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Age and mean platelet volume-based nomogram for predicting the therapeutic efficacy of metoprolol in Chinese pediatric patients with vasovagal syncope

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World Journal of Pediatrics 2024年第9期20卷 957-965页

作者： Xiao-Juan Du ya-qian huang Xue-Ying Li Ying Liao Hong-Fang Jin Jun-Bao Du Department of Pediatrics Peking University First HospitalNo.1 Xi’anmen StreetWest DistrictBeijing100034China State Key Laboratory of Vascular Homeostasis and Remodeling Peking UniversityNo.38Xueyuan RoadHaidian DistrictBeijing100191China Department of Statistics Peking University First HospitalBeijing100034China

Background Vasovagal syncope(VVS)is the most common type of orthostatic intolerance in *** investigated whether platelet-related factors related to treatment efficacy in children suffering from VVS treated with *** Metoprolol-treated VVS patients were *** median duration of therapy was three *** were followed and divided into two groups,treament-effective group and treatment-ineffective *** and least absolute shrinkage selection operator regressions were used to examine treatment outcome ***-operating characteristic(ROC)curves,precision-recall(PR)curves,calibration plots,and decision curve analyses were used to evaluate the nomogram *** Among the 72 patients who complete the follow-up,treatment-effective group and treatment-ineffective group included 42(58.3%)and 30(41.7%)cases,*** patients in the treatment-effective group exhibited higher mean platelet volume(MPV)[(11.0±1.0)fl vs.(9.8±1.0)fl,P<0.01]and platelet distribution width[12.7%(12.3%,14.3%)vs.11.3%(10.2%,12.2%),P<0.01]than those in the treatment-ineffective *** sex ratio was significantly different(P=0.046).A fit model comprising age[odds ratio(OR)=0.766,95%confidence interval(CI)=0.594-0.987]and MPV(OR=5.613,95%CI=2.297-13.711)might predict therapeutic *** area under the curve of the ROC and PR curves was computed to be 0.85 and 0.9,*** P value of the Hosmer-Lemeshow test was *** decision curve analysis confirmed that managing children with VVS based on the predictive model led to a net advantage ranging from 0.01 to *** nomogram is convenient for clinical *** A novel nomogram based on age and MPV can predict the therapeutic benefits of metoprolol in children with VVS.

关键词： Metoprolol Nomogram Retrospective study Therapeutic effect Vasovagal syncope

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Inhibitory Effects of Sulfur Dioxide on Rat Myocardial Fibroblast Proliferation and Migration

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Chinese Medical Journal 2018年第14期131卷 1715-1723页

作者： Lu-Lu Zhang Jun-Bao Du Chao-Shu Tang Hong-Fang Jin ya-qian huang Department of Pediatrics Peking University First Hospital Beijing 100034 China Division of Small Molecules and Cardiovascular Disease Key Laboratory of Molecular Cardiology Ministry of Education Beijing 100083 China Department of Physiology and Pathophysiology Peking University Health Science Centre Beijing 100091 China

