Depression, a prevalent mental disorder with significant socioeconomic burdens, underscores the urgent need for safe and effective non-pharmacological interventions. Recent advances in microbiome research have revealed the pivotal role of gut microbiota dysbiosis in the pathogenesis of depression. Concurrently, exercise, as a cost-effective and accessible intervention, has demonstrated remarkable efficacy in alleviating depressive symptoms. This comprehensive review synthesizes current evidence on the interplay among exercise, gut microbiota modulation, and depression, elucidating the mechanistic pathways through which exercise ameliorates depressive symptoms via the microbiota-gut-brain (MGB) axis. Depression is characterized by gut microbiota alterations, including reduced alpha and beta diversity, depletion of beneficial taxa (e.g., Bifidobacterium, Lactobacillus, and Coprococcus), and overgrowth of pro-inflammatory and pathogenic bacteria (e.g., Morganella, Klebsiella, and Enterobacteriaceae). Metagenomic analyses reveal disrupted metabolic functions in depressive patients, such as diminished synthesis of short-chain fatty acids (SCFAs), impaired tryptophan metabolism, and dysregulated bile acid conversion. For instance, Bifidobacterium longum deficiency correlates with reduced synthesis of neuroactive metabolites like homovanillic acid, while decreased Coprococcus abundance limits butyrate production, exacerbating neuroinflammation. Furthermore, elevated levels of indole derivatives from Clostridium species inhibit serotonin (5-HT) synthesis, contributing to depressive phenotypes. These dysbiotic profiles disrupt the MGB axis, triggering systemic inflammation, neurotransmitter imbalances, and hypothalamic-pituitary-adrenal (HPA) axis hyperactivity. Exercise exerts profound effects on gut microbiota composition, diversity, and metabolic activity. Longitudinal studies demonstrate that sustained aerobic exercise increases alpha diversity, enriches SCFA-producing genera (e.g., Faecalibacterium prausnitzii, Roseburia, and Akkermansia), and suppresses pathobionts (e.g., Desulfovibrio and Streptococcus). For example, a meta-analysis of 25 trials involving 1 044 participants confirmed that exercise enhances microbial richness and restores the Firmicutes/Bacteroidetes ratio, a biomarker of metabolic health. Notably, endurance training promotes Veillonella proliferation, which converts lactate into propionate, enhancing energy metabolism and delaying fatigue. Exercise also strengthens intestinal barrier integrity by upregulating tight junction proteins (e.g., ZO-1, occludin), thereby reducing lipopolysaccharide (LPS) translocation and systemic inflammation. However, excessive exercise may paradoxically diminish microbial diversity and exacerbate intestinal permeability, highlighting the importance of moderate intensity and duration. Exercise ameliorates depressive symptoms through multifaceted interactions with the gut microbiota, primarily via 4 interconnected pathways. First, exercise mitigates neuroinflammation by elevating anti-inflammatory SCFAs such as butyrate, which suppresses NF-κB signaling to attenuate microglial activation and oxidative stress in the hippocampus. Animal studies demonstrate that voluntary wheel running reduces hippocampal TNF‑α and IL-17 levels in stress-induced depression models, while fecal microbiota transplantation (FMT) from exercised mice reverses depressive behaviors by modulating the TLR4/NF‑κB pathway. Second, exercise regulates neurotransmitter dynamics by enriching GABA-producing Lactobacillus and Bifidobacterium, thereby counteracting neuronal hyperexcitability. Aerobic exercise also enhances the abundance of Lactobacillus plantarum and Streptococcus thermophilus, which facilitate 5-HT and dopamine synthesis. Clinical trials reveal that 12 weeks of moderate exercise increases fecal Coprococcus and Blautia abundance, correlating with improved 5-HT bioavailability and reduced depression scores. Third, exercise normalizes HPA axis hyperactivity by reducing cortisol levels and restoring glucocorticoid receptor sensitivity. In rodent models, chronic stress-induced corticosterone elevation is reversed by probiotic supplementation (e.g., Lactobacillus), which enhances endocannabinoid signaling and hippocampal neurogenesis. Furthermore, exercise upregulates brain-derived neurotrophic factor (BDNF) via microbial metabolites like butyrate, promoting histone acetylation and synaptic plasticity. FMT experiments confirm that exercise-induced microbiota elevates prefrontal BDNF expression, reversing stress-induced neuronal atrophy. Fourth, exercise reshapes microbial metabolic crosstalk, diverting tryptophan metabolism toward 5-HT synthesis instead of neurotoxic kynurenine derivatives. Butyrate inhibits indoleamine 2,3-dioxygenase (IDO), a key enzyme in the kynurenine pathway linked to depression. Concurrently, exercise-induced Akkermansia enrichment enhances mucin production, fortifies the gut barrier, and reduces LPS-driven neuroinflammation. Collectively, these mechanisms underscore exercise as a potent modulator of the microbiota-gut-brain axis, offering a holistic approach to alleviating depression through microbial and neurophysiological synergy. Current evidence supports exercise as a potent adjunct therapy for depression, with personalized regimens (e.g., aerobic, resistance, or yoga) tailored to individual microbiota profiles. However, challenges remain in optimizing exercise prescriptions (intensity, duration, and type) and integrating them with probiotics, prebiotics, or FMT for synergistic effects. Future research should prioritize large-scale randomized controlled trials to validate causality, multi-omics approaches to decipher MGB axis dynamics, and mechanistic studies exploring microbial metabolites as therapeutic targets. The authors advocate for a paradigm shift toward microbiota-centric interventions, emphasizing the bidirectional relationship between physical activity and gut ecosystem resilience in mental health management. In conclusion, this review underscores exercise as a multifaceted modulator of the gut-brain axis, offering novel insights into non-pharmacological strategies for depression. By bridging microbial ecology, neuroimmunology, and exercise physiology, this work lays a foundation for precision medicine approaches targeting the gut microbiota to alleviate depressive disorders.

