Phase engineering has proven to be an effective strategy for achieving superior thermoelectric performance,while pressure is an excellent means of expanding the phase space of a material.In this paper,the effect of pr...Phase engineering has proven to be an effective strategy for achieving superior thermoelectric performance,while pressure is an excellent means of expanding the phase space of a material.In this paper,the effect of pressure-induced phase transition on improving the crystal symmetry and enhancing the thermoelectric properties of AgCrSe2 under high pressure and high temperature are reported.A structural phase transition from the low-symmetry R3m phase to the high-symmetry P3m1 phase is discovered below 1 GPa,which increases band degeneracy and contributes to a high electrical conductivity.For the metallic P3m1 phase,the electrons surrounding the Se2−anion gradually transfer to the Ag+and Cr3+cations as the pressure increases,decreasing the density of states around the Fermi level and thus optimizing the carrier concentration,thereby increasing the Seebeck coefficient while maintaining a high electrical conductivity.Consequently,an ultrahigh power factor of 864μW⋅m−1⋅K−2 is achieved at 5 GPa and 297 K.This study provides new insights into improving thermoelectric transport properties by applying physical pressure to enhance crystal symmetry and optimize thermoelectric parameters,and also indicates that phase engineering is a compelling strategy to discover or design novel high-performance thermoelectric materials starting from low-symmetry compounds.展开更多
A new type of extruded nickel-based powder metallurgy(P/M)superalloy was subjected to isothermal compression and tensile experiments to explore its superplasticity.Based on the compression flow curves,the hot working ...A new type of extruded nickel-based powder metallurgy(P/M)superalloy was subjected to isothermal compression and tensile experiments to explore its superplasticity.Based on the compression flow curves,the hot working maps of strain rate sensitivity index(m)were established at various strain levels.When compressing at1020-1110℃,in the strain rate range of 0.001-0.01 s^(-1),the m value was always greater than 0.3,indicating that the superalloy exhibited superplasticity in this deformation region.The tensile results showed that the superalloy exhibited excellent superplasticity under the conditions of 1050℃/0.01 s^(-1),1080℃/0.01 s^(-1)and 1110℃/0.001 s^(-1),with elongation after fracture reaching up to 1011%,1038%and951%,respectively.At low-temperature conditions and hightemperature/low strain rate conditions,both continuous dynamic recrystallization(CDRX)and discontinuous dynamic recrystallization(DDRX)were activated.As the deformation temperature increased,theγphases gradually dissolved into the matrix,and the primaryγ'phase changed from irregular shape to spherical or near-spherical shape.The interaction of theγ'phase with the dislocation promoted dynamic recrystallization(DRX)nucleation and thus slowed down the grain growth rate,which was essential for the superplastic deformation of the alloy.展开更多
BACKGROUND Cervical cancer(CC)stem cell-like cells(CCSLCs),defined by the capacity of differentiation and self-renewal and proliferation,play a significant role in the progression of CC.However,the molecular mechanism...BACKGROUND Cervical cancer(CC)stem cell-like cells(CCSLCs),defined by the capacity of differentiation and self-renewal and proliferation,play a significant role in the progression of CC.However,the molecular mechanisms regulating their self-renewal are poorly understood.Therefore,elucidation of the epigenetic mechanisms that drive cancer stem cell self-renewal will enhance our ability to improve the effectiveness of targeted therapies for cancer stem cells.AIM To explore how DNA methyltransferase 1(DNMT1)/miR-342-3p/Forkhead box M1(FoxM1),which have been shown to have abnormal expression in CCSLCs,and their signaling pathways could stimulate self-renewal-related stemness in CCSLCs.METHODS Sphere-forming cells derived from CC cell lines HeLa,SiHa and CaSki served as CCSLCs.Self-renewal-related stemness was identified by determining sphere and colony formation efficiency,CD133 and CD49f