Haitao Yang

First Affiliated Hospital of Xinjiang Medical University

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Lijie Yan

University of Miami

Jintao Wu

Nanjing Medical University

Xiang Xie

First Affiliated Hospital of Xinjiang Medical University

Xian‐Wei Fan

Guangxi University

Shanling Wang

Zhejiang Center for Disease Control and Prevention

Wen‐Juan Xiu

Tongji University

Ying‐Ying Zheng

First Affiliated Hospital of Zhengzhou University

Hongyan Duan

Lanzhou University of Technology

Xian‐Geng Hou

Xinjiang Medical University

Yi Yang

Beijing University of Chinese Medicine

Cooperative Institutions

Chinese Academy of Sciences

Fujian Medical University

Sun Yat-sen University

Xinjiang Medical University

University of Chinese Academy of Sciences

Nanjing Medical University

Hebei Medical University

Henan Provincial People's Hospital

Shanxi Medical University

First Affiliated Hospital of Xinjiang Medical University

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Usefulness of a Combination of Interatrial Block and a High CHADS<sub>2</sub> Score to Predict New Onset Atrial Fibrillation

International Heart Journal (2016)

Jintao Wu Shanling Wang Yingjie Chu Deyong Long Jianzeng Dong

Interatrial block (IAB) is associated with an increased risk of atrial fibrillation (AF). The aim of this retrospective study was to investigate the association of a combination of IAB and the CHADS2 score, an AF-related risk score for ischemic stroke, with new onset AF in patients in sinus rhythm. A total of 1,571 patients (803 males, 768 females; mean age: 58 ± 16 years) were included in this study. IAB was defined as a P-wave duration > 120 ms in the 12-lead electrocardiogram, and a high CHADS2 score as ≥ 2 points. During the mean follow-up period of 4.8 ± 0.7 years, new onset AF occurred in 122 patients (16.1 per 1,000 patient-years). The incidence of new onset AF was 4.0 per 1,000 patient-years in patients with no IAB and a low CHADS2 score, and 44.0 per 1,000 patient-years in patients with IAB and a high CHADS2 score. In multivariate Cox regression analysis, the hazard ratio for IAB and a high CHADS2 score compared with no IAB and a low CHADS2 score was 12.18 (95% confidence interval: 6.22-23.87, P < 0.001), after adjustment for age, sex, coronary artery disease, valvular heart disease, smoking, medications, and echocardiographic parameters. In conclusion, IAB and a high CHADS2 score independently and synergistically predict new onset AF in patients in sinus rhythm, indicating an approximately 12-fold higher risk in patients with both IAB and a high CHADS2 score. Patients meeting these criteria should have more aggressive early intervention to prevent AF.

Stroke

10.1536/ihj.15-505

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Citations (23)

Predicting disease trait with genomic data: a composite kernel approach

Briefings in Bioinformatics (2016)

Haitao Yang Shaoyu Li Hongyan Cao Chichen Zhang Yuehua Cui

With the advancement of biotechniques, a vast amount of genomic data is generated with no limit. Predicting a disease trait based on these data offers a cost-effective and time-efficient way for early disease screening. Here we proposed a composite kernel partial least squares (CKPLS) regression model for quantitative disease trait prediction focusing on genomic data. It can efficiently capture nonlinear relationships among features compared with linear learning algorithms such as Least Absolute Shrinkage and Selection Operator or ridge regression. We proposed to optimize the kernel parameters and kernel weights with the genetic algorithm (GA). In addition to improved performance for parameter optimization, the proposed GA-CKPLS approach also has better learning capacity and generalization ability compared with single kernel-based KPLS method as well as other nonlinear prediction models such as the support vector regression. Extensive simulation studies demonstrated that GA-CKPLS had better prediction performance than its counterparts under different scenarios. The utility of the method was further demonstrated through two case studies. Our method provides an efficient quantitative platform for disease trait prediction based on increasing volume of omics data.

Kernel (algebra)

Trait

10.1093/bib/bbw043

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Effect of Tongxinluo on nerve regeneration in mice with diabetic peripheral neuropathy.

