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National Science Review 2024年第3期11卷 150-158页

作者： Kun Li Jun Zhang David M.Bell Tiantian Wang Houssni Lamkaddam Tianqu Cui Lu Qi Mihnea Surdu Dongyu Wang Lin Du Imad El Haddad Jay G.Slowik Andre S.H.Prevot Environment research Institute Shandong University Laboratory of Atmospheric Chemistry Paul Scherrer Institute

Organic vapors from biomass burning are a major source of secondary organic aerosols(SOAs). Previous smog chamber studies found that the SOA contributors in biomass-burning emissions are mainly volatile organic compounds(VOCs). While intermediate volatility organic compounds(IVOCs) are efficient SOA precursors and contribute a considerable fraction of biomass-burning emissions, their contribution to SOA formation has not been directly observed. Here, by deploying a newly-developed oxidation flow reactor to study SOA formation from wood burning, we find that IVOCs can contribute ～70% of the formed SOA, i.e.>2 times more than VOCs. This previously missing SOA fraction is interpreted to be due to the high wall losses of semi-volatile oxidation products of IVOCs in smog chambers. The finding in this study reveals that SOA production from biomass burning is much higher than previously thought, and highlights the urgent need for more research on the IVOCs from biomass burning and potentially other emission sources.

关键词： atmospheric chemistry biomass burning secondary organic aerosol intermediate volatility organic compounds

Transient Stability Analysis and Design of VSGs with Different DC-Link Voltage Controllers

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CSEE Journal of Power and Energy Systems 2024年第2期10卷 593-604页

作者： Chao Shen Wei Gu Wanxing Sheng Keyan Liu School of Electrical Engineering Southeast UniversityNanjingChina Power Distribution research Department China Electric Power Research InstituteBeijing 100192China

Virtual synchronous control has been widely studied for the advantages of emulating inertia for voltage source converters (VSCs). A constant dc-link voltage is usually assumed in existing literature to estimate transient stability of virtual synchronous generators (VSGs). However, actual power supply in the dc-side of VSGs is limited and different dc-link voltage controllers are needed to achieve power balance between DC side and AC side. Addition of dc-link voltage controller has great influence on transient behavior of VSGs, which has not been investigated by previous research. To fill this gap, this paper gives insights into the effect of dc-link voltage dynamics on transient stability of VSGs. First, two typical kinds of VSGs with dc-link voltage controllers are introduced. Then, mathematical models considering dc-link dynamics are established and the effect of dc-link voltage controllers on transient synchronization stability of VSGs is revealed through equal area criterion (EAC). It is found that dc-link voltage controller would reduce stability margin of VSGs and design-oriented transient stability analysis is carried out quantitively using critical clearing time (CCT). Finally, simulation results are given to validate correctness of theoretical analysis.

关键词： DC-link voltage dynamics equal area criterion(eac) transient synchronization stability virtual synchronous generator(VSG)

Vaspin alleviates pathological cardiac hypertrophy by regulating autophagy-dependent myocardial senescence

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Emergency and Critical Care Medicine 2024年第1期4卷 4-15页

作者： Haiying Rui Huaxiang Yu Dan Zou Kai Chi Ping Xu Xiaoshuai Song Lulu Liu Xuting Wu Jinxin Wang Li Xue Department of Emergency Medicine and Chest Pain Center Qilu Hospital of Shandong UniversityJinanShandongChina Shandong Provincial Clinical research Center for Emergency and Critical Care Medicine Institute of Emergency and Critical Care Medicine of Shandong UniversityQilu Hospital of Shandong UniversityJinanShandongChina Key Laboratory of Emergency and Critical Care Medicine of Shandong Province Key Laboratory of Cardiopulmonary-Cerebral Resuscitation Research of Shandong ProvinceShandong Provincial Engineering Laboratory for Emergency and Critical Care MedicineQilu Hospital of Shandong UniversityJinanShandongChina The Key Laboratory of cardiovascular Remodeling and Function research Chinese Ministry of EducationChinese Ministry of Health and Chinese Academy of Medical SciencesThe State and Shandong Province Joint Key Laboratory of Translational Cardiovascular MedicineQilu Hospital of Shandong UniversityJinanShandongChina.

