首页期刊导航|当代医学科学(英文)
期刊信息/Journal information
当代医学科学(英文)
当代医学科学(英文)

龚菲力；冯敢生

双月刊

2096-5230

jtmu@tjmu.edu.cn

027-83692514

430030

武汉市航空路13号同济医学院学报

当代医学科学(英文)/Journal Current Medical ScienceSCI
正式出版
收录年代

    The Role of Adipose Tissue-derived Exosomes in Chronic Metabolic Disorders

    Rui HEYong CHEN
    463-474页
    查看更多>>摘要：Excessive fat deposition in obese subjects promotes the occurrence of metabolic diseases,such as type 2 diabetes mellitus(T2DM),cardiovascular diseases,and non-alcoholic fatty liver disease(NAFLD).Adipose tissue is not only the main form of energy storage but also an endocrine organ that not only secretes adipocytokines but also releases many extracellular vesicles(EVs)that play a role in the regulation of whole-body metabolism.Exosomes are a subtype of EVs,and accumulating evidence indicates that adipose tissue exosomes(AT Exos)mediate crosstalk between adipose tissue and multiple organs by being transferred to targeted cells or tissues through paracrine or endocrine mechanisms.However,the roles of AT Exos in crosstalk with metabolic organs remain to be fully elucidated.In this review,we summarize the latest research progress on the role of AT Exos in the regulation of metabolic disorders.Moreover,we discuss the potential role of AT Exos as biomarkers in metabolic diseases and their clinical application.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Immunomodulation of Proton-activated G Protein-coupled Receptors in Inflammation

    Min-shan LIXiang-hong WANGHeng WANG
    475-484页
    查看更多>>摘要：Proton-activated G protein-coupled receptors(GPCRs),initially discovered by Ludwig in 2003,are widely distributed in various tissues.These receptors have been found to modulate the immune system in several inflammatory diseases,including inflammatory bowel disease,atopic dermatitis,and asthma.Proton-activated GPCRs belong to the G protein-coupled receptor family and can detect alternations in extracellular pH.This detection triggers downstream signaling pathways within the cells,ultimately influencing the function of immune cells.In this review,we specifically focused on investigating the immune response of proton-activated GPCRs under inflammatory conditions.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    A Review of Type 1 and Type 2 Intraductal Papillary Neoplasms of the Bile Duct

    Xia-hui HUANGTian-xiang CHENHong-liang LIUMing-wen HUANG...
    485-493页
    查看更多>>摘要：Intraductal papillary neoplasm of the bile duct(IPNB)is a heterogeneous disease similar to intraductal papillary mucinous neoplasm of the pancreas.These lesions have been recognized as one of the three major precancerous lesions in the biliary tract since 2010.In 2018,Japanese and Korean pathologists reached a consensus,classifying IPNBs into type 1 and type 2 IPNBs.IPNBs are more prevalent in male patients in East Asia and are closely related to diseases such as cholelithiasis and schistosomiasis.From a molecular genetic perspective,IPNBs exhibit early genetic variations,and different molecular pathways may be involved in the tumorigenesis of type 1 and type 2 IPNBs.The histological subtypes of IPNBs include gastric,intestinal,pancreaticobiliary,or oncocytic subtypes,but type 1 IPNBs typically exhibit more regular and well-organized histological features than type 2 IPNBs and are more commonly found in the intrahepatic bile ducts with abundant mucin.Due to the rarity of these lesions and the absence of specific clinical and laboratory features,imaging is crucial for the preoperative diagnosis of IPNB,with local bile duct dilation and growth along the bile ducts being the main imaging features.Surgical resection remains the optimal treatment for IPNBs,but negative bile duct margins and the removal of lymph nodes in the hepatic hilum significantly improve the postoperative survival rates for patients with IPNBs.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Association between Serum Ferritin Levels and Metabolic-associated Fatty Liver Disease in Adults:a Cross-sectional Study Based on the NHANES

