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H. S. Jung,R. Sakai 장전수학회 2015 Advanced Studies in Contemporary Mathematics Vol.25 No.3
Let R = (-, ∞), and let Q ∈ C1(R) : R → R+ = [0, ∞) be an even function, which is an exponent. We consider the weight wρ(x) = |x|ρe-Q(x), ρ > 0, x ∈ R, and then we can construct the orthonormal polynomials pn(w2ρ; x) of degree n for w2ρ(x). In this paper we obtain Lp-convergence theorems of even order Hermite-Fejér interpolation polynomials at the zeros {xk,n,ρ}n k=1 of pn(w2 ρ; x). Let R = (-, ∞), and let Q ∈ C1(R) : R → R+ = [0, ∞) be an even function, which is an exponent. We consider the weight wρ(x) = |x|ρe-Q(x), ρ > 0, x ∈ R, and then we can construct the orthonormal polynomials pn(w2ρ; x) of degree n for w2ρ(x). In this paper we obtain Lp-convergence theorems of even order Hermite-Fejer interpolation polynomials at the zeros {xk,n,ρ}n k=1 of pn(w2 ρ; x).
Goda, A.E.,Erikson, R.L.,Sakai, T.,Ahn, J.S.,Kim, B.Y. Elsevier BV 2015 MOLECULAR ONCOLOGY Vol.9 No.1
Novel combinations aiming at maximizing the efficacy of bortezomib are highly valued in the clinic. Therefore the current study investigated the outcomes of combining bortezomib with dipyridamole, a well-known antiplatelet. The co-treatment exerted a synergistic lethality in a panel of human leukemia/lymphoma cell lines of different origin. Mechanistically, dipyridamole did not modulate the proteasome inhibitory activity of bortezomib. However, dipyridamole triggered an endoplasmic reticulum (ER) stress, and co-treatment with bortezomib resulted in higher levels of ER stress than either monotherapies. Relieving ER stress with the protein translation inhibitor, cycloheximide suppressed cell death. Moreover, the enhanced ER stress by the co-treatment was associated with an aggravation of reactive oxygen species (ROS) generation and glutathione (GSH) depletion. Replenishing GSH pools significantly scavenged ROS and rescued the cells. Importantly, the cytotoxicity of the co-treatment was executed mainly via the mitochondrial apoptotic pathway with an efficient suppression of the key anti-apoptotic regulators, Mcl-1, Bcl-xl, Bcl-2 and XIAP, driving the independence of the co-treatment-induced apoptosis of a single apoptotic trigger. Furthermore, the intrinsic potential of bortezomib to inhibit important pro-survival pathways was enhanced by dipyridamole in a GSH/ROS-dependent manner. Interestingly, dipyridamole abrogated JAK2 phosphorylation indirectly and selectively in cancer cells, and the co-treatment-induced cytotoxicity was preserved in a model of stromal-mediated chemoresistance. In nude mice, the antitumor activity of the co-treatment surpassed that of bortezomib monotherapy despite that synergy was lacking. In summary, findings of the present study provided a preclinical rationale which warrants further clinical evaluation of bortezomib/dipyridamole novel combination in hematologic malignancies.
Lee, Y.J.,McPherron, A.,Choe, S.,Sakai, Y.,Chandraratna, R.A.,Lee, S.J.,Oh, S.P. Academic Press 2010 Developmental Biology Vol.347 No.1
Mice deficient in growth differentiation factor 11 (GDF11) signaling display anterior transformation of axial vertebrae and truncation of caudal vertebrae. However, the in vivo molecular mechanisms by which GDF11 signaling regulates the development of the vertebral column have yet to be determined. We found that Gdf11 and Acvr2b mutants are sensitive to exogenous RA treatment on vertebral specification and caudal vertebral development. We show that diminished expression of Cyp26a1, a retinoic acid inactivating enzyme, and concomitant elevation of retinoic acid activity in the caudal region of Gdf11<SUP>-/-</SUP> embryos may account for this phenomenon. Reduced expression or function of Cyp26a1 enhanced anterior transformation of axial vertebrae in wild-type and Acvr2b mutants. Furthermore, a pan retinoic acid receptor antagonist (AGN193109) could lessen the anterior transformation phenotype and rescue the tail truncation phenotype of Gdf11<SUP>-/-</SUP> mice. Taken together, these results suggest that GDF11 signaling regulates development of caudal vertebrae and is involved in specification of axial vertebrae in part by maintaining Cyp26a1 expression, which represses retinoic acid activity in the caudal region of embryos during the somitogenesis stage.
Nagaoka, K.,Yamaguchi, H.,Aida, H.,Yoshioka, K.,Takahashi, M.,Christenson, R.K.,Imakawa, K.,Sakai, S. Asian Australasian Association of Animal Productio 2000 Animal Bioscience Vol.13 No.6
As high as 50% of pregnancies are known to fail and the majority of such losses occur during the peri-implantation period. For the establishment of pregnancy in mammalian species, therefore, implantation of the conceptus to the maternal endometrium must be completed successfully. Physiological events associated with implantation differ among mammals. In ruminant ungulates, an elongation of the trophohlast in early conceptus development is required before the attachment of the conceptus to the uterine endometrium. Moreover, implantation sites are restricted to each uterine caruncula where tissue remodeling, feto-maternal cell fusion and placentation take place in a coordinated manner. These unique events occur under strict conditions and are regulated by numerous factors from the uterine endometrium and trophoblast in a spatial manner. Interferon-tau (IFN-${\tau}$), a conceptus-derived anti-Iuteolytic factor, which rescues corpus luteum from its regression in ruminants, is particularly apt to play an important role as a local regulator in coordination with other factors, such as TGF-${\beta}$, Cox-2 and MMPs at the attachment and placentation sites.