A systematic review and meta-analysis of sex differences in clinical outcomes of hypertrophic cardiomyopathy.

Background: Hypertrophic cardiomyopathy (HCM) is recognized as the most prevalent form of genetic cardiomyopathy, and recent investigations have shed light on the existence of sex disparities in terms of clinical presentation, disease progression, and outcomes. Objectives: This study aimed to systematically review the literature and perform a meta-analysis to comprehensively compare the clinical outcomes between female and male patients with HCM. Methods: A thorough search was conducted in databases including PubMed, Embase, Cochrane Library, and Web of Science, encompassing literature from inception until June 2023. The primary endpoints examined were: (1) all-cause mortality; (2) an arrhythmic endpoint comprising sudden cardiac death (SCD), sustained ventricular tachycardia, ventricular fibrillation, or aborted SCD; and (3) a composite endpoint incorporating either (1) or (2), in addition to hospitalization for heart failure or cardiac transplantation. Pooled estimates were derived using a random-effects meta-analysis model. Results: The analysis encompassed a total of 29 observational studies, involving 44,677 patients diagnosed with HCM, of which 16,807 were female. Baseline characteristics revealed that the female group exhibited an advanced age [55.66 ± 0.04 years vs. 50.38 ± 0.03 years, pooled mean difference (MD) = 0.31, 95% CI: 0.22-0.40, p = 0.000, I2 = 88.89%], a higher proportion of New York Heart Association class III/IV patients [pooled odds ratio (OR) = 1.94, 95% CI: 1.55-2.43, p = 0.000, I2 = 85.92%], and a greater prevalence of left ventricular outflow tract gradient greater than or equal to 30 mmHg (pooled OR = 1.48, 95% CI: 1.27-1.73, p = 0.000, I2 = 68.88%) compared to the male group. The female group were more likely to have a positive genetic test (pooled OR = 1.27, 95% CI: 1.08-1.48, p = 0.000, I2 = 42.74%) and to carry the myosin heavy chain beta 7 mutation (pooled OR = 1.26, 95% CI: 1.04-1.54, p = 0.020, I2 = 0.00%) compared to the male group. Female sex exhibited a significant association with increased risks of all-cause mortality (pooled OR = 1.62, 95% CI: 1.38-1.89, p = 0.000, I2 = 72.78%) and the composite endpoint (pooled OR = 1.47, 95% CI: 1.20-1.79, p = 0.000, I2 = 84.96%), while no substantial difference was observed in the arrhythmic endpoint (pooled OR = 1.08, 95% CI: 0.87-1.34, p = 0.490, I2 = 55.48%). Conclusions: The present findings suggest that female patients with HCM tend to experience poorer clinical outcomes. It is imperative to critically reevaluate disease definitions and enhance awareness to mitigate delays in the diagnosis and treatment of HCM in women, thereby fostering equitable healthcare practices. Systematic Review Registration: https://www.crd.york.ac.uk/, PROSPERO (CRD42023431881).

MCC950 ameliorates ventricular arrhythmia vulnerability induced by heart failure.

MCC950, a specific NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inhibitor, has been reported to play a role in various cardiovascular diseases. However, its role in heart failure (HF)-induced ventricular arrhythmias (VAs) remains unclear. Hence, the present study aimed to clarify the role and underlying mechanisms of MCC950 in HF-induced VAs. Male C57BL/6 mice were induced with HF via transverse aortic constriction (TAC). Histological analysis, echocardiography, electrophysiological investigation, and western blot analysis were conducted to evaluate VA vulnerability induced by TAC and the potential mechanisms underlying the effects. MCC950 markedly improved cardiac function and decreased pulmonary edema induced by HF. Moreover, MCC950 also decreased VA vulnerability, as shown by the shortened QTc duration and action potential duration 90 (APD90), reduced APD alternans threshold, and decreased VA induction rate. Furthermore, MCC950 treatment significantly reversed TAC-induced cardiac hypertrophy and fibrosis. In addition, MCC950 administration increased the protein levels of ion channels (Kv4.2, KChIP2, and Cav1.2). Mechanistically, the above changes induced by MCC950 were due to the inhibition of the NLRP3 inflammasome. As a specific NLRP3 inhibitor, MCC950 significantly decreased HF-induced VA vulnerability by reversing cardiac structural remodeling and electrical remodeling, and the mechanism through which MCC950 exhibited this effect was inhibition of NLRP3 inflammasome activation.