    Jiang-hui LIXue-yao MAYun YILu-rao LI...
    494-502页
    查看更多>>摘要：Objective:Ferritin,initially acting as an iron-storage protein,was found to be associated with metabolic diseases.Our study was designed to investigate the association between serum ferritin and metabolic-associated fatty liver disease(MAFLD)using data from the National Health and Nutrition Examination Survey(NHANES)of the United State of America.Methods:A cross-sectional study was conducted,enrolling a total of 2145 participants from the NHANES in the 2017-2018 cycles.Hepatic steatosis and liver fibrosis were assessed by ultrasound images and several non-invasive indexes.Multiple regression analysis was conducted to determine the associations between serum ferritin concentration and MAFLD and liver fibrosis.Results:The analysis revealed that participants with higher serum ferritin levels(Q3 and Q4 groups)had a higher prevalence of MAFLD than those with the lowest serum ferritin levels[Q3 vs.Q1:OR=2.17(1.33,3.53),P＜0.05 in fatty liver index(FLI);Q4 vs.Q1:OR=3.13(1.91,5.13),P＜0.05 in FLI].Additionally,participants with the highest serum ferritin levels(Q4 group)displayed a higher prevalence of liver fibrosis[Q4 vs.Q1:OR=2.59(1.19,5.62),P＜0.05 in liver stiffness measurement;OR=5.06(1.12,22.94),P＜0.05 in fibrosis-4 index],with significantly increased risk observed in participants with concomitant diabetes[OR=7.45(1.55,35.72),P=0.012].Conclusion:Our study revealed that elevated serum ferritin levels are associated with a higher prevalence of MAFLD and advanced liver fibrosis in patients.Elevated serum ferritin levels combined with diabetes are important risk factors for liver fibrosis.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Long Non-coding RNA PCED1B Antisense RNA 1 Promotes Cell Proliferation and Invasion in Hepatocellular Carcinoma by Regulating the MicroRNA-34a/CD44 Axis

    Jian-gang BIQi LIYu-sheng GUOLi-ping LIU...
    503-511页
    查看更多>>摘要：Objective:This study aimed to examine the role of long non-coding RNA PCED1B antisense RNA 1(PCED1B-AS1)in the development of hepatocellular carcinoma(HCC).Methods:A total of 62 pairs of HCC tissues and adjacent non-tumor tissues were obtained from 62 HCC patients.The interactions of PCED1B-AS1 and microRNA-34a(miR-34a)were detected by dual luciferase activity assay and RNA pull-down assay.The RNA expression levels of PCED1B-AS1,miR-34a and CD44 were detected by RT-qPCR,and the protein expression level of CD44 was determined by Western blotting.The cell proliferation was detected by cell proliferation assay,and the cell invasion and migration by transwell invasion assay.The HCC tumor growth after PCED1B-AS1 was downregulated was determined by in vivo animal study.Results:PCED1B-AS1 was highly expressed in HCC tissues,which was associated with poor survival of HCC patients.Furthermore,PCED1B-AS1 interacted with miR-34a in HCC cells,but they did not regulate the expression of each other.Additionally,PCED1B-AS1 increased the expression level of CD44,which was targeted by miR-34a.The cell proliferation and invasion assay revealed that miR-34a inhibited the proliferation and invasion of HCC in vitro,while CD44 exhibited the opposite effects.Furthermore,PCED1B-AS1 suppressed the role of miR-34a.Moreover,the knockdown of PCED1B-AS1 repressed the HCC tumor growth in nude mice in vivo.Conclusion:PCED1B-AS1 may play an oncogenic role by regulating the miR-34a/CD44 axis in HCC.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    KLF4 Inhibits the Activation of Human Hepatic Stellate Cell In Vitro

    Xing-yu YANGZhe CHENJun TANYin-kai XUE...
    512-518页
    查看更多>>摘要：Objective:Hepatic stellate cells(HSCs)play a crucial role in liver fibrosis.Early-stage liver fibrosis is reversible and intimately associated with the state of HSCs.Kruppel-like factor 4(KLF4)plays a pivotal role in a wide array of physiological and pathological processes.This study aimed to investigate the effect of KLF4 on the proliferation,apoptosis and phenotype of quiescent HSCs.Methods:We designed a KLF4 lentiviral vector and a KLF4 siRNA lentiviral vector,to upregulate and silence KLF4 expression in human HSC LX-2 cells via transfection.Cell proliferation was assessed using the CCK-8 assay.Flow cytometry was used to detect the cell cycle distribution and apoptosis rate.Western blotting was used to determine the levels of some quiescence and activation markers of HSCs.Results:Overexpression of KLF4 significantly increased the levels of E-cadherin and ZO-1,which are quiescent HSC markers,while significantly decreased the levels of N-cadherin and a-SMA,known activated HSC markers.In contrast,cell proliferation and apoptosis rates were elevated in LX-2 cells in which KLF4 expression was silenced.Conclusion:KLF4 inhibits the proliferation and activation of human LX-2 HSCs.It might be a key regulatory protein in the maintenance of HSC quiescence and may serve as a target for the inhibition of hepatic fibrosis.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    TL1A Promotes Fibrogenesis in Colonic Fibroblasts via the TGF-β1/Smad3 Signaling Pathway

