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Jung, In-Hyuk,Choi, Jae-Hoon,Jin, Jing,Jeong, Se-Jin,Jeon, Sejin,Lim, Chaeji,Lee, Mi-Ran,Yoo, Ji-Young,Sonn, Seong-Keun,Kim, Young Ho,Choi, Beom Kyu,Kwon, Byoung S.,Seoh, Ju-Young,Lee, Cheol Whan,Kim, The Federation of American Societies for Experimen 2014 The FASEB Journal Vol.28 No.11
<P>CD137 (4-1BB), a member of the tumor necrosis factor receptor superfamily, has been reported to be expressed in atherosclerotic plaques, and to promote lesion formation. However, the role of CD137 in mediating atherosclerotic plaque stability and the possible underlying molecular and cellular mechanisms are poorly understood. Here, apolipoprotein E-deficient (<I>ApoE</I><SUP>−/−</SUP>) and CD137-deficient <I>ApoE</I><SUP>−/−</SUP> (<I>ApoE</I><SUP>−/−</SUP>CD137<SUP>−/−</SUP>) mice fed a chow diet for 66 wk were used. CD137 induces plaque instability, which is characterized by increased plaque necrosis, decreased collagen content, decreased vascular smooth muscle cell (VSMC) content, and increased macrophage infiltration. CD137 also increases the infiltration of effector T (T<SUB>eff</SUB>) cells into plaque lesion sites, resulting in increased interferon-γ (IFN-γ) expression. Interestingly, T<SUB>eff</SUB>-cell-derived IFN-γ inhibits collagen synthesis in atherosclerotic plaques. Furthermore, CD137 activation increases the apoptosis of VSMCs, possibly by decreasing the antiapoptotic regulator, Bcl-2, and subsequently up-regulating cleaved caspase-3. In macrophages, activation of CD137 signaling boosted the oxidized low density lipoprotein-induced expression of matrix metalloproteinase 9 <I>via</I> the p38 mitogen-activated protein kinase and extracellular signal-regulated kinase1/2 signaling pathways. In summary, activation of CD137 signaling decreases the stability of advanced atherosclerotic plaques <I>via</I> its combined effects on T<SUB>eff</SUB> cells, VSMCs, and macrophages.—Jung, I.-H., Choi, J.-H., Jin, J., Jeong, S.-J., Jeon, S., Lim, C., Lee, M.-R., Yoo, J.-Y., Sonn, S.-K., Kim, Y. H., Choi, B. K., Kwon, B. S., Seoh, J.-Y., Lee, C. W., Kim, D.-Y., Oh, G. T. CD137-inducing factors from T cells and macrophages accelerate the destabilization of atherosclerotic plaques in hyperlipidemic mice.</P>
Lim, Min-Hwa,Park, Mi-Jung,Kim, Sang-Chai,Roh, S. H.,Jung, Seung-Hun,Kim, Hee Tak,Jung, Ho-Young American Scientific Publishers 2017 Journal of Nanoscience and Nanotechnology Vol.17 No.8
<P>Durability test of commercial polymer electrolyte membranes investigated because longer performance of VRFB depends on the membrane's chemical stability. For hydrolytic stability test, distilled water and membrane was placed in the pressurized container, activated for 24 h at 200 degrees C to check the weight loss, and distilled water's pH change. To confirm the chemical degradation, the membrane was impregnated in 0.1 M V(V) solution for 72 h and concentration change was measured by UV-vis Spectrum. Through this experiment, anion exchange membrane in VRFB is considered in terms of chemical degradation.</P>
Derrick, Jeffrey S.,Kerr, Richard A.,Korshavn, Kyle J.,McLane, Michael J.,Kang, Juhye,Nam, Eunju,Ramamoorthy, Ayyalusamy,Ruotolo, Brandon T.,Lim, Mi Hee American Chemical Society 2016 Inorganic Chemistry Vol.55 No.10
<P>The complex and multifaceted pathology of Alzheimer's disease (AD) continues to present a formidable challenge to the establishment of long-term treatment strategies. Multifunctional compounds able to modulate the reactivities of various pathological features, such as amyloid-beta (A beta) aggregation, metal ion dyshomeostasis, and oxidative stress, have emerged as useful tactic. Recently, an incorporation approach to the rational design of multipurpose small molecules has been validated through the production of a multifunctional ligand (ML) as a potential chemical tool for AD. In order to further the development of more diverse and improved multifunctional reagents, essential pharmacophores must be identified. Herein, we report a series of aminoquinoline derivatives (AQ1-4, AQP1-4, and AQDA1-3) based on ML's framework, prepared to gain a structure reactivity understanding of ML's multifunctionality in addition to tuning its metal binding affinity. Our structure reactivity investigations have implicated the dimethylamino group as a key component for supplying the antiamyloidogenic characteristics of ML in both the absence and presence of metal ions. Two-dimensional NMR studies indicate that structural variations of ML could tune its interaction sites along the A beta sequence. In addition, mass spectrometric analyses suggest that the ability of our aminoquinoline derivatives to regulate metal-induced A beta aggregation may be influenced by their metal binding properties. Moreover, structural modifications to ML were also observed to noticeably change its metal binding affinities and metal-to-ligand stoichiometries that were shown to be linked to their antiamyloidogenic and antioxidant activities. Overall, our studies provide new insights into rational design strategies for multifunctional ligands directed at regulating metal ions, A beta, and oxidative stress in AD and could advance the development of improved next-generation multifunctional reagents.</P>
Savelieff, Masha G.,DeToma, Alaina S.,Derrick, Jeffrey S.,Lim, Mi Hee American Chemical Society 2014 Accounts of chemical research Vol.47 No.8
