Objective:To study the effects of WAK on immune function in mice.Methods: After different doses of WAK were given to mice ig, its effects on delayed type hypersensitivity (DTH), hemolysin production, NK and LAK cell killing activity were observed.Results: WAK could enhance DTH and hemolysin production in immunosuppressive mice and improve NK and LAK cell killing activity in mice.Conclusions: WAK could exhibit its antitumor effect by increasing immune function.

This study is to investigate the effect of hydroxyethylpuerarin on the expression of tumor necrosis factor-alpha (TNF-α) and activity of nuclear factor kappa B (NF-κB) after middle cerebral artery occlusion (MCAO) in rats. Rats were subjected to cerebral ischemia-reperfusion injury induced by MCAO. Hydroxyethylpuerarin (10, 20, 40 mg·kg-1, iv) was administered just 30 min before occlusion and immediately after reperfusion. After a 24 h reperfusion following 2 h of MCAO, the number of viable neurons in hippocampal CA1 region was counted by hematoxylin and eosin (HE) staining. TNF-α protein and its mRNA expression were examined with radioimmunoassay (RIA) and reverse transcriptase-polymerase chain reaction (RT-PCR) respectively. NF-κB activity was observed by electrophoretic mobility shift assay (EMSA), and inhibition of NF-κB α (IκBα) protein expression was evaluated by Western blotting analysis. Animals treated with hydroxyethylpuerarin had a significant increase in neuronal survival in comparison with vehicle-treated group. Hydroxyethylpuerarin significantly reduced the protein and mRNA expression of TNF-α following 2 h of ischemia with 24 h of reperfusion. NF-κB DNA binding activity and the degradation of IκBα in the cytoplasm also decreased by hydroxyethylpuerarin treatment. The protective effects of hydroxyethylpuerarin against ischemia-reperfusion injury may be mediated by decreasing the expression of TNF-α and the activity of NF-κB in rats.

Objective To investigate the distribution of ompA gnne in 15 Chinese reference standard strains belonging to 15 serogroups of Leptospira interrogate, and to express recombinant OmpA ( rOmpA ) and to identify immunogenicity and immunoprotection of rOmpA. Methods Genomic DNAs from different leptospiral strains were extracted by phenol-chloroform method. Entire ompA gene fragments from the strains were amplified by PCR and then sequenced after T-A cloning. A prokaryotic expression system of ompA gene from L. interrogans strain 56601 was constructed, and the expression and yield of rOmpA were determined by SOS-PAGE plus Bio-Rad Agarose Image Analyser. Rabbits were immunized with rOmpA for obtaining antiserum, and immunodiffusion test was used to measure the antiserum's titer. Western blot assay was performed to determine the immunoreaetivity of rOmpA with the antiserum against rOmpA and antiserum against whole cell of L. interrogans strain 56601, while mi-croscopic agglutination test (MAT) was applied to detect the cross agglutination to the 15 L. interrogans strains. A leptospire adhering cell model and a leptospire infecting guinea pigs model were used to determine the adhesion-bloc-king effect of rOmpA antiserum and immunoprotection of rOmpA. Results All the 15 L. interrogans strains, but not L. biflexa strain Patoe Ⅰ , had sequence conserved ompA genes. The yield of rOmpA was approximate 20% of the total bacterial proteins, rOmpA could induce rabbits to produce antibody and immunodiffusion titer of the anti-serum was 1:4. Both antisera against rOmpA and against whole cell of L. interrogans strain 56601 were able to pro-duce positive Western blot signs to rOmpA, and the former offered 1 : 20-1 : 320 MAT titers to the 15 L. interrogans strains. 1: 10-1:160 dilutions of rOmpA antiserum could efficiently block L. interrogans strain 56601 adhering to J774A. 1 cells, and 100 μg and 200 μg rOmpA displayed 50.0% and 75.0% immunoprotective rates in the infee-ted guinea pigs. Conclusion ompA gene only exists in genomes of different pathogenic L. interrogans serogroups. rOmpA has relatively stronger antigenicity, cross immunoreactivity and certain immunoprotection, implying that this recombinant protein may be used as a candidate antigen for developing universal genetic engineering vaccine of L. interrogans.

