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当代医学科学(英文)

当代医学科学(英文)

本刊是中华人民共和国教育部主管以英文（或德文）刊登医学及其相关领域科研论文的学术期刊。本刊是我国最早进入美国医学文摘（IM）检索系统的刊物之一，之后进入全球最大数据库PubMed供世界各国研究工作者查询，2005年被世界著名出版公司Springer公司“中国在线图书馆”全文收录，2007年被美国《科学引文索引》（SCI-E）收录。本刊主要刊登基础医学、临床医学、预防医学、环境医学、法医学、药学等方面的论文。读者对象为国内外高级医药、卫生、科技人员。
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  • 发文量：436
  • 被引量：112
  • H指数：0
  • 开始收录时间：-
  • CNKI综合因子：-
  • 维普期刊影响因子： 0.81
  • 万方期刊影响因子：-
  • 创刊时间：-
  • 国内刊号/CN：42-1898/R
    国际刊号/ISSN：2096-5230
  • 发行周期：双月刊
    邮发代号：38-56
  • 主管单位：-
    主办单位：Huazhong University of Science and Technology (HUST)
当代医学科学(英文)-联系信息
  • 主编：Jian-guo CHEN
  • 电话：027-83692513
  • 邮箱：-
  • 地址：13 Hangkonglu, Wuhan, Hubei, PR China
  • 邮编：430030
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当代医学科学(英文) >2023年第5期

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  • 摘要：Objective Restoring the blood perfusion of ischemic heart tissues is the main treatment for myocardial ischemia.However,the accompanying myocardial ischemia reperfusion injury(IRI)would aggravate myocardial damage.Previous studies have confirmed that aryl hydrocarbon receptor(AhR)is closely correlated to kidney and intestinal IRI.The present study aimed to explore the relationship between AhR and myocardial IRI.Methods An oxygen glucose deprivation/reoxygenation(OGD/R)model of H9c2 cells and an ischemia/reperfusion(I/R)model of Sprague-Dawley rat myocardium were established.OGD/R cells and myocardial IRI rats were treated with different concentrations of the AhR antagonist CH-223191 or agonist 6-formylindolo[3,2-b]carbazole(FICZ).Under the conditions of normoxia and hypoxia/reoxygenation,the activity of cardiomyocytes,lactate dehydrogenase(LDH)and cell reactive oxygen species(ROS)were detected.In rats,myocardial pathological damage and markers of myocardial injury were detected.Results According to the results of the cell viability,LDH and ROS tests in vitro,both CH-223191 and FICZ showed no myocardial protection under OGD/R conditions.However,the histological staining and analysis of myocardial injury marker LDH in vitro revealed that CH-223191 could significantly reduce the myocardial IRI.Conclusion AhR exhibited a different effect on myocardial IRI in vitro and in vivo.In vivo,CH-223191 could significantly alleviate the myocardial IRI,suggesting that inhibition of AhR may play a role in myocardial protection,and AhR may serve as a potential treatment target for myocardial IRI.
  • 摘要：Objective Cationic antimicrobial protein of 37 kDa(CAP37),a neutrophil-derived protein originally identified for its antimicrobial activity,is now known to have many regulatory effects on host cells.However,its role in the pathogenesis of chronic obstructive pulmonary disease(COPD)has not been studied.We therefore investigated the expression of CAP37 in COPD and its effects on airway structural cells,including bronchial epithelial cells,smooth muscle cells,and fibroblasts.Methods CAP37 was detected in the lung tissue,sputum,and plasma of COPD patients and the control subjects,as well as in the neutrophils stimulated by cigarette smoke extract(CSE).BEAS-2B cells,human bronchial smooth muscle cells(HBSMCs),and MRC-5 cells were treated with CAP37 or an anti-CAP37 antibody plus CAP37.Interleukin(IL)-6 and IL-8 were detected in the BEAS-2B cells.The cell proliferation was analyzed in the HBSMCs.Collagens were also detected in the MRC-5 cells.Results The expression of CAP37 was increased in the lung tissue and sputum supernatant of the COPD patients compared with the control subjects.The sputum supernatant CAP37 levels were inversely correlated with the forced expiratory volume in the first second percentage predicted in COPD.CAP37 was induced by CSE stimulation in the peripheral blood neutrophils from healthy non-smokers.CAP37 induced expression of IL-6 and IL-8 in BEAS-2B cells,and collagen expression of lung fibroblasts(MRC-5 cells).However,CAP37 did not significantly alter the proliferation of the HBSMCs.Conclusion Our findings indicated that neutrophil-derived CAP37 may be involved in airway inflammation and fibrosis in COPD via affecting the bronchial epithelial cells,and fibroblasts,thus suggesting a possible role of CAP37 in the development and progression of COPD.
