• 제목/요약/키워드: completely positive map

검색결과 10건 처리시간 0.015초

α-COMPLETELY POSITIVE MAPS ON LOCALLY C*-ALGEBRAS, KREIN MODULES AND RADON-NIKODÝM THEOREM

  • Heo, Jaeseong;Ji, Un Cig;Kim, Young Yi
    • 대한수학회지
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    • 제50권1호
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    • pp.61-80
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    • 2013
  • In this paper, we study ${\alpha}$-completely positive maps between locally $C^*$-algebras. As a generalization of a completely positive map, an ${\alpha}$-completely positive map produces a Krein space with indefinite metric, which is useful for the study of massless or gauge fields. We construct a KSGNS type representation associated to an ${\alpha}$-completely positive map of a locally $C^*$-algebra on a Krein locally $C^*$-module. Using this construction, we establish the Radon-Nikod$\acute{y}$m type theorem for ${\alpha}$-completely positive maps on locally $C^*$-algebras. As an application, we study an extremal problem in the partially ordered cone of ${\alpha}$-completely positive maps on a locally $C^*$-algebra.

Obatoclax Regulates the Proliferation and Fusion of Osteoclast Precursors through the Inhibition of ERK Activation by RANKL

  • Oh, Ju Hee;Lee, Jae Yoon;Park, Jin Hyeong;No, Jeong Hyeon;Lee, Na Kyung
    • Molecules and Cells
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    • 제38권3호
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    • pp.279-284
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    • 2015
  • Obatoclax, a pan-Bcl2 inhibitor, shows antitumor activities in various solid malignancies. Bcl2-deficient mice have shown the importance of Bcl2 in osteoclasts, as the bone mass of the mice was increased by the induced apoptosis of osteoclasts. Despite the importance of Bcl2, the effects of obatoclax on the proliferation and differentiation of osteoclast precursors have not been studied extensively. Here, we describe the anti-proliferative effects of obatoclax on osteoclast precursors and its negative role on fusion of the cells. Stimulation with low doses of obatoclax significantly suppressed the proliferation of osteoclast precursors in a dose-dependent manner while the apoptosis was markedly increased. Its stimulation was sufficient to block the activation of ERK MAP kinase by RANKL. The same was true when PD98059, an ERK inhibitor, was administered to osteoclast precursors. The activation of JNK1/2 and p38 MAP kinase, necessary for osteoclast differentiation, by RANKL was not affected by obatoclax. Interestingly, whereas the number of TRAP-positive mononuclear cells was increased by both obatoclax and PD98059, fused, multinucleated cells larger than $100{\pm}m$ in diameter containing more than 20 nuclei were completely reduced. Consistently, obatoclax failed to regulate the expression of osteoclast marker genes, including c-Fos, TRAP, RANK and CtsK. Instead, the expression of DC-STAMP and Atp6v0d2, genes that regulate osteoclast fusion, by RANKL was significantly abrogated by both obatoclax and PD98059. Taken together, these results suggest that obatoclax down-regulates the proliferation and fusion of osteoclast precursors through the inhibition of the ERK1/2 MAP kinase pathway.

A NOTE ON THE OPERATOR EQUATION $\alpha+\alpha^{-1}$=$\beta+\beta^{-1}$

  • Thaheem, A.B.
    • 대한수학회보
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    • 제23권2호
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    • pp.167-170
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    • 1986
  • Let M be a von Neumann algebra and .alpha., .betha. be *-automorphisms of M satisfying the operator equation .alpha.+.alpha.$^{-1}$ =.betha.+.betha.$^{-1}$ This operator equation has been extensively studied and many important decomposition theorems have been obtained by several authors (for instance see [4], [5], [2], [1]). Originally, this operator equation arose in the paper of Van Daele on the new approach of the Tomita-Takesaki theory in the case of modular operators ([7]). In the case of one-parameter automorphism groups, this equation has produced a bounded and completely positive map which can play a role similar to the infinitesimal generator (for details see [6] and [1]). A recent and one of the most important applications of this equation has been in developing an anglogue of the Tomita-Takesaki theory for Jordan algebras by Haagerup [3]. One general result of this theory is the following.