Cardiac adaptation to high altitudes after short- and long-term exposure among Chinese Han lowlanders.

BACKGROUND: Short-term, high altitude (HA) exposure raises pulmonary artery systolic pressure (PASP) and decreases left ventricular volumes. However, relatively little is known of the long-term cardiac consequences of prolonged exposure in Chinese Han lowlanders, a highly adapted HA population. AIMS: We studied cardiac structure and function by echocardiography to investigate short-term adaptation and potential long-term cardiac remodeling. METHODS: This study included 301 healthy subjects of short-term exposure (STE), acclimatized Chinese Han lowlanders (AL) at HA, native Tibetans (NT), and sea level residents (SLR) with 75, 77, 69, and 80 participants, respectively. All groups underwent standard echocardiography. RESULTS: Compared with SLR, systolic blood pressure (SBP) and heart rate of STE and AL did not significantly increase following HA exposure, but SBP in STE was lower than AL. In lowlanders, HA exposure enlarged right heart and pulmonary artery (PA), reduced left ventricular (LV) diastolic function. This decrease in LV diastolic function increased with exposure time. Compared with SLR, ejection fraction did not change significantly in STE, but decreased in AL. Interventricular septal end-diastolic thickness (IVSd) increased both in STE and AL compared with SLR. Compared with NT, AL population had higher SBP and the greater diameter of PA. CONCLUSIONS: In Chinese Han lowlanders, exposure to HA enlarged right ventricle and decreased the diastolic function of LV. LV systolic function was preserved after short-term HA exposure but decreased after long-term HA exposure. It was possible to speculate that ethnicity contributed to the observed difference in heart.

LncRNA MHRT Promotes Cardiac Fibrosis via miR-3185 Pathway Following Myocardial Infarction.

Long-chain noncoding RNA (lncRNA) is a new class of molecular regulators in heart development and disease. However, the role of specific lncRNA in cardiac fibrosis remains to be fully explored. This study aimed to investigate the role and potential mechanism of lncRNA MHRT in myocardial fibrosis after myocardial infarction (MI).Cardiac fibroblasts (CFs) were isolated from a mouse model of MI. The expression levels of MHRT and miR-3185 in the hearts of MI and CFs mice treated with transforming growth factor beta 1 (TGF-ß1) were analyzed by qRT-PCR. The collagen expression was assessed using qRT-PCR and Western blot. Cell proliferation was assessed by performing MTT and EdU assays. The direct interaction between lncRNA and miRNA was analyzed by luciferase assay, RNA-binding protein immunoprecipitation (RIP) assay, and RNA pull-down assay.The expression levels of MHRT were raised in MI and CFs mice treated with TGF-ß1. Overexpression of MHRT promoted collagen production and CF proliferation, while silencing of MHRT showed the opposite effect. MiR-3185 was a target gene of MHRT. In addition, overexpression of MHRT reduced the expression levels of miR-3185, and siMHRT reversed the inhibitory effect of TGF-ß1 on the expression of miR-3185. Overexpression of miR-3185 inhibited the upregulation of Col I and Col III induced by TGF-ß1.MHRT promoted cardiac fibrosis after MI through miR-3185 and increased myocardial collagen deposition and promoted myocardial fibrosis.

Left bundle branch pacing with optimization of cardiac resynchronization treatment: A case report.

BACKGROUND: Cardiac resynchronization therapy (CRT) is a well-established therapy for patients with cardiomyopathy. CASE SUMMARY: The patient underwent left bundle branch area and left ventricular (reaching the left ventricular lateral vein through the coronary sinus) pacing. The optimal CRT was performed under the right bundle branch of the patient by adjusting the optimal a-v and v-v interphases to achieve the maximal benefit of the treatment. CONCLUSION: The patient was diagnosed with left bundle branch block and heart failure. A left bundle branch area pacemaker assisted in correcting the complete left bundle branch block. However, the shorter QRS wave shape after pacemaker implantation through the left bundle branch area indicated a complete right bundle branch block pattern. Hence, the left bundle branch area pacemaker is not always considered as the optimal treatment. The left bundle branch pacing with the optimization of cardiac resynchronization treatment may serve as a new CRT strategy.