BACKGROUND: Myocardial ischemia-reperfusion (I/R) is a serious and irreversible injury. Bone marrow-derived mesenchymal stem cells (MSCs) is considered to be a potential therapy for I/R injury due to the paracrine effects. High-mobility group box 1 (HMGB1) is a novel mediator in MSC and regulates the response of inflammation injury. Signal Transduction and Transcription Activator 3 (STAT3) is a critical transcription factor and important for release of paracrine factors. However, the relationship between HMGB1 and STAT3 in paracrine effect of MSC remains unknown. METHODS: In vitro, hypoxia/reoxygenation injury model was established by AnaeroPack System and examined by Annexin V flow cytometry, CCK8 assay and morphology observation. Detection of apoptotic proteins and protein expression of HMGB1 and STAT3 by Western blot. RESULTS: The conditioned medium of MSCs with or without LPS pretreatment was cocultured with H9C2 cells for 24 h before hypoxia treatment and MSC showed obvious cardiomyocytes protect role, as evidence by decreased apoptosis rate and improved cells viability, and LPS pretreated MSC exhibited better protect role than untreated MSC. However, such effect was abolished in HMGB1 deficiency group, silencing HMGB1 decreased the secretion of vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), insulin growth factor (IGF), cell viability, and the expression of STAT3. Furthermore, STAT3 silence attenuated the protective effect of LPS in MSC. CONCLUSIONS These findings suggested that LPS improved MSC-mediated cardiomyocytes protection by HMGB1/STAT3 signaling.

Objective    To summarize the clinical experience in the treatment of high-risk patients with severe aortic valve disease by transcatheter aortic valve implantation (TAVI) via heart apex approach and to evaluate the early efficacy. Method    Five patients who underwent TAVI via heart apex approach from September 2017 to February 2019 in Henan Thoracic Hospital were retrospectively analyzed, including 3 males and 2 females, aged 65-84 (74.6±4.5) years. Result    All operations were performed through a small left incision into the thoracic cavity (3-5 cm), and then through the J-Valve transport system, the aortic valve was successfully released via heart apex after precise positioning under digital subtraction angiography. One patient developed ventricular fibrillation during the operation, and the operation was completed with the assistance of emergency femoral arteriovenous catheterization cardiopulmonary bypass; one patient underwent percutaneous coronary intervention first because of severe coronary stenosis; one patient had paroxysmal atrial fibrillation during the perioperative period, and had hepatorenal insufficiency and thrombocytopenia after the operation, and was improved after medical treatment; one patient had perivalvular leak during the operation, and was improved after re-implantation of the valve; one patient was in stable condition during operation and recovered smoothly after operation. Surgery was successful in all 5 patients. The follow-up time was 2-19 months, and the early clinical effect was good. Conclusion    The short-term clinical efficacy of TAVI via heart apex approach in the treatment of high-risk severe aortic valve disease is definite and safe, but the long-term and medium-term effects need to be further evaluated.

