 (MMP-9) level at admission for in-hospital mortality in patients who received emergency percutaneous coronary intervention (PCI) following AMI. A single blood sample was collected at admission from 155 consecutive AMI patients who underwent emergent PCI. The plasma levels of MMP-9 value (528.9±191.6 ng/ml) were significantly higher in the patients who died (n=24) than in the survivors (385.4±236.0 ng/ml) during 14 days of hospitalization (P=0.005). The age, left ventricle wall motion score index (WMIS), Global Registry of Acute Coronary Events (GRACE) score and B-type natriuretic peptide (BNP) levels and GENSINI score at admission were significantly different between the patients who died and those who survived (P

Background Rickettsia raoultii is frequently detected in multiple tick species, whereas human infection remains scarcely studied. Methods A surveillance study was performed at 3 sentinel hospitals in China, to recruit participants with suspected tick exposure. Rickettsia raoultii infection was identified through polymerase chain reaction, followed by sequencing, and confirmed serologically. Isolation by cell culture was performed and the isolates were genome sequenced. Results Twenty-six subjects were determined to have R. raoultii infection, including 7 with asymptomatic infection, 15 with mild to moderate illness, and 4 with severe illness. Common nonspecific manifestations in the 19 patients with mild to moderate or severe illness included fever (100%), malaise (95%), myalgia (58%), lymphadenopathy (53%), and nausea (42%). Only 5% of them had rash, and 16% had eschar. Scalp eschar and neck lymphadenopathy after a tick bite syndrome was only seen in 2 patients. Of the 4 patients with severe complications, 3 developed pulmonary edema, and 1 developed clouding of consciousness and lethargy. Frequent abnormalities of laboratory testing included leukopenia, thrombocytopenia, lymphopenia, neutropenia, hypoproteinemia, and elevated levels of total bilirubin, hepatic aminotransferases, lactate dehydrogenase, and creatine kinase. All the 19 patients recovered without sequelae after receiving doxycycline treatment. Two R. raoultii strains were isolated, and a significantly less degraded genome was observed than other more virulent Rickettsia strains, indicating a low pathogenicity of the current strain. Conclusions Human infection with R. raoultii has a wide clinical spectrum that ranged from subclinical infection to severe complications. Physicians need to be aware of the high potential and clinical complexity of R. raoultii infection, to ensure appropriate testing and treatment in endemic regions.

Several studies suggest an important role of Acyl-CoA: cholesterol acyltransferase-1(ACAT-1) in the development of atherosclerosis. The aim of present study was to investigate whether there exists a possible correlation between genetic variations in ACAT-1 genes and coronary artery disease (CAD) risk. Four polymorphisms (rs1044925, rs11545566, rs12121758 and rs10913733) were finally selected and genotyped in 750 CAD patients and 580 health controls, using the improved multiplex ligation detection reaction (iMLDR) method. We found that the rs11545566 G allele was associated with a significantly elevated CAD risk [GG vs. AA: adjusted odds ratio (AOR) = 1.62, 95% confidence interval (CI) = 1.13-2.32, P = 0.008; GA/GG vs. AA: AOR = 1.67, 95% CI = 1.22-2.29, P = 0.001]. The rs10913733 G allele was also associated with a significantly elevated CAD risk (GG vs. TT: AOR = 1.57, 95% CI = 1.08-2.28, P = 0.018; GT/GG vs. TT: AOR = 1.39, 95% CI = 1.07-1.79, P = 0.013). Multivariate linear regression analysis showed that the rs11545566 polymorphism was independently associated with the Gensini scores (P = 0.005). The Gensini score of subjects in the variant GG genotype group and the GG/GA genotype group were higher than the score of subjects in the AA genotype group (32.49 ± 26.60 and 31.26 ± 26.96 vs. 23.45 ± 21.64; P = 0.001 and 0.002, respectively). Our results demonstrate that ACAT-1 rs1154556 and rs10913733 polymorphism are novel genetic factors in the development of CAD. Rs11545566 was also associated with the severity of CAD.

