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| 1 | 2018 Chinese Pediatric Cardiology Society(CPCS) guideline for diagnosis and treatment of syncope in children and adolescents显示文摘Syncope belongs to the transient loss of consciousness(TLOC), characterized by a rapid onset, short duration, and spontaneous complete recovery. It is common in children and adolescents, accounting for 1% to 2% of emergency department visits.Recurrent syncope can seriously affect children's physical and mental health, learning ability and quality of life and sometimes cardiac syncope even poses a risk of sudden death. The present guideline for the diagnosis and treatment of syncope in children and adolescents was developed for guiding a better clinical management of pediatric syncope. Based on the globally recent development and the evidence-based data in China, 2018 Chinese Pediatric Cardiology Society(CPCS) guideline for diagnosis and treatment of syncope in children and adolescents was jointly prepared by the Pediatric Cardiology Society, Chinese Pediatric Society, Chinese Medical Association(CMA)/Committee on Pediatric Syncope, Pediatricians Branch, Chinese Medical Doctor Association(CMDA)/Committee on Pediatric Cardiology, Chinese College of Cardiovascular Physicians, Chinese Medical Doctor Association(CMDA)/Pediatric Cardiology Society, Beijing Pediatric Society, Beijing Medical Association(BMA). The present guideline includes the underlying diseases of syncope in children and adolescents, the diagnostic procedures, methodology and clinical significance of standing test and headup tilt test, the clinical diagnosis vasovagal syncope, postural orthostatic tachycardia syndrome, orthostatic hypotension and orthostatic hypertension, and the treatment of syncope as well as follow-up. | Cheng Wang Yaqi Li Ying Liao Hong Tian Min Huang Xiangyu Dong Lin Shi Jinghui Sun Hongfang Jin Junbao Du Jindou An Jie Chen Mingwu Chen Qi Chen Sun Chen Yonghong Chen Zhi Chen Adolphus Kai-tung Chau Junbao Du Zhongdong Du Junkai Duan Hongyu Duan Xiangyu Dong Lin Feng Lijun Fu Fangqi Gong Yonghao Gui Ling Han Zhenhui Han Bing He Zhixu He Xiufen Hu Yimin Hua Guoying Huang Min Huang Ping Huang Yujuan Huang Hongfang Jin Mei Jin Bo Li Fen Li Tao Li Xiaohui Li Xiaoyan Liu Yan Li Haitao Lv Tiewei Lv Zipu Li Luyi Ma Silin Pan Yusheng Pang Hua Peng Yuming Qin Jie Shen Lin Shi Kun Sun Jinghui Sun Hong Tian Jie Tian Cheng Wang Hong Wang Lei Wang Jinju Wang Wendi Wang Yuli Wang Rongzhou Wu Tianhe Xia Yanyan Xiao Chunhong Xie Yanlin Xing Zhenyu Xiong Baoyuan Xu Yi Xu Hui Yan Shiwei Yang Qijian Yi Xia Yu Xianyi Yu Yue Yuan Hongyan Zhang Huili Zhang Li Zhang Qingyou Zhang Xi Zhang Yanmin Zhang Zhiwei Zhang Cuifen Zhao Bin Zhou Hua Zhu | 2018 | Science Bulletin2018，63，23： | 54 |
| 2 | An EGLN1 mutation may regulate hypoxic response in cyanotic congenital heart disease through the PHD2/HIF-1A pathway显示文摘Cyanotic congenital heart disease(CCHD),a term describing the most severe congenital heart diseases are characterized by the anatomic malformation of a right to left shunt.Although the incidence of CCHD are far less than the that of congenital heart diseases(CHD),patients with CCHD always present severe clinical features such as hypoxia,dyspnea,and heart failure.Chronic hypoxia induces hypoxemia that significantly contributes to poor prognosis in CCHD.Current studies have demonstrated that the prolyl-4-hydroxylase2(PHD2,encoded by EGLN1)/hypoxia-inducible factor-1A(HIF-1A)pathway is a key regulator of hypoxic response.Thus,we aim to assess the associations of single polymorphisms(SNPs)of the EGLN1 gene and hypoxic response in CCHD.A missense variant of EGLN1 c.380G>C(rs1209790)was found in 46 patients(46/126),with lower hypoxia incidence and higher rate of collateral vessel formation,compared with the wild type(P<0.05).In vitro experiments,during hypoxia,EGLN1 mutation reduced EGLN1 expression compared with the wild type,with higher HIF-1A,VEGF and EPO expression levels in the mutant.No difference in HK1 expression was observed between the mutant and wild type.CCHD patients with c.380G>C showed improved response to hypoxia compared with the wild-type counterparts.The EGLN1 c.380G>C mutation improves hypoxic response through the PHD2/HIF-1A pathway,which may provide a molecular mechanism for hypoxic response in CCHD.The effects of the EGLN1 c.380G>C mutation on CCHD prognosis deserve further investigation. | Yuanlin Zhou Na Ouyang Lingjuan Liu Jie Tian Xupei Huang Tiewei Lu | 2019 | Genes & Diseases2019，6，1： | 7 |
