• Title/Summary/Keyword: $A_A_L$1

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UNITARY INTERPOLATION FOR VECTORS IN TRIDIAGONAL ALGEBRAS

  • Jo, Young-Soo
    • Journal of applied mathematics & informatics
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    • v.11 no.1_2
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    • pp.431-436
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    • 2003
  • Given vectors x and y in a Hilbert space, an interpolating operator is a bounded operator T such that Tx = y. An interpolating operator for n vectors satisfies the equation $Tx_i\;:\;y_i,\;for\;i\;=\;1,\;2,\;{\cdots},\;n$. In this article, we obtained the following : $Let\;x\;=\;\{x_i\}\;and\;y=\{y_\}$ be two vectors in a separable complex Hilbert space H such that $x_i\;\neq\;0$ for all $i\;=\;1,\;2;\cdots$. Let L be a commutative subspace lattice on H. Then the following statements are equivalent. (1) $sup\;\{\frac{\$\mid${\sum_{k=1}}^l\;\alpha_{\kappa}E_{\kappa}y\$\mid$}{\$\mid${\sum_{k=1}}^l\;\alpha_{\kappa}E_{\kappa}x\$\mid$}\;:\;l\;\in\;\mathbb{N},\;\alpha_{\kappa}\;\in\;\mathbb{C}\;and\;E_{\kappa}\;\in\;L\}\;<\;\infty\;and\;$\mid$y_n\$\mid$x_n$\mid$^{-1}\;=\;1\;for\;all\;n\;=\;1,\;2,\;\cdots$. (2) There exists an operator A in AlgL such that Ax = y, A is a unitary operator and every E in L reduces, A, where AlgL is a tridiagonal algebra.

Infrared and Radio observations of a small group of protostellar objects in the molecular core, L1251-C

  • Kim, Jungha;Lee, Jeong-Eun;Choi, Minho;Bourke, Tyler L.;Evans II, Neal J.;Di Francesco, James;Cieza, Lucas A.;Dunham, Michael M.
    • The Bulletin of The Korean Astronomical Society
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    • v.40 no.1
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    • pp.67.4-68
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    • 2015
  • We present a multi-wavelength observational study of a low-mass star-forming region, L1251-C, with observational results at wavelengths from the near-infrared to the millimeter. Spitzer Space Telescope observations confirmed that IRAS 22343+7501 is a small group of protostellar objects. The extended emission to east-west direction with its intensity peak at the center of L1251A has been detected at 350 and 850 mm with the CSO and JCMT telescopes, tracing dense envelope materials around L1251A. The single-dish data from the KVN and TRAO telescopes show inconsistencies between the intensity peaks of several molecular line emission and that of the continuum emission, suggesting complex distributions of molecular abundances around L1251A. The SMA interferometer data, however, show intensity peaks of CO 2-1 and $^{13}CO$ 2-1 located at the position of IRS 1, which is both the brightest source in IRAC image and the weakest source in the 1.3 mm dust continuum map. IRS 1 is the strongest candidate for being the driving source of a newly detected the compact CO 2-1 outflow. Over the whole region ($14^{\prime}{\times}14^{\prime}$) of L125l-C, 3 Class I and 16 Class II sources have been detected, including three YSOs in L1251A. A comparison with the average projected distance among 19 YSOs in L1251-C and that among 3 YSOs in L1251A suggests L1251-C is an example of low-mass cluster formation, where protostellar objects are forming in a small group.

