Tissue factor pathway inhibitor-2(TFPI-2) is a matrix-associated Kunitz-type serine proteinase inhibitor,and is considered to play an important role in some pathophysiological processes,including artherosclerosis,tumor metastasis and angiogenesis.Extracellular signals can regulate TFPI-2 gene expression through modulating promoter or signaling pathway or other factors.The mechanism,more over,has become one of the focus in recent years.

Adult ; Heat Stroke ; diagnosis ; Humans ; Male ; Middle Aged ; Occupational Diseases ; diagnosis

Adult ; Benzene ; poisoning ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; chemically induced ; diagnosis ; Male ; Occupational Diseases ; diagnosis ; Physical Examination

Adult ; Cadmium ; Female ; Glomerulonephritis, IGA ; etiology ; Humans ; Occupational Exposure

Adolescent ; Ammonia ; poisoning ; Female ; Humans

Adult ; Aged ; Benzamides ; pharmacology ; Drug Resistance, Neoplasm ; genetics ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; genetics ; Middle Aged ; Piperazines ; pharmacology ; Point Mutation ; Pyrimidines ; pharmacology

Objective To construct, express and identify the anti-idiotypic antibody single chain variable fragment (scFv) against Edwardsiella tarda. Methods By using RT-PCR method, the variable regions of the heavy and light chain of the anti-idiotypic monoclonal antibody (mAb) 1E11 against Edwardsiella tarda were cloned and joined with a (Gly_4ser)_3 linker, and the scFv in the orientation of V_L-linker-V_H was constructed. It was then cloned into vector plasmid pET-28a, expressed in Escherichia coli BL21(DE3), and confirmed by SDS-PAGE, Western blot and ELISA. Results The recombinant scFv could be expressed in E.coli BL21 (DE3) in a fusion protein pattern. The expression product was in the form of an inclusion body and the purified fusion protein was obtained after being purified and refolded. The SDS-PAGE and Western blot analysis showed that the molecular had the binding activity to the antigen. Conclusion The recombinant anti-idiotype scFv has been successfully constructed and expressed in E.coli BL21 (DE3), providing the basis and potential for preparation of genetically engineered vaccine against Edwardsiella tarda.

Accidents, Occupational ; Acute Disease ; Adult ; Aniline Compounds ; poisoning ; Female ; Humans

Eight 1,6-O,O-diacetylbritannilactone (OABL) derivatives (compounds 1-8) were synthesized by esterification or reduction of 1-O-diacetylbritannilactone (ABL) isolated from Inula japonica.All derivatives were evaluated for their anti-inflammation activities through the determination of inhibition of nitric oxide (NO) production in lipopolysaccharide (LPS)-induced macrophages.As results,compounds 5-8 (IC50 ＜ 2 μmol/L) exhibited more potent inhibition of NO production activities than the lead compound OABL.

Aim To investigate the changes in the expression of protein kinase C gamma (PKC?), phosphorylated cAMP response element binding protein(pCREB)and immediate-early gene(c-fos and c-jun) in the spinal cord in formalin-induced inflammatory pain and study the effect of agmatine on the changes of PKC? activation, phosphorylation of CREB and expression of c-fos and c-jun.Methods Rats were decapitated at 10, 20 min or 2 h after intraplantar injection of 50 ?l 5% formalin and L_4, 5 spinal cords were dissected. Immunohistochemistry and western blotting analyses were used to observe the expression of PKC?, pCREB, c-fos and c-jun in the spinal dorsal horn and the effect of agmatine on the changes of their expression. Results Unilateral peripheral inflammation induced PKC? activation and CREB phosphorylation bilaterally while c-fos and c-jun expression ipsilaterally in rat spinal cord. PKC activity increased in membrane fractions with unchanged levels in the cytosolic fractions. Pretreatment intraperitoneally with 160 mg?kg-1 agmatine 15 min before inflammation significantly inhibited the activation of PKC? in the membrane fraction, suppressed the phosphorylation of CREB and the expression of c-fos and c-jun. Conclusion The mechanism of the analgesic effect of agmatine may be associated with inhibiting PKC? activation in the plasma membrane, CREB phosphorylation, c-fos and c-jun up-regulation which play roles in the hyperalgesia with peripheral inflammation.