Based on laws of theory of materials strengthening were discribed the experimentally obtained alloying effect in Mg-Ga system and shown using program for 3d atomic structures.As known from our experiments a homogeneou...Based on laws of theory of materials strengthening were discribed the experimentally obtained alloying effect in Mg-Ga system and shown using program for 3d atomic structures.As known from our experiments a homogeneous"wavy"microstructure of the diffusion zone forms as result of mass-transfer of molten gallium into the volume of magnesium alloys.SEM chemical composition shows Mg 65%wt.and Ga 35%wt.and X-ray spectra diffraction data-Mg5Ga2 intermetallic phase formation.Such intermetallic diffusion zone provides the significant strengthening effect of microstructure which was determined experimentally by the indentation method.The 3-d visualization shows the reaction and changing of an original crystal structure of magnesium atomic lattice upon diffusion doping with foreign atoms of gallium and then is shown the coalescence of Mg5Ga2 intermetallic crystal with crystals surfaces of Mg-matrix.So,investigated Mg-alloy strengthening at alloying with Ga explained by two main factors.At first is the formation of intermetallic phases with the ordering and consolidation of the crystal structure of the matrix by the ligature atoms,which is the key factor of the strengthening mechanism fixed experimentally.Second,when hexagonal and orthorhombic atomic structures growth according to their spatial type,a significant disorientation of structural fragments occurs,an increase in the density of the amorphous transition layer,a twinning of the structure in the interphase boundaries,which leads to the formation of intrinsic mutual deformation and a high level of internal stresses.展开更多
溃疡性结肠炎(ulcerative colitis,UC)是一种以结肠黏膜及黏膜下层炎症为主要特征的慢性非特异性炎症,其致病机制复杂,易反复发作,现代医学研究认为其涉及氧化应激、免疫失衡等多方面因素。信号转导和转录激活因子3(signal transducer a...溃疡性结肠炎(ulcerative colitis,UC)是一种以结肠黏膜及黏膜下层炎症为主要特征的慢性非特异性炎症,其致病机制复杂,易反复发作,现代医学研究认为其涉及氧化应激、免疫失衡等多方面因素。信号转导和转录激活因子3(signal transducer and activator of transcription,STAT3)是调节细胞生长、分化和存活的重要因子,可被相关细胞因子激活,从而介导炎症、氧化应激及免疫反应以影响UC病理进程,并与核因子κB(nuclear factor kappa-B,NF-κB)、NOD样受体热蛋白结构域相关蛋白3(NOD-like receptor thermal protein domain associated protein 3,NLRP3)、细胞因子信号传导抑制因子(suppressor of cytokine signaling,SOCSs)等信号通路存在串扰现象。STAT3作为近年来UC相关研究的热点之一,本文综述了中药通过调控STAT3信号通路防治UC的研究进展,深入探究了STAT3激活及介导UC病理过程的分子机制,以及中药成分如何通过多途径调控STAT3信号通路,发挥其潜在的作用机制。相关研究揭示了中药通过调节STAT3信号通路,不仅有效抑制炎症、氧化应激的发生,还能在调控免疫反应、维持肠道屏障功能及完整性等方面发挥重要作用,有望为治疗UC提供新思路。展开更多