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The Role and Regulation of MCL-1 Proteins in Apoptosis Pathway

  • Bae, Jeehyeon
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 2002.07a
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    • pp.113-113
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    • 2002
  • Phylogenetically conserved Bcl-2 family proteins play a pivotal role in the regulation of apoptosis from virus to human. Members of the Bcl-2 family consist of antiapoptotic proteins such as Bcl-2, Bcl-xL, and Bcl-w, and proapoptotic proteins such as BAD, Bax, BOD, and Bok. It has been proposed that anti- and proapoptotic Bcl-2 proteins regulate cell death by binding to each other and forming heterodimers. A delicate balance between anti- and proapoptotic Bcl-2 family members exists in each cell and the relative concentration of these two groups of proteins determines whether the cell survives or undergoes apoptosis. Mcl-1 (Myeloid cell :leukemia-1) is a member of the Bcl-2 family proteins and was originally cloned as a differentiation-induced early gene that was activated in the human myeloblastic leukemia cell line, ML-1 . Mcl-1 is expressed in a wide variety of tissues and cells including neoplastic ones. We recently identified a short splicing variant of Mcl-1 short (Mcl-IS) and designated the known Mcl-1 as Mcl-1 long (Mcl-lL). Mcl-lL protein exhibits antiapoptotic activity and possesses the BH (Bcl-2 homology) 1, BH2, BH3, and transmembrane (TM) domains found in related Bcl-2 proteins. In contrast, Mcl-1 S is a BH3 domain-only proapoptotic protein that heterodimerizes with Mcl-lL. Although both Mc1-lL and Mcl-lS proteins contain BH domains fecund in other Bcl-2 family proteins, they are distinguished by their unusually long N-terminal sequences containing PEST (proline, glutamic acid, serine, and threonine) motifs, four pairs of arginine residues, and alanine- and glycine-rich regions. In addition, the expression pattern of Mcl-1 protein is different from that of Bcl-2 suggesting a unique role (or Mcl-1 in apoptosis regulation. Tankyrasel (TRF1-interacting, ankyrin-related ADP-related polymerasel) was originally isolated based on its binding to TRF 1 (telomeric repeat binding factor-1) and contains the sterile alpha motif (SAM) module, 24 ankyrin (ANK) repeats, and the catalytic domain of poly(adenosine diphosphate-ribose) polymerase (PARP). Previous studies showed that tankyrasel promotes telomere elongation in human cells presumably by inhibiting TRFI though its poly(ADP-ribosyl)action by tankyrasel . In addition, tankyrasel poly(ADP-ribosyl)ates Insulin-responsive amino peptidase (IRAP), a resident protein of GLUT4 vesicles, and insulin stimulates the PARP activity of tankyrase1 through its phosphorylation by mitogen-activated protein kinase (MAPK). ADP-ribosylation is a posttranslational modification that usually results in a loss of protein activity presumably by enhancing protein turnover. However, little information is available regarding the physiological function(s) of tankyrase1 other than as a PARP enzyme. In the present study, we found tankyrasel as a specific-binding protein of Mcl-1 Overexpression of tankyrasel led to the inhibition of both the apoptotic activity of Mel-lS and the survival action of Mcl-lL in mammalian cells. Unlike other known tankyrasel-interacting proteins, tankyrasel did not poly(ADP-ribosyl)ate either of the Mcl-1 proteins despite its ability to decrease Mcl-1 proteins expression following coexpression. Therefore, this study provides a novel mechanism to regulate Mcl-1-modulated apoptosis in which tankyrasel downregulates the expression of Mcl-1 proteins without the involvement of its ADP-ribosylation activity.

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Structure of [$CoL_2(MeOH)(NO_3)_2$] [L = N1-(1-(pyridin-4-yl)ethylidene)naphthalene-1,5-diamine)] ($CoL_2(MeOH)(NO_3)_2$의 구조 [L=N1-(1-(pyridin-4-yl)ethylidene)naphthalene-1,5-diamine)])

  • Kim, Sung-Hoon;Huh, Hyun-Sue;Lee, Soon-W.
    • Korean Journal of Crystallography
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    • v.18 no.1_2
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    • pp.21-25
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    • 2007
  • When a $CH_2Cl_2$ solution of the dipyridyl species L' (N,N'-bis-(1-pyridin-4-yl-ethylidene)-naphthalene-1,5-diamine) was layered onto the top of a MeOH solution of $Co(NO_3)_2{\cdot}6H_2O$, a molecular cobalt compound [$CoL_2(MeOH)(NO_3)_2$] (1), not a coordination polymer, was formed. X-ray structural analysis of compound 1 revealed that it contains the pyridyl-amine ligand L (N1-(4-imino-1-methyl-but-2-enylidene)-naphthalene-1,5-diamine), instead of L'. Structure of compound 1 strongly suggests that the original ligand L' has been hydrolyzed to ligand L during the reaction.