PubMed (2015)

Xue Li Jing Zhang Weicheng Zhao Haitao Yang Jianxin Ma

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes. This study aims to investigate the effects of Tongxinluo on the nerve regeneration in diabetic peripheral neuropathy mice. Forty Specefic Pathogen Free (SPF) male KK/Upj—Ay mice were divided into diabetes group, diabetes with high dose Tongxinluo (4g/kg) (D+H), diabetes with mid dose Tongxinluo (2g/kg) (D+M), and diabetes with low dose Tongxinluo (1g/kg) (D+L) groups. Fasting blood glucose (FPG), heat pain threshold, motor nerve conduction velocity (MNCV), insulin—like growth factor—1 (IGF1), activator protein 1 (c—fos), nerve growth factor (NGF), and basic fibroblast growth factor (BFGF) were measured. Results indicated that FPG of diabetes group was significantly higher than that of control group. Heat pain threshold and MNCV were significantly lowered in diabetes group. Expression levels of IGF1, NGF and BFGF were significantly lower than that of control, whereas c—fos expression was significantly higher than that of control group. Tongxinluo treatment (D+M and D+H) significantly up—regulated heat pain threshold, MNCV, and IGF1, NGF and BFGF expression, but decreased c—fos expresson when compared to that of diabetes group. In conclusion, Tongxinluo can ameliorate diabetic peripheral neuropathy, improve MNCV, and promote nerve regeneration. The underlying mechanism needs to be further elucidated.

Diabetic Neuropathy

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GW29-e1510 Invasive reperfusion after 12 hours of the symptom onset remains beneficial in patients with ST-segment elevation myocardial infarction: evidence from a meta-analysis of published data

Journal of the American College of Cardiology (2018)

Haitao Yang Yi‐Tong Ma Yining Yang Xiaomei Li Fen Liu

Elevation (ballistics)

10.1016/j.jacc.2018.08.614

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Rcan1-1L overexpression induces mitochondrial autophagy and improves cell survival in angiotensin II-exposed cardiomyocytes

Experimental Cell Research (2015)

Hongyan Duan Yongqiang Li Lijie Yan Haitao Yang Jintao Wu

Cell Survival

10.1016/j.yexcr.2015.05.003

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IGHG1 upregulation promoted gastric cancer malignancy via AKT/GSK-3β/β-Catenin pathway

Cancer Cell International (2021)

Xinyu Li Wen Chen Chunkang Yang Yisen Huang Jing Jia

Abstract Background Despite current advances in gastric cancer treatment, disease metastasis and chemo-resistance remain as major hurdles against better overall prognosis. Previous studies indicated that IGHG1 as well as -Catenin serve as important regulators of tumor cellular malignancy. Therefore, understanding detailed molecular mechanism and identifying druggable target will be of great potentials in future therapeutic development. Methods Surgical tissues and gastric cancer cell lines were retrieved to evaluate IGHG1 expression for patients with or without lymph node/distal organ metastasis. Functional assays including CCK8 assay, Edu assay, sphere formation assay and transwell assay, wound healing assay, etc. were subsequently performed to evaluate the impact of IGHG1/-catenin axis on tumor cell proliferation, migration and chemo-resistance. Results Gastric cancer tissues and tumor cell lines demonstrated significantly higher level of IGHG1. Functional study further demonstrated that IGHG1 promoted proliferative and migration as well as chemo-resistance of gastric cancer tumor cells. Further experiments indicated that IGHG1 activated AKT/GSK-3/-Catenin axis, which played crucial role in regulation of proliferative and chemo-resistance of gastric cancer cells. Conclusion This study provided novel evidences that IGHG1 acted as oncogene by promotion of gastric cancer cellular proliferation, migration and chemo-resistance. Our research further suggested that IGHG1/AKT/GSK-3β/β-Catenin axis acted as novel pathway which regulated gastric cancer cellular malignant behavior. Our research might inspire future therapy development to promote overall prognosis of gastric cancer patients.

10.1186/s12935-021-02098-1

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Mutated CYP17A1 promotes atherosclerosis and early-onset coronary artery disease

Cell Communication and Signaling (2023)

Ting‐Ting Wu Ying‐Ying Zheng Xiang Ma Wen‐Juan Xiu Haitao Yang

Abstract Background Coronary artery disease (CAD) is a multi-factor complex trait and is heritable, especially in early-onset families. However, the genetic factors affecting the susceptibility of early-onset CAD are not fully characterized. Methods In the present study, we identified a rare nonsense variant in the CYP17A1 gene from a Chinese Han family with CAD. To validate the effect of this variation on atherosclerosis and early-onset coronary artery disease, we conducted studies on population, cells, and mice. Results The mutation precisely congregated with the clinical syndrome in all the affected family members and was absent in unaffected family members and unrelated controls. Similar to the human phenotype, the CYP17A1 -deficient mice present the phenotype of metabolic syndrome with hypertension, increased serum glucose concentration, and presentation of central obesity and fatty liver. Furthermore, CYP17A1 knockout mice or CYP17A1 + ApoE double knockout mice developed more atherosclerotic lesions than wild type (WT) with high fat diary. In cell models, CYP17A1 was found to be involved in glucose metabolism by increasing glucose intake and utilization, through activating IGF1/mTOR/HIF1-α signaling way, which was consistent in CYP17A1 knockout mice with impaired glucose tolerance and insulin resistance. Conclusions Through our study of cells, mice and humans, we identified CYP17A1 as a key protein participating in the pathophysiology of the atherosclerotic process and the possible mechanism of CYP17A1 C987X mutation induced atherosclerosis and early-onset CAD involving glucose homeostasis regulation was revealed.