Objective To analyze the clustering of major cardiovascular risk factors among population with different level of fasting blood glucose (FBG) in Jiangsu provincial communities. Methods A population-based screening project was conducted during 2015-2017, with 83 522 residents aged 35-75 years from 6 areas included in the study. Prevalence and the clustering of four cardiovascular risk factors (hypertension, obesity, dyslipidemia and smoking) were analyzed. Binary Logistic regression analysis was performed to explore the relationship between FBG and cardiovascular risk factor clustering. Results The prevalence of diabetes was 18.9% among adults aged 35-75 years in Jiangsu province, and 41.4% of them were aware of their disease. Among undiagnosed population, the odd ratios (OR) of cardiovascular risk factors clustering in impaired fasting glucose (IFG) and hyperglycemia group was 1.29 (OR=1.29，95% CI:1.24-1.36，P<0.001) and 1.99 (OR=1.99，95% CI:1.89-2.08，P<0.001), compared with normal FBG group. The control rate of FBG was 15.5% among diagnosed cases. There was no difference in the risk clustering between diabetes patient with and without control of FBG. Conclusions Hyperglycemia and IFG increase the risk of cardiovascular risk factor clustering. Comprehensive interventions should be served as an important role to keep blood glucose at a normal level in high-risk population.

BACKGROUNDThe patients with early-onset epileptic encephalopathy (EOEE) suffer from neurodevelopmental delay. The aim of this study was to analyze the clinical manifestations and amplitude-integrated encephalogram (aEEG) characteristics of infants with EOEE with onset within the neonatal period, to make early diagnosis to improve the prognosis.

METHODSOne-hundred and twenty-eight patients with neonatal seizure were enrolled and followed up till 1 year old. Sixty-six neonates evolved into EOEE were as the EOEE group, the other 62 were as the non-EOEE (nEOEE) group. Then we compared the clinical and aEEG characteristics between the two groups to analyze the manifestations in neonates with EOEE.

RESULTSCompared to the nEOEE group, the incidence of daily seizure attacks, more than two types of convulsions, more than two antiepileptic drugs (AEDs) application, severely abnormal aEEG background, absence of cyclicity, and more than two seizures detection were significantly higher in the EOEE group (P < 0.05) (97% vs. 54.8%; 30.3% vs. 14.5%; 97.0% vs. 25.4%; 39.4% vs. 3.2%; 57.6% vs. 9.7%; and 56% vs. 3.2%, respectively). Severely abnormal background pattern (odds ratio [OR] = 0.081, 95% confidence interval [CI]: 0.009-0.729, P = 0.025) and more than two seizures detection by aEEG (OR = 0.158, 95% CI: 0.043-0.576, P = 0.005) were the independent risk factors for the evolvement into EOEE. The upper and lower margins of active sleep (AS) and quiet sleep (QS) were significantly higher in EOEE group than those of the control group (P < 0.05) (34.3 ± 13.6 vs. 21.3 ± 6.4; 9.9 ± 3.7 vs. 6.7 ± 2.2; 41.2 ± 15.1 vs. 30.4 ± 11.4; and 11.9 ± 4.4 vs. 9.4 ± 4.0; unit: μV, respectively). AS upper margin was demonstrated a higher diagnostic specificity and sensitivity for EOEE than another three parameters according to the receiver operating characteristic curves; the area under the curve was 0.827.

CONCLUSIONSThe clinical characteristics of the neonatal seizure which will evolve into EOEE were more than two AEDs application, high seizure frequency (daily attack), and more than two types of the seizure. Significant high voltage, severely abnormal background, absence of cyclicity, and more than two seizures detected on aEEG were the meaningful indicators to the prediction of EOEE.

