NF-κB family is a kind of nuclear factors in B lymphocyte that can bind to the immunoglobulin κ-chain enhancer and enhance transcriptional activity. NF-κB/Rel proteins, as a dimeric transcription factor, control th...NF-κB family is a kind of nuclear factors in B lymphocyte that can bind to the immunoglobulin κ-chain enhancer and enhance transcriptional activity. NF-κB/Rel proteins, as a dimeric transcription factor, control the expression of genes that regulate a broad range of biological processes through canonical and non-canonical pathways. In the central nervous system, NF-κB controls inflammatory reactions and the apoptotic cell death following nerve injury. It also contributes to the infarction and cell death in stroke models and patients. However, NF-κB is essential for neurosurvival as well. NF-κB activation is a part of recovery process that may protect neurons against oxidative-stresses or brain ischemia-induced apoptosis and neurodegeneration. Inhibition of NF-κB may reduce its neuroprotection activity. Hence the dual opposite effects of NF-κB on cells. The ultimate survival or death of neurons depends on which, where and when the NF-κB factors are activated.展开更多
Objective To investigate changes of autophagy after traumatic brain injury （TBI） and its possible role. Methods Rat TBI model was established by controlled cortical injury system. Autophagic double membrane structur...Objective To investigate changes of autophagy after traumatic brain injury （TBI） and its possible role. Methods Rat TBI model was established by controlled cortical injury system. Autophagic double membrane structure was detected by transmission electronic microscope. Microtubule-associated protein 1 light chain 3 （LC3） and Beclin 1 were also used to investigate the activation of autophagy post-TBI. Double labeling with LC3 and caspase-3, or Beclin 1 and Fluoro-Jade, to show the relationship between autophagy and apoptosis or neuron degeneration after TBI. Results An increase of autophagic double membrane structure was observed in early stage （1 h）, and the increase lasted for at least 32 d post-TBI. LC3 and Beclin 1 proteins also began to elevate at 1 h time point post-TBI in neurons, 3 d later in astrocytes, and peaked at about 8 d post-TBI. In both cell types, LC3 and Beclin l maintained at a high level until 32 d post-TBI. Most LC3 and Beclin 1 positive cells were near the side （including hippocampus）, but not in the core of the injury. In addition, in the periphery of the injury site, not all caspase-3 positive （＋） cells merged with LC3 （＋） cells post-TBI; In hippocampal area, almost all Beclin 1 （＋） neurons did not merge with Fluoro-Jade （＋） neurons from 1 h to 48 h post-TBI. Conclusion Autophagy is activated and might protect neurons from degeneration at early stage post-TBI and play a continuous role afterwards in eliminating aberrant cell components.展开更多
A damage location method using multi-layer perceptron （MLP） is developed to diagnose the cable damage of a real long span cable-stayed bridge. Firstly, the damage patterns are defined based on dynamical calculation....A damage location method using multi-layer perceptron （MLP） is developed to diagnose the cable damage of a real long span cable-stayed bridge. Firstly, the damage patterns are defined based on dynamical calculation. The analysis of damage pattern reveals that the damage patterns caused by different damage locations have inherent distinctness, while the damage extent only linearly amplifies the damage pattern curves. And 4th, 6th and 7th order frequencies are canceled from the patterns because of their insensitiveness to cable damage. Then a MLP network is designed by trail-error method to describe the 7-D mapping space of damage pattern. Identification results prove that the properly organized MLP can grasp the damage pattern and identify the damage location.展开更多
Objective:To explore the protective mechanisms of nerve growth factor (NGF) on spinal cord injury (SCI) and provide theoretical basis for its clinical application. Methods: The SCI of Wistar rats was done by Allens w...Objective:To explore the protective mechanisms of nerve growth factor (NGF) on spinal cord injury (SCI) and provide theoretical basis for its clinical application. Methods: The SCI of Wistar rats was done by Allens weight dropping way by a 10 g×2.5 cm impact on the posterior of spinal cord T 8. NGF (3 g/L, 20 μl) or normal saline was injected through catheter into subarachnoid space 2, 4, 8, 12 and 24 h after SCI. The expression of N-methyl-D-asparate receptor 1 (NMDAR 1) and neuronal constitutive nitric oxide synthase (ncNOS) mRNA in rat spinal cord was detected by in situ hybridization. Results: Abnormal expression of NMDAR 1 and ncNOS mRNA appeared in spinal ventral horn motorneuron in injured rats, as compared with that in control group. The expression of NMDAR 1 and ncNOS mRNA in NGF group was significantly lower than that in saline group (P<0.01). Conclusion: NGF can protect spinal cord against injury in vivo. One of the mechanisms is that NGF can prohibit NMDAR 1 and nitric oxide (NO) production after spinal cord injury.展开更多
基金National Natural Science Foundation of China （No. 30571909） the Youth Teacher＇s Research Foundation of Jiangsu Province, China （No. BU 134701 ） the Medical Development Foundation of Soochow University （No. EE134615）.