Background:Visceral adipose tissue-derived serine protease inhibitor(vaspin),a secretory adipokine,protects against insulin resistance.Recent studies have demonstrated that serum vaspin levels are decreased in patients with coronary artery disease and that vaspin protects against myocardial ischemia-reperfusion injury and atherosclerosis.However,it remains unclear whether vaspin exerts specific effects on pathological cardiac hypertrophy.Methods:An in vivo study was conducted using a cardiac hypertrophy model established by subcutaneous injection of isoproterenol(ISO)in C57BL/6 and vaspin-ko mice.Rapamycin was administered intraperitoneally to mice,for further study.H9c2 cells and neonatal rat ventricular myocytes(NRVMs)were treated with ISO to induce hypertrophy.Human vaspin fusion protein,the proteasome inhibitor MG132,and chloroquine diphosphate were used for further mechanistic studies.Results:Here,we provide the first evidence that vaspin knockdown results in markedly exaggerated cardiac hypertrophy,fibrosis,and cardiomyocyte senescence in mice treated with ISO.Conversely,the administration of exogenous recombinant human vaspin protected NRVMs in vitro against ISO-induced hypertrophy and senescence.Furthermore,vaspin significantly potentiated the ISO-induced decrease in autophagy.Both rapamycin and chloroquine diphosphate regulated autophagy in vivo and in vitro,respectively,and participated in vaspin-mediated cardioprotection.Moreover,the PI3K-AKT-mTOR pathway plays a critical role in vaspin-mediated autophagy in cardiac tissues and NRVMs.Our data showed that vaspin downregulated the p85 and p110 subunits of PI3K by linking p85 and p110 to NEDD4L-mediated ubiquitination degradation.Conclusion:Our results show,for the first time,that vaspin functions as a critical regulator that alleviates pathological cardiac hypertrophy by regulating autophagy-dependent myocardial senescence,providing potential preventive and therapeutic targets for pathological cardiac hypertrophy.

关键词： Autophagic flux Myocardial senescence Pathological cardiac hypertrophy Ubiquitination Vaspin

Mechanism of pachymic acid in the treatment of gastric cancer based on network pharmacology and experimental verification

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World Journal of Gastrointestinal Oncology 2024年第1期16卷 30-50页

作者： Yu-Hua Du Jian-Jun Zhao Xia Li Shi-Cong Huang Na Ning Guo-Qing Chen Yi Yang Yi Nan Ling Yuan College of Pharmacy Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina Ningxia Chinese Medicine research Center Manufacturing LaboratoryYinchuan 750004Ningxia Hui Autonomous RegionChina College of foundation Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina Key Laboratory of Ningxia Minority Medicine Modernization Ministry of Education Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina

BACKGROUND Pachymic acid(PA)is derived from Poria cocos.PA has a variety of pharmacological and inhibitory effects on various tumors.However,the mechanism of action of PA in gastric cancer(GC)remains unclear.AIM To investigate the mechanism of PA in treating GC via the combination of network pharmacology and experimental verification.METHODS The GeneCards and OMIM databases were used to derive the GC targets,while the Pharm Mapper database provided the PA targets.Utilizing the STRING database,a protein-protein interaction network was constructed and core targets were screened.The analyses of Gene Ontology,Kyoto Encyclopedia of Genes and Genomes(KEGG),and gene set enrichment analysis were conducted,and molecular docking and clinical correlation analyses were performed on the core targets.Ultimately,the network pharmacology findings were validated through in vitro cell assays,encompassing assessments of cell viability,apoptosis,cell cycle,cloning,and western blot analysis.RESULTS According to network pharmacology analysis,the core targets were screened,and the PI3K/AKT signaling pathway is likely to be the mechanism by which PA effectively treats GC,according to KEGG enrichment analysis.The experimental findings showed that PA could control PI3K/AKT signaling to prevent GC cell proliferation,induce apoptosis,and pause the cell cycle.CONCLUSION Network pharmacology demonstrated that PA could treat GC by controlling a variety of signaling pathways and acting on a variety of targets.This has also been supported by in vitro cell studies,which serve as benchmarks for further research.