Background： Myocardial fibrosis is an important pathological change has not yet been fully elucidated. The study was designed to examine fibroblast proliferation and migration inhibitor. in many heart diseases, but its pathogenesis is very complex and whether endogenous sulfur dioxide （SO2） is a novel myocardial Methods： Primary rat myocardial fibroblasts were isolated and transfected with aspartate aminotransferase （AAT1 and AAT2） knockdown lentivirus or empty lentivirus. SO2 content in the supematant was determined with high-performance liquid chromatography, and the expressions of AATI, AAT2, proliferating cell nuclear antigen （PCNA）, phosphorylated extracellular signal-regulated protein kinase （p-ERK）, and total ERK （T-ERK） in the cells were detected. Cell migration was detected by wound healing test. Independent sample t-test （for two groups） and one-way analysis of variance （three or more groups） were used to analyze the results. Results： Both AATI and AAT2 knockdown significantly reduced SO2 levels （F = 31.46, P 〈 0.01） and AATI/2 protein expression （AAT1, t = 12.67, P 〈 0.01 ; AAT2, t = 9.61, P 〈 0.01 ）, but increased PCNA expression and Cell Counting Kit-8 （CCK-8） activity as well as the migration in rat primary myocardial fibroblasts （P 〈 0.01）. Supplementation of SO： rather than pyruvate significantly inhibited the increase in proliferation and migration caused by AAT knockdown （P 〈 0.01）. Mechanistically, the ratio of p-ERK to T-ERK was significantly increased in the AAT1/2 knockdown groups compared with that in the empty lentivirus group （AATI, t = -7.36, P 〈 0.01; AAT2, t = 10.97, P 〈 0.01 ）. Whereas PD98059, an inhibitor of ERK activation, successfully blocked AAT knockdown-induced PCNA upregulation （F = 74.01, P 〉 0.05）, CCK-8 activation （F = 50.14, P 〉 0.05）, and migration augmentation in myocardial fibroblasts （24 h,F= 37.08, P〉 0.05; 48 h, F= 58.60, P〉 0.05）. Conclusion： Endogenous SO2 might be a novel myocardial fibrob/ast proliferation and migra

关键词： Endogenous Fibroblast Migration Proliferation Sulfur Dioxide

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Hydrogen Sulfide Regulating Myocardial Structure and Function by Targeting Cardiomyocyte Autophagy

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Chinese Medical Journal 2018年第7期131卷 839-844页

作者： Qing-You Zhang Hong-Fang Jin Selena Chen Qing-Hua Chen Chao-Shu Tang Jun-Bao Du ya-qian huang Department of Pediatrics Peking University First Hospital Beijing 100034 China Division of Biological Sciences University of California San Diego La Jolla California 92093 USA Small Gaseous Molecules and Cardiovascular Disease Section Key Laboratory of Molecular Cardiology Ministry of Education Beijing 100191 China Department of Physiology and Pathophysiology Health Sciences Center Peking University Beijing 100191 China

Objective： Hydrogen sulfide （H2S）, a gaseous signal molecule, plays a crucial role in many pathophysiologic processes in the cardiovascular system. Autophagy has been shown to participate in the occurrence of many cardiac diseases. Increasing evidences indicated that H,S regulates myocardial structure and function in association with the altered autophagy and plays a ＂switcher＂ role in the autophagy of myocardial diseases. The airn of this review was to summarize these insights and provide the experimental evidence that H2S targets cardiomyocyte autophagy to regulate cardiovascular function. Data Sources： This review was based on data in articles published in the PubMed databases up to October 30, 2017, with the following keywords：＂hydrogen sulfide,＂＂autophagy,＂ and ＂cardiovascular diseases.＂ Study Selection： Original articles and critical reviews on H,S and autophagy were selected for this review. Results： When autophagy plays an adaptive role in the pathogenesis of diseases, H2S restores autophagy; otherwise, when autophagy plays a detrimental role, H2S downregulates autophagy to exert a cardioprotective function. For example, H2S has beneficial effects by regulating autophagy in myocardial ischemia/reperfusion and plays a protective role by inhibiting autophagy during the operation of cardioplegia and cardiopuhnonary bypass. H2S postpones cardiac aging associated with the upregulation of autophagy but improves the left ventricular function of smoking rats by lowering autophagy. Conclusions： H2S exerts cardiovascular protection by regulating autophagy. Cardiovascular autophagy would likely become a potential target of H2S therapy for cardiovascular diseases.

