Objective:The aim is to study the apoptosis and c-fos expression occurred in the rat gut following traumatic brain injury,and to explore the potential role of mucosal apoptosis in the intestinal barrier dysfunction and the relation of c-fos expression with the mucosal apoptosis.Methods:Male Wistar rats were randomly divided into six groups(6 rats each group) including controls with sham operation and TBI groups at hours 3,12,24,and 72,and on day 7.Parietal brain contusion was adopted using weight-dropping method.Rat jejunum was taken at each corresponding time point.Apoptosis was detected by in situ immunohistochemical staining(TUNEL) and c-fos expression by immunohistochemistry.Results:Mucosal epithelium appeared to be the major apoptotic cells,and the number of apoptotic cells increased since 3 h after TBI,peaking at 72 h postinjury.The apoptotic cells initially located at the tip of villus and gradually spread to the whole villus.The c-fos expression of gut mucosa gradually increased after TBI,predominantly in epithelial cells,smooth muscle cells and lymphocytes and with the maximal expression appeared at 24 h,72 h and 7 d postinjury.Conclusion:It is highly suggested that intestinal mucosa apoptosis plays an important role in the pathogenesis of gut barrier damage,and c-fos expression might be highly responsible for the apoptosis,proliferation and renovation of the small intestinal mucosa.

Objective To study the role of the cytokine-mediated inflammation in the pathogenesis of acute intestinal mucosa damage and explore the potential mechanisms of glutamine reducing intestinal inflammatory factors on the intcstines and protecting the structure and barrier of intestinal mucosa after traumatic brain iniury(TBI).Methods A total of 54 male Wistar rats were divided equally into nine groups(6 rats in each group),ie,control group,TBI groups(sacrificed at days 1,3,5 and 7 postinjury,respectively)and Glutamine group.Levels of TNF-α and IL-1β in the intestinal tissues were determined by using ELISA and activity of NF-κB by immunohistochemical method.Results Activity of NF-κB in ileum was significantly increased at day 1 following TBI,reached peak at day 3 and remained hjgh level till at day 7 postinjury.TNF-α and IL-1β levels in the intestinal tissues were also significantly increased after TBI,peaked at day 1 and remained high level at day 3 pestinjury.NF-κB activity and the expressions of TNF-α and IL-1β were all obviously decreased posterior to glutamine administration through stomach tube after TBI,compared with normal foodintake group after TBI.Conclusions TBI can induce a rapid and persistent up-regulation of NF-κB and proinflammatory cytokines in the intestine.Inflammation response may play an important role in the pathogenesis of acute intestinal mucosa injury.Glutamine administration throush stomach tube can inhibit NF-κB activity in ileum and reduce TNF-α and IL-1β levels after TBI,indicating that the intestinal barrier function at stress state may be protected by glutamine administration.

Ethyl pyruvate ( EP) is a stable lipophilic ester derivative of pyruvate with many pharmacological actions confirmed by researches , the anti-tumor effects of EP has attracted the attention of many domestic and foreign scholars .EP exerts antitumor activi-ty through several ways , such as inhibiting proliferation , inducing apoptosis , inhibiting angiogenesis , blocking cell cycle .This paper briefly reviews the rencent findings of antitumor function of EP .

Cerebral vasospasm(CVS) is a common complication following aneurysmal subarachnoid hemorrhage(SAH),and is the leading cause of death and disability in SAH patients.Till now,although there is no special treatmemt for CVS,the clinical intervention of CVS has gotten a rapid progress with the development of basic research in recent years.The clinical advancement of CVS management is reviewed.

[Abstract ] Objective Ubiquitin carboxyl hydrolase L1(UCH-L1) is a neuron cytoplasm protein and increased UCH-L1 lev-el in cerebrospinal fluid( CSF) indicates brain injury.The study aimed to indentify UCH-L1 level in CSF of patients with subarachnoid hemorrhage(SAH) and assess the prognosis value of UCH-L1. Methods Retrospective analysis was made on 40 aneurismal SAH patients hospitalized in our department from August 2014 to February 2015.In the experiment group, CSF was taken by lumbar punc-ture in day1-day3, day5-day7, and day8-day10 after subarachnoid hemorrhage.In the control group, a single CSF sample was collect-ed during spinal anesthesia before surgery in 10 patients without neurologic disease.ELISA was applied to determine the concentration of UCH-L1 in CSF followed by comparison.Analysis was also made on relationship of the changes of UCH-L1 and modified rankins scale( MRS) 6 months later. Results CSF UCH-L1 concentrations in all SAH patients were significantly increased in day1-day3 ( P<0.05) after SAH, peaked in day5-day7 (P<0.01) and elevated un-til days 8-10 ( P<0.01 ) .MRS at 6 months showed a significant correlation with CSF levels of UCH-L1 in day5-day7 ( correlation co-efficient CC=0.691, P=0.001) and day8-day10 (CC=0.583,P=0.03), but not in days1-day3 (CC=0.364,P=0.08).SAH pa-tients with a good outcome at 6 months ( MRS<4) had much lower UCH-L1 levels in day5-day7 ( P=0.001) and day8-day10 ( P=0.041) than those with a poor outcome (MRS≥4).Higher UCH-L1 level at day5-day7 was a predictive marker of poor outcome in bi-nary logistic regression analysis (P=0.003); Conclusion The study suggests that increased CSF UCH-L1 level in day5-day7 after SAH is correlated with higher MRS and predicts an adverse clinical outcome 6 months after SAH.

