Objective To explore the cellular localization of chemokine (C-X-C motif) ligand 1 (CXCL1) in brain tissue and its expres-sion in brain tissue and blood in patients with severe traumatic brain injury (TBI), as well as its correlation with the injury severity. Methods From September, 2013 to October, 2015, 78 cases of TBI with craniotomy admitted to our hospital were involved as TBI group. A total of 78 peripheral blood samples and 19 brain tissue samples were studied. According to the scores of Glasgow Coma Scale (GCS) at admission, the TBI group was classified as severe TBI group (6~8, n=35) and particularly severe TBI group (3~5, n=43). Ten cases of control brain tissue were taken from patients with cerebral aneurysms or benign tumor and also undergoing craniotomy during the same time. Peripheral blood from ten healthy people were involved as the healthy control group. Immunofluorescent double staining was used to detect the cellular local-ization of CXCL1 in brain tissues, and ELISA was used to detect the expression of CXCL1 in brain tissue and blood. The relationship be-tween the level of CXCL1 in peripheral blood at different time and the score of Glasgow Outcome Scale (GOS) was analyzed with Spear-man correlation analysis. Results In normal brain tissue, CXCL1 mainly localized in astrocytes. For severe TBI, CXCL1 mainly expressed in neurons and astrocytes. The level of CXCL1 was higher in brain tissue in the particularly severe TBI group than in the severe TBI group (t=-12.58, P<0.05). In the severe TBI group, the level of CXCL1 in blood reached a peak before surgery, then gradually decreased, and was still higher than that in the healthy control group 14 days after surgery (P<0.05), however, no significant difference was found 30 days after surgery compared to the healthy control group (P>0.05). In the particularly severe TBI group, the level of CXCL1 in blood reached a peak before and one day after surgery, then gradually decreased, and was still higher than that in the healthy control group 30 days after surgery (P<0.05). The level of CXCL1 in blood was higher in the particularly severe TBI group than in the severe TBI group at all time points (P<0.05), and the level before surgery was negatively correlated with the score of GOS in the particularly severe TBI group (r=-0.351, P<0.05). Conclusion The CXCL1 protein of injury brain tissue was mainly colocalized in neurons and astrocytes in severe TBI patients, and the ex-pression was associated with injury severity and outcome.

Objective To evaluate liver injury in patients with hepatitis C virus (HCV)/human immunodeficiency virus (HIV) coinfection in Dehong Prefecture,Yunnan Province.Methods A total of 4 784 HIV-infected patients were enrolled in this study.Baseline aspartate aminotransferase (AST),alanine aminotransferase (ALT) and AST-to-platelet ratio index (APRI) before HIV treatment were collected to analyze the relationship between HCV infection and liver injury.Data were analyzed by x2 test and nonparametric rank sum test when appropriate.Risk factors for liver injury were analyzed by multivariate Logistic regression.Results Totally 4 784 patients were included,of which 30.2％ (1 447/ 4 784) were anti-HCV positive,41.7％ (1 996/4 784) had liver dysfunction and 13.3％ (636/4 784) had liver cirrhosis.Prevalence of liver dysfunction (61.1％,821/1 343) and cirrhosis (24.1 ％,323/1 343) were significantly higher among anti-HCV-positive patients than anti-HCV-negative patients (31.5％,974/3 092,X2=341.223,P＜0.01;7.5％,231/3 092,X2=235.457,P＜0.01,respectively).Multivariate Logistic regression showed that anti-HCV-positive patients suffered significantly higher risk of liver dysfunction (OR=1.99,95％ CI:1.66-2.37) and liver cirrhosis (OR=2.41,95％CI:1.90-3.04).Conclusion Patients with HCV/HIV in Dehong Prefecture coinfection had a higher risk for liver injury.

Objective To study the effectsof rehabilitative training on neural function and the expression of glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule-1 (Iba-1) in rats after traumatic brain injury.Methods A left hemisphere traumatic brain injury model was established in ninety Sprague-Dawley rats.They were then randomly divided into a rehabilitation training group,an immobilization group and a free-running group,with 30 rats in each group.Another thirty rats received sham injury as the shamoperated group.Beginning 4 days post-operation the rats of the rehabilitation training group were given balancing,rotating and walking exercises three times daily,15 min/time,6 d/week.The immobilization group was fixed in mesh cages.The rats of the free-running and sham-operated groups were reared in normal cages without any special training exercise.The rats of all 4 groups were given neural and motor function tests to assess the functional outcome.Immunofluorescence staining was used to evaluate the expressions of GFAP (the marker of astrocytes) and Iba-1 (the marker of microglia) in the cortex close to the iujured region at 3 days,1 week,2 weeks,3 weeks and 4 weeks after injury.Results The average neural and motor function test scores in the rehabilitation training group were significantly better than those in the immobilization and free-running groups at the 2nd week and thereafter.The average scores in the free-running group were significantly better than those in the immobilization group at the 4th week after injury.The immunofluorescence staining showed that the expression of GFAP was lowest in the rehabilitation group at the 2nd week and thereafter.Iba-1 expression was significantly lower only at the 3rd week and beyond.Conclusion Rehabilitative training can improve nerve function recovery in rats after traumatic brain injury,and the functional enhancement may be partially attributed to the downregulation of activated astrocytes and microglia.