A damage prediction method based on FE simulation was proposed to predict the occurrence of hot shortness crocks and surface cracks in liquid-solid extrusion process. This method integrated the critical temperature cr...A damage prediction method based on FE simulation was proposed to predict the occurrence of hot shortness crocks and surface cracks in liquid-solid extrusion process. This method integrated the critical temperature criterion and Cockcroft ＆ Latham ductile damage model, which were used to predict the initiation of hot shortness cracks and surface cracks of products, respectively. A coupling simulation of deformation with heat transfer as well as ductile damage was carried out to investigate the effect of extrusion temperature and extrusion speed on the damage behavior of Csf/AZ91D composites. It is concluded that the semisolid zone moves gradually toward deformation zone with the punch descending. The amplitude of the temperature rise at the exit of die from the initial billet temperature increases with the increase of extrusion speed during steady-state extrusion at a given punch displacement. In order to prevent the surface temperature of products beyond the incipient melting temperature of composites, the critical extrusion speed is decreased with the increase of extrusion temperature, otherwise the hot shortness cracks will occur. The maximum damage values increase with increasing extrusion speed or extrusion temperature. Theoretical results obtained by the Deform^TM-2D simulation agree well with the experiments.展开更多
Objective To investigate alterations in the microtubule-associated protein 2 (MAP-2) of neurons in Wistar rats and the effect of nimodipine (Nim), D-2-amino-5-phosphonovaleric acid (D-AP-5) and mild hypothermia on ne...Objective To investigate alterations in the microtubule-associated protein 2 (MAP-2) of neurons in Wistar rats and the effect of nimodipine (Nim), D-2-amino-5-phosphonovaleric acid (D-AP-5) and mild hypothermia on neuronal MAP-2 following fluid percussion injury (FPI).Methods Alterations of MAP-2 in Wistar rat neurons following FPI were measured by a confocal laserscanning microscope using MAP-2 immunofluorescence staining as a MAP-2 indicator.Results MAP-2 immunofluorescence staining was limited to the cell bodies and dendritic compartments of neurons and more intense in dendrites than in cell bodies. The loss of MAP-2 was marked at 3 h posttrauma ( P ＜ 0.01 ), and reached a maximum at 48 h post-trauma. Afterwards, fluorescence recovered partly at 72 h post-trauma. The application of Nim markedly reduced the loss of MAP-2 immunoreectivity within 1 h post-trauma ( P ＜ 0.01 ), and the application of D-AP-5 markedly reduced the loss of MAP-2immunoreactivity within 10 h post-injury ( P ＜ 0.01 ). The application of mild hypothermia decreased the loss of MAP-2 immunoreactivity within 1 h post-injury (P＜ 0.05).Conclusions The partial recovery of fluorescence at 72 h post-trauma indicate that the partial structure of the neuronal microtubules can be repaired by itself. Nim, D-AP-5 and mild hypothermia reduce the degradation of MAP-2 by different mechanisms. The treatment of neuronal cytoskeleton degradation following FPI must employ multiple therapeutic approaches.展开更多
Objective: To investigate the spatial and temporal profile of neural cell apoptosis following traumatic brain injury (TBI). Methods: In addition to morphological evidence of apoptosis, TUNEL histochemistry assay was u...Objective: To investigate the spatial and temporal profile of neural cell apoptosis following traumatic brain injury (TBI). Methods: In addition to morphological evidence of apoptosis, TUNEL histochemistry assay was used to identify DNA fragmentation in situ at both light and electron microscopic levels, whereas characteristic internucleosomal DNA fragmentation of apoptosis was demonstrated by DNA gel electrophoresis. Results: Using TUNEL method, we detected massive cells with extensive DNA fragmentation in different regions of the brains of rats subjected to experimental traumatic brain injury. Compared with the sham controls, in the injured cortex, the apoptotic cells were detectable for up to 24 h and reached a peak at 1 week after injury. The number of apoptotic cells in the white matter had a significant increase as early as 12 h after injury and peaked at 1 week. The number of apoptotic cells increased in the hippocampus at 72 h, whereas in the thalamus, the peak of apoptotic cells was at 2 weeks after injury. The number of apoptotic cells in most regions returned to sham values 2 months after injury. Gel electrophoresis of DNA extracted from affected areas of the injured brain revealed only internucleosomal fragmentation at 185-bp intervals, a feature originally described in apoptotic cell death. And no DNA ladder was detectable in the cortex and hippocampus contralateral to the injured hemisphere.Conclusions: These data suggest that in addition to the well described necrotic cell death, a temporal course of apoptotic cell death is initiated after brain trauma in selected brain regions.展开更多
基金Project(50972121) supported by the National Natural Science Foundation of China
文摘A damage prediction method based on FE simulation was proposed to predict the occurrence of hot shortness crocks and surface cracks in liquid-solid extrusion process. This method integrated the critical temperature criterion and Cockcroft ＆ Latham ductile damage model, which were used to predict the initiation of hot shortness cracks and surface cracks of products, respectively. A coupling simulation of deformation with heat transfer as well as ductile damage was carried out to investigate the effect of extrusion temperature and extrusion speed on the damage behavior of Csf/AZ91D composites. It is concluded that the semisolid zone moves gradually toward deformation zone with the punch descending. The amplitude of the temperature rise at the exit of die from the initial billet temperature increases with the increase of extrusion speed during steady-state extrusion at a given punch displacement. In order to prevent the surface temperature of products beyond the incipient melting temperature of composites, the critical extrusion speed is decreased with the increase of extrusion temperature, otherwise the hot shortness cracks will occur. The maximum damage values increase with increasing extrusion speed or extrusion temperature. Theoretical results obtained by the Deform^TM-2D simulation agree well with the experiments.