// Asiya Abudesimu 1, * , Dilare Adi 1, * , Dilixiati Siti 1, * , Xiang Xie 1 , Yi-Ning Yang 1 , Xiao-Mei Li 1 , Ying-Hong Wang 1 , Yong-Tao Wang 1 , Ya-Jie Meng 1 , Fen Liu 2 , Bang-Dang Chen 2 , Xiang Ma 1 , Zhen-Yan Fu 1 and Yi-Tong Ma 1 1 Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, PR China 2 Xinjiang Key Laboratory of Cardiovascular Disease, Clinical Medical Research Institute of First Affiliated Hospital of Xinjiang Medical University, Urumqi, PR China * These authors contributed equally to this work Correspondence to: Yi-Tong Ma, email: myt-xj@163.com, myt0991@126.com Zhen-Yan Fu, email: fuzhenyan316@126.com Xiang Ma, email: maxiangxj@163.com Keywords: SREBP family, FBXW7, coronary artery disease, case-control study Received: May 26, 2017 Accepted: September 05, 2017 Published: September 19, 2017 ABSTRACT Background: Hyperlipidemia is a major risk factor for coronary artery disease (CAD). The current study was designed to explore the possible correlation between single nucleotide polymorphisms (SNPs) in the lipid homeostasis regulatory genes F-box and WD repeat domain–containing 7 (FBXW7 ) and sterol regulatory element-binding proteins (SREBPs) with CAD among Han Chinese and Uygur Chinese populations in Xinjiang, China. Results: In the Uygur Chinese population, rs9902941 in SREBP-1 and rs10033601 in FBXW7 were found to be associated with CAD in a recessive model (TT vs. CT + CC, P = 0.032; GG vs. AG + AA, P = 0.010, respectively), and rs7288536 in SREBP-2 was found to be associated with CAD in an additive model (CT vs. CC + TT, P = 0.045). The difference was statistically significant in the Uygur Chinese population after multivariate adjustments [Odds ratio (OR) = 1.803, 95% confidence interval (CI): 1.036~3.137, P = 0.037; OR = 1.628, 95% CI: 1.080~2.454, P = 0.020; OR = 1.368; and 95% CI: 1.018~1.837, P = 0.037, respectively]. There were also significant interactions between the above-mentioned models in the Uygur Chinese population. However, these relationships were not observed before or after multivariate adjustment in the Han Chinese population. Materials and Methods: A total of 1,312 Han Chinese (650 CAD patients and 662 controls) and 834 Uygur Chinese (414 CAD patients and 420 controls) were enrolled in this case-control study. Three SNPs (rs9902941 in SREBP-1, rs7288536 in SREBP-2 and rs10033601 in FBXW7) were selected and genotyped using the improved multiplex ligase detection reaction (iMLDR) method. Conclusions: The results of this study indicate that variations in the lipid regulatory pathway genes FBXW7 and SREBPs (rs9902941 in SREBP-1, rs7288536 in SREBP-2 and rs10033601 in FBXW7) are associated with CAD in the Uygur Chinese population in Xinjiang, China.

This study aimed to systemically review the evidence regarding the relationship between the circulating blood osteoprotegerin (OPG) level and rheumatoid arthritis (RA), as well as the potential influential factors. Research related to plasma/serum OPG levels in RA patients and healthy controls were gathered using PubMed, EMBASE, and The Cochrane Library database (up to Jan. 1, 2017). Pooled standard mean difference (SMD) with 95% confidence interval (CI) was calculated by fixed-effects or random-effect model analysis. Heterogeneity test was performed by the Q statistic and quantified using I 2, and publication bias was evaluated using a funnel plot and Egger's linear regression test. After searching databases, 443 articles were obtained, and 11 studies with 710 RA patients and 561 controls were finally included. Meta-analysis revealed that, compared with the control group, the OPG level was significantly higher in the RA group (P

Systemic lupus erythematosus (SLE) is associated with increased cardiovascular risk. This study aims to derive a more precise estimation on pulse wave velocity (PWV) level in patients with SLE and related factors. A literature search was performed using PubMed, EMBASE, and The Cochrane Library databases, studies published up to February 28, 2017, in English. Pooled standardized mean difference (SMD) with 95% confidence interval (CI) was calculated by fixed-effect or random-effect model analysis. Heterogeneity test was performed by the Q statistic and quantified using I2; publication bias was evaluated using a funnel plot and Egger’s linear regression test. Of 156 studies found, 27 met eligibility criteria, and 14 studies were finally included in the meta-analysis. Meta-analysis revealed that the SLE group had significantly higher PWV levels than the control group; SMD = 0.56 and 95% CI (0.30-0.82). Subgroup analyses showed that body mass index (BMI), sample size, and disease duration were associated with PWV in patients with SLE. Overall, our study suggests that patients with SLE have a higher PWV level, and it is associated with BMI, sample size, and disease duration.

Laparoscopic total gastrectomy (LTG) is frequently performed for treating patients with gastric cancer; however, the absence of anastomotic techniques with greater superiority has impaired its popularization. We have compared two types of anastomotic techniques with regard to technical perspectives and clinical outcomes. We reviewed 43 patients with gastric cancer who underwent LTG. Two types of anastomotic techniques have been applied after LTG—the trans-orally inserted anvil (OrVil™) and the reverse puncture device (RPD). Data on the type of anastomosis, blood loss, operation time, anastomosis time, location of tumors, distance between the top border of tumors and top resection margin, diameter of tumor, length of postoperative hospital stay, early and late postoperative complications, and total cost of surgical consumables were obtained by reviewing patient medical records and analyzed thereafter. We included 32 men and 11 women (mean age 61 years). The loss to follow-up rate was 13.2%. The median survival time for the OrVil™ and RPD groups was 23 and 22 months, respectively. The total rate of complications was 9.3%. The difference in the anastomosis times between the groups was statistically significant. OrVil™ required more time than RPD and cost more than RPD. Both the OrVil™ and RPD techniques showed good safety and applicability in LTG. RPD showed an advantage with regard to lesser operative complexity and lower cost.

