采用冷金属过渡(Cold metal transfer,CMT)焊接技术制备了TC4钛合金件,研究了TC4钛合金增材体的显微组织和力学性能。结果表明:TC4钛合金打印态的表面成形良好,电弧3D打印TC4钛合金高度方向宏观组织上为外延生长的粗大β柱状晶形态,组...采用冷金属过渡(Cold metal transfer,CMT)焊接技术制备了TC4钛合金件,研究了TC4钛合金增材体的显微组织和力学性能。结果表明:TC4钛合金打印态的表面成形良好,电弧3D打印TC4钛合金高度方向宏观组织上为外延生长的粗大β柱状晶形态,组织由α相和β相组成。增材体的顶部为针状马氏体区,中部为细小的层片状网篮组织,基材结合处主要由层片状组织、β相以及少量残余α'相组成。所制备的成形件硬度较基材的高,表层部分硬度最大。室温拉伸性能呈现出明显的各向异性,水平方向拉伸强度较高,沿增材高度方向的塑性较高。室温冲击韧度未呈现出明显的各向异性,Aku2均达到70 J/cm2。展开更多
BACKGROUND Acute liver failure(ALF)has a high mortality with widespread hepatocyte death involving ferroptosis and pyroptosis.The silent information regulator sirtuin 1(SIRT1)-mediated deacetylation affects multiple b...BACKGROUND Acute liver failure(ALF)has a high mortality with widespread hepatocyte death involving ferroptosis and pyroptosis.The silent information regulator sirtuin 1(SIRT1)-mediated deacetylation affects multiple biological processes,including cellular senescence,apoptosis,sugar and lipid metabolism,oxidative stress,and inflammation.AIM To investigate the association between ferroptosis and pyroptosis and the upstream regulatory mechanisms.METHODS This study included 30 patients with ALF and 30 healthy individuals who underwent serum alanine aminotransferase(ALT)and aspartate aminotransferase(AST)testing.C57BL/6 mice were also intraperitoneally pretreated with SIRT1,p53,or glutathione peroxidase 4(GPX4)inducers and inhibitors and injected with lipopolysaccharide(LPS)/D-galactosamine(D-GalN)to induce ALF.Gasdermin D(GSDMD)^(-/-)mice were used as an experimental group.Histological changes in liver tissue were monitored by hematoxylin and eosin staining.ALT,AST,glutathione,reactive oxygen species,and iron levels were measured using commercial kits.Ferroptosis-and pyroptosis-related protein and mRNA expression was detected by western blot and quantitative real-time polymerase chain reaction.SIRT1,p53,and GSDMD were assessed by immunofluorescence analysis.RESULTS Serum AST and ALT levels were elevated in patients with ALF.SIRT1,solute carrier family 7a member 11(SLC7A11),and GPX4 protein expression was decreased and acetylated p5,p53,GSDMD,and acyl-CoA synthetase long-chain family member 4(ACSL4)protein levels were elevated in human ALF liver tissue.In the p53 and ferroptosis inhibitor-treated and GSDMD^(-/-)groups,serum interleukin(IL)-1β,tumour necrosis factor alpha,IL-6,IL-2 and C-C motif ligand 2 levels were decreased and hepatic impairment was mitigated.In mice with GSDMD knockout,p53 was reduced,GPX4 was increased,and ferroptotic events(depletion of SLC7A11,elevation of ACSL4,and iron accumulation)were detected.In vitro,knockdown of p53 and overexpression of GPX4 reduced AST and ALT levels,the cytostatic rate,and GSDMD expression,restoring SLC7A11 depletion.Moreover,SIRT1 agonist and overexpression of SIRT1 alleviated acute liver injury and decreased iron deposition compared with results in the model group,accompanied by reduced p53,GSDMD,and ACSL4,and increased SLC7A11 and GPX4.Inactivation of SIRT1 exacerbated ferroptotic and pyroptotic cell death and aggravated liver injury in LPS/D-GalNinduced in vitro and in vivo models.CONCLUSION SIRT1 activation attenuates LPS/D-GalN-induced ferroptosis and pyroptosis by inhibiting the p53/GPX4/GSDMD signaling pathway in ALF.展开更多
文摘虚拟仿真实训和传统教学方法在4D盆底超声这项高阶医学技术教学培训中应用的情况。方法 采用问卷调查以两种教学方法随机分组进行4D盆底超声技术学习的体验感,调查对象为昆明医科大学影像医学及超声医学研二、研三学生,采用完全随机设计的t检验进行分析评价。结果 ① 本次调查两组学生中,虚拟仿真实训组的学生重复检查吻合率较带教实操组的学生高,2组之间存在统计学差异;②而对于课后自主学习情况,虚拟仿真实训组的学生较带教实操组的学生进行的也更好,2组之间存在统计学差异。结论 虚拟仿真实训对于高阶4D盆底超声医学技术的学习较传统的带教实操学习更有帮助;作为创新的教学方法可以研究推广,以帮助医学生提升学习效率,缩短学习时间,以达到事半功倍的学习效果。
基金This work was supported by the National Key R&D Program of China(No.2022YFB4300905)the National Natural Science Foundation of China(No.61903187)the Natural Science Foundation of Jiangsu Province(No.BK20190414).