  • 摘要：Objective Vascular endothelial growth factor A(VEGFA)is a key regulator of angiogenesis,which is a hallmark of cancer that promotes cancer growth and metastasis.It is of great significance to find new intervention targets and related regulatory mechanisms of VEGFA related angiogenesis for the treatment of tumors.This study focuses on the role of tribbles pseudokinase 3(TRIB3)/signal transducer and activator of transcription 3(STAT3)/VEGFA signaling axis in colon cancer angiogenesis.Methods This study investigated the expression level of TRIB3 in colon cancer through database analysis and tissue microarray analysis.The effect of TRIB3 on proliferation,migration and tube formation ability of human umbilical vein endothelial cells(HUVECs)was further confirmed by CCK8 assay,scratch-wound assay/migration assay and tube formation assay respectively.The regulatory relationship of TRIB3/VEGFA signaling axis was identified by qPCR and Western blotting,which was further confirmed through animal experiments,and the specific regulatory mechanism was explored by immunoprecipitation(IP)and chromatin immunoprecipitation(ChIP)with colon cancer cell lines.Results TRIB3 was increased in colon cancer tissues compared to normal tissues,and elevated TRIB3 expression indicated a poor prognosis in colon cancer patients.Moreover,it was found that silencing TRIB3 could inhibit cancer angiogenesis,whereas overexpressing TRIB3 promoted cancer angiogenesis in vitro and in vivo.Mechanistically,TRIB3 physically interacted with STAT3 and enhanced STAT3-mediated transcriptional activity.Furthermore,the function of TRIB3 in cancer angiogenesis was through cooperating with STAT3 to increase the VEGFA expression.Conclusion Our study provides insights into cancer angiogenesis and offers a potential therapeutic strategy for TRIB3-overexpressed cancer.
  • 摘要：Gene therapy refers to introducing normal exogenous genes into target cells to correct or compensate for the diseases caused by defective and abnormal genes for the purpose of therapy.It holds out hope of a cure for single-gene genetic diseases such as thalassemia,hemophilia,etc.At present,gene therapy is performed in two ways:introducing exogenous genes,and gene editing.A great number of clinical trials of gene therapy in hemophilia have been carried out using viral vectors to introduce foreign genes into target cells.However,the production of neutralizing antibodies following injection and the inability to prepare viral vectors in large quantities limit their application.Although gene-editing methods like CRISPR avoid the above problems,the potential risks of off-target effects are still unknown.More trials and evidence are needed to elucidate the safety and accuracy of gene therapy.This paper will review the bench and clinical work of gene therapy in hemophilia in recent years,and summarize the challenges and prospects of gene therapy,so as to provide directions for future scientific research in this field.
  • 摘要：Objective The occurrence and development of inflammation are closely correlated to the polarization of macrophages.All-trans retinoic acid(ATRA)has been proven to promote the polarization of macrophages from M1 to M2,but this lacks an effective carrier to participate in the biological response.The present study aims to determine whether retinoic acid-incorporated glycol chitosan(RA-GC)nanoparticles can regulate macrophage polarization in Porphyromonas gingivalis-lipopolysaccharide(Pg-LPS)-induced inflammation.Methods Mouse 264.7 cell lines were treated with 1µg/mL Pg-LPS to induce inflammation.After the effects of ATRA and RA-GC on the activity of macrophages were detected by CCK-8 assay,cells induced with Pg-LPS were assigned to the blank control group(GC)nanoparticles without ATRA,and experimental groups(GC nanoparticles loaded with different concentrations of ATRA:1,10 and 100µg/mL).The effects of RA-GC on inflammatory cytokines tumor necrosis factor-α,interleukin(IL)-10 and IL-12 in macrophages were detected by enzyme-linked immunosorbent assay(ELISA).Subsequently,the effects of GC nanoparticles loaded with/without ATRA on macrophage polarization in an inflammatory environment were detected by RT-PCR and Western blotting.Results The results revealed that RA-GC had no significant effect on macrophage activity.However,RA-GC could effectively inhibit the Pg-LPS-induced inflammatory factor expression in macrophages.Meanwhile,the experimental results confirmed that RA-GC could downregulate the expression of inducible nitric oxide synthase(iNOS)(a marker of M1 macrophages)and upregulate the expression of mannose receptor and Arginase-1(a marker of M2 macrophages)in a dose-dependent manner.Conclusion The present study confirms that RA-GC can promote the M2 polarization of macrophages in an inflammatory environment,and proposes this as a promising target for the clinical treatment of Pg-LPS-related diseases.
  • 摘要：Drug-induced interstitial lung disease(DILD)is the most common pulmonary adverse event of anticancer drugs.In recent years,the incidence of anticancer DILD has gradually increased with the rapid development of novel anticancer agents.Due to the diverse clinical manifestations and the lack of specific diagnostic criteria,DILD is difficult to diagnose and may even become fatal if not treated properly.Herein,a multidisciplinary group of experts from oncology,respiratory,imaging,pharmacology,pathology,and radiology departments in China has reached the“expert consensus on the diagnosis and treatment of anticancer DILD”after several rounds of a comprehensive investigation.This consensus aims to improve the awareness of clinicians and provide recommendations for the early screening,diagnosis,and treatment of anticancer DILD.This consensus also emphasizes the importance of multidisciplinary collaboration while managing DILD.
  • 摘要：Objective Endothelial dysfunction is one candidate for triggering neointima formation after arteriovenous grafts(AVGs),but the factors mediating this process are unclear.The purpose of this study was to investigate the role of endoplasmic reticulum stress(ERS)-induced endothelial dysfunction in neointima formation following AVGs in high-fat diet(HFD)mice.Methods CCAAT-enhancer-binding protein-homologous protein(CHOP)knockout(KO)mice were created.Mice were fed with HFD to produce HFD model.AVGs model were applied in the groups of WT ND,WT HFD,and CHOP KO HFD.Human umbilical vein endothelial cells(HUVECs)were cultured with oxidized low density lipoprotein(ox-LDL)(40 mg/L)for the indicated time lengths(0,6,12,24 h).ERS inhibitor tauroursodeoxycholic acid(TUDCA)was used to block ERS.Immunohistochemical staining was used to observe the changes of ICAM1.Changes of ERS were detected by real-time RT-PCR.Protein expression levels and ERS activation were detected by Western blotting.Endothellial cell function was determined by endothelial permeability assay and transendothelial migration assay.Results HFD increased neointima formation in AVGs associated with endothelial dysfunction.At the same time,ERS was increased in endothelial cells(ECs)after AVGs in mice consuming the HFD.In vitro,ox-LDL was found to stimulate ERS,increase the permeability of the EC monolayer,and cause endothelial dysfunction.Blocking ERS with TUDCA or CHOP siRNA reversed the EC dysfunction caused by ox-LDL.In vivo,knockout of CHOP(CHOP KO)protected the function of ECs and decreased neointima formation after AVGs in HFD mice.Conclusion Inhibiting ERS in ECs could improve the function of AVGs.
