BACKGROUND:Studies have demonstrated that the mechanisms underlying cellular apoptosis signal transduction focus on two pathways:intracellular mitochondria and extracellular death receptor.The current evidence support...BACKGROUND:Studies have demonstrated that the mechanisms underlying cellular apoptosis signal transduction focus on two pathways:intracellular mitochondria and extracellular death receptor.The current evidence supports that signal transduction of cellular apoptosis also includes endoplasmic reticulum stress signal transduction. OBJECTIVE:To observe Caspase-12 expression and cellular apoptosis following ischemia in rats with progressive spinal cord compression,and to verify the influence of endoplasmic reticulum stress on the apoptosis induced by spinal cord injury. DESIGN,TIME AND SETTING:A randomized,controlled,animal trial was performed at the Institute of Neuroscience in Chongqing Medical University between January and October in 2006. MATERIALS:Immunohistochemical kit,diaminobenzidine,and TUNEL kit were purchased from Beijing Zhongshan Biotechnology,China;rabbit anti-rat Caspase-12 monoclonal antibody was provided by Santa Cruz,USA. METHODS:Sixty Wistar rats,aged 3-4 months,were randomly assigned to a model group(n=50), which underwent spinal cord compression in the L_1 segment following L_1 laminectomy and articular process excision to establish a model of progressive spinal cord compression,and a sham-surgery group(n=10),which underwent only laminectomy.Starting with the first day after surgery,the rats were locally anesthetized,the skin was opened,and the screw was rotated by 1/4 of a cycle,twice weekly. MAIN OUTCOME MEASURES:At 3,7,14,21,and 28 days after surgery,rats from each group were anesthetized,and the spinal cords were resected.Pathological changes following spinal cord compression were determined using hematoxylin-eosin staining,Nissl dye,and transmission electron microscopy.The TUNEL method was used to observe neuronal apoptosis in the compressed spinal cord segments.Immunohistochemistry and Western blot were utilized to detect Caspase-12 expression in the compressed segments. RESULTS:Cellular swelling,neural degeneration,and altered endoplasmic reticulum structures were observed at 3 days following compression.Symptoms became gradually aggravated with increasing compression time.Compared with the sham-surgery group,the number of apoptotic neurons was remarkably increased in compressed segments of the model group(P<0.05),and Caspase-12 expression was also shown to increase(P<0.05). CONCLUSION:Neuronal apoptosis was a predominant pathological factor resulting in secondary spinal cord injury during progressive spinal cord compression,and Caspase-12 was shown to be possibly involved in neuronal apoptosis induced by progressive spinal cord compression.展开更多
本文报道了一种在蓝宝石衬底上NaOH辅助化学气相沉积(CVD)生长有序排列单层MoS2条带的方法.MoS2条带具有优良的单晶性,其载流子迁移率为~150 cm^2V^-1s^-1,在550 nm波长下的光学响应为103 mA W^-1.单层MoS2条带在蓝宝石衬底上具有两种...本文报道了一种在蓝宝石衬底上NaOH辅助化学气相沉积(CVD)生长有序排列单层MoS2条带的方法.MoS2条带具有优良的单晶性,其载流子迁移率为~150 cm^2V^-1s^-1,在550 nm波长下的光学响应为103 mA W^-1.单层MoS2条带在蓝宝石衬底上具有两种生长方式,其中一种为受层间范德华力以及晶格影响的取向生长,另一种为受蓝宝石台阶约束的平行生长.NaOH的引入量对MoS2形态与取向起重要作用,可以实现从取向性三角形晶畴,受衬底晶格影响的取向MoS2条带,受衬底台阶约束的平行条带,再到大尺寸杂乱取向三角形晶畴的连续可调.本文的结果有利于推动MoS2的基础研究及器件应用,也为合成其他一维和二维纳米结构开辟了新途径.展开更多
基金the National Natural Science Foundation of China,No.30270437Chunhui Program of the Ministry of Education in 2003, No.200407
文摘BACKGROUND:Studies have demonstrated that the mechanisms underlying cellular apoptosis signal transduction focus on two pathways:intracellular mitochondria and extracellular death receptor.The current evidence supports that signal transduction of cellular apoptosis also includes endoplasmic reticulum stress signal transduction. OBJECTIVE:To observe Caspase-12 expression and cellular apoptosis following ischemia in rats with progressive spinal cord compression,and to verify the influence of endoplasmic reticulum stress on the apoptosis induced by spinal cord injury. DESIGN,TIME AND SETTING:A randomized,controlled,animal trial was performed at the Institute of Neuroscience in Chongqing Medical University between January and October in 2006. MATERIALS:Immunohistochemical kit,diaminobenzidine,and TUNEL kit were purchased from Beijing Zhongshan Biotechnology,China;rabbit anti-rat Caspase-12 monoclonal antibody was provided by Santa Cruz,USA. METHODS:Sixty Wistar rats,aged 3-4 months,were randomly assigned to a model group(n=50), which underwent spinal cord compression in the L_1 segment following L_1 laminectomy and articular process excision to establish a model of progressive spinal cord compression,and a sham-surgery group(n=10),which underwent only laminectomy.Starting with the first day after surgery,the rats were locally anesthetized,the skin was opened,and the screw was rotated by 1/4 of a cycle,twice weekly. MAIN OUTCOME MEASURES:At 3,7,14,21,and 28 days after surgery,rats from each group were anesthetized,and the spinal cords were resected.Pathological changes following spinal cord compression were determined using hematoxylin-eosin staining,Nissl dye,and transmission electron microscopy.The TUNEL method was used to observe neuronal apoptosis in the compressed spinal cord segments.Immunohistochemistry and Western blot were utilized to detect Caspase-12 expression in the compressed segments. RESULTS:Cellular swelling,neural degeneration,and altered endoplasmic reticulum structures were observed at 3 days following compression.Symptoms became gradually aggravated with increasing compression time.Compared with the sham-surgery group,the number of apoptotic neurons was remarkably increased in compressed segments of the model group(P<0.05),and Caspase-12 expression was also shown to increase(P<0.05). CONCLUSION:Neuronal apoptosis was a predominant pathological factor resulting in secondary spinal cord injury during progressive spinal cord compression,and Caspase-12 was shown to be possibly involved in neuronal apoptosis induced by progressive spinal cord compression.
基金This work was financially supported by the Science and Technology Commission of Shanghai Municipality(18511110700).
文摘本文报道了一种在蓝宝石衬底上NaOH辅助化学气相沉积(CVD)生长有序排列单层MoS2条带的方法.MoS2条带具有优良的单晶性,其载流子迁移率为~150 cm^2V^-1s^-1,在550 nm波长下的光学响应为103 mA W^-1.单层MoS2条带在蓝宝石衬底上具有两种生长方式,其中一种为受层间范德华力以及晶格影响的取向生长,另一种为受蓝宝石台阶约束的平行生长.NaOH的引入量对MoS2形态与取向起重要作用,可以实现从取向性三角形晶畴,受衬底晶格影响的取向MoS2条带,受衬底台阶约束的平行条带,再到大尺寸杂乱取向三角形晶畴的连续可调.本文的结果有利于推动MoS2的基础研究及器件应用,也为合成其他一维和二维纳米结构开辟了新途径.