    Jia SONGDong-lei SUNChen-yang LIYu-xin LUO...
    519-528页
    查看更多>>摘要：Objective:Intestinal fibrosis is a refractory complication of inflammatory bowel disease(IBD).Tumor necrosis factor ligand-related molecule-1A(TL1A)is important for IBD-related intestinal fibrosis in a dextran sodium sulfate(DSS)-induced experimental colitis model.This study aimed to explore the effects of TL1A on human colonic fibroblasts.Methods:A trinitrobenzene sulfonic acid(TNBS)-induced experimental colitis model of LCK-CD2-TL1A-GFP transgenic(Tg)or wild-type(WT)mice was established to determine the effect and mechanism of TL1A on intestinal fibrosis.The human colonic fibroblast CCD-18Co cell line was treated concurrently with TL1A and human peripheral blood mononuclear cell(PBMC)supernatant.The proliferation and activation of CCD-18Co cells were detected by BrdU assays,flow cytometry,immunocytochemistry and Western blotting.Collagen metabolism was tested by Western blotting and real-time quantitative polymerase chain reaction(RT-qPCR).Results:The level of collagen metabolism in the TNBS+ethyl alcohol(EtOH)/Tg group was greater than that in the TNBS+EtOH/WT group.Transforming growth factor-β1(TGF-β1)and p-Smad3 in the TNBS+EtOH/Tg group were upregulated as compared with those in the TNBS+EtOH/WT group.The proliferation of CCD-18Co cells was promoted by the addition of human PBMC supernatant supplemented with 20 ng/mL TL1 A,and the addition of human PBMC supernatant and TL1A increased CCD-18Co proliferation by 24.4％at 24 h.TL1A promoted cell activation and increased the levels of COL1A2,COL3A1,and TIMP-1 in CCD-18Co cells.Treatment of CCD-18Co cells with TL1A increased the expression of TGF-β1 and p-Smad3.Conclusion:TL1A promotes TGF-β1-mediated intestinal fibroblast activation,proliferation,and collagen deposition and is likely related to an increase in the TGF-β1/Smad3 signaling pathway.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Identification and Validation of SLC9A2 as A Potential Tumor Suppressor in Colorectal Cancer:Integrating Bioinformatics Analysis with Experimental Confirmation

    Yan-min LIUTie-cheng YANGXiao-chang FANGLi-jie YANG...
    529-544页
    查看更多>>摘要：Objective:To uncover the mechanisms underlying the development of colorectal cancer(CRC),we applied bioinformatic analyses to identify key genes and experimentally validated their possible roles in CRC onset and progression.Methods:We performed Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis on differentially expressed genes(DEGs),constructed a protein-protein interaction(PPI)network to find the top 10 hub genes,and analyzed their expression in colon adenocarcinoma(COAD)and rectum adenocarcinoma(READ).We also studied the correlation between these genes and immune cell infiltration and prognosis and validated the expression of SLC9A2 in CRC tissues and cell lines using qRT-PCR and Western blotting.Functional experiments were conducted in vitro to investigate the effects of SLC9A2 on tumor growth and metastasis.Results:We found 130 DEGs,with 45 up-regulated and 85 down-regulated in CRC.GO analysis indicated that these DEGs were primarily enriched in functions related to the regulation of cellular pH,zymogen granules,and transmembrane transporter activity.KEGG pathway analysis revealed that the DEGs played pivotal roles in pancreatic secretion,rheumatoid arthritis,and the IL-17 signaling pathway.We identified 10 hub genes:CXCL1,SLC26A3,CXCL2,MMP7,MMP1,SLC9A2,SLC4A4,CLCA1,CLCA4,and ZG16.GO enrichment analysis showed that these hub genes were predominantly involved in the positive regulation of transcription.Gene expression analysis revealed that CXCL1,CXCL2,MMP1,and MMP7 were highly expressed in CRC,whereas CLCA1,CLCA4,SLC4A4,SLC9A2,SLC26A3,and ZG16 were expressed at lower levels.Survival analysis revealed that 5 key genes were significantly associated with the prognosis of CRC.Both mRNA and protein expression levels of SLC9A2 were markedly reduced in CRC tissues and cell lines.Importantly,SLC9A2 overexpression in SW480 cells led to a notable inhibition of cell proliferation,migration,and invasion.Western blotting analysis revealed that the expression levels of phosphorylated ERK(p-ERK)and phosphorylated JNK(p-JNK)proteins were significantly increased,whereas there were no significant changes in the expression levels of ERK and JNK following SLC9A2 overexpression.Correlation analysis indicated a potential link between SLC9A2 expression and the MAPK signaling pathway.Conclusion:Our study suggests that SLC9A2 acts as a tumor suppressor through the MAPK pathway and could be a potential target for CRC diagnosis and therapy.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    TOPK Inhibition Enhances the Sensitivity of Colorectal Cancer Cells to Radiotherapy by Reducing the DNA Damage Response