背景:骨代谢紊乱会引起骨相关疾病的发生,而叉头框转录因子O3可以通过调节氧化应激、自噬水平等来影响骨组织细胞增殖、分化与凋亡,调控骨代谢过程。目的:系统性分析叉头框转录因子O3调控骨代谢及其在骨科疾病中作用机制的相关研究文献...背景:骨代谢紊乱会引起骨相关疾病的发生,而叉头框转录因子O3可以通过调节氧化应激、自噬水平等来影响骨组织细胞增殖、分化与凋亡,调控骨代谢过程。目的:系统性分析叉头框转录因子O3调控骨代谢及其在骨科疾病中作用机制的相关研究文献,为后续以叉头框转录因子O3为靶点治疗骨疾病的研究提供参考。方法:以“(SU=FoxO3a OR SU=Foxo3 OR SU=Forkhead box O3 OR SU=叉头框转录因子O3)AND SU=骨”为检索句在中国知网进行检索,以“主题:(“FoxO3a”)OR主题:(“Foxo3”)OR主题:(“Forkhead box O3”)OR主题:(“叉头框转录因子O3”)AND主题:(“骨”)”为检索句在万方医学数据库进行检索;以“((FoxO3a)OR(Foxo3)OR(Forkhead box O3))AND((bone)OR(Skeleton))”为检索句在PubMed数据库进行检索,排除陈旧、重复、质量较差以及不相关的文献,最终纳入56篇文献进行综述分析。结果与结论:①叉头框转录因子O3与骨髓间充质干细胞:叉头框转录因子O3能够促进成骨谱系的形成,还可通过激活自噬促进早期成骨分化。同时,叉头框转录因子O3在骨髓间充质干细胞中体现抗氧化特性,保护细胞免受氧化应激诱导的衰老。②叉头框转录因子O3与成骨细胞:叉头框转录因子O3在成骨细胞中能通过干扰Wnt/β-连环蛋白通路抑制成骨,同时能激活抗氧化酶保护成熟成骨细胞。叉头框转录因子O3能促进成骨祖细胞的增殖,并通过激活自噬促进成骨分化。③叉头框转录因子O3与破骨细胞:叉头框转录因子O3表达可抵抗氧化应激和激活自噬抑制破骨细胞生成。④叉头框转录因子O3与骨细胞:叉头框转录因子O3可通过抗氧化作用保护骨细胞,还可通过抑制p16和p53信号通路和抑制衰老相关分泌表型来减少骨流失。⑤叉头框转录因子O3与软骨细胞:叉头框转录因子O3在骨关节炎中对软骨细胞起到保护作用,抑制软骨细胞分解或凋亡,促进软骨细胞外基质合成,可抑制软骨细胞肥大;然而,叉头框转录因子O3与Runt相关转录因子1在软骨细胞中高度共表达却会促进软骨祖细胞的早期软骨形成和终末肥大。⑥叉头框转录因子O3通过参与氧化应激抵抗与调控自噬等过程影响骨代谢,参与多类骨相关疾病的病理进程。展开更多
文摘Based on laws of theory of materials strengthening were discribed the experimentally obtained alloying effect in Mg-Ga system and shown using program for 3d atomic structures.As known from our experiments a homogeneous"wavy"microstructure of the diffusion zone forms as result of mass-transfer of molten gallium into the volume of magnesium alloys.SEM chemical composition shows Mg 65%wt.and Ga 35%wt.and X-ray spectra diffraction data-Mg5Ga2 intermetallic phase formation.Such intermetallic diffusion zone provides the significant strengthening effect of microstructure which was determined experimentally by the indentation method.The 3-d visualization shows the reaction and changing of an original crystal structure of magnesium atomic lattice upon diffusion doping with foreign atoms of gallium and then is shown the coalescence of Mg5Ga2 intermetallic crystal with crystals surfaces of Mg-matrix.So,investigated Mg-alloy strengthening at alloying with Ga explained by two main factors.At first is the formation of intermetallic phases with the ordering and consolidation of the crystal structure of the matrix by the ligature atoms,which is the key factor of the strengthening mechanism fixed experimentally.Second,when hexagonal and orthorhombic atomic structures growth according to their spatial type,a significant disorientation of structural fragments occurs,an increase in the density of the amorphous transition layer,a twinning of the structure in the interphase boundaries,which leads to the formation of intrinsic mutual deformation and a high level of internal stresses.