Correlation among high salt intake, blood pressure variability, and target organ damage in patients with essential hypertension: Study protocol clinical trial (SPIRIT compliant).

BACKGROUND: Essential hypertension is a multifactorial disease, which is affected by genetic and environmental factors, and can cause diseases such as cerebrovascular disease, heart failure, coronary heart disease, and chronic renal failure. High salt intake is a risk factor for hypertension, stroke, and cardiovascular disease. Blood pressure variability (BPV) is a reliable independent predictor of cardiovascular events and death. At present, there are few studies about the correlation among high salt intake, BPV, and target organ damage (TOD) in patients with hypertension. OBJECTIVE: The purpose of this study is to compare 24-hour urine sodium excretion, BPV, carotid intima-media thickness, left ventricular mass index, and serum creatinine or endogenous creatinine clearance rate. To clarify the relationship between high salt load and BPV and TOD in patients with hypertension.This study is a cross-sectional study. It will recruit 600 patients with essential hypertension in the outpatient and inpatient department of cardiovascular medicine of Chengdu Fifth People's Hospital. Researchers will obtain blood and urine samples with the patient's informed consent. In addition, we will measure patient's blood pressure and target organ-related information. TRIAL REGISTRY: The study protocol was approved by the Chengdu Fifth People's Hospital. Written informed consent will be obtained from all the participants. The trial was registered in the Chinese Clinical trial registry, ChiCTR2000029243. This trial will provide for the correlation among high salt intake, BPV, and TOD in patients with essential hypertension.

Chinese herbal preparations for chronic heart failure: Study protocol for an umbrella review of systematic reviews and meta-analyses.

BACKGROUND: Chinese herbal preparations (CHPs) have been reported to be effective in the management of chronic heart failure (CHF); they are beneficial in improving cardiac function, reducing hospital stays and readmission. However, the credibility of their effectiveness evidence has not been evaluated. We aim to summarize and evaluate current effectiveness evidence of traditional Chinese medicine in the management of CHF. METHODS: We will search PubMed, Embase, the Cochrane Database of Systemic Review (CDSR), and Web of Science from inception to December 2019 for systematic reviews that assessing the effectiveness of CHPs for CHF. The search will be performed without language restriction. Experimental interventions will include any type of CHPs, and control interventions will include placebo, sham interventions, usual care, or no controls. The primary outcome will be the changes in heart function classification defined by the New York Heart Association. Secondary outcomes include left ventricular ejection fraction, Six Minute Walk Test, other efficacy outcomes, and adverse events. We will use I statistics to assess the between-study heterogeneity in each meta-analysis, Eager test to detect publication bias, and the ratio of observed versus expected number of trials with positive findings. We will summarize the evidence and classify them into convincing, highly suggestive, suggestive, or weak. RESULTS: The results of this study will be published in a peer-reviewed journal. ETHICS AND DISSEMINATION: No ethical approval and patient consent are required since this study data is based on published literature. The results of the study will be submitted to a peer-reviewed journal. PROTOCOL REGISTRATION NUMBER: PROSPERO CRD 42019139649 (https://www.crd.york.ac.uk/PROSPERO/#joinuppage).

An ultrasensitive electrochemical sensing platform for the detection of cTnI based on aptamer recognition and signal amplification assisted by TdT.

We have developed an ultrasensitive and highly specific electrochemical sensing platform for the detection of cardiac troponin I (cTnI), a recognized biomarker for the diagnosis of acute myocardial infarction (AMI) and related cardiovascular diseases (CVDs). This strategy is based on the assists of terminal deoxynucleotidyl transferase (TdT)-mediated signal amplification and the specific recognition between cTnI and the aptamer of cTnI. In this experiment, we prepared a gold electrode that modified with probe 2 (P2), in the presence of cTnI, the aptamer of cTnI that in probe 1 (P1)/aptamer complexes bond with cTnI specifically and release the free P1. P1 would bind with P2, resulting in the formation of 3'-OH of DNA. In the presence of terminal deoxynucleotidyl transferase (TdT) and dTTP, TdT mediated P1 to extend and formed the structure of poly T. Methylene blue (MB)-poly A hybridized with the extended poly T and generated an electrochemical signal. The detection limit can be as low as 40 pg mL-1. This sensor was also successfully applied to the detection of cTnI in numerous spiked biological samples, and it can be a great reference for the clinical diagnosis, prognosis, and treatment of CVDs and AMI.