  • 摘要：Objective Numerous studies have indicated that excitatory amino acid toxicity,such as glutamate toxicity,is involved in glaucoma.In addition,excessive glutamate can lead to an intracellular calcium overload,resulting in regulated necrosis.Our previous studies have found that the calpastatin(CAST)-calpain pathway plays an important role in retinal neuron-regulated necrosis after glutamate injury.Although inhibition of the calpain pathway can decrease regulated necrosis,necrotic cells remain.It has been suggested that there are other molecules that participate in retinal neuron-regulated necrosis.CAST is an important regulator of dynamin-related protein 1(Drp1)-mediated mitochondrial defects.Thus,the aim of this study was to determine whether the CAST-Drp1 pathway may be an underlying signaling axis in neuron-regulated necrosis.Methods Using cultured retinal neurons and in an in-vivo glaucoma model induced by glutamate overload,members of the CAST-Drp1 pathway were assessed by immunofluorescence,Western blotting,Phos-tagTM SDS-PAGE,and co-immunoprecipitation assays.Moreover,the black and white box test was performed on the rats.Results We found that more retinal neuron-regulated necrosis and Drp1 activation as well as lower CAST levels were present in the glutamate-induced glaucoma model.Rats with glutamate-induced glaucoma exhibited impaired visual function.We also observed retinal neuron-regulated necrosis and Drp1 activity decreased,and impaired vision recovered after CAST active peptide application,indicating that the CAST-Drp1 pathway plays a critical role in retinal neuron-regulated necrosis and visual function.Conclusion The results of this study indicate that the CAST-Drp1 pathway protects against retinal neuron-regulated necrosis,which may expand the therapeutic targets for the treatment of neurodegenerative disorders involving dysfunction of glutamate metabolism,such as glaucoma.
  • 摘要：Objective The prevalence of carbapenem-resistant Klebsiella pneumoniae(CR-KP)is a global public health problem.It is mainly caused by the plasmid-carried carbapenemase gene.Outer membrane vesicles(OMVs)contain toxins and other factors involved in various biological processes,includingβ-lactamase and antibiotic-resistance genes.This study aimed to reveal the transmission mechanism of OMV-mediated drug resistance of Klebsiella(K.)pneumoniae.Methods We selected CR-KP producing K.pneumoniae carbapenemase-2(KPC-2)to study whether they can transfer resistance genes through OMVs.The OMVs of CR-KP were obtained by ultracentrifugation,and incubated with carbapenem-sensitive K.pneumoniae for 4 h.Finally,the carbapenem-sensitive K.pneumoniae was tested for the presence of bla_(KPC-2)resistance gene and its sensitivity to carbapenem antibiotics.Results The existence of OMVs was observed by the electron microscopy.The extracted OMVs had bla_(KPC-2)resistance gene.After incubation with OMVs,bla_(KPC-2)resistance gene was detected in sensitive K.pneumoniae,and it became resistant to imipenem and meropenem.Conclusion This study demonstrated that OMVs isolated from KPC-2-producing CR-KP could deliver bla_(KPC-2)to sensitive K.pneumoniae,allowing the bacteria to produce carbapenemase,which may provide a novel target for innovative therapies in combination with conventional antibiotics for treating carbapenem-resistant Enterobacteriaceae.
  • 摘要：Objective This study analyzed the role of G1 to S phase transition 1 protein(GSPT1)in promoting progression of liver cancer cells.Methods A bioinformatics database was used to analyze the expression levels of GSPT1 in liver cancer tissues and the prognosis of patients.Subsequently,Western blotting and quantitative PCR were used to verify the expression levels of GSPT1 between normal hepatocytes and hepatoma cells.We used a CRISPR/Cas9 system to construct knockouts of GSPT1 in HepG2 and HCCLM9 liver cancer cells.The effect of GSPT1 on liver cancer cell migration and invasion was analyzed using flow cytometry,migration,and tumor formation assays.Results The Cancer Genome Atlas Liver Hepatocellular Carcinoma dataset indicated that GSPT1 expression was upregulated in liver cancer cell lines,and patients with liver cancer had poor prognosis.Knockout of GSPT1 in cells significantly inhibited tumor proliferation,cell migration,and growth in vivo.Conclusion In this study,we found that GSPT1 promotes the migration and invasion of liver cancer cells.
  • 摘要：Objective The National Natural Science Foundation of China(NSFC)has made great progress in promoting the development of aortic dissection research in recent years.This study aimed to examine the development and research status of aortic dissection research in China so as to provide references for future research.Methods The NSFC projects data from 2008 to 2019 were collected from the Internet-based Science Information System and other websites utilized as search engines.The publications and citations were retrieved by Google Scholar,and the impact factors were checked by the InCite Journal Citation Reports database.The investigator’s degree and department were identified from the institutional faculty profiles.Results A total of 250 grant funds totaling 124.3 million Yuan and resulting in 747 publications were analyzed.The funds in economically developed and densely populated areas were more than those in underdeveloped and sparsely populated areas.There was no significant difference in the amount of funding per grant between different departments’investigators.However,the funding output ratios of the grants for cardiologists were higher than those for basic science investigators.The amount of funding for clinical researchers and basic scientific researchers in aortic dissection was also similar.Clinical researchers were better in terms of the funding output ratio.Conclusion These results suggest that the medical and scientific research level of aortic dissection in China has been greatly improved.However,there are still some problems that urgently need to be solved,such as the unreasonable regional allocation of medical and scientific research resources,and the slow transition from basic science to clinical practice.
