[Synergistic effect of deficiency in thrombosis-related genes].

Objective: To investigate the interaction of deficiency in thrombosis-related gene in a mouse model.

Methods: To generate mice carrying mutations in alpha-galactosidase A (Gla) and factor V Leiden (Fvl) and analyze the phenotypes, namely, tissue fibrin deposition and thrombus formation in organs.

Results: Fibrin deposition in organs of mice carrying both mutations in Gla and Fvl was significantly increased compared with that in mice with single mutaton: [Gla(-/0) Fv(Q/Q)+Gla(-/-)Fv(Q/Q)] vs.

[Leptin promotes neointimal formation by stimulating vascular smooth muscle cell proliferation through leptin receptor].

Objective: To evaluate the role of leptin in neointimal formation and related mechanisms.

Methods: Femoral arterial injury was induced in wild-type (Wt, n = 10), leptin-deficient (Lep(-)/-, n = 12), and leptin receptor-deficient (LepR(-)/-, n = 10) mice. Leptin treatment studies (tail vein injection of adenovirus expressing murine leptin on the RSV promoter, ad-leptin) were performed on Lep(-)/- (n = 5) and LepR(-)/- (n = 4) mice.

[Factor V Leiden mutation leads to enhanced atherosclerosis in apolipoprotein E deficient mice].

Objective: Factor V Leiden (FvL) causing activated protein C resistance is a genetic risk factor for venous thrombosis in humans, and it's effect on atherosclerosis is controversial. We evaluated the effect of FvL mutation on atherosclerosis in apolipoprotein E deficient mice fed with normal diet.

Methods: Degree of atherosclerosis and tissue fibrin deposition were determined in Fv+/+ApoE-/-, FvQ/+ApoE-/- and FvQ/QApoE-/- mice.

[Effect of alpha-galactosidase A deficiency on FV leiden fibrin deposition and thrombosis in mice].

Objective: To evaluate the effect of alpha-galactosidase A (Gla) deficiency on FV Leiden (FVL) associated thrombosis in vivo.

Methods: To generate the mice carrying mutations in Gla and FVL and analyze the tissue fibrin deposition in organs and thrombosis.

Results: In the presence of FVL, Gla deficiency greatly increased tissue fibrin deposition compared with that in wild-type [Gla(-/0) FV(Q/Q) vs.

High efficient mammalian expression and secretion of a functional humanized single-chain Fv/human interleukin-2 molecules.

Aim: To construct and produce a recombinant bispecific humanized single-chain Fv (sFv) /Interleukin-2 (IL-2) fusion protein by using mammalian cells.

Methods: The sFv/IL-2 protein was genetically engineered, and transfected to mammalian cells to determine whether the mammalian protein folding machinery can produce and secrete active sFv/IL-2 with high efficiency.

Results: The fusion protein was constructed and high efficiently expressed with yields up to 102 +/- 4.