文摘采用冷金属过渡(Cold metal transfer,CMT)焊接技术制备了TC4钛合金件,研究了TC4钛合金增材体的显微组织和力学性能。结果表明:TC4钛合金打印态的表面成形良好,电弧3D打印TC4钛合金高度方向宏观组织上为外延生长的粗大β柱状晶形态,组织由α相和β相组成。增材体的顶部为针状马氏体区,中部为细小的层片状网篮组织,基材结合处主要由层片状组织、β相以及少量残余α'相组成。所制备的成形件硬度较基材的高,表层部分硬度最大。室温拉伸性能呈现出明显的各向异性,水平方向拉伸强度较高,沿增材高度方向的塑性较高。室温冲击韧度未呈现出明显的各向异性,Aku2均达到70 J/cm2。
基金Supported by National Natural Science Foundation of China,No.82060123Doctoral Start-up Fund of Affiliated Hospital of Guizhou Medical University,No.gysybsky-2021-28+1 种基金Fund Project of Guizhou Provincial Science and Technology Department,No.[2020]1Y299Guizhou Provincial Health Commission,No.gzwjk2019-1-082。
文摘BACKGROUND Acute liver failure(ALF)has a high mortality with widespread hepatocyte death involving ferroptosis and pyroptosis.The silent information regulator sirtuin 1(SIRT1)-mediated deacetylation affects multiple biological processes,including cellular senescence,apoptosis,sugar and lipid metabolism,oxidative stress,and inflammation.AIM To investigate the association between ferroptosis and pyroptosis and the upstream regulatory mechanisms.METHODS This study included 30 patients with ALF and 30 healthy individuals who underwent serum alanine aminotransferase(ALT)and aspartate aminotransferase(AST)testing.C57BL/6 mice were also intraperitoneally pretreated with SIRT1,p53,or glutathione peroxidase 4(GPX4)inducers and inhibitors and injected with lipopolysaccharide(LPS)/D-galactosamine(D-GalN)to induce ALF.Gasdermin D(GSDMD)^(-/-)mice were used as an experimental group.Histological changes in liver tissue were monitored by hematoxylin and eosin staining.ALT,AST,glutathione,reactive oxygen species,and iron levels were measured using commercial kits.Ferroptosis-and pyroptosis-related protein and mRNA expression was detected by western blot and quantitative real-time polymerase chain reaction.SIRT1,p53,and GSDMD were assessed by immunofluorescence analysis.RESULTS Serum AST and ALT levels were elevated in patients with ALF.SIRT1,solute carrier family 7a member 11(SLC7A11),and GPX4 protein expression was decreased and acetylated p5,p53,GSDMD,and acyl-CoA synthetase long-chain family member 4(ACSL4)protein levels were elevated in human ALF liver tissue.In the p53 and ferroptosis inhibitor-treated and GSDMD^(-/-)groups,serum interleukin(IL)-1β,tumour necrosis factor alpha,IL-6,IL-2 and C-C motif ligand 2 levels were decreased and hepatic impairment was mitigated.In mice with GSDMD knockout,p53 was reduced,GPX4 was increased,and ferroptotic events(depletion of SLC7A11,elevation of ACSL4,and iron accumulation)were detected.In vitro,knockdown of p53 and overexpression of GPX4 reduced AST and ALT levels,the cytostatic rate,and GSDMD expression,restoring SLC7A11 depletion.Moreover,SIRT1 agonist and overexpression of SIRT1 alleviated acute liver injury and decreased iron deposition compared with results in the model group,accompanied by reduced p53,GSDMD,and ACSL4,and increased SLC7A11 and GPX4.Inactivation of SIRT1 exacerbated ferroptotic and pyroptotic cell death and aggravated liver injury in LPS/D-GalNinduced in vitro and in vivo models.CONCLUSION SIRT1 activation attenuates LPS/D-GalN-induced ferroptosis and pyroptosis by inhibiting the p53/GPX4/GSDMD signaling pathway in ALF.
