Objective:To investigate the effects of Acanthopanax Senticosus polysaccharides (ASPS) on TLR4 signaling pathway in Lewis tumor-bearing mice,and to explore the immunomodulatory mechanism of ASPS.Methods:Lewis lung carcinoma cells and C57BL/6 mice were used to establish the animal model for solid tumor.The tumor-bearing mice were divided into five groups:normal saline (NS) group,Adriamycin (ADM) group,ASPS low-dose group,ASPS middle-dose group and ASPS high-dose group.Mter 25 d treatment,the weight of tumor,tumor inhibition rate and immune organ index were measured.ELISA were applied to detected the cytokines in peripheral blood of tumor-bearing mice.Quantitative real-time PCR (Q-PCR) and Western blot were selectively used to detect the gene and protein expression of TLR4 signaling pathway in splenocytes.Results:The tumor inhibition rate,immune organ index and the secretion of TNF-α,IL-1β and IL-6 were increased by ASPS,compared with NS group (P＜0.05).The gene and protein expression of TLR4,MyD88,TRAF6,NF-κB p65 and AP-1 were also induced by ASPS (P＜0.05).Meanwhile,ASPS had no obvious effects on the secretion of IL-12p70 and the expression of TRAM (P＞0.05).Conclusion:TLR4 signaling pathway may be involved in the immunomodulatory effects of ASPS on Lewis tumor-bearing mice.

Background Excessive production,deposition and contraction of extracellular matrix (ECM) of human lens endothelial cells (LECs) is one of main causes to posterior capsular opacification (PCO).Researches indicated that Wnt3a protein was involved in production of ECM and fibrosis in epithelial cells,but its effect on LECs is still unclear.Objective This study aimed to elucidate the roles of Wnt3a in production of ECM and gel contraction of LECs.Methods Lipofectamine-mediated transient transfection technique was used to introduce cDNA of Wnt3a gene and pcDNA3-HA vector into the LEC cell line SRA01/04 to act as Wnt3a transfection group and control group respectively.After 48 h of transfection,Western blot was used to detect the expression of Wnt3a,main components of ECM Col-Ⅰ,Col-Ⅳ and integrin β1.Immunofluorescence was used to detect the expression and distrubition of α-SMA and F-actin;collagen contraction was observed by mingling SRA01/04 cells with Col-Ⅰ.Results After 48 hours of transfection using lipofectamine 2000,the expressions of wnt3a protein in SRA01/04 cells was 0.703 ±0.105 in the wnt3a transfected group,and that in the control group was 0.290 ± 0.066,showing a significant difference between the two groups (t =5.782,P＜0.01).Western blot assay showed that the expression levels of Col-Ⅰ and Integrin β1 was 0.697±0.021 and 0.875±0.055 in the Wnt3a transfected group,and which was significantly higher than 0.370±0.020 and 0.580±0.030 in the control group (t =19.600,8.156,both P＜0.01).The expression level of Col Ⅳ in the Wnt3a transfected group was higher than that of the control group (0.430±0.020 vs 0.383 ±0.031),but the difference was not significant (t =2.514,P＞0.05).Immunofluorescence assay revealed that F-actin and α-SMA were weakly expressed in the cell membrane primarily in the control group,while they were strongly expressed in the cell membrane,cytoplasma in the Wnt3a transfected group.Tewnty-four hours after addtion of Col-Ⅰ,the gel contraction area ratio appeared to be more obvious in comparison with the 8 hours (64.1％ ±2.3％ vs 98.9％ ± 1.0％),and gel contraction area ratio was lower in the Wnt3a transfected group than that in the control group (64.1％ ± 2.3％ vs 93.9％ ± 3.1％).Conclusions The overexpression of Wnt3a activates the production of ECM,and the remodeling of celluar skeleton and cellular contraction.

