作为未来对于物体的识别技术,射频识别在人们生活中占有越来越重要的地位.这项技术将不断深入社会生活,在人们周围无处不在.由于这项技术的广泛应用,它的安全性以及涉及到个人生活的隐私问题不得不引起各界的关注.最初考虑到读卡器和标...作为未来对于物体的识别技术,射频识别在人们生活中占有越来越重要的地位.这项技术将不断深入社会生活,在人们周围无处不在.由于这项技术的广泛应用,它的安全性以及涉及到个人生活的隐私问题不得不引起各界的关注.最初考虑到读卡器和标签之间通讯的可视性以及因特网络潜在的诸多攻击,研究者主要针对读卡器和后端数据库的通讯安全问题,做出了很多的工作.随着UHF标签的推行,读卡器和射频标签通讯范围增大,它们之间的通讯不再安全.本文针对读卡器和标签之间通讯中可能受到的攻击进行分析,建立了一个保证它们通讯安全的模型,依据该模型对EPC C lass1 G en2(EPC C 1G 2)协议进行分析,指出了协议可能受到的攻击,并提出了具有身份验证功能的协议修改方案.展开更多
Background:KIT proto-oncogene,receptor tyrosine kinase(KIT,CD117)and platelet-derived growth factor-alpha(PDGFRA)are key drivers of gastrointestinal stromal tumors(GIST),but resistance to targeted therapy often arises...Background:KIT proto-oncogene,receptor tyrosine kinase(KIT,CD117)and platelet-derived growth factor-alpha(PDGFRA)are key drivers of gastrointestinal stromal tumors(GIST),but resistance to targeted therapy often arises from tumor protein p53(p53)alterations and loss of cell cycle control.However,the role of p53 status in GIST therapeutic potential has rarely been studied,so this study aimed to employ both wild-type andmutant p53 GIST models to investigate how p53 dysfunction influences the efficacy of p53 pathway-targeted therapies.Methods:The efficacy of the mouse double minute 2 homolog(MDM2)inhibitor(HDM201)and the Wee1 G2 checkpoint kinase(Wee1)inhibitor(adavosertib)was confirmed in both p53 wild-type(p53 WT)and p53 mutant(p53 MT)GIST cells.The anti-proliferative effects were assessed using the Cell Counting Kit-8(CCK-8)assay.Flow cytometry(FACS)and immunoblotting were employed to evaluate apoptosis and the expression of proteins related to drug efficacy.These findings were further validated in a xenograft model.Results:HDM201 selectively inhibited growth and triggered apoptosis in p53WT GIST cells,while adavosertib was effective mainly in p53 MT cells.Western blot analysis revealed thatHDM201 increased p53 and p21 levels in p53WT cells,and adavosertib affectedWee1 and phospho-cdc2 expression in both p53WT and p53 MT cells.In a xenograft mouse model,HDM201 significantly reduced the tumor volume and weight in p53WTGIST cells,whereas p53MT tumors showed only a moderate size reduction with adavosertib,without significant changes.Conclusions:Our results highlight the importance of p53 status in guiding GIST treatment.p53 WT tumors respond toMDM2 inhibitors,while p53 MTtumors show greater sensitivity toWee1 inhibitors,supporting p53 pathway targeting as a promising strategy for GIST patients.展开更多
文摘作为未来对于物体的识别技术,射频识别在人们生活中占有越来越重要的地位.这项技术将不断深入社会生活,在人们周围无处不在.由于这项技术的广泛应用,它的安全性以及涉及到个人生活的隐私问题不得不引起各界的关注.最初考虑到读卡器和标签之间通讯的可视性以及因特网络潜在的诸多攻击,研究者主要针对读卡器和后端数据库的通讯安全问题,做出了很多的工作.随着UHF标签的推行,读卡器和射频标签通讯范围增大,它们之间的通讯不再安全.本文针对读卡器和标签之间通讯中可能受到的攻击进行分析,建立了一个保证它们通讯安全的模型,依据该模型对EPC C lass1 G en2(EPC C 1G 2)协议进行分析,指出了协议可能受到的攻击,并提出了具有身份验证功能的协议修改方案.
基金financially supported by grants from the Chang-Gung Memorial Hospital(CMRPG3J0971~3,CMRPVVP0111,and CMRPVVQ0041 to CEWCMRPG3P0101 to HJS)the National Science and Technology Council(113-2628-B-182-001-MY3 and 113-2811-B-182-024 to CEW).
文摘Background:KIT proto-oncogene,receptor tyrosine kinase(KIT,CD117)and platelet-derived growth factor-alpha(PDGFRA)are key drivers of gastrointestinal stromal tumors(GIST),but resistance to targeted therapy often arises from tumor protein p53(p53)alterations and loss of cell cycle control.However,the role of p53 status in GIST therapeutic potential has rarely been studied,so this study aimed to employ both wild-type andmutant p53 GIST models to investigate how p53 dysfunction influences the efficacy of p53 pathway-targeted therapies.Methods:The efficacy of the mouse double minute 2 homolog(MDM2)inhibitor(HDM201)and the Wee1 G2 checkpoint kinase(Wee1)inhibitor(adavosertib)was confirmed in both p53 wild-type(p53 WT)and p53 mutant(p53 MT)GIST cells.The anti-proliferative effects were assessed using the Cell Counting Kit-8(CCK-8)assay.Flow cytometry(FACS)and immunoblotting were employed to evaluate apoptosis and the expression of proteins related to drug efficacy.These findings were further validated in a xenograft model.Results:HDM201 selectively inhibited growth and triggered apoptosis in p53WT GIST cells,while adavosertib was effective mainly in p53 MT cells.Western blot analysis revealed thatHDM201 increased p53 and p21 levels in p53WT cells,and adavosertib affectedWee1 and phospho-cdc2 expression in both p53WT and p53 MT cells.In a xenograft mouse model,HDM201 significantly reduced the tumor volume and weight in p53WTGIST cells,whereas p53MT tumors showed only a moderate size reduction with adavosertib,without significant changes.Conclusions:Our results highlight the importance of p53 status in guiding GIST treatment.p53 WT tumors respond toMDM2 inhibitors,while p53 MTtumors show greater sensitivity toWee1 inhibitors,supporting p53 pathway targeting as a promising strategy for GIST patients.
