Nel Noddings’ethics of care is an important lineage of Western moral education thought,which contains deep humanistic values.Service-learning advocates the equal importance of service and learning,and emphasizes more...Nel Noddings’ethics of care is an important lineage of Western moral education thought,which contains deep humanistic values.Service-learning advocates the equal importance of service and learning,and emphasizes more on the discovery of educational connotations in practice.Based on the social background of aging,this paper takes the“Care for the Elderly”service-learning program as an example,attempts to take the care ethics as the entry point,adopts interviews,questionnaires,and other research methods,and opens-up the service-learning practice path under the threshold of Nel Noddings’care education theory.展开更多
The emergence of nodding syndrome (NS) in Northern Uganda has generated controversial views with respect to patterns, natural history, and aetiology of the disease which is yet unknown. This study explored spatial pat...The emergence of nodding syndrome (NS) in Northern Uganda has generated controversial views with respect to patterns, natural history, and aetiology of the disease which is yet unknown. This study explored spatial patterns of NS using spatial-temporal methods to establish its clustering patterns across both space and time. Village and year of NS onset for individual patients between the years 1990 and 2014 were entered as input for spatial and temporal analysis in the 6 districts in northern Uganda where it is prevalent. Our temporal results showed that NS onset started before the population was moved in Internally Displaced People’s (IDPs) camps. It also shows that NS continued to be reported during the IDPs and after people had left the IDPs. Our spatial and spatiotemporal analysis showed that two periods had persistent NS clusters. These were 2000-2004 and 2010-2014, coinciding with the period when the population was in the IDP camps and when the population was already out of the camps, respectively. Our conclusion is that the view of associating NS outbreak with living conditions in IDP camps is thus coincidental. We, therefore, contend that the actual aetiological factor of NS is still at large.展开更多
目的观察电针对缺血性脑卒中大鼠神经行为学及脑组织结构的影响,探讨电针通过调控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)炎性小体途径改善缺血性脑卒中大鼠神经功能的...目的观察电针对缺血性脑卒中大鼠神经行为学及脑组织结构的影响,探讨电针通过调控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)炎性小体途径改善缺血性脑卒中大鼠神经功能的机制。方法36只健康雄性SD大鼠采用随机数字表随机分为假手术组12只及手术组24只,手术组大鼠采用Longa等改良线栓法制备大鼠脑缺血再灌注损伤(MCAO)模型。术后2 h行神经行为学评分,造模成功的大鼠再随机分为模型组及电针组。电针组予电针“曲池”“足三里”连续干预7 d,假手术组及模型组不做干预。干预完成后分别评估各组大鼠神经功能缺损情况,HE染色观察脑组织病理学变化,QPCR及Western blot法检测炎性小体相关蛋白NLRP3、ASC、Caspase-1的表达水平,ELISA检测各组大鼠血清IL-1β和IL-18炎性因子表达。结果与假手术组相比,模型组大鼠神经功能评分均显著提高,差异有高度统计学意义(P<0.01),脑组织缺血皮质区神经元胞体缩小变形,核固缩明显,大鼠脑组织缺血周围区炎性因子相关蛋白NLRP3、ASC、Caspase-1的mRNA及蛋白表达水平升高,差异有高度统计学意义(P<0.01),血清IL-1β和IL-18炎症因子表达增加,差异有高度统计学意义(P<0.01);经电针干预7 d后,电针组神经评分功能较模型组显著下降,差异有统计学意义(P<0.05),所见的病理损伤减少;炎性小体相关蛋白NLRP3、ASC、Caspase-1的表达下降,差异有统计学意义(P<0.05),且电针下调了血清IL-1β和IL-18的表达,差异有统计学意义(P<0.05)。结论电针“曲池”“足三里”可减轻缺血性脑卒中大鼠神经功能缺损症状,减少脑组织病理损伤,下调NLRP3、ASC、Caspase-1表达水平,其机制可能与调控NLRP3炎性小体途径抗细胞焦亡,减轻脑缺血再灌注损伤有关。展开更多