Introducing information-knowledge-wisdom transformation law and its four sub processes including information acquisition,recognition,decision and implementation,the paper summarizes the process of Evidence-based Medicine (EBM) information services,analyzes the scope of carrying out EBM information services by the hospital library under the guidance of new perspective,and discusses the specific forms of EBM information services by exampling the practice of EBM information services carried out by the library of the First Affiliated Hospital of Chongqing University of Medical Sciences.

Aim To observe the influence of carvedilol on the injury and expression of intercellular adhesion molecule-1 induced by hydrogen peroxide in ECV-304 cells and investigate the anti-atherosclerotic effect of carvedilol.Methods: The viability of ECV-304 cells was detected by MTT assay.Morphological changes of ECV-304 cells were observed under converse microscope.The level of lactate dehydrogenase released to the extracellular medium,the intracellular superoxide dismutase activity and the extracellular and intracellular Malondialdelyde level were determined using automatic biochemistry analyser.The expression of ICAM-1 in protein level and mRNA level was detected with flow cytometric technique and RT-PCR.Results Pretreated with carvidilol(1.0?10~(-5)～1.0?10~(-9)mol?L~(-1)) for 24 h,the cell survival rate was increased significantly in a concentration-dependent manner.Pre-incubation for 24 h with carvedilol results in a significant concentration-dependent decline of LDH release from hydrogen peroxide(1.0?10~(-6)mol?L~(-1))injured cells.While ECV-304 cells were pre-incubated with carvedilol,the level of MDA decreased and the activity of SOD increased significantly.Carvedilol produced a concentration-dependent inhibition of the expression of ICAM-1 protein and mRNA in hydrogen peroxide injured ECV-304 cells in a similar manner.Conclusion: These experiments demonstrated that carvedilol was able to protect ECV-304 cells from the oxidative stress injury and inhibit ICAM-1expression in ECV-304 cells induced by hydrogen peroxide.Therefore,we can consider that carvedilol maintains and improves the function of endothelium damaged by hydrogen peroxide from many aspects,which does indicate extensive antioxidant effects on the hydrogen peroxide-injured vascular endothelial cells and suggest promising effects in atherogenesis process.

The aim of this study is to investigate the effect and mechanism of angiotensin (Ang) II on E-selectin and vascular cell adhesion molecule-1 (VCAM-1) expression in rat brain microvascular endothelial cells (BMEC) and evaluate the effect of compound EXP-2528, a novel Ang Ⅱ type 1 (AT1) receptor antagonist. The experiment was performed in cultured BMEC of rat. The mRNA and protein expression of E-selectin and VCAM-1 in BMEC was analyzed by RT-PCR and Western blotting, respectively. The results showed that the mRNA and protein expression of E-selectin and VCAM-1 in BMEC were significantly upregulated by 4 h or 18 h exposure to 1×10-7 mol·L-1 Ang Ⅱ. These effects were abolished by pretreatment with the selective AT1 receptor antagonists losartan and compound EXP-2528, but not with the AT2 selective antagonist PD123319. Combining losartan with PD123319 also significantly inhibited Ang Ⅱ-induced E-selectin and VCAM-1 expression in BMEC, but there was no significant difference compared with losartan group. These findings indicated that Ang Ⅱ upregulated E-selectin and VCAM-1 in BMEC by activating AT1 receptor and then involved in the development of cerebrovascular disease.

