An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
Background: Cancer gene therapy using a nonviral vector is expected to be repeatable, safe, and inexpensive, and to have longterm effectiveness.Gene therapy using the E3 and C1 (E3C1) domain of developmental endothelial locus-1 (Del1) has been shown to improve prognosis in a mouse transplanted tumor model.Objective: In this study, we examined how this treatment affects angiogenesis in mouse transplanted tumors.Materials and methods: Mouse transplanted tumors (SCCKN human squamous carcinoma cell line) were injected locally with a nonviral plasmid vector encoding E3C1 weekly.Histochemical analysis of the transplanted tumors was then performed to assess the effects of E3C1 on prognosis.Results: All mice in the control group had died or reached an endpoint within 39 days.In contrast, one of ten mice in the E3C1 group had died by day 39, and eight of ten had died or reached an endpoint by day 120 (p < 0.01).Enhanced apoptosis in tumor stroma was seen on histochemical analyses, as was inhibited tumor angiogenesis in E3C1-treated mice.In addition, western blot analysis showed decreases in active Notch and HEY1 proteins.Conclusion: These findings indicate that cancer gene therapy using a nonviral vector encoding E3C1 significantly improved life-span by inhibiting tumor angiogenesis.(
We consider $2+1$ flavor Wilson chiral perturbation theory including the lattice spacing contributions of $\mathrm{O}({a}^{2})$. We adopt a power counting appropriate for the unquenched lattice simulations carried out by the CP-PACS/JLQCD Collaboration and compute the pseudoscalar meson masses to one loop. These expression are required to perform the chiral extrapolation of the CP-PACS/JLQCD lattice data.
We discuss the perturbative O(a{sub s}a) matching in the static heavy and domain-wall light quark system. The gluon action is the Iwasaki action and the link smearing is performed in the static heavy action. The chiral symmetry of the light quark realized by using the domain-wall fermion formulation does not prohibit the mixing of the operators at O(a). The application of O(a) improvement to the actual data shows that the B meson decay constant f{sub B}, the matrix elements M{sub B} and the B parameter B{sub B} have non-negligible effects, while the effect on the SU(3) breaking ratio {zeta} is small.
CP-PACS and JLQCD Collaborations are carrying out a joint project of the 2+1 flavor full QCD with the RG-improved gauge action and the non-perturbatively ${\cal O}(a)$-improved Wilson quark action. This simulation removes quenching effects of all three light quarks, which is the last major uncertainty in lattice QCD. In this report we present our results for the light meson spectrum and quark masses on a $20^3\times 40$ lattice at the lattice spacing $a\simeq 0.10$ fm.
Abstract Using symmetry properties, we determine the mixing pattern of a class of nonlocal quark bilinear operators containing a straight Wilson line along a spatial direction. We confirm the previous study that mixing among the lowest dimensional operators, which have a mass dimension equal to three, can occur if chiral symmetry is broken in the lattice action. For higher dimensional operators, we find that the dimension-three operators will always mix with dimension-four operators, even if chiral symmetry is preserved. Also, the number of dimension-four operators involved in the mixing is large, and hence it is impractical to remove the mixing by the improvement procedure. Our result is important for determining the Bjorken- x dependence of the parton distribution functions using the quasi-distribution method on a Euclidean lattice. The requirement of using large hadron momentum in this approach makes the control of errors from dimension-four operators even more important.
Abstract Coagulation factor IX is thought to circulate in the blood as an inactive zymogen before being activated in the coagulation process. The effect of coagulation factor IX on cells is poorly understood. This study aimed to evaluate the effects of intact coagulation factor IX and its cleavage fragments on cell behavior. A431 cells (derived from human squamous cell carcinoma), Pro5 cells (derived from mouse embryonic endothelial cells), Cos7 cells, and human umbilical vein endothelial cells were utilized in this study. The effects of coagulation factor IX and its cleavage fragments on cell behavior were investigated in several types of experiments, including wound‐healing assays and modified Boyden chamber assays. The effect of coagulation factor IX depended on its processing; full‐length coagulation factor IX suppressed cell migration, increased adhesion to matrix, and enhanced intercellular adhesion. In contrast, activated coagulation factor IX enhanced cell migration, suppressed adhesion to matrix, and inhibited intercellular adhesion. An activation peptide that is removed during the coagulation process was found to be responsible for the activity of full‐length coagulation factor IX, and the activity of activated coagulation factor IX was localized to an EGF domain of the coagulation factor IX light chain. Full‐length coagulation factor IX has a sedative effect on cells, which is counteracted by activated coagulation factor IX in vitro. Thus, coagulation factor IX may play roles before, during, and after the coagulation process.