10.1186/s12964-023-01061-z

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Effects of simvastatin on inflammation in patients with chronic obstructive pulmonary diseases

China Modern Medicine (2011)

Haitao Yang

Objective:To investigate the nature of simvastatin on chronic obstructive pulmonary disease(COPD) patients with nasal lavage,sputum and serum inflammatory cells and(or) inflammation and clinical indices of neurotransmitter.Methods:44 patients with COPD in remission,20 patients received conventional treatment with simvastatin 40 mg/d treatment of 24 patients compared 10 weeks before treatment and after treatment of serum IL-8,IL-6,CRP,VEGF levels and to observe the lung function,clinical symptoms and respiratory questionnaire(SGRQ) score changes.Results:After 10 weeks of simvastatin in serum IL-8 [(6.0 ±2.3) ng/L] than before treatment [(6.9 ±1.9) ng/L] slightly decreased,VEGF [(687.9±30.2) ng/L vs(650.8±32.2) ng/L] slightly elevated,but the difference was not statistically significant(all P0.05);serum CRP,IL-6 levels were significantly reduced [before treatment were(4.2 ±3.6) mg/L,(4.7±1.7) ng/L;treatment were(2.2±2.0) mg/L,(4.3±1.8) ng/L],the difference was statistically significant(P0.05);Clinical score and the SGRQ scores in the symptom score was significantly lower [(3.9±1.0) vs(3.2±0.9);(28.7±11.4) vs(27.9±10.2)],the difference was statistically significant(P0.05),no obvious improvement in lung function(all P0.05).Conventional treatment group,all inflammatory markers and quality of life score,lung function were not significantly improved(all P0.05).Conclusion:Simvastatin can reduce systemic inflammation in COPD patients and relieve symptoms.

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The higher the serum albumin, the better? Findings from the PRACTICE study

European Journal of Internal Medicine (2023)

Ying‐Ying Zheng Tingting Wu Xian‐Geng Hou Yi Yang Haitao Yang

Hypoalbuminemia

Mace

Ischemia-modified albumin

10.1016/j.ejim.2023.07.023

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Impact of XPF rs2276466 polymorphism on cancer susceptibility: a meta-analysis

Bioscience Reports (2019)

Yezhou Liu Kun Liu Xueru Zhao Yidan Sun Ning Ma

Association between the xeroderma pigmentosum complementation group F (XPF)rs2276466 located in the excision repair cross complementation group 4 (ERCC4) gene and cancer susceptibility has been widely investigated. However, results thus far have remained controversial. A meta-analysis was performed to identify the impact of this polymorphism on cancer susceptibility. PubMed, Embase and Science-Web databases were searched systematically up to May 20, 2018, to obtain all the records evaluating the association between the rs2276466 polymorphism and the risk of all types of cancers. We used the odds ratio (OR) as a measure of effect, and pooled the data in a Mantel-Haenszel weighed random-effects meta-analysis to provide a summary estimate of the impact of this polymorphism on gastrointestinal cancer, neurogenic cancer and other cancers (breast cancer and SCCHN). All the analyses were carried out in STATA 14.1.11 case-control studies that consisted of 5730 cases and 6756 controls, were eventually included in our meta-analysis. The significant association was observed between the XPFrs2276466 polymorphism and neurogenic cancer susceptibility (recessive model: OR = 1.648, 95% CI = 1.294-2.098, P<0.001). Furthermore, no significant impact of this polymorphism was detected on decreased gastrointestinal cancer risk (dominant model: OR = 1.064, 95%CI = 0.961-1.177, P = 0.233). The rs2276466 polymorphism might play different roles in carcinogenesis of various cancer types. Current evidence did not suggest that this polymorphism was directly associated with gastrointestinal susceptibility. However, this polymorphism might contribute to increased neurogenic cancer risk. More preclinical and epidemiological studies are still imperative for further evaluation.

10.1042/bsr20181785

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Citations (3)