Aim To investigate the antiarrhythmic mechanism of taurine-magnesium coordination com-pound on abnormal sodium current channel ( INa ) in-duced by hypoxia-reoxygenation in ventricular myocytes of rats. Methods Single ventricular myocytes were i-solated from each rat heart using enzymatic dissociation through Langendorff retrograde aortic perfusion. Whole-cell patch clamp was applied in voltage clamp mode to record INa both in normal ventricular myocytes and single ventricular myocytes of arrhythmia induced by hypoxia-reoxygenation. Results The peak density of INa was changed from ( 56. 89 ± 2. 07 ) pA/pF to (35. 05 ± 1. 52) pA/pF( n=6, P <0. 01 vs control) by hypoxia-reoxygenation with the INa I-V curve shifting upward. TMCC(200, 400 μmol·L-1)was able to re-store the reduction caused by H/R to (35. 78 ± 1. 95) pA/pF, (41. 52 ± 0. 86) pA/pF, (n=6,P <0. 01) and (48. 34 ± 0. 99) pA/pF(n=6,P<0. 01) respec-tively, but not at 100 μmol·L-1(n=6, P>0. 05), in a concentration-dependent manner, while amioda-rone restored it to (39. 44 ± 1. 24) pA/pF (n=6,P<0. 01 ) . Both high concentration of TMCC and amioda-rone could shift the I-V curve downward. In addition, TMCC and amiodarone could restore the INa inactivation curve and slow down its inactivation, whereas the acti-vation curves showed no significant differences among groups. Conclusion TMCC(200,400 μmol·L-1) could restore the H/R induced INa reduction and shift the I-V curve downward by inhibiting steady-state inac-tivation, which is suggested to be one of the mecha-nisms of the antiarrhythmic effects of TMCC in hypoxia-reoxygenation model.

Objective To investigate characteristics of free fatty acid (FFA) and high-sensitivity Creactive protein (hs-CRP) in patients with type 2 diabetes mellitus and metabolic syndrome (MS) compared to those with type 2 diabetes mellitus without MS.Methods Totally 120 patients with type 2 diabetes mellitus who received blood glucose control in Shaoxing People's Hospital from January to June 2013 were recruited and divided into MS group (n =56) and non-MS group (n =64).The serum FFA profile of the patients was measured by enzymatic assay, and the serum hs-CRP level measured by particle-enhanced immuno-precipitation assay.Results The level of FFA was higher in the MS group than that in the non-MS group [(0.60 ±0.25) mmoL/L vs.(0.45 ±0.21) mmol/L, P =0.033].The level of hs-CRP was higher in the MS group than that in the non-MS group [5.29 (4.69-5.82) mg/L vs.0.73 (0.42-1.26) mg/L, P =0.000].The level of hs-CRP was higher in the patients with central obesity than that in those without central obesity [4.34 (0.91-5.46) mg/L vs.1.80 (0.82-3.27) mg/L, P=0.014], also higher in hypertensive patients than in non-hypertensive patients [5.21 (3.18-5.96) mg/L vs.2.93 (0.89-4.98) mg/L, P =0.012].Conclusions Serum FFA and hs-CRP concentrations may be significantly higher in type 2 diabetes mellitus patients with MS.The increased levels of FFA and hs-CRP may play an important role in the pathogenesis of type 2 diabetes mellitus and MS.

Objective To investigate the relationship between serum phospholipid polyunsaturated fatty acids (PUFA) and interleukin-6 (IL-6) in patients with metabolic syndrome.Methods Serum phospholipid PUFA profiles of 61 patients with metabolic syndrome and 55 healthy controls was analyzed with high performance gas chromatography.Enzyme-linked immunosorbent assay was used to measure serum IL-6 levels.Results The IL-6 concentration was significantly higher in the MS group than in the control group [(16.0 ± 4.7) pg/ml vs.(9.2 ± 2.6) pg/ml,P =0.000].The total PUFA percentage was lower in the MS group than in the control group [(47.2±2.4)％ vs.(50.8 ±2.5)％,P=0.001].The serum IL-6 concentration was negatively correlated with n-3 PUFA,n-6 PUFA,and total PUFA (r =-0.51,P ＜0.01;r=-0.27,P＜0.01;r=-0.38,P＜0.01).Conclusions Serum PUFA in patients with metabolic syndrome is lower than in healthy people.Serum IL-6 concentration may be negatively correlated with total PUFA concentration.

The information-knowledge-intelligence transformation rules were introduced as the theory for the transformation of information service main body for evidence-based medicine according to the analysis of domestic and foreign institutional main body and personal main body for the information service of evidence-based medicine.It was proposed that medical library as the institutional main body should be transformed into information repository + thinking library and clinical medical librarians as the personal main body should be transformed into evidence witness + decision making adviser with associated literacy.