protein level,and SRY-box transcription factor 2 and octamer-binding transcription factor 4 mRNA level.The microRNA expression profiles between HeLa cells and HeLa-derived CCSLCs or mRNA expression profiles that HeLaderived CCSLCs were transfected with or without miR-342-3p mimic were compared using quantitative PCR analysis.The expression levels of DNMT1 mRNA,miR-342-3p,and FoxM1 protein were examined by quantitative real-time PCR and western blotting.In vivo carcinogenicity was assessed using a mouse xenograft model.The functional effects of the DNMT1/miR-342-3p/FoxM1 axis were examined by in vivo and in vitro gain-of-activity and loss-of-activity assessments.Interplay among DNMT1,miR-342-3p,and FoxM1 was tested by methylationspecific PCR and a respective luciferase reporter assay.RESULTS CCSLCs derived from the established HeLa cell lines displayed higher self-renewal-related stemness,including enhanced sphere and colony formation efficiency,increased CD133 and CD49f protein level,and heightened transcriptional quantity of stemness-related factors SRY-box transcription factor 2 and octamer-binding transcription factor 4 in vitro as well as a stronger tumorigenic potential in vivo compared to their parental cells.Moreover,quantitative PCR showed that the miR-342-3p level was downregulated in HeLa-derived CCSLCs compared to HeLa cells.Its mimic significantly decreased DNMT1 and FoxM1 mRNA expression levels in CCSLCs.Knockdown of DNMT1 or miR-342-3p mimic transfection suppressed DNMT1 expression,increased miR-342-3p quantity by promoter demethylation,and inhibited CCSLC self-renewal.Inhibition of FoxM1 by shRNA transfection also resulted in the attenuation of CCSLC self-renewal but had little effect on the DNMT1 activity and miR-342-3p expression.Furthermore,the loss of CCSLC self-renewal exerted by miR-342-3p mimic was inverted by the overexpression of DNMT1 or FoxM1.Furthermore,DNMT1 and FoxM1 were recognized as straight targets by miR-342-3p in HeLa-derived CCSLCs.CONCLUSION Our findings suggested that a novel DNMT1/miR-342-3p/FoxM1 signal axis promotes CCSLC self-renewal and presented a potential target for the treatment of CC through suppression of CCSLC self-renewal.However,this pathway has been previously implicated in CC,as evidenced by prior studies showing miR-342-3p-mediated downregulation of FoxM1 in cervical cancer cells.Additionally,research on liver cancer further supports the involvement of miR-342-3p in suppressing FoxM1 expression.While our study contributed to this body of knowledge,we did not present a completely novel axis but reinforced the therapeutic potential of targeting the DNMT1/miR-342-3p/FoxM1 axis to suppress CCSLC self-renewal in CC treatment.展开更多
Objective miR-34c-3p is down-regulated in nasopharyngeal carcinoma(NPC).The biological role of miR-34c-3p in NPC and its underlying mechanisms are unknown and were explored in this study.Methods Flow cytometry and imm...Objective miR-34c-3p is down-regulated in nasopharyngeal carcinoma(NPC).The biological role of miR-34c-3p in NPC and its underlying mechanisms are unknown and were explored in this study.Methods Flow cytometry and immunohistochemical staining were employed to detect cluster of differentiation 86(CD86)and cluster of differentiation 206(CD206)expression;quantitative real-time polymerase chain reaction(qRT-PCR)and western blotting were employed to examine mRNA expression and protein levels;cell counting kit-8(CCK8)and transwell assays were employed to assess cell proliferation,migration,and invasion;and hematoxylin-eosin(HE)staining was employed to assess pathological changes in tumor tissues.Results Our results revealed that the miR-34c-3p mimic markedly inhibited M2 polarization of macrophages by targeting SLC7A11,and M2 macrophages transfected with the miR-34c-3p mimic inhibited the proliferation,migration,and invasion of NPC cells.The in vivo experiments further confirmed that miR-34c-3p mimics blocked tumor growth and reduced inflammatory infiltration in tumor tissues.Conclusion This study provides novel insights into the pathogenesis of NPC and a new treatment strategy.展开更多
基金supported by the Jilin Province Science and Technology Development Program,China(Grant No.20250102013JC).
