随着全球工业化程度不断加深,各国对矿产资源的需求持续攀升,全球各国普遍面临矿产资源供不应求、供需失衡的问题,而传统矿山开采模式资源开采效率低下、人员安全事故频发、安全风险高、环境破坏严重,这促进了矿山开采模式从传统方式向...随着全球工业化程度不断加深,各国对矿产资源的需求持续攀升,全球各国普遍面临矿产资源供不应求、供需失衡的问题,而传统矿山开采模式资源开采效率低下、人员安全事故频发、安全风险高、环境破坏严重,这促进了矿山开采模式从传统方式向智能化、信息化方向加速转变。近些年,移动通信技术的飞速演进促进了智慧矿山进一步发展。因此,综述了新一代信息通信技术赋能智慧矿山的技术途径,包括无人驾驶技术,远程控制技术,智能传感技术,超高清(Ultra High Definition,UHD)视频技术,无线雷管技术等关键技术对智慧矿山的使能作用。通过部署融合了移动通信、云计算、大数据、人工智能、组件式软件等设施的B5G矿山专用网络,满足智慧矿山超大带宽,超低网络时延,大规模接入等核心需求,解决当前矿山通信及智能化发展面临的通信效率低、覆盖盲区范围广、智能化程度不足、安全保障薄弱等问题,为建设安全,高效,经济,绿色的智慧矿山提供了技术支持。展开更多
Background:Hepatocellular carcinoma(HCC)is a prevalent liver malignancy.This study examined the roles of transforming growth factor beta(TGF-β)and cytochrome b5 domain containing 2(CYB5D2)in HCC etiology and their pr...Background:Hepatocellular carcinoma(HCC)is a prevalent liver malignancy.This study examined the roles of transforming growth factor beta(TGF-β)and cytochrome b5 domain containing 2(CYB5D2)in HCC etiology and their prognostic biomarker potential.Methods:Key modules and prognostic genes were identified by analyzing the GSE101685 dataset by weighted gene co-expression network analysis(WGCNA)and Least absolute shrinkage and selection operator(LASSO)Cox regression.The expression levels of CYB5D2 and TGF-βin HCC cell lines were quantified using Quantitative reverse transcription polymerase chain reaction(qRT-PCR)and Western blotting(WB)assays.Effects of CYB5D2 overexpression on cell proliferation,migration,invasion,and epithelial-mesenchymal transition(EMT)marker regulation were assessed in vitro,while in vivo tumorigenicity was evaluated using a xenograft model of HCC in nude mice.Results:In this study,WGCNA identified the turquoise module as significantly associated with HCC,containing 452 DEGs.LASSO Cox regression analysis revealed 9 key prognostic genes,with CYB5D2 being underexpressed in HCC cells and tissues.TGF-βwas negatively correlated with CYB5D2 expression,resulting in poor patient prognosis.Functional assays demonstrated that CYB5D2 overexpression inhibited proliferation,migration,and invasion of HCC cell lines,and altered EMT marker expression.Furthermore,the addition of TGF-βpartially reversed the suppressive effects caused by CYB5D2 overexpression.In vivo,CYB5D2 overexpression significantly reduced tumor growth,indicating its potential as a therapeutic target for HCC.Conclusion:The tumor suppressor function of CYB5D2 in HCC and its interaction with TGF-βoffered fresh information on the molecular pathophysiology of HCC and possible treatment avenues.展开更多
Background:Oral squamous cell carcinoma(OSCC)is the most common head and neck malig-nancy with a low five-year survival rate.ATP-binding cassette subfamily B member 5(ABCB5)has been linked to tumorigenesis.However,its...Background:Oral squamous cell carcinoma(OSCC)is the most common head and neck malig-nancy with a low five-year survival rate.ATP-binding cassette subfamily B member 5(ABCB5)has been linked to tumorigenesis.However,its role in inducing OSCC remains unclear.Methods:Quantitative reverse transcription polymerase chain reaction(qRT-PCR),western blot,and immunocytochemistry(ICC)were performed to examine the level of ABCB5 in OSCC(CAL27 and HSC-3)and human oral keratinocyte(HOK).ABCB5 was knocked down in CAL27 cells using ABCB5-specific small interfering RNA(ABCB5 siRNA),and its contribution to migration,invasion,and epithelial-mesenchymal transition(EMT),a process by which epithelial cells lose their tight junction and acquire an increased migratory and invasive phenotype resembling that of mesenchymal cells,were evaluated by three-dimension and transwell migration and invasion assays,qRT-PCR and ICC.An in vivo OSCC model was established using 4-nitroquinoline-1-oxide(4NQO),a carcinogenic chemical that is commonly used to develop OSCC by destroying DNA synthesis and oxidative stress.Pathological alterations,ABCB5,and EMT markers were evaluated by H&E staining,immunohistochemistry,and qRT-PCR.Results:ABCB5 was significantly upregulated in CAL27 and HSC-3 cells as compared to HOK.Knockdown of ABCB5 significantly reduced the number of migrated and invaded CAL27 cells,accompanied by the significantly increased E-cadherin and decreased Vimentin and N-cadherin under Transforming growth factorβ(TGF-β)treatment.In vivo,as OSCC advanced,a notable rise in the expressions of ABCB5,N-cadherin,and Vimentin,while a statistical decrease in E-cadherin was demonstrated.Conclusion:ABCB5 promotes the migration,invasion,and EMT of OSCC.ABCB5 might be a new biomarker and potential therapeutic target for OSCC.展开更多
文摘随着全球工业化程度不断加深,各国对矿产资源的需求持续攀升,全球各国普遍面临矿产资源供不应求、供需失衡的问题,而传统矿山开采模式资源开采效率低下、人员安全事故频发、安全风险高、环境破坏严重,这促进了矿山开采模式从传统方式向智能化、信息化方向加速转变。近些年,移动通信技术的飞速演进促进了智慧矿山进一步发展。因此,综述了新一代信息通信技术赋能智慧矿山的技术途径,包括无人驾驶技术,远程控制技术,智能传感技术,超高清(Ultra High Definition,UHD)视频技术,无线雷管技术等关键技术对智慧矿山的使能作用。通过部署融合了移动通信、云计算、大数据、人工智能、组件式软件等设施的B5G矿山专用网络,满足智慧矿山超大带宽,超低网络时延,大规模接入等核心需求,解决当前矿山通信及智能化发展面临的通信效率低、覆盖盲区范围广、智能化程度不足、安全保障薄弱等问题,为建设安全,高效,经济,绿色的智慧矿山提供了技术支持。
基金National Natural Science Foundation of China Youth Training Project(2021GZR003)Medical-Engineering Interdisciplinary Research Youth Training Project(2022YGJC001).