Objective To analyze the association of the morbidity,the management of blood glucose,and the prognosis of patients with hyperglycemia in the medical intensive care units(ICU).Methods Medical records of ICU patients of Renji Hospital from 2002 to 2009 were reviewed using Medical Record Inquiry System,and the data were retrospectively analyzed.Results(1)2631 subjects were included in the present study,blood glucose was determined at least once during hospitalization in 2168 of them.The incidence of hyperglycemia was 26.3%,in which 12.9% presented a known history of diabetes and 13.4% without.In the patients with diabetes history,93.2% of them received anti-diabetic treatment during hospitalization.mainly with oral anti-hyperglyeemic agents (53.0%)or subcutaneous insulin injection(24.9%).However,in the patients without diabetes history,84.4% were not treated against hyperglycemia.The mortality was increased in the latter group(30.4% vs13.9%,P<0.01).(2)In the patients with diabetes history,the mortality in patients whose blood glucose>10 mmol/L was higher than those with blood glucose≤7.0 mmol/L(20.5% vs 9.9%,P<0.05):while in the patients without diabetes history,the mortality began to rise as blood glucose>7.0 mmol/L(P<0.01).(3)Multiple stepwise regression analysis revealed that the average blood glucose level was an independent risk factor for death(OR=1.26).Conclusions The ICU patients showed a high prevalence of hyperglycemia,the management of hyperglycemia should be emphasized.Hyperglycemia in critically ill patients might be an independent risk factor of increased mortality.

Objective: To explore the effect of Sijunzi decoction(SJZD) at different time points on gastrin(GAS) gene expression level in spleen-qi deficiency rats.Methods: Spleen-qi deficiency syndrome was induced in rats by compound methods which including rhubarb,exhaust and hunger.Spleen-qi deficiency rats were randomly divided into the model control group and SJZD group.Reverse transcriptase polymerase chain reaction was applied to observe the GAS mRNA of gastric antrum in rats treated by SJZD.Results: Serum gastrin and GAS mRNA were both decreasing significantly in the model control group.After being treated by SJZD,serum gastrin and GAS mRNA of spleen-qi deficiency rats began to recover.Especially,after 21 days' treatment,GAS mRNA and serum gastrin were both increasing significantly when compared with those in the model control group.Conclusion: The regulation on GAS mRNA is one of the mechanisms of SJZD for spleen-qi deficiency.

Objective To investigate the change of HO-1 expression in adipose tissue of obese young SD rats as well as its relationship with macrophage infiltration and polarization. Methods Three-week old SD rats (n=24) were randomly divided into 2 groups, routine diet group (NC) and high fat diet group (FC). After feeding 4 weeks, triglyceride (TG), high den?sity lipoprotein (HDL-C), fasting glucose and insulin were compared between these two groups and the insulin resistance in?dex was calculated. The gene expressions of HO-1, IL-6, IL-10 and MCP-1 were assessed by quantitative PCR. Infiltration and polarization of macrophages and M2 macrophages in the visceral adipose tissue were examined by immunohistochemis?try. Results The levels of FINS, FBG and HOMA-IR in rats of FC group were higher than those of rats in NC group after 4 weeks feeding (P<0.05). The level of HO-1, IL-6, MCP-1 in rats from FC group were significantly higher while level of IL-10 were lower compared with those in rats from NC group after 4 weeks of feeding (P<0.05). In samples from FC groups, more macrophages were detected in adipose tissue by DAB staining than those from NC group. There was no significant dif?ference (P>0.05) in MOD value of F4/80 and CD206 between these two groups (P>0.05). Conclusion The infiltration of macrophage in visceral adipose tissue of obese young SD rats significantly increased while HO-1 expression was reactively increased. This insinuated that HO-1 might play an important role in anti-inflammatory mechanism through regulating polar?ization of macrophages.

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Objective:To investigate the role of suppressor of cytokine signaling 1 (SOCS1) in berberine (BBR) mediated-inhibition of microglial activation.Methods:The combination of lipopolysaccharide (LPS) and interferon-γ (IFN-γ) activated N9 microglia to mimic neuroinflammation. The cells were divided into control group, simulated neuroinflammation group (10 ng/ml LPS+ 10 U/ml IFN-γ), BBR treatment group (1 μmol/L BBR+ LPS/IFN-γ), SOCS1-siRNA treatment group (SOCS1-siRNA+ BBR+ LPS/IFN-γ), and scrambled siRNA treatment group (SC-siRNA+ BBR+ LPS/IFN-γ). After incubation for 24 h, the expression levels of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) in cell culture medium were detected by enzyme-linked immunosorbent assay. Western blotting was used to detect the expression levels of inducible nitric oxide synthase (iNOS) and nuclear factor κB (NF-κB). Immunocytochemical method was used to observe cell morphology and iNOS expression.Results:Compared with the control group, LPS/IFN-γ significantly increased the levels of TNF-α and IL-6 in the medium, up-regulated the expression levels of iNOS and NF-κB (all P<0.05), and increased the volume of microglia. 1 μmol/L-BBR significantly inhibited the release of TNF-α and IL-6 from microglia, decreased the expression levels of iNOS and NF-κB (all P<0.05), and improved cell morphology. SOCS1-siRNA significantly reversed the inhibitory effect of BBR on microglia activation (all P<0.05). Conclusions:BBR may inhibit LPS and IFN-γ-induced microglial activation through SOCS1 molecule.