Comparing Compliance and Efficacy of Isocaloric Oral Nutritional Supplementation Using 1.5 kcal/mL or 1 kcal/mL Sip Feeds in Mildly to Moderately Malnourished Indonesian Children: A Randomized Controlled Trial

  • Devaera, Yoga;Syaharutsa, Danny Maesadatu;Jatmiko, Herwasto Kuncoroyakti;Sjarif, Damayanti Rusli
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.21 no.4
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    • pp.315-320
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    • 2018
  • Purpose: This study set out to evaluate the compliance to, and efficacy of oral supplementation, using a 1.5 kcal/mL or 1 kcal/mL sip feed, in children with mild to moderate malnutrition. Methods: This was a parallel, randomized, controlled open-label trial in children aged 3 to 6 years with a weight for height Z (WHZ) score <-1 and ${\geq}-3$, who were randomized to receive a total of 600 kcal/day from either a 1.5 kcal/mL or a 1.0 kcal/mL pediatric sip feed for 28 days. Assessments included daily study product intake, body weight, tolerance and dietary intake from solid food. Results: Of 110 children recruited, 98 ($mean{\pm}standard$ deviation of age $49{\pm}7months$) completed the study. Both sip feeds were well tolerated, with high compliance ($80{\pm}24%$ and $81{\pm}22%$ of prescribed volume in 1.5 kcal/mL and 1.0 kcal/mL groups respectively, p=0.79). Both study groups gained similar weight during the 28 days intervention period ($0.42{\pm}0.40kg$ in 1.5 kcal/mL group vs. $0.49{\pm}0.49kg$ in 1.0 kcal/mL group, p=0.43). There were no significant differences between the groups in weight gain and in the change in WHZ score over the intervention period. Dietary analysis at the end of the study did not show replacement of solid food by the oral nutritional supplements. Conclusion: In children with mild to moderate malnutrition, both 1.5 kcal/mL and 1 kcal/mL pediatric sip feeds had high compliance and were well tolerated, and were equally effective in promoting weight gain in the 28 days study period.

A STUDY ON HTGH-EFFICIENCY ATOMIZATION OF MOLTEN MATERIALS (PART 3 : MECHANISM AND CHARACTERISTICS OF ATOMIZATION) (Atomize법에 의한 용융소재의 고효율 미세화에 관한 연구 (제3보 : 애토마이저의 미립화 기구와 특성))

  • Oh, J.G.;Kwon, S.I.
    • Journal of ILASS-Korea
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    • v.4 no.1
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    • pp.19-26
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    • 1999
  • An experimental study of twin-fluid atomization for powder metallurgy has been conducted using a specially designed atomizer in which liquid is first spread into a thin sheet and then exposed on both sides to high-velocity air. Inner air jet worked for supplying liquid and outer air jets disintegrated liquid sheet. The first result of this study were confined to the effect of atomizing quality through experiments with water. The experimental data will be extend to include the influence of atomizing air velocities on mean particle size through experiments with molten material. An experimental equation on the relationship between SMD and the related parameters was taken out; $$SMD=0.00302\frac{{(\sigma_L\;\rho_L\;D_L)}^{0.5}}{\rho_A(V_1+1.155\;V_2)/2}(1+\frac{W_L}{(W_{A1}/3.33)+W_{A2}})+0.0148(\frac{{\mu_L}^2}{\sigma_L\;\rho_L})^{0.425} \;{D_L}^{0.575}(1+\frac{W_L}{(W_{A1}/3.33)+W_{A2}})^2$$.