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Up-Regulation of RANK Expression via ERK1/2 by Insulin Contributes to the Enhancement of Osteoclast Differentiation

  • Oh, Ju Hee;Lee, Na Kyung
    • Molecules and Cells
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    • 제40권5호
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    • pp.371-377
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    • 2017
  • Despite the importance of the receptor activator of nuclear factor (NF)-kappaB ligand (RANKL)-RANK signaling mechanisms on osteoclast differentiation, little has been studied on how RANK expression is regulated or what regulates its expression during osteoclastogenesis. We show here that insulin signaling increases RANK expression, thus enhancing osteoclast differentiation by RANKL. Insulin stimulation induced RANK gene expression in time- and dose-dependent manners and insulin receptor shRNA completely abolished RANK expression induced by insulin in bone marrow-derived monocyte/macrophage cells (BMMs). Moreover, the addition of insulin in the presence of RANKL promoted RANK expression. The ability of insulin to regulate RANK expression depends on extracellular signal-regulated kinase 1/2 (ERK1/2) since only PD98059, an ERK1/2 inhibitor, specifically inhibited its expression by insulin. However, the RANK expression by RANKL was blocked by all three mitogen-activated protein (MAP) kinases inhibitors. The activation of RANK increased differentiation of BMMs into tartrate-resistant acid phosphatase-positive ($TRAP^+$) osteoclasts as well as the expression of dendritic cell-specific transmembrane protein (DC-STAMP) and d2 isoform of vacuolar ($H^+$) ATPase (v-ATPase) Vo domain (Atp6v0d2), genes critical for osteoclastic cell-cell fusion. Collectively, these results suggest that insulin induces RANK expression via ERK1/2, which contributes to the enhancement of osteoclast differentiation.

Molecular Cloning of Chitinase Genes Family from Serratia marcescens

  • Song, Young-Hwan;Kweon, Oh-Gun
    • 한국어병학회지
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    • 제6권2호
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    • pp.103-110
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    • 1993
  • Sau3AI으로 부분절단한 Serratia marcescens genomic DNA(5Kb 이상)을 pUC19의 BamHI site에 삽입하여 total genomic library를 준비하였다. Swollen colloidal chitin media에서 halo를 형성하는 2개의 E.coli 형질전환주를 선별하였다. 이들 colony가 chitinase 유전자를 갖음을 재확인하기 위하여 4-methylumbelliferyl N-acetyl-$\beta$-D-glucosaminide(4-MuFGlcNAc)를 이용하였다. 4-MuFGlcNAc는 chitinase에 대한 기질특이성을 나타내며 형광을 나타내는 기질로서 positive clone들은 360nm의 자외선을 조사하였을 경우 밝은 형광을 나타낸다. pUC19으로 부터 유래된 2 종류의 다른 chitinase clone, pCH1(11.0Kb) 및 pCH2(7.5Kb)를 genomic DNA library로 부터 분리하였으며, 이들의 제한효소지도를 작성한 결과 서로 다른 제한효소지도를 나타내었다. pCH1EA 및 pCH2로 부터 각각의 EcoRI-Xbal fragment를 subcloning함으로써 두개의 다른 chitinase 유전자의 위치를 결정하였다. pCH1EA 및 pCH2를 cross hybridization 한 결과 hybridization signal을 나타내지 않아 서로 유사성이 없는 것으로 사료된다.

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Dobutamine-Induced Perioperative Anaphylaxis in a Dog

  • Jeong, Youngeun;Jang, Yunseol;Moon, Changhwan;Jeong, Jaemin;Roh, Yoonho;Lee, Haebeom;Jeong, Seong-Mok
    • 한국임상수의학회지
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    • 제37권3호
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    • pp.145-148
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    • 2020
  • A 9-years old spayed female Maltese was referred for the treatment of mass on the right 1st mammary gland and acute weight bearing lameness of right hindlimb. It was diagnosed as malignant mammary tumor and cranial cruciate ligament rupture of right stifle joint. Right upper regional mastectomy followed by cranial closing wedge osteotomy (CCWO) of the right tibia were planned for the present problems. Preanesthetic work-up did not show any remarkable abnormalities. Forty-five minutes after induction of anesthesia dobutamine was administered at a rate of 5 ㎍/kg/min by constant rate infusion due to gradual decrease of blood pressure below MAP 60 mmHg during surgical procedure. Despite of the increase of dobutamine infusion rate up to 20 ㎍/kg/min, blood pressure didn't recover. At the end of regional mastectomy generalized skin redness and eyelid edema were identified. Anesthesia was stopped and CCWO procedure was cancelled. To recover from the anaphylactic reactions dexamethasone and diphenhydramine were administered. After about one hour, the patient completely recovered from hypotension and anaphylactic reactions. After 4 weeks, intradermal skin test (IDST) was performed for all the drugs used during anesthesia. Only dobutamine showed positive reaction in IDST. Therefore, dobutamine was considered as the causative agent of anaphylaxis in this patient during the anesthesia. In case of perioperative anaphylactic reaction, postoperative investigation should be performed to identify causative agent and to provide safe recommendations for future anesthetic procedure.