Impairment of Circulating CD4⁺CD25⁺GARP⁺ regulatory T cells in patients with acute coronary syndrome.

BACKGROUND: Atherosclerosis (AS) is an inflammatory and immune disease. Regulatory T cells (Tregs) suppress the activation of T cells and have been shown to play a protective role during the pathogenesis of AS. However, specific markers for Tregs are lacking. Recently, glycoprotein A repetitions predominant (GARP) was discovered as a specific marker of activated Tregs, and we therefore utilized GARP as a specific surface marker for Tregs in the current study. METHODS: To assess whether GARP(+) Tregs are downregulated in patients with acute coronary syndrome (ACS), we examined CD4(+)CD25(+)GARP(+) T cell frequencies as well as their associated cytokines and suppressive function. Additionally, we compared GARP expression to that of FOXP3, which may be more sensitive as a marker of activated Tregs in patients with ACS. RESULTS: Patients with ACS demonstrated a significant decrease in circulating CD4(+)CD25(+)GARP(+) Tregs. Moreover, the suppressive function of Tregs and levels of related cytokines were also impaired in ACS patients compared to those with stable angina (SA) or normal coronary artery (NCA). Additionally, after TCR stimulation, peripheral blood mononuclear cells (PBMCs) from patients with ACS exhibited a decrease in CD4(+)CD25(+)GARP(+) Tregs. CONCLUSIONS: These fnding indicate that circulating CD4(+)CD25(+)GARP(+) Tregs are impaired in patients withACS. Thus, targeting GARP may promote the protective function of Tregs in ACS.

A genome-wide association study identifies common variants influencing serum uric acid concentrations in a Chinese population.

BACKGROUND: Uric acid (UA) is a complex phenotype influenced by both genetic and environmental factors as well as their interactions. Current genome-wide association studies (GWASs) have identified a variety of genetic determinants of UA in Europeans; however, such studies in Asians, especially in Chinese populations remain limited. METHODS: A two-stage GWAS was performed to identify single nucleotide polymorphisms (SNPs) that were associated with serum uric acid (UA) in a Chinese population of 12,281 participants (GWAS discovery stage included 1452 participants from the Dongfeng-Tongji cohort (DFTJ-cohort) and 1999 participants from the Fangchenggang Area Male Health and Examination Survey (FAMHES). The validation stage included another independent 8830 individuals from the DFTJ-cohort). Affymetrix Genome-Wide Human SNP Array 6.0 chips and Illumina Omni-Express platform were used for genotyping for DFTJ-cohort and FAMHES, respectively. Gene-environment interactions on serum UA levels were further explored in 10,282 participants from the DFTJ-cohort. RESULTS: Briefly, we identified two previously reported UA loci of SLC2A9 (rs11722228, combined P = 8.98 × 10-31) and ABCG2 (rs2231142, combined P = 3.34 × 10-42). The two independent SNPs rs11722228 and rs2231142 explained 1.03% and 1.09% of the total variation of UA levels, respectively. Heterogeneity was observed across different populations. More importantly, both independent SNPs rs11722228 and rs2231142 were nominally significantly interacted with gender on serum UA levels (P for interaction = 4.0 × 10-2 and 2.0 × 10-2, respectively). The minor allele (T) for rs11722228 in SLC2A9 has greater influence in elevating serum UA levels in females compared to males and the minor allele (T) of rs2231142 in ABCG2 had stronger effects on serum UA levels in males than that in females. CONCLUSIONS: Two genetic loci (SLC2A9 and ABCG2) were confirmed to be associated with serum UA concentration. These findings strongly support the evidence that SLC2A9 and ABCG2 function in UA metabolism across human populations. Furthermore, we observed these associations are modified by gender.

A genome wide association study of genetic loci that influence tumour biomarkers cancer antigen 19-9, carcinoembryonic antigen and α fetoprotein and their associations with cancer risk.