  • 摘要：Objective Type A acute aortic dissection(TAAAD)is a dangerous and complicated condition with a high death rate before hospital treatment.Patients who are fortunate to receive prompt surgical treatment still face high in-hospital mortality.A series of post-operative complications further affects the prognosis.Post-operative pneumonia(POP)also leads to great morbidity and mortality.This study aimed to identify the prevalence as well as the risk factors for POP in TAAAD patients and offer references for clinical decisions to further improve the prognosis of patients who survived the surgical procedure.Methods The study enrolled 89 TAAAD patients who underwent surgical treatment in Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan,Hubei province,China from December 2020 to July 2021 and analyzed the perioperative data and outcomes of these patients.Logistic regression analyses were used to identify the risk factors for POP.Results In the study,31.5%of patients developed POP.Patients with POP had higher proportions of severe oxygenation damage,pneumothorax,reintubation,tracheotomy,renal replacement therapy,arrhythmia,gastrointestinal bleeding,and longer duration of mechanical ventilation,fever,ICU stay,and length of stay(all with P<0.05).The in-hospital mortality was 2.3%.Smoking,preoperative white blood cells,and intraoperative transfusion were the independent risk factors for POP in TAAAD.Conclusion Patients who underwent TAAAD surgery suffered poorer outcomes when they developed POP.Furthermore,patients with risk factors should be treated with caution.
  • 摘要：Objective:This study aimed to explore the effects of tea polyphenols(TP)on inflammation of orbital fibroblasts in Graves’ophthalmopathy(GO)and to provide new ideas for GO treatment.Methods:Primary orbital fibroblasts were extracted from orbital adipose/connective tissues of patients with and without GO.Real-time quantitative PCR(RT-qPCR)was used to detect the expression of interleukin(IL)-6,IL-1β,and monocyte chemotactic protein(MCP)-1 in non-GO and GO orbital fibroblasts.The CCK-8 assay was used to determine the appropriate concentration of TP for subsequent experiments.RT-qPCR and enzyme-linked immunosorbent assay(ELISA)were performed to investigate the effects of TP on lipopolysaccharide(LPS)-induced production of inflammatory cytokines.Nuclear factor-κB(NF-κB)expression was measured using Western blotting analysis.NOD-like receptor 3(NLRP3)expression was detected using both Western blotting analysis and immunofluorescence staining.Results:The mRNA levels of IL-6,IL-1β,and MCP-1 in GO orbital fibroblasts were significantly higher than those in non-GO cells.TP treatment significantly inhibited LPS-induced production of inflammatory factors,including IL-6,IL-1β,and MCP-1.TP also inhibited the expression levels of NF-κB and NLRP3.Inflammation in the GO orbital fibroblasts was higher than that in non-GO cells.TP inhibited the production of inflammatory cytokines in GO orbital fibroblasts in vitro through the NF-κB/NLRP3 pathway.Conclusion:These findings suggest that TP may have a potential role in GO treatment.
  • 摘要：Objective Y-Chromosomal short tandem repeat polymorphism(Y-STR)analysis plays an indispensable role in the identification of male individuals,population genetics,and biogeographic research.While profiles of many populations based on Y-STR markers in human genomes are ample,haplotype data for the Wuwei Han are still scarce.Methods In this study,2180 unrelated Wuwei Han male individuals residing in Gansu Province,China were collected and genotyped using the novel Microreader™40Y Plus ID system.Phylogenetic relationship reconstructions,multidimensional scaling(MDS),and heatmap analysis were performed based on the genetic distance(Rst)values between our studied population and other populations of the Ymax module in the Y-STR Haplotype Reference Database(YHRD).Results A total of 2129 unique haplotypes were obtained,and the haplotype diversity(HD)and discrimination capacity(DC)for the Wuwei Han were 0.9999 and 0.9931,respectively.Conclusion Our results demonstrate that the Wuwei Han population had intimate genetic relationships with East Asians,especially the geographically close Han populations.Overall,this Y-Chromosomal assay gives valuable information about paternal lineages in male individual tracking and genealogical database construction.
  • 摘要：Objective Disc calcification is strongly associated with disc degeneration;however,the underlying mechanisms driving its pathogenesis are poorly understood.This study aimed to provide a gene expression profile of nucleus pulposus cells(NPCs)from calcified discs,and clarify the potential mechanism in disc degeneration.Methods Primary NPCs were isolated from calcified and control discs(CAL-NPC and CON-NPC),respectively.The proliferation and extracellular matrix(ECM)metabolism capacities of the cells were evaluated using MTT and Western blotting,respectively.RNA sequencing was used to identify differentially expressed genes(DEGs)in the CAL-NPCs.The biological functions of the DEGs were analyzed using the Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)databases.The transcription factor database and Cytoscape software were used to construct the transcription factor-DEGs regulatory network.The role of the verified transcription factor in NPC proliferation and ECM metabolism was also investigated.Results The CAL-NPCs exhibited a lower proliferation rate and higher ECM degradation capacity than the CON-NPCs.In total,375 DEGs were identified in the CAL-NPCs.The GO and KEGG analyses showed that the DEGs were primarily involved in the regulation of ribonuclease activity and NF-kappa B and p53 signaling pathways.GATA-binding protein 3(GATA3)with the highest verified levels was selected for further studies.Overexpression of GATA3 in the CON-NPCs significantly inhibited their proliferation and promoted their ECM degradation function,while the knockdown of GATA3 in the CAL-NPCs resulted in the opposite phenotypes.Conclusion This study provided a comprehensive gene expression profile of the NPCs from the calcified discs and supported that GATA3 could be a potential target for reversing calcification-associated disc degeneration.
