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 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 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.