目的通过脂多糖(Lipopolysaccharide,LPS)诱导的脓毒症模型验证G蛋白偶联受体120(G-protein coupled receptor120,GPR120)基因对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...目的通过脂多糖(Lipopolysaccharide,LPS)诱导的脓毒症模型验证G蛋白偶联受体120(G-protein coupled receptor120,GPR120)基因对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)炎症小体及肺损伤的影响,并探索其调控分子机制。方法通过C57BL/6小鼠构建体内脓毒症模型,通过GPR120基因激动剂TUG891进行干预,验证GPR120基因对脓毒症小鼠肺损伤的保护作用;然后进行转录组测序,筛选差异信号通路,并在动物模型中验证NLRP3炎症小体及调控蛋白的差异表达。通过慢病毒转染构建GPR120基因过表达/低表达的Raw264.7单核巨噬细胞株,观察GPR120基因对NLRP3炎症小体的调控作用。结果与脓毒症组相比,LPS+TUG891组小鼠肺组织中包括cAMP通路基因在内的77个基因表达显著上调,37个基因表达下降。LPS组的GPR120水平较正常对照组显著降低,同时cAMP/PKA信号通路关键蛋白CREB及PKA表达减少,NLRP3、Caspase-1及IL-1β等炎症小体激活相关蛋白水平升高(P<0.01),予以TUG891处理后,组织内GPR120表达回升,cAMP/PKA信号通路重新被激活(P<0.01),NLRP3炎症小体蛋白活化程度下降(P<0.05)。体外实验中,LPS诱导的脓毒症可引起细胞增殖活性下降,GPR120基因在脓毒症巨噬细胞中表达减低(P<0.001),通过干预GPR120基因表达,证实GPR120基因可负性调控NLRP3炎症小体的活化程度及细胞炎症反应(P<0.01)。结论脓毒症中GPR120基因的激活可通过抑制NLRP3炎症小体的活化,减轻脓毒症的炎症反应及肺损伤。展开更多
文摘Nel Noddings’ethics of care is an important lineage of Western moral education thought,which contains deep humanistic values.Service-learning advocates the equal importance of service and learning,and emphasizes more on the discovery of educational connotations in practice.Based on the social background of aging,this paper takes the“Care for the Elderly”service-learning program as an example,attempts to take the care ethics as the entry point,adopts interviews,questionnaires,and other research methods,and opens-up the service-learning practice path under the threshold of Nel Noddings’care education theory.
文摘The emergence of nodding syndrome (NS) in Northern Uganda has generated controversial views with respect to patterns, natural history, and aetiology of the disease which is yet unknown. This study explored spatial patterns of NS using spatial-temporal methods to establish its clustering patterns across both space and time. Village and year of NS onset for individual patients between the years 1990 and 2014 were entered as input for spatial and temporal analysis in the 6 districts in northern Uganda where it is prevalent. Our temporal results showed that NS onset started before the population was moved in Internally Displaced People’s (IDPs) camps. It also shows that NS continued to be reported during the IDPs and after people had left the IDPs. Our spatial and spatiotemporal analysis showed that two periods had persistent NS clusters. These were 2000-2004 and 2010-2014, coinciding with the period when the population was in the IDP camps and when the population was already out of the camps, respectively. Our conclusion is that the view of associating NS outbreak with living conditions in IDP camps is thus coincidental. We, therefore, contend that the actual aetiological factor of NS is still at large.
文摘目的通过脂多糖(Lipopolysaccharide,LPS)诱导的脓毒症模型验证G蛋白偶联受体120(G-protein coupled receptor120,GPR120)基因对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)炎症小体及肺损伤的影响,并探索其调控分子机制。方法通过C57BL/6小鼠构建体内脓毒症模型,通过GPR120基因激动剂TUG891进行干预,验证GPR120基因对脓毒症小鼠肺损伤的保护作用;然后进行转录组测序,筛选差异信号通路,并在动物模型中验证NLRP3炎症小体及调控蛋白的差异表达。通过慢病毒转染构建GPR120基因过表达/低表达的Raw264.7单核巨噬细胞株,观察GPR120基因对NLRP3炎症小体的调控作用。结果与脓毒症组相比,LPS+TUG891组小鼠肺组织中包括cAMP通路基因在内的77个基因表达显著上调,37个基因表达下降。LPS组的GPR120水平较正常对照组显著降低,同时cAMP/PKA信号通路关键蛋白CREB及PKA表达减少,NLRP3、Caspase-1及IL-1β等炎症小体激活相关蛋白水平升高(P<0.01),予以TUG891处理后,组织内GPR120表达回升,cAMP/PKA信号通路重新被激活(P<0.01),NLRP3炎症小体蛋白活化程度下降(P<0.05)。体外实验中,LPS诱导的脓毒症可引起细胞增殖活性下降,GPR120基因在脓毒症巨噬细胞中表达减低(P<0.001),通过干预GPR120基因表达,证实GPR120基因可负性调控NLRP3炎症小体的活化程度及细胞炎症反应(P<0.01)。结论脓毒症中GPR120基因的激活可通过抑制NLRP3炎症小体的活化,减轻脓毒症的炎症反应及肺损伤。