OBJECTIVE: Tumour biomarkers are used as indicators for cancer screening and as predictors for therapeutic responses and prognoses in cancer patients. We aimed to identify genetic loci that influence concentrations of cancer antigen 19-9 (CA19-9), carcinoembryonic antigen (CEA) and α fetoprotein (AFP), and investigated the associations between the significant single nucleotide polymorphisms (SNPs) with risks of oesophageal squamous cell (OSCC), pancreatic and hepatocellular cancers. DESIGN: We carried out a genome wide association study on plasma CA19-9, CEA and AFP concentrations in 3451 healthy Han Chinese and validated the results in 10 326 individuals. Significant SNPs were further investigated in three case control studies (2031 OSCC cases and 2044 controls; 981 pancreatic cancer cases and 1991 controls; and 348 hepatocellular cancer cases and 359 controls). RESULTS: The analyses showed association peaks on three genetic loci for CA19-9 (FUT6-FUT3 at 19p13.3, FUT2-CA11 at 19q13.3 and B3GNT3 at 19p13.1; p=1.16×10(-13)-3.30×10(-290)); four for CEA (ABO at 9q34.2, FUT6 at 19p13.3, FUT2 at 19q13.3 and FAM3B at 21q22.3; p=3.33×10(-22)-5.81×10(-209)); and two for AFP (AFP at 4q11-q13 and HISPPD2A at 15q15.3; p=3.27×10(-18) and 1.28×10(-14)). These explained 17.14% of the variations in CA19-9, 8.95% in CEA and 0.57% in AFP concentrations. Significant ABO variants were also associated with risk of OSCC and pancreatic cancers, and AFP variants with risk of hepatocellular cancer (p<0.05). CONCLUSIONS: This study identified several loci associated with CA19-9, CEA and AFP concentrations. The ABO variants were associated with risk of OSCC and pancreatic cancers and AFP variants with risk of hepatocellular cancer.

Higher carbohydrate antigen 125 levels are associated with increased risk of coronary heart disease in elderly chinese: a population-based case-control study.

BACKGROUND: High carbohydrate antigen 125 (CA-125) level was reported to be associated with some cardiac dysfunctions, such as chronic heart failure, but the relationship between CA-125 level and coronary heart disease (CHD) risk remains unclear. The aim of this study was to explore the potential association in a Chinese older population. METHODS: In a population-based case-control study conducted in a Chinese older population, serum CA-125 levels were measured in 1177 diagnosed CHD patients and 3531 age and sex matched control subjects without CHD. RESULTS: Serum CA-125 level was significantly higher in CHD patients than controls (P < 0.001) with adjustment for age, gender, smoking, drinking, BMI, physical activity, hypertension, dyslipidemia, diabetes mellitus, medication history and family history of CHD and myocardial infarction. CHD risk was doubled (OR: 2.10, 95%CI: 1.69-2.60) among subjects in the highest quartile compared to those in the lowest quartile of CA-125 level (P trend < 0.001). Furthermore, CA-125 levels were associated with CHD risks in subjects with age over 60 years (OR: 2.19, 95%CI: 1.75-2.73), current smokers (OR: 2.29, 95%CI: 1.50-3.49), current drinkers (OR: 2.35, 95%CI: 1.57-3.53) and subjects with hypertension (OR: 2.04, 95%CI: 1.71-2.43). CONCLUSIONS: Elevated serum CA-125 level might be associated with increased risk of coronary heart disease in the Chinese older population. Further investigations are needed to identify the possible biological role of CA-125 in CHD development in the future.

Genome-wide association study on serum alkaline phosphatase levels in a Chinese population.

BACKGROUND: Serum alkaline phosphatase (ALP) is a complex phenotype influenced by both genetic and environmental factors. Recent Genome-Wide Association Studies (GWAS) have identified several loci affecting ALP levels; however, such studies in Chinese populations are limited. We performed a GWAS analyzing the association between 658,288 autosomal SNPs and serum ALP in 1,461 subjects, and replicated the top SNPs in an additional 8,830 healthy Chinese Han individuals. The interactions between significant locus and environmental factors on serum ALP levels were further investigated. RESULTS: The association between ABO locus and serum ALP levels was replicated (P = 2.50 × 10⁻²¹, 1.12 × 10⁻56 and 2.82 × 10⁻²7 for SNP rs8176720, rs651007 and rs7025162 on ABO locus, respectively). SNP rs651007 accounted for 2.15% of the total variance of serum ALP levels independently of the other 2 SNPs. When comparing our findings with previously published studies, ethnic differences were observed across populations. A significant interaction between ABO rs651007 and overweight and obesity was observed (FDR for interaction was 0.036); for individuals with GG genotype, those with normal weight and those who were overweight or obese have similar serum ALP concentrations; minor allele A of rs651007 remarkably reduced serum ALP levels, but this effect was attenuated in overweight and obese individuals. CONCLUSIONS: Our findings indicate that ABO locus is a major determinant for serum ALP levels in Chinese Han population. Overweight and obesity modifies the effect of ABO locus on serum ALP concentrations.

