Objective To detect the levels of tumor necrosis factor (TNF)-a,interleukin (IL)-1β,IL-2,1L-6,IL-8,1L-10,IL-12 and interferon (IFN)-α in the serum and cerebrospinal fluid of the patients with epidemic encephalitis B,and to investigate the roles in pathogenesis of epidemic encephalitis B.Methods Approximately of 2 mL serum and 2 mL cerebrospinal fluid from 24 patients with epidemic encephalitis B during acute phase were collected,and 2 mL serum from 20 healthy controls were collected.The levels of eytokines in serum and cerebrospinal fluid were detected by enzyme linked immunosorbent assay (ELISA).Means of multi-sample were compared by analysis of variance and means of two-sample were compared by t test.Results The levels of TNF-α,IL-1β,IL-6,IL-8,IL-10 and IFN-α in eerebrospinal fluid were (24.5±6.6),(7.8±2.4),(16.0±5.7),(17.6±4.8),(130.2±33.6) and (45.2±10.8) ng/L,respectively,and in serum were (25.3±11.2),(7.1±3.2),(14.5±6.2),(16.0±6.5),(82.0±27.8) and (42.5±16.2) ng/L,respectively.The levels of TNF-α,IL-1β,IL-6,IL-8,IL-10 and IFN-α in serum and cerebrospinal fluid from patients with epidemic encephalitis B were all higher than those in serum of healthy controls [(12.7±7.9),(2.6±1.0),(6.2±2.2),(9.6±3.3),(71.4±12.8) and (30.0±14.0) ng/L;F value was 14.10,29.46,23.38,14.78,32.59,7.52;all P＜0.01];while the levels of IL-2 and IL-12 were not increased significantly.The levels of IL-1β,IL-6,IL-8,IL-10,IL-12 and IFN-α in cerebrospinal fluid were higher than those in serum,while the levels of TNF-± and IL-2 in cerebrospinal fluid were lower than those in serum.The levels of IL-6 and IL-8 in cerebrospinal fluid from patients with severe type of epidemic encephalitis B were (18.8±5.4) ng/L and (20.7±2.7) ng/L,and were higher than those with common type [(12.1±3.0) and (13.3±3.3) ng/L;t=3.50,t=5.96;P＜0.05],while the levels of IL-2 in serum and in cerebrospinal fluid from patients with severe type were lower than those with common type. Conclusions Oversecretions of TNF-α,IL-1β,IL-6,IL-8,IL-10 and IFN-a are involved in the inflammatory damage of epidemic encephalitis B,while under-secretions of IL 2 and ILl2 may be involved in cellular immune responses.

Objective To observe the effect of nerve growth factor(NGF) on CCL4‐induced hepatic fibrosis in mice .Methods The hepatic fibrosis model was induced by subcutaneous injection of CCL 4 in mice .Thirty female Kunming mice were equally and randomly divided into three groups :fibrosis model group (A) ,NGF intervention group (B) and normal saline control group (C) .At 8 weeks following the initiation of experiment ,the samples were collected to measure ALT ,AST ,TBIL ,ALB by the fully automativ biochemical analyzer ,an the liver fibrosis indices (HA ,LN ,PC Ⅲ ) by radioimmunoassay .The Ishaki scoring system was adopted to assess the severity of hepatic inflammation and fibrosis degree .Results Serum levels of ALT ,AST ,HA and LN in the group A and B were significantly higher than those in the group C (F= 111 .45 ,658 .80 ,157 .43 ,167 .99 ;P< 0 .05) ,the levels of ALT 、AST and LN in the group B were significantly lower than those in the group A (P< 0 .05) .The HE staining ,reticular fiber staining and Masson staining showed that the liver fibrosis degree and the liver tissue inflammation in the group A were most obvious ,the liver tissue inflamation in the group B were significantly alleviated as compared with the group A .No fibrous septum was formed and the fiber tissues were fine and short .No obvious inflammatory cells infiltration and fibers formation were found in the liver tissue of the group C .The scores of liver inflamation grade and fibrosis staging in the group C were higher than those in the group B and C ,moreover the scores of liver inflammation grade and fibsosis had statstical differences among 3 groups (P < 0 .05) .Conclusion NGF can block hepatic fibrosis induced by CCL4 and relieve the liver inflammation .

Objective To study biological characteristics of R5 tropic human immunodeficiency virus (HIV)-1 strains in different disease stage. Methods Primary clinical viruses were isolated from fresh peripheral blood mononuclear cells (PBMC) using co-culture methods; meanwhile, viral co receptor usage and infectivity were tested using flow cytometry on GHOST (3) cell lines,which expressed CD4 receptor and CC ehemokine receptor 5 (CCR5) or CXCR4 eoreceptor; to identified CCR5 tropic viruses(R5 tropic strains). Viral replication kinetics was detected in PBMCs. Plasma viral load was measured using an HIV-1 nucleotide fluorescence quantification assay kit. Results There were 22 individuals with HIV-1 subtype B' infection, in which 11 were CD4>0. 2 × 109/L and 11 were CD4≤0. 2 × 109/L. All isolated viruses used CCR5 coreceptor and therefore were HIV-1 R5 tropic strains. The infectivity of R5 tropic strains isolated from patients with CD4≤0.2 × 109/L was (7.392 7 ± 4. 584 2) % ; while the infectivity of R5 tropic strain from patients with CD4>0. 2 × 109/L was (2. 613 6 ± 1. 610 5)%. There were significant statistical difference(t= 3. 262, P<0.05). The possibility of viral replication became strong after the day 7 post-infection. There was a significant difference of viral replication between two groups in the day 7,10, 15 post-infection(t value was 3. 771, 2. 509 and 2. 260 respectively, P<0. 05). The possibility of viral replication was higher in CD4≤0.2 ×109/L group than that of CD4>0.2 × 109/L group. The logarithm of viral load was (5. 606 8 ± 0. 815 1 ) copies/mL in CD4≤0.2 × 109/L group and (4. 729 8 ± 0. 431 6) copies/mL in CD4> 0.2 × 109/L group. There was a significant difference between two groups(t = 3. 771 ; P<0.05). Conclusion Viral infection and replication are enhanced during progression of disease, even if viral coreceptor usage do not switch from CCR5 to CXCR4.