基金ThisstudywassupportedbyagrantfromtheFoundationofHeilongjiangDevelopmentinMedicalSciences (No G98C19 13)
文摘Objective To investigate alterations in the microtubule-associated protein 2 (MAP-2) of neurons in Wistar rats and the effect of nimodipine (Nim), D-2-amino-5-phosphonovaleric acid (D-AP-5) and mild hypothermia on neuronal MAP-2 following fluid percussion injury (FPI).Methods Alterations of MAP-2 in Wistar rat neurons following FPI were measured by a confocal laserscanning microscope using MAP-2 immunofluorescence staining as a MAP-2 indicator.Results MAP-2 immunofluorescence staining was limited to the cell bodies and dendritic compartments of neurons and more intense in dendrites than in cell bodies. The loss of MAP-2 was marked at 3 h posttrauma ( P ＜ 0.01 ), and reached a maximum at 48 h post-trauma. Afterwards, fluorescence recovered partly at 72 h post-trauma. The application of Nim markedly reduced the loss of MAP-2 immunoreectivity within 1 h post-trauma ( P ＜ 0.01 ), and the application of D-AP-5 markedly reduced the loss of MAP-2immunoreactivity within 10 h post-injury ( P ＜ 0.01 ). The application of mild hypothermia decreased the loss of MAP-2 immunoreactivity within 1 h post-injury (P＜ 0.05).Conclusions The partial recovery of fluorescence at 72 h post-trauma indicate that the partial structure of the neuronal microtubules can be repaired by itself. Nim, D-AP-5 and mild hypothermia reduce the degradation of MAP-2 by different mechanisms. The treatment of neuronal cytoskeleton degradation following FPI must employ multiple therapeutic approaches.
文摘Objective: To investigate the spatial and temporal profile of neural cell apoptosis following traumatic brain injury (TBI). Methods: In addition to morphological evidence of apoptosis, TUNEL histochemistry assay was used to identify DNA fragmentation in situ at both light and electron microscopic levels, whereas characteristic internucleosomal DNA fragmentation of apoptosis was demonstrated by DNA gel electrophoresis. Results: Using TUNEL method, we detected massive cells with extensive DNA fragmentation in different regions of the brains of rats subjected to experimental traumatic brain injury. Compared with the sham controls, in the injured cortex, the apoptotic cells were detectable for up to 24 h and reached a peak at 1 week after injury. The number of apoptotic cells in the white matter had a significant increase as early as 12 h after injury and peaked at 1 week. The number of apoptotic cells increased in the hippocampus at 72 h, whereas in the thalamus, the peak of apoptotic cells was at 2 weeks after injury. The number of apoptotic cells in most regions returned to sham values 2 months after injury. Gel electrophoresis of DNA extracted from affected areas of the injured brain revealed only internucleosomal fragmentation at 185-bp intervals, a feature originally described in apoptotic cell death. And no DNA ladder was detectable in the cortex and hippocampus contralateral to the injured hemisphere.Conclusions: These data suggest that in addition to the well described necrotic cell death, a temporal course of apoptotic cell death is initiated after brain trauma in selected brain regions.