    Shi-gui PANGXin ZHANGZhao-xin LILi-fei HE...
    545-553页
    查看更多>>摘要：Objective:Abnormal expression of T-lymphokine-activated killer cell-originated protein kinase(TOPK)was reported to be closely related to the resistance of prostate cancer to radiotherapy and to targeted drug resistance in lung cancer.However,the role of TOPK inhibition in enhancing radiosensitivity of colorectal cancer(CRC)cells is unclear.This study aimed to evaluate the radiosensitization of TOPK knockdown in CRC cells.Methods:The expression of TOPK was detected in CRC tissues by immunohistochemistry,and the effect of TOPK knockdown was detected in CRC cells by Western blotting.CCK-8 and clonogenic assays were used to detect the growth and clonogenic ability of CRC cells after TOPK knockdown combined with radiotherapy in CRC cells.Furthermore,proteomic analysis showed that the phosphorylation of TOPK downstream proteins changed after radiotherapy.DNA damage was detected by the comet assay.Changes in the DNA damage response signaling pathway were analyzed by Western blotting,and apoptosis was detected by flow cytometry.Results:The expression of TOPK was significantly greater in CRC tissues at grades 2-4 than in those at grade 1.After irradiation,CRC cells with genetically silenced TOPK had shorter comet tails and reduced expression levels of DNA damage response-associated proteins,including phospho-cyclin-dependent kinase 1(p-CDK1),phospho-ataxia telangiectasia-mutated(p-ATM),poly ADP-ribose polymerase(PARP),and meiotic recombination 11 homolog 1(MRE11).Conclusions:TOPK was overexpressed in patients with moderately to poorly differentiated CRC.Moreover,TOPK knockdown significantly enhanced the radiosensitivity of CRC cells by reducing the DNA damage response.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Standard-definition White-light,High-definition White-light versus Narrow-band Imaging Endoscopy for Detecting Colorectal Adenomas:A Multicenter Randomized Controlled Trial

    Chang-wei DUANHui-hong ZHAIHui XIEXian-zong MA...
    554-560页
    查看更多>>摘要：Objective:This study aimed to compare the performance of standard-definition white-light endoscopy(SD-WL),high-definition white-light endoscopy(HD-WL),and high-definition narrow-band imaging(HD-NBI)in detecting colorectal lesions in the Chinese population.Methods:This was a multicenter,single-blind,randomized,controlled trial with a non-inferiority design.Patients undergoing endoscopy for physical examination,screening,and surveillance were enrolled from July 2017 to December 2020.The primary outcome measure was the adenoma detection rate(ADR),defined as the proportion of patients with at least one adenoma detected.The associated factors for detecting adenomas were assessed using univariate and multivariate logistic regression.Results:Out of 653 eligible patients enrolled,data from 596 patients were analyzed.The ADRs were 34.5％in the SD-WL group,33.5％in the HD-WL group,and 37.5％in the HD-NBI group(P=0.72).The advanced neoplasm detection rates(ANDRs)in the three arms were 17.1％,15.5％,and 10.4％(P=0.17).No significant differences were found between the SD group and HD group regarding ADR or ANDR(ADR:34.5％vs.35.6％,P=0.79;ANDR:17.1％vs.13.0％,P=0.16,respectively).Similar results were observed between the HD-WL group and HD-NBI group(ADR:33.5％vs.37.7％,P=0.45;ANDR:15.5％vs.10.4％,P=0.18,respectively).In the univariate and multivariate logistic regression analyses,neither HD-WL nor HD-NBI led to a significant difference in overall adenoma detection compared to SD-WL(HD-WL:OR 0.91,P=0.69;HD-NBI:OR 1.15,P=0.80).Conclusion:HD-NBI and HD-WL are comparable to SD-WL for overall adenoma detection among Chinese outpatients.It can be concluded that HD-NBI or HD-WL is not superior to SD-WL,but more effective instruction may be needed to guide the selection of different endoscopic methods in the future.Our study's conclusions may aid in the efficient allocation and utilization of limited colonoscopy resources,especially advanced imaging technologies.
      原文链接:
    • NETL
    • NSTL
    • 万方数据