关键词： Autophagy Cardioprotective Function Cardiovascular System Hydrogen Sulfide

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Sulfur Dioxide Inhibits Extracellular Signal-regulated Kinase Signaling to Attenuate Vascular Smooth Muscle Cell Proliferation in Angiotensin II-induced Hypertensive Mice

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Chinese Medical Journal 2016年第18期129卷 2226-2232页

作者： Hui-Juan Wu ya-qian huang Qing-Hua Chen Xiao-Yu Tian Jia Liu Chao-Shu Tang Hong-Fang Jin Jun-Bao Du Department of Pediatrics Peking University First Hospital Beijing 100034 China Department of Physiology and Pathophysiology Peking University Health Science Centre Beijing 100191 China Key Laboratory of Molecular Cardiology Ministry of Education Beijing 100091 China

Background： Clarifying the mechanisms underlying vascular smooth muscle cell （VSMC） proliferation is important for the prevention and treatment of vascular remodeling and the reverse of hyperplastic lesions. Previous research has shown that the gaseous signaling molecule sulfur dioxide （SO2） inhibits VSMC proliferation, but the mechanism for the inhibition of the angiotensin Ⅱ （Angll）-induced VSMC proliferation by SO, has not been fully elucidated. This study was designed to investigate if SO2 inhibited VSMC proliferation in mice with hypertension induced by Angll. Methods： Thirty-six male C57 mice were randomly divided into control, Angll, and Angll ＋ SO2 groups. Mice in Angll group and Angl I ＋ SO2 group received a capsule-type Angll pump implanted under the skin of the back at a slow-release dose of 1000 ng-kg^-1min In addition, mice in Angll ＋ SO2 received intraperitoneal injections of SO., donor. Arterial blood pressure of tail artery was determined. The thickness of the aorta was measured by elastic fiber staining, and proliferating cell nuclear antigen （PCNA） and phosphorylated-extracellular signal-regulated kinase （P-ERK） were detected in aortic tissues. The concentration of SO~ in serum and aortic tissue homogenate supernatant was measured using high-performance liquid chromatography with fluorescence determination. In the in vio＇o study, VSMC of A7R5 cell lines was divided into six groups： control, Angll, Angll ＋ SO2 PD98059 （an inhibitor of ERK phosphorylation）, Angll ＋ PD98059, and Angll ＋ SO, ＋ PD98059. Expression of PCNA, ERK, and P-ERK was determined by Western blotting. Results： In animal experiment, compared with the control group, Angll markedly increased blood pressure （P 〈 0.01 ） and thickened the aortic wall in mice （P 〈 0.05） with an increase in the expression of PCNA （P 〈 0.05）. SO2 however, reduced the systemic hypertension and the wall thickness induced by AnglI （P 〈 0.05）. It inhibited the increased expression of PCNA and P-ERK induced by A

关键词： Angiotensin II Hypertension Proliferation Sulfur Dioxide Vascular Smooth Muscle Cell

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Baseline left ventricular ejection fraction associated with symptom improvements in both children and adolescents with postural tachycardia syndrome under metoprolol therapy

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Chinese Medical Journal 2021年第16期134卷 1977-1982页

作者： Yuan-Yuan Wang Zhen-Hui Han Yu-Li Wang Ying Liao Chun-Yu Zhang Ping Liu Chao-Shu Tang Jun-Bao Du Hong-Fang Jin ya-qian huang Department of Pediatrics Peking University First HospitalBeijing 100034China Department of Pediatrics Children’s Hospital of KaifengHenan 475000China Key Laboratory of Molecular Cardiovascular Sciences Ministry of EducationBeijing 100191China Department of Physiology and Pathophysiology Health Science CentrePeking UniversityBeijing 100191China.