The proliferation of cardiac fibroblasts (CFs) is a key pathological process in the cardiac remodeling. To establish an objective, quantitative method for the analysis of cell proliferation and cell cycle, we applied the high-content screening (HCS) and flow cytometry (FCM) techniques. CFs, isolated by enzyme digestion from newborn C57BL/6J mice, were serum starved for 12 h and then given 10% fetal bovine serum (FBS) for 24 h. Followed by BrdU and DAPI (or 7-AAD) staining, CFs proliferation and cell cycle were analyzed by HCS and FCM, respectively. Discoidin domain receptor 2 (DDR2) staining indicated that the purity of isolated CFs was over 95%. (1) HCS analysis showed that the ratio of BrdU-positive cells was significantly increased in 10% FBS treated group compared with that in serum-free control group [(12.96 ± 0.67)% vs (2.77 ± 0.33)%; P < 0.05]. Cell cycle analysis showed that CFs in G0/G1 phase were diploid, and CFs in S phase were companied with proliferation, DNA replication and enlarged nuclei; CFs in G2 phase were tetraploid, and CFs in M phase produced two identical cells (2N). (2) FCM analysis showed that the ratio of BrdU-positive cells was increased in 10% FBS treated group compared with that in the control group [(11.10 ± 0.42)% vs (2.22 ± 0.31)%; P < 0.05]; DNA content histogram of cell cycle analysis indicated that the platform of S phase elevated in 10% FBS group compared with control group. (3) There were no differences between the two methods in the results of proliferation and cell cycle analysis. In conclusion, HCS and FCM methods are reliable, stable and consistent in assessment of the proliferation and cell cycle in CFs.
Animals ; Cell Cycle ; Cell Proliferation ; Fibroblasts ; cytology ; Flow Cytometry ; Mice ; Mice, Inbred C57BL ; Mitosis ; Myocardium ; cytology

OBJECTIVETo investigate cholesteryl ester transfer protein (CETP) gene polymorphism -629C/A among Han Chinese patients with coronary heart disease (CHD) in Tianjin region, and to assess the influence of genetic factors on therapeutic effect of atorvastatin and clinical outcome in order to provide a pharmacogenomic basis for personalized treatment.

METHODSFrom October 2010 to July 2011, 232 patients with angiographically confirmed CHD were recruited. Polymorphism of position -629 of CETP gene promoter was determined with polymerase chain reaction - restricted fragment length polymorphism (PCR-RFLP) method. Serum level of CETP was determined with enzyme-linked immunosorbent assay (ELISA). Lipid level in all patients was determined at baseline and after 12 months of treatment with 20 mg/d atorvastatin. Clinical follow-up was carried out for more than a year (12-23 months). Major adverse cardiac events including death, non-fatal infarction, revascularization and stroke (MACE) were recorded. A Kaplan-Meier log-rank test was used to compare MACE-free survival for individuals with various genotypes.

RESULTSThe frequency of -629A allele was 0.408. Compared with CC or CA genotypes, individuals with AA genotype had lower CETP levels and higher high-density lipoprotein cholesterol (HDL-C) levels, albeit without statistical significance (F = 0.893, P = 0.411 and F = 1.279, P = 0.282, respectively). There also appeared to be a negative correlation between serum HDL-C and CETP levels, though no statistical significance was detected (r = -0.151, P = 0.081). After 12 months atorvastatin therapy, individuals with CC genotype had greater reduction of low-density lipoprotein cholesterol (LDL-C), reduced LP(a) and elevated HDL-C compared with CA or AA genotypes. LDL-C level has decreased by 35.41% in CC homozygotes, 18.84% in CA heterozygotes and 8.15% in AA homozygotes (P = 0.001). HDL-C level has increased by 14.37% in CC homozygotes, 10.48% in CA heterozygotes and 6.64% in AA homozygotes, respectively. However, above changes did not reach statistical significance (P = 0.470). The incidence of MACE after a mean follow-up of (18.66 ± 5.99) months was 7.76%, which included 2 (0.86%) deaths, 5 (2.16%) non-fatal infarctions, 9 (3.88%) revascularizations and 2 (0.86%) strokes. The cumulative MACE-free survival rates were 92.4%, 85.3% and 65.0% for CC, CA and AA genotypes, respectively (Log-rank P = 0.444).

CONCLUSIONOur results suggested that AA variant for the -629A allele of CETP gene had higher HDL-C levels and reduced CETP levels, though patients with CC genotype appeared to have better benefited from statin therapy with reduction in LDL-C and LP(a) levels. Long-term clinical prognosis was however not affected by the 3 genotypes.