Acute brain injury is usually complicated by systemic inflammatory response syndrome (SIRS) which is initiated by cytokines and inflammatory mediators and induces a series of adverse physiological changes, culminating in the development of multiple organ failure. SIRS plays a pivotal role on the function of brain and extra cerebral organs, exacerbates the brain edema, and increases the septic rate. The diagnostic criteria and pathological courses of SIRS, and its relationship with acute brain injury and sepsis are briefly reviewed.

The metabolic response to traumatic brain injury includes hypermetabolism, hypercatabolism, hyperglycemia, acute phase response and immunosuppression, which are mediated mainly by hypothalamus pituitary adrenal axis and cytokines. Sufficient nutritional support and appropriate metabolic intervention are believed clinically to play an important role on the mitigation of secondary brain damage, reduction of septic rate and improvement of patient′s outcomes.

Objective To assess the feasibility and safety of transradial puncture route for digital subtraction angiography (DSA)in young patients with ischemic cerebrovascular disease. Methods One hundred young patients with cerebrovascular disease who underwent whole brain angiography at the Department of Neurology,the 81 st Hospital of PLA were enrolled. They were divided into either a radial group (n =50)or a femoral group (n = 50)using a computer random number method. The time of puncture,success rate of puncture,success rate of selective angiography,exposure time,and incidence of complications were compared and analyzed. Results (1)The puncture time of the radial group was significantly longer than that of the femoral group,they were 3. 00 ± 0. 50 min and 1. 50 ± 0. 25 min respectively. There was significant difference (t = 18. 97,P < 0. 05). There were no significant differences in the success rate of puncture (98% vs. 100%),success rate of selective angiography (100% vs. 100%),and exposure time (5. 3 ± 2. 2 vs. 4. 8 ± 1. 7 min)between the two groups (all P > 0. 05). (2)The incidence of complications of the radial group (4%,n = 2)was significantly 1ower than that of the femoral group (18%,n = 9 ). There was significant difference between the two groups (χ2 = 5. 01,P < 0. 05 ). Conclusion Transradial route puncture for whole brain DSA in young patients with cerebrovascular disease is safely and feasible.

Objectives: The aim of the current study was to explore the alterations of intestinal mucosa morphology and barrier function, and to determine how rapidly impairment of gut barrier function occurs and how long it persists following traumatic brain injury. Methods: Male Wistar rats were randomly divided into six groups (6 rats each group) including controls without brain injury and traumatic brain injury groups at hours 3, 12, 24, 72 and days 7. The intestinal mucosa structure was detected by histopathological examination and electron microscopy. Gut barrier dysfunction was evaluated by detecting serum endotoxin and intestinal permeability. The level of serum endotoxin and intestinal permeability were measured by using chromogenic limulus amebocyte lysate and lactulose/mannitol (L/M) ratio, respectively. Results: After traumatic brain injury, the histopathological alterations of gut mucosa occurred rapidly as early as 3 hours and progressed to a serious state, including shedding of epithelial cells, fracture of villi, focal ulcer, fusion of adjacent villi, dilation of central chyle duct, mucosal atrophy, and vascular dilation, congestion and edema in the villous interstitium and lamina propria. Apoptosis of epithelial cells, fracture and sparseness of microvilli, loss of tight junction between enterocytes, and damage of mitochondria and endoplasm were found by electron microscope. The villous height, crypt depth and surface area in jejunum decreased progressively with the time of brain injury. The level of serum endotoxin and L/M ratio were significantly higher in traumatic brain injury groups than that in control (P

Objective:The aim of the current study was to investigate the expression of nuclear factor-?B(NF-?B) and metalloproteinase-9(MMP-9) in the small intestine and to explore the potential role of NF-?B and MMP-9 in the damage of gut mucosal barrier after traumatic brain injury.Methods:The trauma was produced by a free-falling weight on the exposed dura of right parietal lobe.The rats were randomly divided into control group and traumatic brain injury groups at hours 3,12,24 and 72,and on day 7.NF-?B binding activity in the small intestine was studied by electrophoretic mobility shift assay(EMSA),and the expression of MMP-9 was studied by immunohistochemistry.Results:The results showed that NF-?B binding activity and MMP-9 expression in the small intestine was progressively increased,reached the maximum at 72 h and kept at high level up to 7 d after TBI.Concomitant upregulation of NF-?B~()and MMP-9 was observed.MMP-9 positively immunostained cells were mainly located at villous interstitium,lamina propria,crypt and submucosal layer,including endothelial cells,lymphocytes and neutrophils.Conclusion:It was concluded that cortical contusion trauma could induce a concomitant and persistent upregulation of NF-?B binding activity and MMP-9 expression in the small intestine which might play a central role in the~()damage of gut mucosal barrier.