During the recent conflicts in Iraq and Afghanistan,traumatic brain injury (TBI)has become the most prev-alent military injury that is described as the signature injuryof the current military operations.It usually causes no or mild external injury but results in serious long-lasting neuropsychiatric abnormalities,which have far-reaching impact on veterans,their families and the American society.Here we describeol the investment in TBI from the US government and the development in the diagnosis and treatment of mild TBI on the battlefield before putting forward some proposals for the Chinese army.

Objective To investigate the effect of adenosine A2A receptor on pituitary-adrenal axis response in acute phase of moderate craniocerebral trauma.Methods Eighteen adenosine A2A receptor knock-out mice in a C57BL/6 background and another eighteen their wild-type littermates were divided into normal control group and craniocerebral trauma for 4 hours group,and craniocerebral trauma for 24 hours group according to random number table,with siμ mice per group.Plasma levels of adrenocorticotropic-hormone (ACTH) and corticosterone at hours 4 and 24 postinjury were determined using ELISA method.Results At 4 and 24 hours,brain water content in wild-type mice [(80.950 ± 0.184) ％,(82.178 ± 0.255)％ respectively] was higher than that in gene knock-out mice [(80.006 ± 0.199)％,(81.091 ± 0.295)％ respectively,P ＜ 0.01].Besides,brain water content in both wild-type and gene knock-out mice increased after injury (P ＜ 0.01).Plasma levels of ACTH and corticosterone were higher in geneknock-out sham mice than in wild-type sham mice [(120.214 ± 2.472) ng/L vs (91.767 ±7.395) ng/L,(27.814 ±0.888) μg/L vs (11.430 ±0.644) μg/L respectively,P ＜0.0l].At 4 and 24 hours,plasma levels of ACTH [(174.776-± 5.040) ng/L,(189.613 ± 4.802) ng/L respectively] in geneknock-out mice showed a higher increase than those in wild-type mice [(119.594 ± 6.945) ng/L,(124.93-± 11.001 7) ng/L respectively,P ＜ 0.05].Moreover,plasma levels of corticosterone [(40.138 ±-0.805) μg/L] at 4 hours and [(37.440-0.485)μg/L] at 24 hours in gene knock-out mice showed a same result as compared with that in wild-type mice [(19.702 ± 0.804) μg/L,(17.602 ± 0.743) μg/L respectively,P ＜ 0.05].Conclusions Knock-out of adenosine A2A receptor increases the release of ACTH and corticosterone in acute stage of moderate craniocerebral trauma and promotes pituitary-adrenal stress response.This may provide a novel explanation for the neuroprotective effect of A2A receptor deficiency.

ObjectiveTo investigate the mechanism of dexamethasone (Dex) in inhibiting monocyte adhesion and phagocytose function.Methods Under the stimulation of phorbo1-12-myristate-13-acetate (PMA),U937 monocytes cultured in vitro were treated with Dex and Fasudil respectively.The adhesion rate of U937 monocles to human umbilical vein endothelial cells (HUVECs) and their phagocytic ability of India ink were studied.The protein content and activity of rho-associated coiled-coil protein kinase 1 ( ROCK1 ) as well as the effects of mifepristone and cycloheximide on Dex were determined.ResultsBoth DEX and Fasudil could significantly inhibit the adhesion tate and phagocytosis of U937 cells stimulated by PMA and suppressed the activity of ROCK1.While mifepristone and cycloheximide could not alter these effects of DEX.ConclusionDEX interferes with the adhesion and phagocytosis function of U937 cells by inhibiting ROCKI activity.