| 3 | Acetylation of H3K4,H3K9,and H3K27 mediated by p300 regulates the expression of GATA4 in cardiocytes显示文摘GATA4 is a particularly important cardiogenic transcription factor and serves as a potent driver of cardiogenesis.Recent progress in the field has made it clear that histone acetylation can influence gene expression through changing the structure of chromatin.Our previous research had revealed that hypo-acetylation could repress gata4 expression in cardiocytes,however the underlying mechanism by which this occurred was still unclear.To reveal the mechanism of histone acetylation involved in the regulation of gata4 transcription,we concentrated on P300,one of the important histone acetyltransferase associated with cardiogenesis.We found that P300 participated in gata4 expression through regulating histone acetylation in embryonic mouse hearts.RNAi-mediated downregulation of P300 modulated the global acetylation of H3 and the acetylation of H3K4,H3K9,and H3K27 in gata4 and Tbx5 promoters.Interestingly,there was an obvious inhibition of gata4 transcription,whereas Tbx5 was not influenced.Furthermore,SGC-CBP30,the selective inhibitor of the bromodomain in CBP/P300,downregulated gata4 transcription by repressing the acetylation of H3K4,H3K9,and H3K27 in the gata4 promoters.Taken together,our results identified that acetylation of H3K4,H3K9,and H3K27 mediated by P300 plays an important role in regulation of gata4 expression in cardiogenesis. | Wei Zhou Dagui Jiang Jie Tian Lingjuan Liu Tiewei Lu Xupei Huang Huichao Sun | 2019 | Genes & Diseases2019，6，3： | 3 |
| 4 | miR-429 Modulates the expression of c-myc in human gastric carcinoma cells 显示文摘 | Tiewei Sun Chunmei Wang Jun Xing | 2011 | Eur J Cancer2011，16，： | 1 |
| 5 | Identification of Distinct Basal and Luminal Subtypes of Muscle-Invasive Bladder Cancer with Different Sensitivities to Frontline Chemotherapy显示文摘 | Woonyoung Choi Sima Porten Seungchan Kim Daniel Willis Elizabeth R. Plimack Jean Hoffman-Censits Beat Roth Tiewei Cheng Mai Tran I-Ling Lee Jonathan Melquist Jolanta Bondaruk Tadeusz Majewski Shizhen Zhang Shanna Pretzsch Keith Baggerly Arlene Siefker-Rad | 2014 | Cancer Cell2014，，： | 1 |
| 6 | Effect of chloride source concentration on chloride diffusion in concrete显示文摘 | ZHANG Tiewei GJORV O E | 2005 | ACI Materials Journal2005，102，5： | 1 |
| 7 | Electrochemical method for accelerated testing of chloride diffusivity in concrete显示文摘 | ZHANG Tiewei GJORV O E | 1994 | Cement and Concrete Research1994，24，8： | 1 |
| 8 | miR-429 Modulates the expression of c-myc in human gastric carcinoma cells显示文摘 | Tiewei Sun Chunmei Wang Jun Xing Dequan Wu | 2011 | European Journal of Cancer2011，，17： | 1 |
| 9 | Nanoparticle carriers based on copolymers of poly (e-caprolactone) andhyperbranched polymers for drug delivery显示文摘 | Wang Tiewei Li Mingjun Gao Hongxia | 2011 | J Colloid Inter{ Sci2011，353，1： | 1 |
| 10 | Diffusion behavior of chloride ions in concrete 显示文摘 | Zhang Tiewei Odd E | 1996 | Cement and Concrete Research1996，26，6： | 1 |
| 11 | Carotid cavernous fistulas treated by endovascular covered stent grafts with follow-up results 显示文摘 | Tiewei Q Ali A Shaolei G | 2010 | Br J Neurosurg2010，24，： | 1 |
| 12 | Hydroxypropyl-β-cyclodextrin copolymers and their nanoparticles as doxorubicin delivery system 显示文摘 | Wang Tiewei Zhang Chunling Liang Xingjie | 2011 | J Pharm Sci2011，100，3： | 1 |
| 13 | Gjorv, An electrochemical methods for accelerated testing of chloride diffusivity in concrete显示文摘 | Zhang Tiewei and Odd E | 1994 | Cement and Concrete Research1994，24，8： | 1 |
| 14 | An eIF3a gene mutation dysregulates myocardium growth with left ventricular noncompaction via the p-ERK1/2 pathway显示文摘Left ventricular noncompaction(LVNC)is a heterogeneous disorder with undlear genetic causes and an unknown mechanism.elF3a,an important member of the Eukaryotic translation initiation factor 3(elF3)family,is involved in multiple biological processes,indluding cell prolif eration and migration during myocardial development,suggesting it could play a role in LVNC development.To investigate the association between a novel variant(C.1145 A->G)in elF3a and LVNC,and explore potential mechanisms that could lead to the development of LVNC.A novel elF3a variant,C.1145 A->G,was identified by whole-exome sequencing in a familial pedigree with LVNC.Adenovirus vectors containing wild-type elF 3a and the mutated version were constructed and co-infected into H9C2 cells.Cell proliferation,apoptosis,cell migration,and differentiation,as well as phosphorylation of ERK1/2 were stud-ied and were measured by proliferation assays,flow cytometry,real-time PCR and Westem blot,respectively.The elF3a mutation inhibited the proliferation of H9C2 cells,induced apoptosis,promoted cell migration,and inhibited the dif ferentiation of human induced plurip-otent stem cell-derived cardiomyocytes(hiPSC-CMs).The effect of the elF3a mutation may be attributed to a decrease in expression of p-ERK1/2.A novel elF3a gene mutation disrupted the p-ERK1/2 pathway and caused decreased myocardium proliferation,differentiation,acceler-ated migration.This finding may provide some insight into the mechanism involved in LVNC development. | Mei Ge Xuehan Bai Aoyi Liu Lingjuan Liu Jie Tian Tiewei Lu | 2021 | Genes & Diseases2021，8，4： | 1 |