Aim: Although immunohistochemistry (IHC) and reverse transcription-PCR can detect ALK rearrangements, the ALK break-apart FISH assay is currently considered the standard method. Materials & methods: Five patients with advanced non-small-cell lung cancer, who had an ALK-negative FISH result that was later confirmed as positive by the Ventana IHC assay, were studied. Four had previously received chemotherapy or radiotherapy. All five were subsequently treated with Crizoitinib 250 mg twice daily. Results & conclusion: Four patients had a partial response to Crizotinib and one had stable disease. IHC is an efficient technique for diagnosing ALK rearrangements in patients with non-small-cell lung cancer, and may serve as an alternative to FISH in clinical practice.

// Jing-Zhan Zhang 1,2 , Ying Gao 3 , Ying-Ying Zheng 1 , Fen Liu 1 , Yi-Ning Yang 1 , Xiao-Mei Li 1 , Xiang Ma 1 , Yi-Tong Ma 1 and Xiang Xie 1 1 Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China 2 Department of Dermatology, People’s Hospital of Xinjiang Uygur Autonomous Region, Urumqi, China 3 Department of Cadre Ward, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China Correspondence: Xiang Xie, email: // Keywords : coronary heart disease; serum resistin; meta-analysis Received : November 24, 2016 Accepted : January 24, 2017 Published : February 25, 2017 Abstract To explore the relationship between the serum resistin level and different types of coronary heart diseases (CHD). Literature was retrieved by formal searching of PubMed, Web of Science, Google Scholar, the Cochrane Library, Wanfang Data, China Biological Medicine Database (SinoMed) and China National Knowledge Infrastructure (CNKI) and by hand searching of reference lists of related articles. RevMan5.3 statistical software was utilized for processing and analysis. A total of 22 literatures involving 2070 subjects were included. Meta-analysis showed that the level of serum resistin in the patients with stable angina (SA), unstable angina(UA) or acute myocardial infarction (AMI) were significantly higher than those of normal controls, respectively [SMD(95% CI)were 1.97(1.15, 2.79), 2.54(1.76, 3.31), and 3.62(2.62, 4.62), all P

Gastric schwannoma (GS) is a rare neoplasm of the stomach. It accounts for 0.2% of all gastric tumors and is mostly benign, slow-growing, and asymptomatic. Due to its rarity, GS is not widely recognized by clinicians, and the precise differential diagnosis between GS and other gastric submucosal tumors remains difficult preoperatively. The present study reports a case of GS misdiagnosed as gastrointestinal stromal tumor and reviews the clinical, imaging, and pathological features, treatment, and follow-up of 221 patients with GS previously reported in the English literature. Although GS is rare, the case reported in the current study highlights the importance of including GS in differential diagnoses of gastric submucosal tumors. Furthermore, the findings of the review suggest that although many cases are asymptomatic, the most common symptoms are abdominal pain or discomfort, not gastrointestinal bleeding, and malignant GSs present with clinical symptoms more commonly. Although large-sample multicenter studies on the efficacy, safety, and oncological outcomes of minimally invasive techniques are required, the findings presented herein may be helpful for clinicians when diagnosing or treating GS.

To identify medication adherence and its influencing factors among patients of 14 methadone maintenance treatment (MMT) clinics in Xi'an, China.Data were obtained from the National AIDS Information System-Community Methadone Maintenance Treatment. All patients registered in the system were not permitted to take methadone at home without professionals' supervision. Medication adherence was assessed using categorical (ie, dropout or retained) and continuous (ie, treatment time, methadone use time, and percentage of methadone use days) variables. Percentages of methadone use days of90%, 50% to 90%, or50% indicated good, moderate, and poor adherence, respectively. Multivariate Cox stepwise regression analysis was used to identify the influencing factors.Of the 10,398 patients, 52.2% had dropped out of MMT by December 31, 2013, whereas only 11.8% regularly visited the clinic for daily methadone (ie,90% methadone use days) during a certain period. Protective factors were older age (30 years); female sex; having no contact with peer drug users over the past month; no needle-sharing experience; a negative initial morphine urine test; and a higher average daily methadone dose (20 mg) (P 0.05). Risk factors were answering "others" for marital status; being employed; having a lack of stable income; not living with family; answering "others" for drug use type; frequently engaging in unauthorized drug use during MMT; no readmission; long travel times to the MMT clinic (30 minutes); having no convenient MMT service time; and being dissatisfied with MMT service (P 0.05).Based on our findings, multimodal intervention and management programs can be developed to improve poor medication adherence among the MMT patient population.