  • 摘要：Objective This study aimed to determine whether the prevalence of thyroid nodules(TNs)increased due to modern lifestyles or other factors,despite the advances in screening and diagnostic tools.Methods This study included 3474 pairs of participants,who were matched by gender and age(±3 years)from two cross-sectional sampling surveys:(1)the program on the iodine nutritional status and related health status of residents in Shanghai in 2009;(2)the thyroid disease screening program for adults in Shanghai between 2017 and 2018.The prevalence of TNs and thyroid diseases in 2009 and 2017–2018 were compared,and the potential risk factors of TNs were detected.Results The prevalence of TNs in 2009 was 28.9%:22.5%in males and 34.5%in females.In 2017,this increased to 43.8%:37.9%in males and 49.1%in females.The prevalence of TNs significantly increased from 2009 to 2017(odds ratio,1.486;95%confidence interval,1.238–1.786).In addition,female gender,thyroid disease history,and age were the main risk factors for TNs after adjusting for confounders in the logistic regression across the time period.Conclusion The prevalence of TNs significantly increased across nearly 10 years in Shanghai.
  • 摘要：Objective Contact precautions,especially the initiation of isolation,are important measures to prevent and control multidrug-resistant organisms(MDROs).However,the implementation in clinical practice remains weak.This study aimed to analyze the impact of multidisciplinary collaborative intervention on isolation implementation in multidrug-resistant infection,and determine the factors that affect the implementation of isolation measures.Methods A multidisciplinary collaborative intervention related to isolation was conducted at a teaching tertiary hospital in central China on November 1,2018.The information of 1338 patients with MDRO infection and colonization at 10 months before and after the intervention was collected.Then,the issuance of isolation orders was retrospectively analyzed.Univariate analysis and multivariate logistic regression analysis were performed to analyze the factors that affected the isolation implementation.Results The overall issuance rate of isolation orders was 61.21%,which increased from 33.12%to 75.88%(P<0.001)after the implementation of the multidisciplinary collaborative intervention.The intervention(P<0.001,OR=0.166)was a promoting factor for the issuance of isolation orders,in addition to the length of stay(P=0.004,OR=0.991),department(P=0.004),and microorganism(P=0.038).Conclusion The isolation implementation remains far lower than policy standards.Multidisciplinary collaborative interventions can effectively improve the compliance to isolation measures implemented by doctors,thereby promoting the standardized management of MDROs,and providing reference for further improving the quality of hospital infection management.
  • 摘要：Objective Thyroid-associated ophthalmopathy(TAO)is an autoimmune disorder involving the orbital tissue.This study aimed to understand the role of regulatory T cells(Tregs)in TAO during 12-week systemic glucocorticoid(GC)treatment.Methods Thirty-two moderate-severe TAO patients with a clinical activity score(CAS)≥3/7 or with prolonged T2 relaxation time(T2RT)on at least one side of extraocular muscle(EOM)were enrolled.The percentage of the peripheral CD4+CD25(high)CD127(−/low)Tregs was analyzed using flow cytometry before and after the GC treatment.The activity and severity of TAO,T2RT,and the clinical outcomes after the GC treatment were assessed.Their correlation with the peripheral Tregs was investigated.Results There was no significant association between the baseline Treg fraction and the activity and severity of TAO or the treatment response.A significant reduction of Tregs was observed after the GC therapy merely in patients without any clinical improvement.Conclusion Treg reduction after systemic GC therapy is indicative of a poor therapeutic response.Accordingly,dynamic alterations of Tregs could help to evaluate the effectiveness of the GC treatment.
  • 摘要：Objective Schizophrenia(SZ)is associated with cognitive impairment,and it is known that the activity of cAMP response element binding protein(CREB)decreases in the brain of SZ patients.The previous study conducted by the investigators revealed that the upregulation of CREB improves the MK801-related SZ cognitive deficit.The present study further investigates the mechanism on how CREB deficiency is associated with SZ-related cognitive impairment.Methods MK-801 was used to induce SZ in rats.Western blotting and immunofluorescence were performed to investigate CREB and the CREB-related pathway implicated in MK801 rats.The long-term potentiation and behavioral tests were performed to assess the synaptic plasticity and cognitive impairment,respectively.Results The phosphorylation of CREB at Ser133 decreased in the hippocampus of SZ rats.Interestingly,among the upstream kinases of CREB,merely ERK1/2 was downregulated,while CaMKII and PKA remained unchanged in the brain of MK801-related SZ rats.The inhibition of ERK1/2 by PD98059 reduced the phosphorylation of CREB-Ser133,and induced synaptic dysfunction in primary hippocampal neurons.Conversely,the activation of CREB attenuated the ERK1/2 inhibitor-induced synaptic and cognitive impairment.Conclusion These present findings partially suggest that the deficiency of the ERK1/2-CREB pathway is involved in MK801-related SZ cognitive impairment.The activation of the ERK1/2-CREB pathway may be therapeutically useful for treating SZ cognitive deficits.
