In this study,a binder based 3D-printing technology viz.Fused Granular Fabrication(FGF)technique was used to produce interconnected and open porous Mg-6.3Gd bone scaffolds for compression test analyses.The consolidati...In this study,a binder based 3D-printing technology viz.Fused Granular Fabrication(FGF)technique was used to produce interconnected and open porous Mg-6.3Gd bone scaffolds for compression test analyses.The consolidation of the green parts(as printed scaffolds)was performed using solvent debinding in cyclohexane and subsequent conventional sintering in argon atmosphere.Compression tests were performed on as sintered parts.Additionally,a simulation strategy was developed for modeling the compression behavior of the sintered parts,utilizing the data from the experimental results.The experimental compression test results and the simulation strategy for the compression behavior of the 3D-printed scaffolds demonstrated good agreement.展开更多
目的:探讨益胃消瘀颗粒治疗萎缩性胃炎胃黏膜肠化的治疗作用与机制。方法:8周龄雄性SD大鼠60只,按随机数字表法分为空白组、模型组、胃复春组、益胃消瘀颗粒高剂量组、益胃消瘀颗粒中剂量组、益胃消瘀颗粒低剂量组共6组,N-甲基-N’-硝基...目的:探讨益胃消瘀颗粒治疗萎缩性胃炎胃黏膜肠化的治疗作用与机制。方法:8周龄雄性SD大鼠60只,按随机数字表法分为空白组、模型组、胃复春组、益胃消瘀颗粒高剂量组、益胃消瘀颗粒中剂量组、益胃消瘀颗粒低剂量组共6组,N-甲基-N’-硝基-N-亚硝基胍(MNNG)和法莫替丁联合造模。6个月及7个月后分次抽检3只,造模成功后开始进入实验给药阶段,给药3个月后观察大鼠胃黏膜组织学改变,RT-qPCR检测胃黏膜标本中尾型同源盒转录因子2(caudal-related homeobox transcription factor2,CDX2)、干细胞转录调控因子性别决定相关基因簇2(Sex de-termining region Y-box 2,SOX2)的表达,Western blot检测胃黏膜中NK6同源框蛋白3(NK6 Homeobox Protein 3,NKX6.3)、骨形成蛋白4(bone morphogenic protein 4,BMP4)的表达。结果:光镜下观察胃黏膜病理组织,模型组可见黏膜萎缩及肠化,益胃消瘀颗粒高、中剂量组及胃复春组萎缩及肠化均较模型组明显改善,低剂量组萎缩及肠化有所减轻;与空白组比较,模型组NKX6.3、Sox2表达明显下降,BMP4、CDx2表达明显升高;与模型组比较,益胃消瘀颗粒高、中剂量组和胃复春组NKX6.3表达明显上升,益胃消瘀颗粒高、中、低剂量组及胃复春组Sox2表达明显升高,BMP4、CDx2表达明显下降。结论:益胃消瘀颗粒能够改善萎缩性胃炎肠化大鼠胃黏膜组织病理形态,其机制可能与激活NKX6.3、下调Cdx2、上调Sox2和抑制BMP4表达有关。展开更多
基金Alexander von Humboldt Foundation for the award of the Post-Doctoral Fellowship to M.Marvi-Mashhadi to undertake this research workthe support from the Bundesministerium für Bildung und Forschung(BMBF)through Bio Mag3D project code Nr.03VP09852 to undertake this research。
文摘In this study,a binder based 3D-printing technology viz.Fused Granular Fabrication(FGF)technique was used to produce interconnected and open porous Mg-6.3Gd bone scaffolds for compression test analyses.The consolidation of the green parts(as printed scaffolds)was performed using solvent debinding in cyclohexane and subsequent conventional sintering in argon atmosphere.Compression tests were performed on as sintered parts.Additionally,a simulation strategy was developed for modeling the compression behavior of the sintered parts,utilizing the data from the experimental results.The experimental compression test results and the simulation strategy for the compression behavior of the 3D-printed scaffolds demonstrated good agreement.
文摘目的:探讨益胃消瘀颗粒治疗萎缩性胃炎胃黏膜肠化的治疗作用与机制。方法:8周龄雄性SD大鼠60只,按随机数字表法分为空白组、模型组、胃复春组、益胃消瘀颗粒高剂量组、益胃消瘀颗粒中剂量组、益胃消瘀颗粒低剂量组共6组,N-甲基-N’-硝基-N-亚硝基胍(MNNG)和法莫替丁联合造模。6个月及7个月后分次抽检3只,造模成功后开始进入实验给药阶段,给药3个月后观察大鼠胃黏膜组织学改变,RT-qPCR检测胃黏膜标本中尾型同源盒转录因子2(caudal-related homeobox transcription factor2,CDX2)、干细胞转录调控因子性别决定相关基因簇2(Sex de-termining region Y-box 2,SOX2)的表达,Western blot检测胃黏膜中NK6同源框蛋白3(NK6 Homeobox Protein 3,NKX6.3)、骨形成蛋白4(bone morphogenic protein 4,BMP4)的表达。结果:光镜下观察胃黏膜病理组织,模型组可见黏膜萎缩及肠化,益胃消瘀颗粒高、中剂量组及胃复春组萎缩及肠化均较模型组明显改善,低剂量组萎缩及肠化有所减轻;与空白组比较,模型组NKX6.3、Sox2表达明显下降,BMP4、CDx2表达明显升高;与模型组比较,益胃消瘀颗粒高、中剂量组和胃复春组NKX6.3表达明显上升,益胃消瘀颗粒高、中、低剂量组及胃复春组Sox2表达明显升高,BMP4、CDx2表达明显下降。结论:益胃消瘀颗粒能够改善萎缩性胃炎肠化大鼠胃黏膜组织病理形态,其机制可能与激活NKX6.3、下调Cdx2、上调Sox2和抑制BMP4表达有关。