文摘Phase engineering has proven to be an effective strategy for achieving superior thermoelectric performance,while pressure is an excellent means of expanding the phase space of a material.In this paper,the effect of pressure-induced phase transition on improving the crystal symmetry and enhancing the thermoelectric properties of AgCrSe2 under high pressure and high temperature are reported.A structural phase transition from the low-symmetry R3m phase to the high-symmetry P3m1 phase is discovered below 1 GPa,which increases band degeneracy and contributes to a high electrical conductivity.For the metallic P3m1 phase,the electrons surrounding the Se2−anion gradually transfer to the Ag+and Cr3+cations as the pressure increases,decreasing the density of states around the Fermi level and thus optimizing the carrier concentration,thereby increasing the Seebeck coefficient while maintaining a high electrical conductivity.Consequently,an ultrahigh power factor of 864μW⋅m−1⋅K−2 is achieved at 5 GPa and 297 K.This study provides new insights into improving thermoelectric transport properties by applying physical pressure to enhance crystal symmetry and optimize thermoelectric parameters,and also indicates that phase engineering is a compelling strategy to discover or design novel high-performance thermoelectric materials starting from low-symmetry compounds.
基金financially supported by Shandong Provincial Natural Science Foundation of China(Nos.ZR2024JQ020 and ZR2021QE102)Taishan Scholars Program of Shandong Province(Nos.tsqn202211115 and tsqn202306162)+2 种基金Yantai high-end talent introduction"Double Hundred Plan"(2021)the Science Foundation Program for Distinguished Young Scholars of Shandong(Overseas)(No.2022HWYQ-084)the Talent Training Program for Shandong Province Higher Educational Youth Innovative Teams(2021)
文摘A new type of extruded nickel-based powder metallurgy(P/M)superalloy was subjected to isothermal compression and tensile experiments to explore its superplasticity.Based on the compression flow curves,the hot working maps of strain rate sensitivity index(m)were established at various strain levels.When compressing at1020-1110℃,in the strain rate range of 0.001-0.01 s^(-1),the m value was always greater than 0.3,indicating that the superalloy exhibited superplasticity in this deformation region.The tensile results showed that the superalloy exhibited excellent superplasticity under the conditions of 1050℃/0.01 s^(-1),1080℃/0.01 s^(-1)and 1110℃/0.001 s^(-1),with elongation after fracture reaching up to 1011%,1038%and951%,respectively.At low-temperature conditions and hightemperature/low strain rate conditions,both continuous dynamic recrystallization(CDRX)and discontinuous dynamic recrystallization(DDRX)were activated.As the deformation temperature increased,theγphases gradually dissolved into the matrix,and the primaryγ'phase changed from irregular shape to spherical or near-spherical shape.The interaction of theγ'phase with the dislocation promoted dynamic recrystallization(DRX)nucleation and thus slowed down the grain growth rate,which was essential for the superplastic deformation of the alloy.
基金Supported by Guangzhou Basic and Applied Basic Research Foundation,No.202201010121Medical Joint Fund of Jinan University,No.YXZY2024014 and No.YXJC2022001+2 种基金Hospital Achievement Transformation and Cultivation Project,No.ZH201911the Key Discipline Project of Guangdong Province,No.2019-GDXK-0016and the Medical Science and Technology Research Foundation of Guangdong Province,No.B2021145.