  • 摘要：Objective Primary Sjogren’s syndrome(pSS)is a systemic autoimmune disease that mainly affects the exocrine gland,especially in women.Currently,the results of studies on the menstruation or fertility of pSS patients remain controversial.This study aimed to examine the menstrual and reproductive characteristics of pSS patients.Methods Clinical data of 449 pSS patients who were admitted to Tongji Hospital in Hubei,China,from January 2015 to November 2021 were obtained and their menstrual and reproductive information analyzed.In addition,the clinical features of pSS patients with premenopausal or postmenopausal onset were compared.Results The spontaneous abortion rate of pSS patients was not higher than the reported rate of the general population and that the age of menarche,menstrual cycle,and menstrual period of pSS patients did not significantly differ from those reported in the general population;however,early menopause seemed to be more common in pSS patients.Skin involvement(27.96%vs.15.00%,P=0.005)and hyperglobulinemia(10.64%vs.4.16%,P=0.033)were more common in patients with premenopausal pSS onset,but patients with postmenopausal onset had a significantly greater incidence of interstitial lung disease(32.50%vs.17.02%,P=0.0004).Also,erythropenia(47.00%vs.31.25%,P=0.002),hypoalbuminemia(19.49%vs.8.22%,P=0.0009),and prevalence of high hypersensitive C-reactive protein levels(21.67%vs.10.94%,P=0.005)were more common in pSS patients with postmenopausal onset.Notably,the rate of abnormal pregnancy was significantly greater in patients with premenopausal onset(9.72%vs.2.50%,P=0.011).Conclusion Patients with pSS onset before or after menopause may have different risks in pulmonary involvement and laboratory manifestations.
  • 摘要：Objective To construct and verificate an RNA-binding protein(RBP)-associated prognostic model for gliomas using integrated bioinformatics analysis.Methods RNA-sequencing and clinic pathological data of glioma patients from The Cancer Genome Atlas(TCGA)database and the Chinese Glioma Genome Atlas database(CGGA)were downloaded.The aberrantly expressed RBPs were investigated between gliomas and normal samples in TCGA database.We then identified prognosis related hub genes and constructed a prognostic model.This model was further validated in the CGGA-693 and CGGA-325 cohorts.Results Totally 174 differently expressed genes-encoded RBPs were identified,containing 85 down-regulated and 89 up-regulated genes.We identified five genes-encoded RBPs(ERI1,RPS2,BRCA1,NXT1,and TRIM21)as prognosis related key genes and constructed a prognostic model.Overall survival(OS)analysis revealed that the patients in the high-risk subgroup based on the model were worse than those in the low-risk subgroup.The area under the receiver operator characteristic curve(AUC)of the prognostic model was 0.836 in the TCGA dataset and 0.708 in the CGGA-693 dataset,demonstrating a favorable prognostic model.Survival analyses of the five RBPs in the CGGA-325 cohort validated the findings.A nomogram was constructed based on the five genes and validated in the TCGA cohort,confirming a promising discriminating ability for gliomas.Conclusion The prognostic model of the five RBPs might serve as an independent prognostic algorithm for gliomas.
  • 摘要：Objective:To investigate whether human short interspersed nuclear element antisense RNA(Alu antisense RNA;Alu asRNA)could delay human fibroblast senescence and explore the underlying mechanisms.Methods:We transfected Alu asRNA into senescent human fibroblasts and used cell counting kit-8(CCK-8),reactive oxygen species(ROS),and senescence-associated beta-galactosidase(SA-β-gal)staining methods to analyze the anti-aging effects of Alu asRNA on the fibroblasts.We also used an RNA-sequencing(RNA-seq)method to investigate the Alu asRNA-specific mechanisms of anti-aging.We examined the effects of KIF15 on the anti-aging role induced by Alu asRNA.We also investigated the mechanisms underlying a KIF15-induced proliferation of senescent human fibroblasts.Results:The CCK-8,ROS and SA-β-gal results showed that Alu asRNA could delay fibroblast aging.RNA-seq showed 183 differentially expressed genes(DEGs)in Alu asRNA transfected fibroblasts compared with fibroblasts transfected with the calcium phosphate transfection(CPT)reagent.The KEGG analysis showed that the cell cycle pathway was significantly enriched in the DEGs in fibroblasts transfected with Alu asRNA compared with fibroblasts transfected with the CPT reagent.Notably,Alu asRNA promoted the KIF15 expression and activated the MEK-ERK signaling pathway.Conclusion:Our results suggest that Alu asRNA could promote senescent fibroblast proliferation via activation of the KIF15-mediated MEK-ERK signaling pathway.
  • 摘要：Objective Cardiac fibroblasts(CFs)proliferation and extracellular matrix deposition are important features of cardiac fibrosis.Various studies have indicated that vitamin D displays an anti-fibrotic property in chronic heart diseases.This study explored the role of vitamin D in the growth of CFs via an integrin signaling pathway.Methods MTT and 5-ethynyl-2′-deoxyuridine assays were performed to determine cell viability.Western blotting was performed to detect the expression of proliferating cell nuclear antigen(PCNA)and integrin signaling pathway.The fibronectin was observed by ELISA.Immunohistochemical staining was employed to evaluate the expression of integrinβ3.Results The PCNA expression in the CFs was enhanced after isoproterenol(ISO)stimulation accompanied by an elevated expression of integrin beta-3(β3).The blockade of the integrinβ3 with a specific integrinβ3 antibody reduced the PCNA expression induced by the ISO.Decreasing the integrinβ3 by siRNA reduced the ISO-triggered phosphorylation of FAK and Akt.Both the FAK inhibitor and Akt inhibitor suppressed the PCNA expression induced by the ISO in the CFs.Calcitriol(CAL),an active form of vitamin D,attenuated the ISO-induced CFs proliferation by downregulating the integrinβ3 expression,and phosphorylation of FAK and Akt.Moreover,CAL reduced the increased levels of fibronectin and hydroxyproline in the CFs culture medium triggered by the ISO.The administration of calcitriol decreased the integrinβ3 expression in the ISO-induced myocardial injury model.Conclusion These findings revealed a novel role for CAL in suppressing the CFs growth by the downregulation of the integrinβ3/FAK/Akt pathway.