The g0/g1 switch gene 2 is an important regulator of hepatic triglyceride metabolism.

Nonalcoholic fatty liver disease is associated with obesity and insulin resistance. Factors that regulate the disposal of hepatic triglycerides contribute to the development of hepatic steatosis. G0/G1 switch gene 2 (G0S2) is a target of peroxisome proliferator-activated receptors and plays an important role in regulating lipolysis in adipocytes. Therefore, we investigated whether G0S2 plays a role in hepatic lipid metabolism. Adenovirus-mediated expression of G0S2 (Ad-G0S2) potently induced fatty liver in mice. The liver mass of Ad-G0S2-infected mice was markedly increased with excess triglyceride content compared to the control mice. G0S2 did not change cellular cholesterol levels in hepatocytes. G0S2 was found to be co-localized with adipose triglyceride lipase at the surface of lipid droplets. Hepatic G0S2 overexpression resulted in an increase in plasma Low-density lipoprotein (LDL)/Very-Low-density (VLDL) lipoprotein cholesterol level. Plasma High-density lipoprotein (HDL) cholesterol and ketone body levels were slightly decreased in Ad-G0S2 injected mice. G0S2 also increased the accumulation of neutral lipids in cultured HepG2 and L02 cells. However, G0S2 overexpression in the liver significantly improved glucose tolerance in mice. Livers expressing G0S2 exhibited increased 6-(N-(7-nitrobenz-2-oxa-1-3-diazol-4-yl) amino)-6-deoxyglucose uptake compared with livers transfected with control adenovirus. Taken together, our results provide evidence supporting an important role for G0S2 as a regulator of triglyceride content in the liver and suggest that G0S2 may be a molecular target for the treatment of insulin resistance and other obesity-related metabolic disorders.

A genome-wide association study for serum bilirubin levels and gene-environment interaction in a Chinese population.

Bilirubin is an effective antioxidant and is influenced by both genetic and environmental factors. Recent genome-wide association studies (GWAS) have identified multiple loci affecting serum total bilirubin levels. However, most of the studies were conducted in European populations and little attention has been devoted either to genetic variants associated with direct and indirect bilirubin levels or to the gene-environment interactions on bilirubin levels. In this study, a two-stage GWAS was performed to identify genetic variants associated with all types of bilirubin levels in 10,282 Han Chinese individuals. Gene-environment interactions were further examined. Briefly, two previously reported loci, UGT1A1 on 2q37 (rs6742078 and rs4148323, combined P = 1.44 × 10(-89) and P = 5.05 × 10(-69) , respectively) and SLCO1B3 on 12p12 (rs2417940, combined P = 6.93 × 10(-19) ) were successfully replicated. The two loci explained 9.2% and 0.9% of the total variations of total bilirubin levels, respectively. Ethnic genetic differences were observed between Chinese and European populations. More importantly, a significant interaction was found between rs2417940 in SLCO1B3 gene and smoking on total bilirubin levels (P = 1.99 × 10(-3) ). Single nucleotide polymorphism (SNP) rs2417940 had stronger effects on total bilirubin levels in nonsmokers than in smokers, suggesting that the effects of SLCO1B3 genotype on bilirubin levels were partly dependent on smoking status. Consistent associations and interactions were observed for serum direct and indirect bilirubin levels.

Different physical activity subtypes and risk of metabolic syndrome in middle-aged and older Chinese people.