文摘溃疡性结肠炎(ulcerative colitis,UC)是一种以结肠黏膜及黏膜下层炎症为主要特征的慢性非特异性炎症,其致病机制复杂,易反复发作,现代医学研究认为其涉及氧化应激、免疫失衡等多方面因素。信号转导和转录激活因子3(signal transducer and activator of transcription,STAT3)是调节细胞生长、分化和存活的重要因子,可被相关细胞因子激活,从而介导炎症、氧化应激及免疫反应以影响UC病理进程,并与核因子κB(nuclear factor kappa-B,NF-κB)、NOD样受体热蛋白结构域相关蛋白3(NOD-like receptor thermal protein domain associated protein 3,NLRP3)、细胞因子信号传导抑制因子(suppressor of cytokine signaling,SOCSs)等信号通路存在串扰现象。STAT3作为近年来UC相关研究的热点之一,本文综述了中药通过调控STAT3信号通路防治UC的研究进展,深入探究了STAT3激活及介导UC病理过程的分子机制,以及中药成分如何通过多途径调控STAT3信号通路,发挥其潜在的作用机制。相关研究揭示了中药通过调节STAT3信号通路,不仅有效抑制炎症、氧化应激的发生,还能在调控免疫反应、维持肠道屏障功能及完整性等方面发挥重要作用,有望为治疗UC提供新思路。
文摘背景:骨代谢紊乱会引起骨相关疾病的发生,而叉头框转录因子O3可以通过调节氧化应激、自噬水平等来影响骨组织细胞增殖、分化与凋亡,调控骨代谢过程。目的:系统性分析叉头框转录因子O3调控骨代谢及其在骨科疾病中作用机制的相关研究文献,为后续以叉头框转录因子O3为靶点治疗骨疾病的研究提供参考。方法:以“(SU=FoxO3a OR SU=Foxo3 OR SU=Forkhead box O3 OR SU=叉头框转录因子O3)AND SU=骨”为检索句在中国知网进行检索,以“主题:(“FoxO3a”)OR主题:(“Foxo3”)OR主题:(“Forkhead box O3”)OR主题:(“叉头框转录因子O3”)AND主题:(“骨”)”为检索句在万方医学数据库进行检索;以“((FoxO3a)OR(Foxo3)OR(Forkhead box O3))AND((bone)OR(Skeleton))”为检索句在PubMed数据库进行检索,排除陈旧、重复、质量较差以及不相关的文献,最终纳入56篇文献进行综述分析。结果与结论:①叉头框转录因子O3与骨髓间充质干细胞:叉头框转录因子O3能够促进成骨谱系的形成,还可通过激活自噬促进早期成骨分化。同时,叉头框转录因子O3在骨髓间充质干细胞中体现抗氧化特性,保护细胞免受氧化应激诱导的衰老。②叉头框转录因子O3与成骨细胞:叉头框转录因子O3在成骨细胞中能通过干扰Wnt/β-连环蛋白通路抑制成骨,同时能激活抗氧化酶保护成熟成骨细胞。叉头框转录因子O3能促进成骨祖细胞的增殖,并通过激活自噬促进成骨分化。③叉头框转录因子O3与破骨细胞:叉头框转录因子O3表达可抵抗氧化应激和激活自噬抑制破骨细胞生成。④叉头框转录因子O3与骨细胞:叉头框转录因子O3可通过抗氧化作用保护骨细胞,还可通过抑制p16和p53信号通路和抑制衰老相关分泌表型来减少骨流失。⑤叉头框转录因子O3与软骨细胞:叉头框转录因子O3在骨关节炎中对软骨细胞起到保护作用,抑制软骨细胞分解或凋亡,促进软骨细胞外基质合成,可抑制软骨细胞肥大;然而,叉头框转录因子O3与Runt相关转录因子1在软骨细胞中高度共表达却会促进软骨祖细胞的早期软骨形成和终末肥大。⑥叉头框转录因子O3通过参与氧化应激抵抗与调控自噬等过程影响骨代谢,参与多类骨相关疾病的病理进程。