<title>Conspectus</title><P>The development of a cure for Alzheimer’s disease (AD) has been impeded by an inability to pinpoint the root cause of this disorder. Although numerous potential pathological factors have been indicated, acting either individually or mutually, the molecular mechanisms leading to disease onset and progression have not been clear. Amyloid-β (Aβ), generated from proteolytic processing of the amyloid precursor protein (APP), and its aggregated forms, particularly oligomers, are suggested as key pathological features in AD-affected brains. Historically, highly concentrated metals are found colocalized within Aβ plaques. Metal binding to Aβ (metal–Aβ) generates/stabilizes potentially toxic Aβ oligomers, and produces reactive oxygen species (ROS) in vitro (redox active metal ions; plausible contribution to oxidative stress). Consequently, clarification of the relationship between Aβ, metal ions, and toxicity, including oxidative stress via metal–Aβ, can lead to a deeper understanding of AD development.</P><P>To probe the involvement of metal–Aβ in AD pathogenesis, rationally designed and naturally occurring molecules have been examined as chemical tools to target metal–Aβ species, modulate the interaction between the metal and Aβ, and subsequently redirect their aggregation into nontoxic, off-pathway unstructured aggregates. These ligands are also capable of attenuating the generation of redox active metal–Aβ-induced ROS to mitigate oxidative stress. One rational design concept, the incorporation approach, installs a metal binding site into a framework known to interact with Aβ. This approach affords compounds with the simultaneous ability to chelate metal ions and interact with Aβ. Natural products capable of Aβ interaction have been investigated for their influence on metal-induced Aβ aggregation and have inspired the construction of synthetic analogues. Systematic studies of these synthetic or natural molecules could uncover relationships between chemical structures, metal/Aβ/metal–Aβ interactions, and inhibition of Aβ/metal–Aβ reactivity (i.e., aggregation modes of Aβ/metal–Aβ; associated ROS production), suggesting mechanisms to refine the design strategy.</P><P>Interdisciplinary investigations have demonstrated that the designed molecules and natural products control the aggregation pathways of metal–Aβ species transforming their size/conformation distribution. The aptitude of these molecules to impact metal–Aβ aggregation pathways, either via inhibition of Aβ aggregate formation, most importantly of oligomers, or disaggregation of preformed fibrils, could originate from their formation of complexes with metal–Aβ. Potentially, these molecules could direct metal–Aβ size/conformational states into alternative nontoxic unstructured oligomers, and control the geometry at the Aβ-ligated metal center for limited ROS formation to lessen the overall toxicity induced by metal–Aβ. Complexation between small molecules and Aβ/metal–Aβ has been observed by nuclear magnetic resonance spectroscopy (NMR) and ion mobility-mass spectrometry (IM-MS) pointing to molecular level interactions, validating the design strategy. In addition, these molecules exhibit other attractive properties, such as antioxidant capacity, prevention of ROS production, potential blood-brain barrier (BBB) permeability, and reduction of Aβ-/metal–Aβ-induced cytotoxicity, making them desirable tools for unraveling AD complexity. In this Account, we summarize the recent development of small molecules, via both rational design and the selection and modification of natural products, as tools for investigating metal–Aβ complexes, to advance our understanding of their relation to AD p
Lim, Jung Mi,Lee, Kyung S.,Woo, Hyun Ae,Kang, Dongmin,Rhee, Sue Goo The Rockefeller University Press 2015 The Journal of cell biology Vol.210 No.1
<P>Proteins associated with the centrosome play key roles in mitotic progression in mammalian cells. The activity of Cdk1-opposing phosphatases at the centrosome must be inhibited during early mitosis to prevent premature dephosphorylation of Cdh1—an activator of the ubiquitin ligase anaphase-promoting complex/cyclosome—and the consequent premature degradation of mitotic activators. In this paper, we show that reversible oxidative inactivation of centrosome-bound protein phosphatases such as Cdc14B by H<SUB>2</SUB>O<SUB>2</SUB> is likely responsible for this inhibition. The intracellular concentration of H<SUB>2</SUB>O<SUB>2</SUB> increases as the cell cycle progresses. Whereas the centrosome is shielded from H<SUB>2</SUB>O<SUB>2</SUB> through its association with the H<SUB>2</SUB>O<SUB>2</SUB>-eliminating enzyme peroxiredoxin I (PrxI) during interphase, the centrosome-associated PrxI is selectively inactivated through phosphorylation by Cdk1 during early mitosis, thereby exposing the centrosome to H<SUB>2</SUB>O<SUB>2</SUB> and facilitating inactivation of centrosome-bound phosphatases. Dephosphorylation of PrxI by okadaic acid–sensitive phosphatases during late mitosis again shields the centrosome from H<SUB>2</SUB>O<SUB>2</SUB> and thereby allows the reactivation of Cdk1-opposing phosphatases at the organelle.</P>
Mi, J.W.,Won, S.J.,Kim, M.J.,Lim, B.S. The Korean Society of Automotive Engineers 2000 International journal of automotive technology Vol.1 No.2
High temperature materials in service are subjected to mechanical damage due to operating load and metallurgical damage due to operating temperature. Therefore, when designing or assessing life of high temperature components, both factors must be considered. In this paper, the effect of tensile hold time on high temperature fatigue crack growth and long term prior thermal aging heat treatment on creep rupture behavior were investigated using STS 316L and STS 316 austenitic stainless steels, which are widely used for high temperature components like in automotive exhaust and piping systems. In high temperature fatigue crack growth tests using STS 316L, as tensile hold time increased, crack growth rate decreased in relatively short tensile hold time region. In long term aged specimens, cavity type microcracks have been observed at the interface of grain boundary and coarsened carbide.