ObjectiveThe study is to investigate the predictive values of dosimetric parameters and patient related factors in severe acute radiation pneumonitis (SARP) after concurrent chemoradiotherapy in non-small cell lung cancer (NSCLC).Methods In all,147 NSCLC patients treated with concurrent chemotherapy and 3DCRT between 2006 and 2010 was collected.Independent sample t test was used to compare parameter values between patients with SARP and those without SARP.Logistic regression was used to identify significant determined factor.Predictive value of each parameter was tested by ROC analysis.Pearson correlation was used to analyze correlations between parameters.Represent factors were identified by factor analysis.ResultsThe incidence of SARP was 9.5％ ( 14/147 ).The means lung dose (MLD),V20,V30,V40,and V50 ( x2 =4.87 -6.84,P =0.009 -0.025,respectively ) were determining factors for SARP.Our datasets shows that for SARP ＜5％,MLD,V20,V30,V40 and V50 should be ≤16.77 Gy,V20≤34.15％,.V30 ≤23.62％,.V40 ≤ 18.57％,V50 ≤ 13.02％.ROC analysis show that areas under MLD,V20,V30,V40 and V50 curves was corresponding to 0.678,0.661,0.667,0.677,and 0.651,respectively.In addition,the sensitivity and specificity of each parameter at cutoff values are:78.0％ and 48.1％ for MLD;42.9％ and 82.0％ for V2o ;78.6％ and 52.9％ for V30 ;71.4％ and 61.7％ for V40,and 57.1％ and 67.7％ for V50.Factor analysis suggest that we can choose 1 or 2 parameters from MLD,V20,or V30,and another from V40 or V50 for predicting.The incidence of SARP was greater in patients with tumorsin right lower lung than other locations ( 22.2％ vs 6.7％,x2 =6.19,P =0.0 2 3 ).Conclusions The MLD,V20,V30,V40 and V50 are determining factors for SARP.As predictive value of each parameter alone is relatively week,using two or more parameters to predict SARP is recommended.

Objective: To explore the molecular mechanism of Taoren-Honghua herb pair (THP) on syndrome of bloodstasis based on the network pharmacology. Methods: We collected THP's compounds from traditional Chinese Medicinedatabases and input them into Pharm Mapper to get their potential targets, and collected the known targets of compoundsby Scifinder. Then we did KEGG-pathway analysis by DAVID database. Finally draw and analyze the network byCytoscape by information above. Results: Seventeen compounds of THP acquired 74 known targets, which was associatedwith four modules: improving the hemodynamics, anticoagulation, anti-inflammation, regulating apoptosis andproliferation. We also got 317 potential targets through PharmMapper and got 128 signaling pathway through pathwayenrichment including 39 disease-related pathways, 25 endocrine-related pathways, 11 immune-related pathways and soon. Conclusion: The four modules of the known target are exactly related to the four characteristics of the syndrome ofblood stasis. The potential targets and the 128 signal pathways involve a variety of pathophysiological processes of thesyndrome of blood stasis. These reflect the molecular mechanism of THP intervention in the syndrome of blood stasis

Objective To describe the clinical features,ancillary tests,treatments and outcomes of adult male patients with anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis.Methods Observational study of clinical data,ancillary tests,treatments and outcomes of 5 adult male patients,admitted to our hospital from August 2014 to May 2016 and diagnosed as having anti-NMDAR encephalitis,was carried out.And the pathologic mechanism was discussed combining with literature review.Results All of the 5 adult male patients were not associated with treatoma,4 patients had significant relevant past medical histories,including purulent meningitis,drug abuse,colon descendens adenocarcinoma after radical resection and idiopathic inflammatory demyelinating disease (IIDD).For ancillary tests,positive virus antibodies were detected in two patients,and one of them presented positive EBV-DNA in CSF sample;one patient presented elevated thyroid autoantibodies in sera sample;four patients presented atypical abnormal brain contrast enhancement MRI,and three of them exhibited punctiform and/or patchy enhancement in brain parenchyma;one of them showed gliacyte proliferation after necrosis and another one presented demyelination.All patients had favorable outcomes after timely immune therapies.Conclusion Adult male patients who are rarely associated with teratomas may trigger by virus infection,other autoimmune or demyelinating diseases;the earlier application of immune therapies,the better the prognosis.