| 15 | Assessment of Building Physical Vulnerability in Earthquake‑Debris Flow Disaster Chain显示文摘Large earthquakes not only directly damage buildings but also trigger debris fows,which cause secondary damage to buildings,forming a more destructive earthquake-debris fow disaster chain.A quantitative assessment of building vulnerability is essential for damage assessment after a disaster and for pre-disaster prevention.Using mechanical analysis based on pushover,a physical vulnerability assessment model of buildings in the earthquake-debris fow disaster chain is proposed to assess the vulnerability of buildings in Beichuan County,China.Based on the specifc sequence of events in the earthquake-debris fow disaster chain,the seismic vulnerability of buildings is 79%,the fow impact and burial vulnerabilities of damaged buildings to debris fow are 92%and 28%respectively,and the holistic vulnerability of buildings under the disaster chain is 57%.By comparing diferent vulnerability assessment methods,we observed that the physical vulnerability of buildings under the disaster chain process is not equal to the statistical summation of the vulnerabilities to independent hazards,which implies that the structural properties and vulnerability of buildings have changed during the disaster chain process.Our results provide an integrated explanation of building vulnerability,which is essential for understanding building vulnerability in earthquake-debris fow disaster chain and building vulnerability under other disaster chains. | Hao Zheng Zhifei Deng Lanlan Guo Jifu Liu Lianyou Liu Tiewei Li Huan Zheng Tao Zheng | 2023 | International Journal of Disaster Risk Science2023，14，4： | 0 |
| 16 | An Improved Immune Clone Selection Algorithm for Parameters Optimization of Marine Electric Power System Stabilizer显示文摘In themarine electric power system,the marine generators will be disturbed by the large change of loads or the fault of the power system.The marine generators usually installed power system stabilizers to damp power system oscillations through the excitation control.This paper proposes a novel method to obtain optimal parameter values for Power System Stabilizer(PSS)to suppress low-frequency oscillations in the marine electric power system.In this paper,a newly developed immune clone selection algorithm was improved from the three aspects of the adaptive incentive degree,vaccination,and adaptive mutation strategies.Firstly,the typical PSS implementation type of leader-lag structure was adopted and the objective function was set in the optimization process.The performance of PSS tuned by improved immune clone selection algorithm was compared with PSS tuned by basic immune clone selection algorithm(ICSA)under various operating conditions and disturbances.Then,an improved immune clone selection algorithm(IICSA)optimization technique was implemented on two test systems for test purposes.Based on the simulations,it is found that an improved immune clone selection algorithm demonstrates superiority over the basic immune clone selection algorithm in getting a smaller number of iterations and fast convergence rates to achieve the optimal parameters of the power system stabilizers.Moreover,the proposed approach improves the stability and dynamic performance under various loads conditions and disturbances of the marine electric power system. | Zong Bi Weifeng Shi Tiewei Song | 2022 | Energy Engineering2022，119，3： | 0 |
