| Missile craniocerebral injury (MCI), a kind of serious injury that leads to high mortality and disabled rates, is an important project for study in military medicine. MCI sometimes occurs in the special environment, such as in cold or high temperature. At present there is no research reports about MCI in high temperature (HT) and high humidity (HH) environment. However, Southeast China is under HT and HH all around the year, The further study on MCI in such special environment will promote to investigate the pathophysiologic changes and its mechanism, and improve the cure level of MCI in HT and HH, which lead to doing well in sanitarian and safeguard, having realistic guide significance.Heat shock proteins (HSPs), also known as stress protein, are a set of highly conserved proteins that are induced by heat stress and a variety of stressful stimuli, such as hypoxia, ischemia, cold, and nitric oxide, et al. HSPs enable organisms or cells to survive potentially lethal insult, which protective roles process is called heat shock response. In mammals, 70,000 molecular wt heat shock protein (HSP70), its identical potential (pI) is between pH 5.2 and pH 6.3, is among the most abundant and important stress protein, is called HSP70 family. HSP70 may function as molecularchaperones to facilitate protein folding, processing and trafficking. HSP70 plays a critical biological role in cells' stress protection, heat endurance, apoptosis, inflammation, and immunity reaction.Aggravating original brain injury by secondary neural cells death after brain injury is an important cause that affects recovery of brain injury. At present it is found that many changes of neural biochemical factors take part in the development process of neuron death, but the mechanism of their effects remains unclear. It has proved in these years that many signal transduction pathways take roles in the pathophysiologic process of secondary damage after primary brain injury. Among them mitogen-activated protein kinases (MAPKs) series signal transduction are the common pathways that transduce the extracellular stimuli to the nuclei or other compartments, and induce the cells response. P38 MAPK, one of the four present determined signal pathways, takes part in cells growing, developing, differentiating, functional in-phase among cells and so on. In the effect of ex-environment stress, such as heat injury, hyperosmotic, inflammatory factor, p38 MAPK is activated by phosphorylated, which mediate the special gene expression through phosphorylate-activated transcriptional factor, thereby transduce the extracellular signal to the nuclei, participates cell apoptosis causing by ill-stimuli. The recent research has demonstrated that the transient activation p38 MAPK triggers cardioprotection in early phase of ischemic preconditioning (IP), or that the deactivation of p38 MAPK after the onset of lethal ischemia mediates cardioprotection. The mechanism of the phasic pattern effect of p38 MAPK remain unclear. The suppression of the activation of p38 MAPK is considered to be one of the important neuroprotective mechanism against ischemia-reperfussion induced neuronal injury in the gerbil ischemia. The activation, changes, and function of p38 MAPK in MCI under special environment, such as high temperature (HT) combining high humidity (HH) are still not reported.Research Object:1. To establish rabbit MCI model in HT and HH environment, by using simulated climate cabin to simulate actual environment.2. To explore the feature of change for HSP70 protein and activation of p38 MAPK in MCI under HT and HH environment.3. To explore special pathophysiologic change and its mechanism in MCI under HT and HH environment, which by experimental treatment to affect the changes of HSP protein and activation of p38 MAPK. Providing theory base for traumatic cure by understanding the speciality of MCI under HT and HH environment.The experiment includes four parts to reach the above research object.Part One: Establishment of MCI model under HT and HH environment a...
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