Background:Postural tachycardia syndrome(POTS)is a common childhood disease that seriously affects the patient’s physical and mental *** study aimed to investigate whether pre-treatment baseline left ventricular ejection fraction(LVEF)and left ventricular fractional shortening(LVFS)values were associated with symptom improvement after metoprolol therapy for children and adolescents with ***:This retrospective study evaluated 51 children and adolescents with POTS who received metoprolol therapy at the Peking University First Hospital between November 2010 and July *** patients had completed a standing test or basic head-up tilt test and cardiac echocardiography before *** response was evaluated 3 months after starting metoprolol *** pre-treatment baseline LVEF and LVFS values were evaluated for correlations with decreases in the symptom score after treatment(DSS).Multivariable analysis was performed using factors with a P value of0.050).However,responders had significantly higher baseline LVEF(71.09%±4.44%vs.67.17%±4.88%,t=2.789,P=0.008)and LVFS values(40.00[38.00,42.00]%vs.36.79%±4.11%,Z=2.542,P=0.010)than the *** baseline LVEF and LVFS were positively correlated with DSS(r=0.378,P=0.006;r=0.363,P=0.009),*** regression analysis revealed that LVEF was independently associated with the response to metoprolol therapy in children and adolescents with POTS(odds ratio:1.201,95%confidence interval:1.039–1.387,P=0.013).Conclusions:Pre-treatment baseline LVEF was associated with symptom improvement after metoprolol treatment for children and adolescents with POTS.

关键词： Children Left ventricular ejection fraction Left ventricular fractional shortening Metoprolol Postural tachycardia syndrome

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Synergistically enhanced ORR and HER performance on Co-N-C coupled in-situ generated PtCo intermetallic

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Journal of Energy Chemistry 2025年第1期100卷 721-729页

作者： Guanyu Luo Min Song Lulu An Xiao huang qian Zhang Chenhao Zhang Tao Shen Shuang Wang Deli Wang Key Laboratory of Material Chemistry for Energy Conversion and Storage (Huazhong University of Science and Technology) Ministry of Education School of Chemistry and Chemical Engineering Huazhong University of Science and Technology

Integrating multi-scale sites in a composite catalyst is vital to realize efficient ***,a synergistic composite catalyst consisting of Co atomic sites and in-situ generated PtCo intermetallic compounds （IMCs）(o-PtCo@CoNC) is proposed through Co pre-anchoring and subsequent impregnation-reduction *** loading of Co atoms provides a chance for in-situ generating PtCo ordered intermetallic *** remaining Co single atoms and PtCo IMCs construct synergistic electrocatalytic *** from the ordered structure,synergistic effect of Pt Co IMCs and Co single atoms,o-PtCo@CoNC exhibits excellent electrocatalytic performance for oxygen reduction reaction （ORR） and hydrogen evolution reaction （HER） with mass activity of 1.21 A mgPt-1（at 0.9 V） and5.70 A mgPt-1（at an overpotential of 100 mV）,***,o-PtCo@CoNC delivers negligible loss of half-wave potential and overpotential during long-term stability test in acid solutions,with 13 mV decay after 50,000 potential cycles for ORR and a 2.7 mV decay after 20,000 potential cycles for *** integration strategy of single-atomic sites coupled IMCs paves the way for enhancing the activity and durability of Pt-based electrocatalysts.

关键词： Electrolytic reduction

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Cartilage Oligomeric Matrix Protein Protects Angiotensin Ⅱ-induced Abdominal Aortic Aneurysms

Cartilage Oligomeric Matrix Protein Protects Angiotensin Ⅱ-...

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第八届海峡两岸心血管科学研讨会

作者： ya-qian huang,Bo Liu,Xian Wang,Wei Kong (Department of Physiology and Pathophysiology,Basic Mecical Collagen of Peking University,Beijing 100191,China)