| 17 | A Case of Pediatric Heart Failure Caused by Anomalous Origin of the Left Coronary Artery from the Pulmonary Artery: Case Report and Literature Review显示文摘A female patient aged 3 months and 10 days was admitted to the cardiology department because of symptoms of heart failure.According to the echocardiography results,the patient received a diagnosis of primary endocardial fi broelastosis and was treated withγ-globulin,prednisone,digoxin,and diuretics.Coronary computed tomographic angiography and coronary angiography were performed as there was no improvement after 2 months of treatment.Finally,the patient received a diagnosis of anomalous origin of the left coronary artery from the pulmonary artery(ALCAPA).ALCAPA is a rare congenital heart defect that can cause severe heart failure during infancy,and is easily misdiagnosed clinically.In this report,we show the process of misdiagnosis of the case and consult the relevant literature,hoping to improve the understanding and early diagnosis of ALCAPA. | Lei Zhang Tiewei Lv Xiaoyan Liu Chuan Feng Min Zheng Jie Tian Huichao Sun | 2021 | Cardiovascular Innovations and Applications2021，，2： | 0 |
| 18 | Intranuclear cardiac troponin I plays a functional role in regulating Atp2a2 expression in cardiomyocytes显示文摘In the past studies,it is shown that cardiac troponin I(cTnI,encoded by TNNI3),as a cytoplasmic protein,is an inhibitory subunit in troponin complex,and involves in cardiomyocyte diastolic regulation.Here,we assessed a novel role of cTnI as a nucleoprotein.Firstly,the nuclear translocation of cTnI was found in mouse,human fetuses and rat heart tissues.In addition,there were differences in percentage of intranuclear cTnI in different conditions.Based on weighted gene co-expression network analyses(WGCNA)and verification in cell experiments,a strong expression correlation was found between TNNI3 and Atp2a2,which encodes sarco-endoplasmic reticulum Ca2t ATPase isoform 2a(SERCA2a),and involves in ATP hydrolysis and Ca2t transient.TNNI3 gain and loss caused Atpa2a2 increase/decrease in a dosedependent manner both in mRNA and protein levels,in vivo and in vitro.By using ChIP-sequence we demonstrated specific binding DNA sequences of cTnI were enriched in ATP2a2 promoter239we889 region and the specific binding sequence motif of cTnI was analyzed by software as'CCAT',which has been reported to be required for YY1 binding to the promoter region of YY1-related genes.Moreover,it was further verified that pcDNA3.1()-TNNI3 could express cTnI proteins and increase the promoter activity of Atp2a2 through luciferase report assay.In the end,we evaluated beat frequencies,total ATP contents,Ca2t transients in TNNI3-siRNA myocardial cells.These findings indicated,for the first time,cTnI may regulate Atp2a2 in cardiomyocytes as a co-regulatory factor and participate in the regulation of intracellular Ca ions. | Qian Lu Bo Pan Haobo Bai Weian Zhao Lingjuan Liu Gu Li Ruimin Liu Tiewei Lv Xupei Huang Xi Li Jie Tian | 2022 | Genes & Diseases2022，9，6： | 0 |
| 19 | Expression of histone deacetylase (HDAC) family members in bortezomib-refractory multiple myeloma and modulation by panobinostat显示文摘Aim:Multiple myeloma(MM)is a hematological malignancy of antibody-producing mature B cells or plasma cells.The proteasome inhibitor,bortezomib,was the first-in-class compound to be FDA approved for MM and is frequently utilized in induction therapy.However,bortezomib refractory disease is a major clinical concern,and the efficacy of the pan-histone deacetylase inhibitor(HDACi),panobinostat,in bortezomib refractory disease indicates that HDAC targeting is a viable strategy.Here,we utilized isogenic bortezomib resistant models to profile HDAC expression and define baseline and HDACi-induced expression patterns of individual HDAC family members in sensitive vs.resistant cells to better understanding the potential for targeting these enzymes.Methods:Gene expression of HDAC family members in two sets of isogenic bortezomib sensitive or resistant myeloma cell lines was examined.These cell lines were subsequently treated with HDAC inhibitors:panobinostat or vorinostat,and HDAC expression was evaluated.CRISPR/Cas9 knockdown and pharmacological inhibition of specific HDAC family members were conducted.Results:Interestingly,HDAC6 and HDAC7 were significantly upregulated and downregulated,respectively,in bortezomib-resistant cells.Panobinostat was effective at inducing cell death in these lines and modulated HDAC expression in cell lines and patient samples.Knockdown of HDAC7 inhibited cell growth while pharmacologically inhibiting HDAC6 augmented cell death by panobinostat.Conclusion:Our data revealed heterogeneous expression of individual HDACs in bortezomib sensitive vs.resistant isogenic cell lines and patient samples treated with panobinostat.Cumulatively our findings highlight distinct roles for HDAC6 and HDAC7 in regulating cell death in the context of bortezomib resistance. | Tiewei Cheng Kendall Kiser Leslie Grasse Lakesla Iles Geoffrey Bartholomeusz Felipe Samaniego Robert Z.Orlowski Joya Chandra | 2021 | Cancer Drug Resistance2021，4，4： | 0 |
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