文摘Background:Hepatocellular carcinoma(HCC)is a prevalent liver malignancy.This study examined the roles of transforming growth factor beta(TGF-β)and cytochrome b5 domain containing 2(CYB5D2)in HCC etiology and their prognostic biomarker potential.Methods:Key modules and prognostic genes were identified by analyzing the GSE101685 dataset by weighted gene co-expression network analysis(WGCNA)and Least absolute shrinkage and selection operator(LASSO)Cox regression.The expression levels of CYB5D2 and TGF-βin HCC cell lines were quantified using Quantitative reverse transcription polymerase chain reaction(qRT-PCR)and Western blotting(WB)assays.Effects of CYB5D2 overexpression on cell proliferation,migration,invasion,and epithelial-mesenchymal transition(EMT)marker regulation were assessed in vitro,while in vivo tumorigenicity was evaluated using a xenograft model of HCC in nude mice.Results:In this study,WGCNA identified the turquoise module as significantly associated with HCC,containing 452 DEGs.LASSO Cox regression analysis revealed 9 key prognostic genes,with CYB5D2 being underexpressed in HCC cells and tissues.TGF-βwas negatively correlated with CYB5D2 expression,resulting in poor patient prognosis.Functional assays demonstrated that CYB5D2 overexpression inhibited proliferation,migration,and invasion of HCC cell lines,and altered EMT marker expression.Furthermore,the addition of TGF-βpartially reversed the suppressive effects caused by CYB5D2 overexpression.In vivo,CYB5D2 overexpression significantly reduced tumor growth,indicating its potential as a therapeutic target for HCC.Conclusion:The tumor suppressor function of CYB5D2 in HCC and its interaction with TGF-βoffered fresh information on the molecular pathophysiology of HCC and possible treatment avenues.
基金the financial support from the Sichuan Science and Technology Program(No.2024JDRC0040)Luzhou Science and Technology Program(No.2023JYJ002,No.2023SYF139)+4 种基金Southwest Medical University Technology Program(No.2024ZKY018,No.2023ZD001,No.2024KQZX09)National Natural Science Foundation of China(No.82403404)NHCKey Laboratory ofNuclear TechnologyMedical Transformation(Mianyang Central Hospital)(No.2023HYX028)The Science and Technology Strategic Cooperation Programs of Deyang Stomatological Hospital and Southwest Medical University(No.2024DYKQXNYD03)the Affiliated Stomatology Hospital of Southwest Medical University Program(No.2022KQ03)。
文摘Background:Oral squamous cell carcinoma(OSCC)is the most common head and neck malig-nancy with a low five-year survival rate.ATP-binding cassette subfamily B member 5(ABCB5)has been linked to tumorigenesis.However,its role in inducing OSCC remains unclear.Methods:Quantitative reverse transcription polymerase chain reaction(qRT-PCR),western blot,and immunocytochemistry(ICC)were performed to examine the level of ABCB5 in OSCC(CAL27 and HSC-3)and human oral keratinocyte(HOK).ABCB5 was knocked down in CAL27 cells using ABCB5-specific small interfering RNA(ABCB5 siRNA),and its contribution to migration,invasion,and epithelial-mesenchymal transition(EMT),a process by which epithelial cells lose their tight junction and acquire an increased migratory and invasive phenotype resembling that of mesenchymal cells,were evaluated by three-dimension and transwell migration and invasion assays,qRT-PCR and ICC.An in vivo OSCC model was established using 4-nitroquinoline-1-oxide(4NQO),a carcinogenic chemical that is commonly used to develop OSCC by destroying DNA synthesis and oxidative stress.Pathological alterations,ABCB5,and EMT markers were evaluated by H&E staining,immunohistochemistry,and qRT-PCR.Results:ABCB5 was significantly upregulated in CAL27 and HSC-3 cells as compared to HOK.Knockdown of ABCB5 significantly reduced the number of migrated and invaded CAL27 cells,accompanied by the significantly increased E-cadherin and decreased Vimentin and N-cadherin under Transforming growth factorβ(TGF-β)treatment.In vivo,as OSCC advanced,a notable rise in the expressions of ABCB5,N-cadherin,and Vimentin,while a statistical decrease in E-cadherin was demonstrated.Conclusion:ABCB5 promotes the migration,invasion,and EMT of OSCC.ABCB5 might be a new biomarker and potential therapeutic target for OSCC.