  • 摘要：Objective Ubiquitin conjugate enzyme E2O(UBE2O)is a ubiquitin-conjugating enzyme that has been reported to be involved in tumorigenesis.This study investigated the role of UBE2O in hepatocellular carcinoma(HCC).Methods The expression of UBE2O was detected using qRT-PCR,Western blotting,and immunohistochemical staining.Cell proliferation and Transwell assays were used to detect proliferation,migration,and invasion of HCC cells,respectively.Bioinformatic analysis was performed to analyze the relationship between UBE2O and the clinical features,prognosis,and immune cell infiltration of HCC.Results UBE2O was significantly over-expressed in HCC tissues.High expression of UBE2O was associated with poor tumor grade and poor prognosis.Functional experiments showed that down-regulation of UBE2O inhibited HCC cell proliferation,migration,and invasion.Co-expression gene analysis and gene set enrichment analysis showed that UBE2O was associated with protein hydrolysis,cell cycle,and cancer-related pathways in HCC.The results of immune analysis revealed that the expression of UBE2O was positively correlated with the immune infiltration and expression of immune-related chemokines of HCC.Conclusions UBE2O is significantly correlated with the prognosis of HCC and may be a valuable prognostic biomarker for HCC.
  • 摘要：Objective The ATP responsive P2 purinergic receptors can be subdivided into metabotropic P2X family and ionotropic P2Y family.Among these,P2X3 is a type of P2X receptor which is specifically expressed on nerves,especially on pre-ganglionic sensory fibers.This study investigates whether gefapixant possesses the potential of inhibiting cardiac sympathetic hypersensitivity to protect against cardiac remodeling in the context of myocardial infarction.Methods The Sprague-Dawley rats were divided randomly into three groups:sham group-myocardial infarction group,and myocardial infarction with gefapixant treatment group.Myocardial infarction was induced by left anterior descending branch ligation.The gefapixant solution was intraperitoneally injected each time per day for 7 days and the appropriate dosage of gefapixant was determined according to the results of hematoxylin-eosin(HE)staining and myocardial injury biomarkers.Conditions of cardiac function were assessed by echocardiograph and cardiac fibrosis was evaluated by Western blotting and immunofluorescence staining of collagen I and collagen III.The sympathetic innervation was detected by norepinephrine concentration(pg/mL),in-vivo electrophysiology,and typical sympathetic biomarkers.Inflammatory cell infiltration was shown from immunofluorescence staining and pro-inflammatory signaling pathway activation was checked by immunohistology,quantitative realtime PCR(qPCR)and Western blotting.Results It was found that gefapixant injection of 10 mg/kg per day had the highest dosage-efficacy ratio.Furthermore,gefapixant treatment improved cardiac pump function as shown by increased LVEF and LVFS,and decreased LVIDd and LVIDs.The expression levels of collagen I and collagen III,and TNF-αwere all decreased by P2X3 inhibition.Mechanistically,the decreased activation of nucleotide-binding and oligomerization domain-like receptors family pyrin-domain-containing 3(NLRP3)inflammasome and subsequent cleavage of caspase-1 which modulated interleukin-1β(IL-1β)and IL-18 level in heart after gefapixant treatment were associated with the suppressed cardiac inflammation.Conclusion It is suggested that P2X3 inhibition by gefapixant ameliorates post-infarct autonomic nervous imbalance,cardiac dysfunction,and remodeling possibly via inactivating NLRP3 inflammasome.
  • 摘要：Objective Despite the recent advances in diagnosis and treatment,sepsis continues to lead to high morbidity and mortality.Early diagnosis and prompt treatment are essential to save lives.However,most biomarkers can only help to diagnose sepsis,but cannot predict the development of septic shock in high-risk patients.The present study determined whether the combined measurement of procalcitonin(PCT),thromboelastography(TEG)and platelet(PLT)count can predict the development of septic shock.Methods A retrospective study was conducted on 175 septic patients who were admitted to the intensive care unit between January 2017 and February 2021.These patients were divided into two groups:73 patients who developed septic shock were assigned to the septic shock group,while the remaining 102 patients were assigned to the sepsis group.Then,the demographic,clinical and laboratory data were recorded,and the predictive values of PCT,TEG and PLT count for the development of septic shock were analyzed.Results Compared to the sepsis group,the septic shock group had statistically lower PLT count and TEG measurements in the R value,K value,αangle,maximum amplitude,and coagulation index,but had longer prothrombin time(DT),longer activated partial thromboplastin time(APTT),and higher PCT levels.Furthermore,the Sequential Organ Failure Assessment(SOFA)score was higher in the septic shock group.The multivariate logistic regression analysis revealed that PCT,TEG and PLT count were associated with the development of septic shock.The area under the curve analysis revealed that the combined measurement of PCT,TEG and PLT count can be used to predict the development of septic shock with higher accuracy,when compared to individual measurements.Conclusion The combined measurement of PCT,TEG and PLT count is a novel approach to predict the development of septic shock in high-risk patients.