BACKGROUND: The prevalence of metabolic syndrome (MetS) is growing rapidly in China. Tai chi and dancing are common types of exercise among middle-aged and elderly Chinese. It remains unclear whether these activities are associated with a lower risk of MetS. METHODOLOGY/PRINCIPAL FINDINGS: A total of 15,514 individuals (6,952 men, 8,562 women) aged 50 to 70 years from the Dongfeng-Tongji Cohort in Shiyan, China participated in a cross-sectional study. Physical activity and other lifestyle factors were assessed with semi-structured questionnaires during face-to-face interviews. MetS was defined by the current National Cholesterol Education Program/Adult treatment Panel III criteria for Asian Americans. The prevalence of MetS was 33.2% in the study population. In the multivariable-adjusted logistic regression analyses, total physical activity levels were monotonically associated with a lower odds of MetS [OR 0.75 comparing extreme quintiles, 95% confidence interval (CI) 0.66-0.86, P<0.001]. Compared with non-exercisers in a specific exercise type, jogging (OR 0.82, 95% CI 0.68-1.00, P = 0.046), tai chi (OR 0.72, 95% CI 0.60-0.88, P<0.001), and dancing (OR 0.56, 95% CI 0.47-0.67, P<0.001) were associated with significantly lower odds of MetS. Furthermore, each 1-h/week increment in tai chi and dancing was associated with a 5% (95% CI 2%-9%) and a 9% (95% CI 6%, 12%) lower risk of MetS. CONCLUSIONS/SIGNIFICANCE: Jogging, tai chi and dancing are associated with a significantly lower risk of having MetS in middle-aged and older Chinese. Future intervention studies should consider the role of jogging, tai chi and dancing in preventing MetS.

A genome wide association study identifies common variants associated with lipid levels in the Chinese population.

Plasma lipid levels are important risk factors for cardiovascular disease and are influenced by genetic and environmental factors. Recent genome wide association studies (GWAS) have identified several lipid-associated loci, but these loci have been identified primarily in European populations. In order to identify genetic markers for lipid levels in a Chinese population and analyze the heterogeneity between Europeans and Asians, especially Chinese, we performed a meta-analysis of two genome wide association studies on four common lipid traits including total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL) and high-density lipoprotein cholesterol (HDL) in a Han Chinese population totaling 3,451 healthy subjects. Replication was performed in an additional 8,830 subjects of Han Chinese ethnicity. We replicated eight loci associated with lipid levels previously reported in a European population. The loci genome wide significantly associated with TC were near DOCK7, HMGCR and ABO; those genome wide significantly associated with TG were near APOA1/C3/A4/A5 and LPL; those genome wide significantly associated with LDL were near HMGCR, ABO and TOMM40; and those genome wide significantly associated with HDL were near LPL, LIPC and CETP. In addition, an additive genotype score of eight SNPs representing the eight loci that were found to be associated with lipid levels was associated with higher TC, TG and LDL levels (P = 5.52 × 10(-16), 1.38 × 10(-6) and 5.59 × 10(-9), respectively). These findings suggest the cumulative effects of multiple genetic loci on plasma lipid levels. Comparisons with previous GWAS of lipids highlight heterogeneity in allele frequency and in effect size for some loci between Chinese and European populations. The results from our GWAS provided comprehensive and convincing evidence of the genetic determinants of plasma lipid levels in a Chinese population.

miR-146a in PBMCs modulates Th1 function in patients with acute coronary syndrome.

The upregulation of Th1 cells has been suggested to have an essential function in the development of atherosclerosis (AS). Recent studies indicate that miR-146a is a microRNA specifically and highly expressed in Th1-driven autoimmune disease. The aim of the study was to investigate the possible mechanisms of the miR-146a in the onset of acute coronary syndrome (ACS). The results showed that the expression of miR-146a in peripheral blood mononuclear cells (PBMCs) was significantly increased in patients with ACS. We showed that overexpression of miR-146a in PBMCs could significantly upregulate the function of Th1 cells. Furthermore, we showed that miR-146a treatment could modulate the Th1 differentiation through posttranscriptional enhancing the T-bet pathway in PBMCs. In addition, this study also provided evidence that miR-146a treatment in vitro could induce the protein expression of TNF-alpha, MCP-1, NF-kappaB p65, which are key pro-inflammatory cytokines and critical transcription factor in AS. In contrast, miR-146a inhibitor could attenuate these phenomena significantly. The results support the concept that miR-146a may be a novel regulatory factor in Th1 differentiation and a new therapeutic target for AS and ACS.