文摘NF-κB family is a kind of nuclear factors in B lymphocyte that can bind to the immunoglobulin κ-chain enhancer and enhance transcriptional activity. NF-κB/Rel proteins, as a dimeric transcription factor, control the expression of genes that regulate a broad range of biological processes through canonical and non-canonical pathways. In the central nervous system, NF-κB controls inflammatory reactions and the apoptotic cell death following nerve injury. It also contributes to the infarction and cell death in stroke models and patients. However, NF-κB is essential for neurosurvival as well. NF-κB activation is a part of recovery process that may protect neurons against oxidative-stresses or brain ischemia-induced apoptosis and neurodegeneration. Inhibition of NF-κB may reduce its neuroprotection activity. Hence the dual opposite effects of NF-κB on cells. The ultimate survival or death of neurons depends on which, where and when the NF-κB factors are activated.
基金This work was supported by the National Natural Science Foundation of China （No. 30571909） the Youth Teacher Foundation of Jiangsu Province （No. BU134701）+1 种基金 Medical Development Foundation of Soochow University （No. EE 134615） We also thank Jin-Sheng YANG for his help in polishing the English language.
文摘Objective To investigate changes of autophagy after traumatic brain injury （TBI） and its possible role. Methods Rat TBI model was established by controlled cortical injury system. Autophagic double membrane structure was detected by transmission electronic microscope. Microtubule-associated protein 1 light chain 3 （LC3） and Beclin 1 were also used to investigate the activation of autophagy post-TBI. Double labeling with LC3 and caspase-3, or Beclin 1 and Fluoro-Jade, to show the relationship between autophagy and apoptosis or neuron degeneration after TBI. Results An increase of autophagic double membrane structure was observed in early stage （1 h）, and the increase lasted for at least 32 d post-TBI. LC3 and Beclin 1 proteins also began to elevate at 1 h time point post-TBI in neurons, 3 d later in astrocytes, and peaked at about 8 d post-TBI. In both cell types, LC3 and Beclin l maintained at a high level until 32 d post-TBI. Most LC3 and Beclin 1 positive cells were near the side （including hippocampus）, but not in the core of the injury. In addition, in the periphery of the injury site, not all caspase-3 positive （＋） cells merged with LC3 （＋） cells post-TBI; In hippocampal area, almost all Beclin 1 （＋） neurons did not merge with Fluoro-Jade （＋） neurons from 1 h to 48 h post-TBI. Conclusion Autophagy is activated and might protect neurons from degeneration at early stage post-TBI and play a continuous role afterwards in eliminating aberrant cell components.
文摘A damage location method using multi-layer perceptron （MLP） is developed to diagnose the cable damage of a real long span cable-stayed bridge. Firstly, the damage patterns are defined based on dynamical calculation. The analysis of damage pattern reveals that the damage patterns caused by different damage locations have inherent distinctness, while the damage extent only linearly amplifies the damage pattern curves. And 4th, 6th and 7th order frequencies are canceled from the patterns because of their insensitiveness to cable damage. Then a MLP network is designed by trail-error method to describe the 7-D mapping space of damage pattern. Identification results prove that the properly organized MLP can grasp the damage pattern and identify the damage location.
文摘Objective:To explore the protective mechanisms of nerve growth factor (NGF) on spinal cord injury (SCI) and provide theoretical basis for its clinical application. Methods: The SCI of Wistar rats was done by Allens weight dropping way by a 10 g×2.5 cm impact on the posterior of spinal cord T 8. NGF (3 g/L, 20 μl) or normal saline was injected through catheter into subarachnoid space 2, 4, 8, 12 and 24 h after SCI. The expression of N-methyl-D-asparate receptor 1 (NMDAR 1) and neuronal constitutive nitric oxide synthase (ncNOS) mRNA in rat spinal cord was detected by in situ hybridization. Results: Abnormal expression of NMDAR 1 and ncNOS mRNA appeared in spinal ventral horn motorneuron in injured rats, as compared with that in control group. The expression of NMDAR 1 and ncNOS mRNA in NGF group was significantly lower than that in saline group (P<0.01). Conclusion: NGF can protect spinal cord against injury in vivo. One of the mechanisms is that NGF can prohibit NMDAR 1 and nitric oxide (NO) production after spinal cord injury.