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The Construction and Viterbi Decoding of New (2k, k, l) Convolutional Codes

  • Peng, Wanquan;Zhang, Chengchang
    • Journal of Information Processing Systems
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    • v.10 no.1
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    • pp.69-80
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    • 2014
  • The free distance of (n, k, l) convolutional codes has some connection with the memory length, which depends on not only l but also on k. To efficiently obtain a large memory length, we have constructed a new class of (2k, k, l) convolutional codes by (2k, k) block codes and (2, 1, l) convolutional codes, and its encoder and generation function are also given in this paper. With the help of some matrix modules, we designed a single structure Viterbi decoder with a parallel capability, obtained a unified and efficient decoding model for (2k, k, l) convolutional codes, and then give a description of the decoding process in detail. By observing the survivor path memory in a matrix viewer, and testing the role of the max module, we implemented a simulation with (2k, k, l) convolutional codes. The results show that many of them are better than conventional (2, 1, l) convolutional codes.

ON f-DERIVATIONS FROM SEMILATTICES TO LATTICES

  • Yon, Yong Ho;Kim, Kyung Ho
    • Communications of the Korean Mathematical Society
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    • v.29 no.1
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    • pp.27-36
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    • 2014
  • In this paper, we introduce the notion of f-derivations from a semilattice S to a lattice L, as a generalization of derivation and f-derivation of lattices. Also, we define the simple f-derivation from S to L, and research the properties of them and the conditions for a lattice L to be distributive. Finally, we prove that a distributive lattice L is isomorphic to the class $SD_f(S,L)$ of all simple f-derivations on S to L for every ${\wedge}$-homomorphism $f:S{\rightarrow}L$ such that $f(x_0){\vee}f(y_0)=1$ for some $x_0,y_0{\in}S$, in particular, $$L{\simeq_-}=SD_f(S,L)$$ for every ${\wedge}$-homomorphism $f:S{\rightarrow}L$ such that $f(x_0)=1$ for some $x_0{\in}S$.

L1 Cell Adhesion Molecule Promotes Migration and Invasion via JNK Activation in Extrahepatic Cholangiocarcinoma Cells with Activating KRAS Mutation

  • Kim, Haejung;Hwang, Haein;Lee, Hansoo;Hong, Hyo Jeong
    • Molecules and Cells
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    • v.40 no.5
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    • pp.363-370
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    • 2017
  • Extrahepatic cholangiocarcinoma (ECC), a malignant tumor of biliary origin, has a poor prognosis with limited treatment options. The KRAS oncogene is the most commonly mutated gene in ECC and one of the factors that predicts a poor prognosis and low survival rate. L1 cell adhesion molecule (L1CAM) is expressed in ECC cells and acts as an independent poor prognostic factor in predicting patient survival. In this study we investigate the functional significance of L1CAM in ECC cells with activating KRAS mutation. We selected an ECC cell line, EGI-1, with activating KRAS mutation, and then confirmed its expression of L1CAM by RT-PCR, western blot analysis, and flow cytometry. The suppression of L1CAM expression (using a specific lentivirus-delivered shRNA) significantly decreased the migratory and invasive properties of EGI-1 cells, without altering their proliferation or survival. Analyses of signaling effectors in L1CAM-depleted and control EGI-1 cells indicated that L1CAM suppression decreased the levels of both phosphorylated MKK4 and total MKK4, together with c-Jun N-terminal kinase (JNK) phosphorylation. Further, exposure to a JNK inhibitor (SP600125) decreased migration and invasion of EGI-1 cells. These results suggest that L1CAM promotes cellular migration and invasion via the induction of MKK4 expression, leading to JNK activation. Our study is the first to demonstrate a functional role for L1CAM in ECC carrying the activating KRAS mutation. Given that KRAS is the most commonly mutated oncogene in ECC, L1CAM may serve as an attractive therapeutic target for ECC cells with activating KRAS mutation.