文摘BACKGROUND Cervical cancer(CC)stem cell-like cells(CCSLCs),defined by the capacity of differentiation and self-renewal and proliferation,play a significant role in the progression of CC.However,the molecular mechanisms regulating their self-renewal are poorly understood.Therefore,elucidation of the epigenetic mechanisms that drive cancer stem cell self-renewal will enhance our ability to improve the effectiveness of targeted therapies for cancer stem cells.AIM To explore how DNA methyltransferase 1(DNMT1)/miR-342-3p/Forkhead box M1(FoxM1),which have been shown to have abnormal expression in CCSLCs,and their signaling pathways could stimulate self-renewal-related stemness in CCSLCs.METHODS Sphere-forming cells derived from CC cell lines HeLa,SiHa and CaSki served as CCSLCs.Self-renewal-related stemness was identified by determining sphere and colony formation efficiency,CD133 and CD49f protein level,and SRY-box transcription factor 2 and octamer-binding transcription factor 4 mRNA level.The microRNA expression profiles between HeLa cells and HeLa-derived CCSLCs or mRNA expression profiles that HeLaderived CCSLCs were transfected with or without miR-342-3p mimic were compared using quantitative PCR analysis.The expression levels of DNMT1 mRNA,miR-342-3p,and FoxM1 protein were examined by quantitative real-time PCR and western blotting.In vivo carcinogenicity was assessed using a mouse xenograft model.The functional effects of the DNMT1/miR-342-3p/FoxM1 axis were examined by in vivo and in vitro gain-of-activity and loss-of-activity assessments.Interplay among DNMT1,miR-342-3p,and FoxM1 was tested by methylationspecific PCR and a respective luciferase reporter assay.RESULTS CCSLCs derived from the established HeLa cell lines displayed higher self-renewal-related stemness,including enhanced sphere and colony formation efficiency,increased CD133 and CD49f protein level,and heightened transcriptional quantity of stemness-related factors SRY-box transcription factor 2 and octamer-binding transcription factor 4 in vitro as well as a stronger tumorigenic potential in vivo compared to their parental cells.Moreover,quantitative PCR showed that the miR-342-3p level was downregulated in HeLa-derived CCSLCs compared to HeLa cells.Its mimic significantly decreased DNMT1 and FoxM1 mRNA expression levels in CCSLCs.Knockdown of DNMT1 or miR-342-3p mimic transfection suppressed DNMT1 expression,increased miR-342-3p quantity by promoter demethylation,and inhibited CCSLC self-renewal.Inhibition of FoxM1 by shRNA transfection also resulted in the attenuation of CCSLC self-renewal but had little effect on the DNMT1 activity and miR-342-3p expression.Furthermore,the loss of CCSLC self-renewal exerted by miR-342-3p mimic was inverted by the overexpression of DNMT1 or FoxM1.Furthermore,DNMT1 and FoxM1 were recognized as straight targets by miR-342-3p in HeLa-derived CCSLCs.CONCLUSION Our findings suggested that a novel DNMT1/miR-342-3p/FoxM1 signal axis promotes CCSLC self-renewal and presented a potential target for the treatment of CC through suppression of CCSLC self-renewal.However,this pathway has been previously implicated in CC,as evidenced by prior studies showing miR-342-3p-mediated downregulation of FoxM1 in cervical cancer cells.Additionally,research on liver cancer further supports the involvement of miR-342-3p in suppressing FoxM1 expression.While our study contributed to this body of knowledge,we did not present a completely novel axis but reinforced the therapeutic potential of targeting the DNMT1/miR-342-3p/FoxM1 axis to suppress CCSLC self-renewal in CC treatment.
文摘Objective miR-34c-3p is down-regulated in nasopharyngeal carcinoma(NPC).The biological role of miR-34c-3p in NPC and its underlying mechanisms are unknown and were explored in this study.Methods Flow cytometry and immunohistochemical staining were employed to detect cluster of differentiation 86(CD86)and cluster of differentiation 206(CD206)expression;quantitative real-time polymerase chain reaction(qRT-PCR)and western blotting were employed to examine mRNA expression and protein levels;cell counting kit-8(CCK8)and transwell assays were employed to assess cell proliferation,migration,and invasion;and hematoxylin-eosin(HE)staining was employed to assess pathological changes in tumor tissues.Results Our results revealed that the miR-34c-3p mimic markedly inhibited M2 polarization of macrophages by targeting SLC7A11,and M2 macrophages transfected with the miR-34c-3p mimic inhibited the proliferation,migration,and invasion of NPC cells.The in vivo experiments further confirmed that miR-34c-3p mimics blocked tumor growth and reduced inflammatory infiltration in tumor tissues.Conclusion This study provides novel insights into the pathogenesis of NPC and a new treatment strategy.