Adult ; Aged ; Atorvastatin Calcium ; Cholesterol Ester Transfer Proteins ; blood ; genetics ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Coronary Artery Disease ; blood ; drug therapy ; genetics ; Female ; Heptanoic Acids ; therapeutic use ; Humans ; Male ; Middle Aged ; Mutation, Missense ; Polymorphism, Single Nucleotide ; Pyrroles ; therapeutic use ; Treatment Outcome

Objective To investigate the geographical characteristics of single nucleotide polymorphism(SNP) of candidate genes associated with coronary artery disease in Chinese Han population.Methods Study population were Chinese Han nationality recruited from Xi'an,Shiyan and Ningbo districts.Patients with coronary artery disease were defined by coronary angiography with stenosis ≥ 50% and control subjects with stenosis ＜10%,respectively.The DNA was extracted from peripheral white blood cell by approach comprised proteinase K digestion,phenol and chloroform extraction as well as isopropanol precipitation.The SNP of ATP-binding cassette transporter(ABCA1)-G596A,cholesteryl ester transfer protein(CETP)-Taq1B,Lipoprotein lipase(LPL)-Hind Ⅲ and LPL-Pvu Ⅱ were genotyped by PCR-RFLPs,and verified by gene sequencing.Results A Total of 615 patients undertaken coronary angiography were recruited from cardiac center in Xi'an(220),Ningbo(209)and Shiyan district(186),China (mean age 60±10 years,75.9% males).Diabetes melitus was more prevalent in Xi'an Cohort population than Shiyan and Ningbo cohort(P＜0.01).Plasma total cholesterol,LDL cholestcol and trigtyceride levels in Xi'an Cohort population were significantly higher,and HDL-C siginificantly lower than in Shiyan and Ningbo cohort population [HDL-C:(1.17±0.48)mmol/L vs.(1.25±0.33)mmol/L and (1.29±0.44)mmol/L,P＜0.05].Distribution differences for ABCA1-G596A and CETP-Taq1B genotypes were found in Xi'an Cohort population compared to Ningbo and Shiyan cohorts(for ABCA1,Xi'an:0.24,0.53,0.23 and Shiyan:0.17,0.62,0.21 and Ningbo:0.34,0.37,0.29,for GG,AG,AA,respectively,P＜0.01;and for CETP,Xi'an:0.29,0.54,0.17 and Shiyan:0.38,0.40,0.22 and Ningbo:0.39,0.49,0.12 for B181,B182,B282,respectively,P＜0.01),but not for LPL variants.ABCA1-G596A variant predicted HDL-C [Xi'an:(1.2±0.3)mmol/L,(1.3±0.2)mmol/L and(1.4±0.4)mmol/L,P=0.01;Shiyan:(1.1±0.4)mmol/L:(1.2±0.3)mmol/L and(1.3±0.4)mmol/L,P=0.03;Ningbo,(1.2±0.3)mmol/L,(1.3±0.4)mmol/L and(1.4±0.3)mmol/L,across GG,Gato AA genotype,respectively,P=0.01]and TG levels[Xi'an:(2.4±1.3)mmol/L,(1.9±0.9)mmol/L and(1.6±0.8)mmol/L,P＜0.01;Shiyan:(2.1±1.0)mmol/L,(1.9±0.8)mmol/L and(1.8±0.7)mmol/L,P=0.03;Ningbo:(1.9±1.1) mmol/L,(1.8±0.9) mmol/L and(1.6±0.7)mmol/L,across GG,GA to AA genotype,P=0.05] with dose-dependent relationship.LPL-Hind Ⅲ(+)carriers had higher triglycerides in three cohort population[Xi'an:(2.2±1.0)mmol/L,(1.8±0.9)mmol/L,(1.6±0.7)mmol/L,P=0.01;Shiyan:(2.1±0.7)mmol/L,(1.9±1.0)mmol/L,(1.7±0.6)mmol/L,P=0.01;Ningbo:(1.8±1.0)mmol/L,(1.6±0.6)mmol/L and(1.4±0.5)mmol/L,for +/+,+/-and-/-genotypes,respectively,P=0.001].SNP of CETP-Taq1B,LPL-Hind Ⅲ and LPL-Pvu Ⅱ predicted HDL-C and/or TG levels in different cohort population with different manners.All these SNP were not significantly associated with the development of coronary artery disease (all P＞0.05).Conclusion A geographical heterogeneity of environmental and genetic risk factors related to the development of coronary artery disease exists in Chinese Han population.Irrespective of the different geographical cohort of Chinese Han population,the SNP of candidate genes can partly predict the differences in risk-related plasma HDL-C and/or TG levels rather than angiographic coronary artery disease.