Objective Abdominal aortic aneurysm(AAA) is a significant contributor of mortality in elderly *** inflammation,oxidative stress,aberrant matrix degradation and vascular smooth muscle cells (VSMCs) apoptosis are crucial for AAA *** recently reported that macromolecular cartilage oligomeric matrix protein(COMP) is pivotal for maintaining the homeostasis of *** COMP is involved in AAA formation is not *** we aimed to test the effect of COMP on Ang Ⅱ -induced AAA formation. Methods 5 - month - old male COMP mice on a C57BL/6J background and COMP littermate control C57 mice on a normal chow diet were infused with 1,000 ng·min·kg Ang Ⅱ or saline for 4 ***, adenovirus(Ad) - COMP or Ad - LacZ mixed with plurogenic gel were applied to the suprarenal aorta of 4 - month - old male ApoE mice three days prior to infusion with 1,000 ng·min·kg Ang Ⅱ or saline for additional 4 *** In animals infused with Ang Ⅱ ,suprarenal AAAs were present in 69% (9/13) of COMP mice but in only 10%(1/10) of the COMP mice(P<0.05).The maximal diameter of the suprarenal aorta was markedly increased(C57 ***(0.9±0.1) mm vs.(1.7±0.1) mm,P<0.05).COMP mice infused with Ang Ⅱ had more disrupted elastic lamellae than that of littermate. In addition,COMP deficiency aggravated vascular ROS production,macrophages and T cells accumulation, increased proinflammatory cytokines MCP-1 and IL-6 secretion by vascular smooth muscle cells (VSMC),and enhanced in situ zymography of *** contrast,the incidence of AAA was reduced in Ad - COMP treated ApoE mice infusion of Ang Ⅱ (Ad-LacZ *** - COMP:42%vs.8%,n=12,P<0.05).The diameter of the suprarenal aorta was reduced from(1.6±0.1) mm to(1.0±0.2) mm(P<0.05).Histopathological examination revealed that Ad - COMP attenuated elastin destruction,inflammatory cells(macrophages and T cells) infiltration,proinflammatory factors such as MCP-1 and IL-6 secretion, MMP-9 activation and expression,and ROS *** Re

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AZD1775 synergizes with SLC7A11 inhibition to promote ferroptosis

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Science China Life Sciences 2025年第1期 204-218页

作者： Chen Xiong Hong Ling Yingdan huang Hanzhi Dong Bangxiang Xie qian Hao Xiang Zhou Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences Fudan University Department of Oncology Shanghai Medical CollegeFudan University Department of Breast Surgery Fudan University Shanghai Cancer CenterFudan University Department of Oncology First Affiliated Hospital of Nanchang University Beijing Institute of Hepatology Beijing Youan HospitalCapital Medical University Beijing Engineering Research Center for Precision Medicine and Transformation of Hepatitis and Liver Cancer Key Laboratory of Breast Cancer in Shanghai Fudan University Shanghai Cancer CenterFudan University Shanghai Key Laboratory of Medical Epigenetics International Co-laboratory of Medical Epigenetics and Metabolism (Ministry of Science and Technology)Institutes of Biomedical SciencesFudan University

Tumor suppressor p53-mediated cell cycle arrest and DNA damage repair may exert cytoprotective effects against cancer therapies, including WEE1 inhibition. Considering that p53 activation can also lead to multiple types of cell death, the role of this tumor suppressor in WEE1 inhibitor-based therapies remains disputed. In this study, we reported that nucleolar stress-mediated p53 activation enhanced the WEE1 inhibitor AZD1775-induced ferroptosis to suppress lung cancer growth. Our findings showed that AZD1775 promoted ferroptosis by blocking cystine uptake, an action similar to that of Erastin. Meanwhile, inhibition of WEE1 by the WEE1 inhibitors or si RNAs induced compensatory upregulation of SLC7A11, which conferred resistance to ferroptosis. Mechanistically, AZD1775 prevented the enrichment of H3K9me3, a histone marker of transcriptional repression, on the SLC7A11 promoter by repressing the expression of the histone methyltransferase SETDB1, thereby enhancing NRF2-mediated SLC7A11 transcription. This finding was also validated using the H3K9me3 inhibitor BRD4770. Remarkably, we found that the nucleolar stress-inducing agent Actinomycin D(Act. D) inhibited SLC7A11 expression by activating p53, thus augmenting AZD1775-induced ferroptosis. Moreover, the combination of AZD1775 and Act. D synergistically suppressed wild-type p53-harboring lung cancer cell growth both in vitro and in vivo. Altogether, our study demonstrates that AZD1775 promotes ferroptosis by targeting cystine uptake but also mediates the adaptive activation of SLC7A11 through the WEE1-SETDB1 cascade and NRF2-induced transcription, and inhibition of SLC7A11 by Act. D boosts the anti-tumor efficacy of AZD1775 by enhancing ferroptosis in cancers with wild-type p53.

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Exploring the interaction between the gut microbiota and cyclic adenosine monophosphate-protein kinase A signaling pathway:a potential therapeutic approach for neurodegenerative diseases

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Neural Regeneration Research 2025年第11期20卷 3095-3112页

作者： Fengcheng Deng Dan yang Lingxi Qing Yifei Chen Jilian Zou Meiling Jia qian Wang Runda Jiang Lihua huang College of Pharmacy Chengdu University of Traditional Chinese MedicineChengduSichuan ProvinceChina State Key Laboratory of Southwestern Chinese Medicine Resources Chengdu University of Traditional Chinese MedicineChengduSichuan ProvinceChina

The interaction between the gut microbiota and cyclic adenosine monophosphate(cAMP)-protein kinase A(PKA)signaling pathway in the host's central nervous system plays a crucial role in neurological diseases and enhances communication along the gut–brain *** gut microbiota influences the cAMP-PKA signaling pathway through its metabolites,which activates the vagus nerve and modulates the immune and neuroendocrine ***,alterations in the cAMP-PKA signaling pathway can affect the composition of the gut microbiota,creating a dynamic network of microbial-host *** reciprocal regulation affects neurodevelopment,neurotransmitter control,and behavioral traits,thus playing a role in the modulation of neurological *** coordinated activity of the gut microbiota and the cAMP-PKA signaling pathway regulates processes such as amyloid-β protein aggregation,mitochondrial dysfunction,abnormal energy metabolism,microglial activation,oxidative stress,and neurotransmitter release,which collectively influence the onset and progression of neurological *** study explores the complex interplay between the gut microbiota and cAMP-PKA signaling pathway,along with its implications for potential therapeutic interventions in neurological *** pharmacological research has shown that restoring the balance between gut flora and cAMP-PKA signaling pathway may improve outcomes in neurodegenerative diseases and emotional *** can be achieved through various methods such as dietary modifications,probiotic supplements,Chinese herbal extracts,combinations of Chinese herbs,and innovative dosage *** findings suggest that regulating the gut microbiota and cAMP-PKA signaling pathway may provide valuable evidence for developing novel therapeutic approaches for neurodegenerative diseases.

关键词： cyclic adenosine monophosphate emotional disorders gut microbiota neurodegenerative diseases neurological diseases protein kinase A reciprocal regulation signaling pathway strategy therapies

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电视体育娱乐节目的体育功能及未来发展

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体育科学研究 2018年第4期22卷 41-44页

作者：陈亚运黄倩魏德样福建师范大学体育科学学院福建福州350108

为了对未来电视体育娱乐节目的发展有所裨益,实现社会效益与经济价值的最大化,研究以电视体育娱乐节目为对象,采用了文献法、逻辑分析等研究方法,对其体育功能及其影响进行了探讨。研究认为:电视体育娱乐节目的体育功能主要分为生理功... 详细信息

为了对未来电视体育娱乐节目的发展有所裨益,实现社会效益与经济价值的最大化,研究以电视体育娱乐节目为对象,采用了文献法、逻辑分析等研究方法,对其体育功能及其影响进行了探讨。研究认为:电视体育娱乐节目的体育功能主要分为生理功能、心理功能和社会功能,生理功能的影响主要体现在全民健身、医疗方面;心理功能的影响则体现在娱乐、审美、教育等方面;社会功能的影响作用于在经济、政治方面。基于此,对电视体育娱乐节目的未来发展提出应满足观众需求、把握节目底线,内容为王、主动创新,提升节目的本土化和专业化程度,确立与节目风格匹配的主持人等建议。

关键词：体育传播电视体育娱乐节目体育娱乐体育功能

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