  • 摘要：Objective To investigate the etiology,clinical characteristics,diagnosis,and treatment strategies and efficacy of pulsatile tinnitus(PT)caused by vascular anatomy abnormality.Methods The clinical data of 45 patients with PT in our hospital from 2012 to 2019 were collected and retrospectively analyzed.Results All 45 patients had vascular anatomical abnormalities.The patients were divided into 10 categories according to the different locations of vascular abnormalities:sigmoid sinus diverticulum(SSD),sigmoid sinus wall dehiscence(SSWD),SSWD with high jugular bulb,pure dilated mastoid emissary vein,aberrant internal carotid artery(ICA)in the middle ear,transverse-sigmoid sinus(TSS)transition stenosis,TSS transition stenosis with SSD,persistent occipital sinus stenosis,petrous segment stenosis of ICA,and dural arteriovenous fistula.All patients complained of PT synchronous with heartbeat rhythm.Endovascular interventional therapy and extravascular open surgery were used according to the location of the vascular lesions.Tinnitus disappeared in 41 patients,was significantly relieved in 3 patients,and was unchanged in 1 patient postoperatively.Except for one patient with transient headache postoperatively,no obvious complications occurred.Conclusion PT caused by vascular anatomy abnormalities can be identified by detailed medical history and physical and imaging examination.PT can be relieved or even completely alleviated after appropriate surgical treatments.
  • 摘要：Objective:This study aimed to describe,optimize and evaluate a method for preparing multivalent conjugate vaccines by simultaneous conjugation of two different bacterial capsular polysaccharides(CPs)with tetanus toxoid(TT)as bivalent conjugates.Methods:Different molecular weights(MWs)of polysaccharides,activating agents and capsular polysaccharide/protein(CP/Pro)ratio that may influence conjugation and immunogenicity were investigated and optimized to prepare the bivalent conjugate bulk.Using the described method and optimized parameters,a 20-valent pneumococcal conjugate vaccine and a bivalent meningococcal vaccine were developed and their effectiveness was compared to that of corresponding licensed vaccines in rabbit or mouse models.Results:The immunogenicity test revealed that polysaccharides with lower MWs were better for Pn1-TT-Pn3 and MenA-TT-MenC,while higher MWs were superior for Pn4-TT-Pn14,Pn6A-TT-Pn6B,Pn7F-TT-Pn23F and Pn8-TT-Pn11A.For activating polysaccharides,1-cyano-4-dimethylaminopyridinium tetrafluoroborate(CDAP)was superior to cyanogen bromide(CNBr),but for Pn1,Pn3 and MenC,N-(3-dimethylaminopropyl)-N’-ethylcarbodiimide hydrochloride(EDAC)was the most suitable option.For Pn6A-TT-Pn6B and Pn8-TT-Pn11A,rabbits immunized with bivalent conjugates with lower CP/Pro ratios showed significantly stronger CP-specific antibody responses,while for Pn4-TT-Pn14,higher CP/Pro ratio was better.Instead of interfering with the respective immunological activity,our bivalent conjugates usually induced higher IgG titers than their monovalent counterparts.Conclusion:The result indicated that the described conjugation technique was feasible and efficacious to prepare glycoconjugate vaccines,laying a solid foundation for developing extended-valent multivalent or combined conjugate vaccines without potentially decreased immune function.
  • 摘要：Objective Kidney renal clear cell carcinoma(KIRC)is a common renal malignancy that has a poor prognosis.As a member of the F box family,cyclin F(CCNF)plays an important regulatory role in normal tissues and tumors.However,the underlying mechanism by which CCNF promotes KIRC proliferation still remains unclear.Methods Bioinformatics methods were used to analyze The Cancer Genome Atlas(TCGA)database to obtain gene expression and clinical prognosis data.The CCK8 assay,EdU assay,and xenograft assay were used to detect cell proliferation.The cell senescence and potential mechanism were assessed by SA-β-gal staining,Western blotting,as well as ELISA.Results Our data showed that CCNF was highly expressed in KIRC patients.Meanwhile,downregulation of CCNF inhibited cell proliferation in vivo and in vitro.Further studies showed that the reduction of CCNF promoted cell senescence by decreasing cyclin-dependent kinase 1(CDK1),increasing the proinflammatory factors interleukin(IL)-6 and IL-8,and then enhancing the expression of p21 and p53.Conclusion We propose that the high expression of CCNF in KIRC may play a key role in tumorigenesis by regulating cell senescence.Therefore,CCNF shows promise as a new biomarker to predict the clinical prognosis of KIRC patients and as an effective therapeutic target.
  • 摘要：Temporal bone malignant tumors are characterized by atypical clinical symptoms,and easy recurrence and metastasis.They account for 0.2%of head and neck tumors,and the most common pathological type is squamous cell carcinoma.Patients with squamous cell carcinoma of the temporal bone are often at advanced stages when diagnosed,and lose the chance for surgery.Neoadjuvant immunotherapy has recently been approved as the first-line treatment for refractory recurrent/metastatic squamous cell carcinoma of the head and neck.However,it remains to be determined whether neoadjuvant immunotherapy can be used as the first-line treatment for temporal bone squamous cell carcinoma to reduce the tumor stage before surgery,or as a palliative treatment for patients with unresectable advanced stage carcinoma.The present study reviews the development of immunotherapy and its clinical application in head and neck squamous cell carcinoma,summarizes the treatment of temporal bone squamous cell carcinoma,and prospects the neoadjuvant immunotherapy as the first-line treatment for temporal bone squamous cell carcinoma.

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