关键词： Pachymic acid Gastric cancer Network pharmacology Enrichment analysis Cell proliferation

Advances in Zika virus vaccines and therapeutics:A systematic review

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Asian Pacific Journal of Tropical Medicine 2024年第3期17卷 97-109页

作者： Shiza Malik Khalid Muhammad Omar Ahsan Muhammad Tahir Khan Ranjit Sah Yasir Waheed Bridging Health foundation Rawalpindi 46000Pakistan Department of Biology College of SciencesUAE University15551Al AinUnited Arab Emirates Department of Medicine Foundation University Medical CollegeFoundation University IslamabadIslamabad 44000Pakistan INTI International University Persiaran Perdana BBN Putra Nilai71800 NilaiNegeri SembilanMalaysia Institute of Molecular Biology and Biotechnology the University of LahoreKM Defence RoadLahore 58810Pakistan Zhongjing research and Industrialization Institute of Chinese Medicine Zhongguancun Scientific ParkNanyang 473006China Department of Microbiology Tribhuvan University Teaching HospitalInstitute of MedicineKathmandu 44600Nepal Department of Microbiology Dr.D.Y.Patil Medical CollegeHospital and Research CentreDr.D.Y.Patil VidyapeethPune 411018MaharashtraIndia Department of Public Health Dentistry Dr.D.Y.Patil Dental College and HospitalDr.D.Y.Patil VidyapeethPune 411018MaharashtraIndia Gilbert and Rose-Marie Chagoury School of Medicine Lebanese American UniversityByblos 1401Lebanon

Zika virus(ZIKV)is the causative agent of a viral infection that causes neurological complications in newborns and adults worldwide.Its wide transmission route and alarming spread rates are of great concern to the scientific community.Numerous trials have been conducted to develop treatment options for ZIKV infection.This review highlights the latest developments in the fields of vaccinology and pharmaceuticals developments for ZIKV infection.A systematic and comprehensive approach was used to gather relevant and up-to-date data so that inferences could be made about the gaps in therapeutic development.The results indicate that several therapeutic interventions are being tested against ZIKV infection,such as DNA vaccines,subunit vaccines,live-attenuated vaccines,virus-vector-based vaccines,inactivated vaccines,virus-like particles,and mRNA-based vaccines.In addition,approved anti-ZIKV drugs that can reduce the global burden are discussed.Although many vaccine candidates for ZIKV are at different stages of development,none of them have received Food and Drug Authority approval for use up to now.The issue of side effects associated with these drugs in vulnerable newborns and pregnant women is a major obstacle in the therapeutic pathway.

关键词： Zika virus Infection Therapeutics Antiviral agents Vaccines Therapies Treatment Novel therapeutic Clinical management

DNA Methylation Variation Is Identified in Monozygotic Twins Discordant for Congenital Heart Diseases

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Congenital Heart Disease 2024年第2期19卷 247-256页

作者： Shuliang Xia Huikang Tao Shixin Su Xinxin Chen Li Ma Jianru Li Bei Gao Xumei Liu Lei Pi Jinqing Feng Fengxiang Li Jia Li Zhiwei Zhang Guangdong Provincial People’s Hospital Southern Medical UniversityGuangzhou510100China Department of cardiovascular Surgery Guangzhou Women and Children’s Medical CenterGuangzhou Medical UniversityGuangdong Provincial Clinical Research Center for Child HealthGuangzhou510623China Department of Pediatric Cardiology Guangdong Cardiovascular InstituteGuangdong Provincial Key Laboratory of South China Structural Heart DiseaseGuangzhou510100China Clinical Physiology Laboratory Institute of PediatricsGuangzhou Women and Children’s Medical CenterGuangzhou Medical UniversityGuangdong Provincial Key Laboratory of Research in Structural Birth Defect DiseaseGuangzhou510623China Department of Echocardiogram Guangzhou Women and Children’s Medical CenterGuangzhou Medical UniversityGuangdong Provincial Clinical Research Center for Child HealthGuangzhou510623China Department of Pediatrics Washington University School of MedicineSt.LouisMO63130USA Clinical Biological Resource Bank of Guangzhou Women and Children’s Medical Center Guangzhou Medical UniversityGuangzhou510623China

Aims:Multiple genes and environmental factors are known to be involved in congenital heart disease(CHD),but epigenetic variation has received little attention.Monozygotic(MZ)twins with CHD provide a unique model for exploring this phenomenon.In order to investigate the potential role of Deoxyribonucleic Acid(DNA)methyla-tion in CHD pathogenesis,the present study examined DNA methylation variation in MZ twins discordant for CHD,especially ventricular septal defect(VSD).Methods and Results:Using genome-wide DNA methylation profiles,we identified 4004 differentially methylated regions(DMRs)in 18 MZ twin pairs discordant for CHD,and 2826 genes were identified.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)analysis revealed a list of CHD-associated pathways.To further investigate the role of DNA methylation in VSD,data from 7 pairs of MZ twins with VSD were analyzed.We identified 1614 DMRs corresponding to 1443 genes associated with arrhythmogenic right ventricular cardiomyopathy,cyclic guanosine monopho-sphate-protein kinase G(cGMP-PKG)signaling pathway by KEGG analysis,and cell-cell adhesion,calcium ion transmembrane transport by GO analysis.A proportion of DMR-associated genes were involved in calcium signaling pathways.The methylation changes of calcium signaling genes might be related to VSD pathogenesis.Conclusion:CHD is associated with differential DNA methylation in MZ twins.CHD may be etiologically linked to DNA methylation,and methylation of calcium signaling genes may be involved in the development of VSD.

关键词： Congenital heart disease monozygotic twins methylation modification epigenetics

Mitochondrial carrier homolog 2 increases malignant phenotype of human gastric epithelial cells and promotes proliferation,invasion,and migration of gastric cancer cells

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World Journal of Gastrointestinal Oncology 2024年第3期16卷 991-1005页

作者： Jing-Wen Zhang Ling-Yan Huang Ya-Ning Li Ying Tian Jia Yu Xiao-Fei Wang School of Basic Medical Science NHC Key Laboratory of Metabolic Cardiovascular Diseases ResearchNingxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina Department of Pathology General Hospital of Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina School of Clinical Medicine Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina Department of Pathology North China University of Science and Technology Affiliated HospitalTangshan 063000Hebei ProvinceChin

BACKGROUND The precise role of mitochondrial carrier homolog 2(MTCH2)in promoting malignancy in gastric mucosal cells and its involvement in gastric cancer cell metastasis have not been fully elucidated.AIM To determine the role of MTCH2 in gastric cancer.METHODS We collected 65 samples of poorly differentiated gastric cancer tissue and adjacent tissues,constructed MTCH2-overexpressing and MTCH2-knockdown cell models,and evaluated the proliferation,migration,and invasion of human gastric epithelial cells(GES-1)and human gastric cancer cells(AGS)cells.The mito-chondrial membrane potential(MMP),mitochondrial permeability transformation pore(mPTP)and ATP fluorescence probe were used to detect mitochondrial function.Mitochondrial function and ATP synthase protein levels were detected via Western blotting.RESULTS The expression of MTCH2 and ATP2A2 in gastric cancer tissues was significantly greater than that in adjacent tissues.Overexpression of MTCH2 promoted colony formation,invasion,migration,MMP expression and ATP production in GES-1 and AGS cells while upregulating ATP2A2 expression and inhibiting cell apoptosis;knockdown of MTCH2 had the opposite effect,promoting overactivation of the mPTP and promoting apoptosis.CONCLUSION MTCH2 can increase the malignant phenotype of GES-1 cells and promote the proliferation,invasion,and migration of gastric cancer cells by regulating mitochondrial function,providing a basis for targeted therapy for gastric cancer cells.

关键词： Gastric cancer Mitochondrial carrier homolog 2 ATP synthase ATP2A2 Mitochondrial permeability transformation pore

Equilibrium Arrivals to Preemptive Queueing System with Fixed and Random Population Size

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Journal of the Operations research Society of China 2024年第1期12卷 77-92页

作者： Julia Chirkova Vladimir Mazalov Institute of Applied Mathematical research Karelian Research Centre of RASPetrozavodsk185910Russia School of Mathematics and Statistics Qingdao UniversityQingdao266071ShandongChina

A single-server queueing system with preemptive access is considered.Each customer has one attempt to enter the system at its working interval[0,T].As soon as the customer request enters the system,the server immediately starts the service.But when the next request arrives in the system,the previous one leaves the system even he has not finished his service yet.We study a non-cooperative game in which the customers wish to maximize their probability of obtaining service within a certain period of time.We characterize the Nash equilibrium and the price of anarchy,which is defined as the ratio between the optimal and equilibrium social utility.Two models are considered.In the first model the number of players is fixed,while in the second it is random and obeys the Poisson distribution.We demonstrate that there exists a unique symmetric equilibrium for both models.Finally,we calculate the price of anarchy for both models and show that the price of anarchy is not monotone with respect to the number of customers.

关键词： Service system Preemptive priorities Strategic users Random number of players Optimal arrivals Kolmogorov backward equations Nash equilibrium Price of anarchy

Shuxuening Injection Inhibits Apoptosis and Reduces Myocardial Ischemia-Reperfusion Injury in Rats through PI3K/AKT Pathway

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Chinese Journal of Integrative Medicine 2024年第5期30卷 421-432页

作者： YUE Tong-tong CAO Ying-jie CAO Ya-xuan LI Wei-xia WANG Xiao-yan SI Chun-ying XIA Han ZHU Ming-jun TANG Jin-fa WANG He The First Clinical Medical College of Henan University of Chinese Medicine Zhengzhou 450046China Department of Pharmacy the First Affiliated Hospital of Henan University of Chinese MedicineZhengzhou 451200China Department of cardiovascular Diseases the First Affiliated Hospital of Henan University of Chinese MedicineZhengzhou 451200China

Objective: To investigate the main components and potential mechanism of Shuxuening Injection(SXNI) in the treatment of myocardial ischemia-reperfusion injury(MIRI) through network pharmacology and in vivo research. Methods: The Traditional Chinese Medicine Systems Pharmacology(TCMSP) and Pharm Mapper databases were used to extract and evaluate the effective components of Ginkgo biloba leaves, the main component of SXNI. The Online Mendelian Inheritance in Man(OMIM) and Gene Cards databases were searched for disease targets and obtain the drug target and disease target intersections. The active ingredient-target network was built using Cytoscape 3.9.1 software. The STRING database, Metascape online platform, and R language were used to obtain the key targets and signaling pathways of the anti-MIRI effects of SXNI. In order to verify the therapeutic effect of different concentrations of SXNI on MIRI in rats, 60 rats were first divided into 5 groups according to random number table method: the sham operation group, the model group, SXNI low-dose(3.68 mg/kg), medium-dose(7.35 mg/kg), and high-dose(14.7 mg/kg) groups, with 12 rats in each group. Then, another 60 rats were randomly divided into 5 groups: the sham operation group, the model group, SXNI group(14.7 mg/kg), SXNI+LY294002 group,and LY294002 group, with 12 rats in each group. The drug was then administered intraperitoneally at body weight for 14 days. The main biological processes were validated using in vivo testing. Evans blue/triphenyltetrazolium chloride(TTC) double staining, hematoxylin-eosin(HE) staining, terminal deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay, enzyme-linked immunosorbent assay(ELISA), and Western blot analysis were used to investigate the efficacy and mechanism of SXNI in MIRI rats. Results: Eleven core targets and 30 Kyoto Encyclopedia of Genes and Genomes(KEGG) pathways were selected. Among these, the phosphoinositide 3-kinase(PI3K)/protein kinase B(AKT) pathway was closely related to SXNI treatment of MIRI. In v

关键词： myocardial ischemia reperfusion injury PI3K/AKT signaling pathway Shuxuening Injection apoptosis Ginkgo biloba leaves

Screening for metabolic dysfunction-associated fatty liver disease:Time to discard the emperor’s clothes of normal liver enzymes?

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World Journal of Gastroenterology 2024年第22期30卷 2839-2842页

作者： Chen-Xiao Huang Xiao-Dong Zhou Calvin Q Pan Ming-Hua Zheng Metabolic Dysfunction-Associated Fatty Liver Disease research Center Department of HepatologyThe First Affiliated Hospital of Wenzhou Medical UniversityWenzhou 325000Zhejiang ProvinceChina Department of cardiovascular Medicine The Key Laboratory of Cardiovascular Diseases of WenzhouThe First Affiliated Hospital of Wenzhou Medical UniversityWenzhou 325000Zhejiang ProvinceChina Division of Gastroenterology and Hepatology Department of MedicineNew York University Langone HealthNew York University Grossman School of MedicineNew YorkNY 11355United States Institute of Hepatology Wenzhou Medical UniversityKey Laboratory of Diagnosis and Treatment for the Development of Chronic Liver Disease in Zhejiang ProvinceWenzhou 325000Zhejiang ProvinceChina

Metabolic dysfunction-associated fatty liver disease(MAFLD)is the most prevalent chronic liver condition worldwide.Current liver enzyme-based screening methods have limitations that may missed diagnoses and treatment delays.Regarding Chen et al,the risk of developing MAFLD remains elevated even when alanine aminotransferase levels fall within the normal range.Therefore,there is an urgent need for advanced diagnostic techniques and updated algorithms to enhance the accuracy of MAFLD diagnosis and enable early intervention.This paper proposes two potential screening methods for identifying individuals who may be at risk of developing MAFLD:Lowering these thresholds and promoting the use of noninvasive liver fibrosis scores.

关键词： Metabolic dysfunction-associated fatty liver disease Non-alcoholic fatty liver disease Alanine aminotransferase Liver enzymes Screening Noninvasive liver fibrosis scores