OBJECTIVETo investigate the levels of cardiovascular disease risk factors and their relations to clinical phenotype associated with coronary artery disease (CAD).

METHODSThe subjects were recruited from five independent cardiovascular centers. Coronary angiography was employed to define the CAD with stenosis in each major vessel > or = 70% and control with stenosis < 10% in every lesion. The classic risk factors including family history, body mass index, smoking habits, hypertension, diabetes mellitus, and serum lipid levels were surveyed according to established criteria. Associations between risk levels and clinical phenotypes were assessed by case control and correlation analysis.

RESULTSA total of 762 individuals were collected, including 481 men and 281 women, aged from 17 to 81 (mean 60 +/- 10) years. The patients with CAD accounted for 55.5% of all participants, and controls 44.5%, respectively. Compared with the pattern in published data, our study showed that mean serum high density lipoprotein cholesterol (HDL-C) level was significantly lower (P < 0.001) and triglycerides was significantly higher (P < 0.001), while total cholesterol (TC) and low density lipoprotein cholesterol levels were comparative (both P > 0.05). The prevalence of low HDL-C (< 40 g/L) and hypertriglyceridemia (> 150 g/L) were 27.2% and 41.4%, respectively. Mean serum levels of HDL-C and apolipoprotein A1 were significantly higher in female subjects than in male (P < 0.001). Lower HDL-C functioned as an independent risk factor for CAD only in men (RR = 2.8, 95% CI: 1.5-4. 2, P < 0.001), yet increased non-HDL cholesterol combined with diabetes mellitus and obesity seemed to play a key role in the development of CAD in women. Similarity in risk association with CAD was found for hypertension and TC/HDL ratio in male and female subjects, while family history had no relationship with the presence of CAD.

CONCLUSIONIt is remarkable that emphasis of intervention in future should be given on the prevalent low serum HDL-C and its strong risk correlation with the presence of CAD in male subjects of Chinese Han population.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; China ; epidemiology ; Coronary Artery Disease ; epidemiology ; Ethnic Groups ; Female ; Humans ; Male ; Middle Aged ; Risk Factors

OBJECTIVETo study the single nucleotide polymorphisms in genes associated with the high density lipoprotein (HDL) metabolism in Chinese population.

METHODSTwo hundred and nine normal Han ethnic subjects, aged 59+/-10 years, were recruited from 5 medical centers in western part of China. DNA was extracted by proteinase K digestion, phenol and chloroform extraction as well as isopropanol precipitation. The polymerase chain reaction (PCR)-restriction fragment length polymorphisms (RFLP) in conjunction with sequencing were employed to test the single nucleotide polymorphisms (SNPs) in ATP-binding cassette transporter (ABCA1), cholesteryl ester transfer protein (CETP) and lipoprotein lipase (LPL) genes.

RESULTSThe allelic frequencies of A and G of ABCA1 gene are 53.4% and 46.6%; of B2 and B1 allele of CETP, 41.0% and 59.0%; of HindIII (-) and (+) allele of LPL, 18.9% and 81.1%; and of PvuII(+) and (-) allele of LPL, 66.0% and 34.0%, respectively. All genotype frequencies fit well with the Hardy-Weinberg equilibrium; the significant linkage disequilibrium exists between LPL HindIII(+)and PvuII(+) polymorphisms. All of the RFLP in these genes result from the single nucleic substitution in fragment recognized by corresponding restriction enzymes.

CONCLUSIONThe genetic polymorphisms of ABCA1, LPL-HindIII and LPL-PvuII in Chinese Han ethnic population are significantly different from Caucasians residing in USA or Europe.

ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters ; genetics ; Aged ; Asian Continental Ancestry Group ; genetics ; Base Sequence ; China ; Cholesterol Ester Transfer Proteins ; genetics ; Female ; Gene Frequency ; Genotype ; Humans ; Linkage Disequilibrium ; Lipoprotein Lipase ; genetics ; Lipoproteins, HDL ; metabolism ; Male ; Middle Aged ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA