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Rogozin, E. A.,Lee, K. W.,Kang, N. J.,Yu, H.,Nomura, M.,Miyamoto, K.-I.,Conney, A. H.,Bode, A. M.,Dong, Z. Oxford University Press 2008 Carcinogenesis Vol.29 No.6
<P>Some xanthine analogues, including 1,3,7-trimethylxanthine (caffeine) and 1,3-dimethylxanthine (theophylline), have been shown to exert anticancer activities in both cell culture and animal models. The present study focused on the relationship of structure and activity of 50 different caffeine analogues in preventing epidermal growth factor (EGF)-induced malignant transformation of mouse epidermal JB6 promotion-sensitive (P+) Cl41 (JB6 P+) cells. Results indicated that the inhibition of cell transformation by the 1,3,7-trialkylxanthines depends on the number of carbons at the alkyl groups R1 and R3, but not R7. Notably, 1-ethyl-3-hexylxanthine (xanthine 70) was the most effective compound for inhibiting EGF-induced neoplastic transformation among the 50 xanthine analogues tested. The 50% inhibition of cell transformation (ICT(50)) value for xanthine 70 was 48- or 75-fold less than the ICT(50) value of caffeine or theophylline, respectively. Further study revealed that xanthine 70 (5-40 muM) dose dependently inhibited EGF-induced transactivation of activator protein 1 (AP-1), whereas theophylline or caffeine (up to 500 muM) had no effect on AP-1 activity. In addition, xanthine 70 (10 muM) inhibited 12-O-tetradecanoylphorbol-13-acetate- or H-Ras-induced neoplastic transformation in JB6 P+ cells by 78.2 or 62.0%, respectively. Collectively, these results indicated that the number of carbons at R1 and R3 is important for the antitumor-promoting activity of the trialkylxanthines and xanthine 70 might be a promising anticancer agent.</P>
Tuning of magnetic and transport properties in Bi2Te3by divalent Fe doping
Jo, N. H.,Lee, K. J.,Kim, C. M.,Okamoto, K.,Kimura, A.,Miyamoto, K.,Okuda, T.,Kim, Y. K.,Lee, Z.,Onimaru, T.,Takabatake, T.,Jung, M. H. American Physical Society 2013 Physical review. B, Condensed matter and materials Vol.87 No.20
Age-Related Decline in Oligodendrogenesis Retards White Matter Repair in Mice
Miyamoto, Nobukazu,Pham, Loc-Duyen D.,Hayakawa, Kazuhide,Matsuzaki, Toshinori,Seo, Ji Hae,Magnain, Caroline,Ayata, Cenk,Kim, Kyu-Won,Boas, David,Lo, Eng H.,Arai, Ken American Heart Association, Inc. 2013 Stroke Vol.44 No.9
<P><B>Background and Purpose—</B></P><P>Aging is one of the major risk factors for white matter injury in cerebrovascular disease. However, the effects of age on the mechanisms of injury/repair in white matter remain to be fully elucidated. Here, we ask whether, compared with young brains, white matter regions in older brains may be more vulnerable in part because of decreased rates of compensatory oligodendrogenesis after injury.</P><P><B>Methods—</B></P><P>A mouse model of prolonged cerebral hypoperfusion was prepared by bilateral common carotid artery stenosis in 2-month and 8-month-old mice. Matching in vitro studies were performed by subjecting oligodendrocyte precursor cells to sublethal 7-day CoCl<SUB>2</SUB> treatment to induce chemical hypoxic stress.</P><P><B>Results—</B></P><P>Baseline myelin density in the corpus callosum was similar in 2-month and 8-month-old mice. But after induction of prolonged cerebral hypoperfusion, older mice showed more severe white matter injury together with worse deficits in working memory. The numbers of newborn oligodendrocytes and their precursors were increased by cerebral hypoperfusion in young mice, whereas these endogenous responses were significantly dampened in older mice. Defects in cyclic AMP response element-binding protein signaling may be involved because activating cyclic AMP response element-binding protein with the type-III phosphodiesterase inhibitor cilostazol in older mice restored the differentiation of oligodendrocyte precursor cells, alleviated myelin loss, and improved cognitive dysfunction during cerebral hypoperfusion. Cell culture systems confirmed that cilostazol promoted the differentiation of oligodendrocyte precursor cells.</P><P><B>Conclusions—</B></P><P>An age-related decline in cyclic AMP response element-binding protein–mediated oligodendrogenesis may compromise endogenous white matter repair mechanisms, and therefore, drugs that activate cyclic AMP response element-binding protein signaling provide a potential therapeutic approach for treating white matter injury in aging brains.</P>
Oxidative Stress Interferes With White Matter Renewal After Prolonged Cerebral Hypoperfusion in Mice
Miyamoto, Nobukazu,Maki, Takakuni,Pham, Loc-Duyen D.,Hayakawa, Kazuhide,Seo, Ji Hae,Mandeville, Emiri T.,Mandeville, Joseph B.,Kim, Kyu-Won,Lo, Eng H.,Arai, Ken American Heart Association, Inc. 2013 Stroke Vol.44 No.12
<P><B>Background and Purpose—</B></P><P>White matter injury caused by cerebral hypoperfusion may contribute to the pathophysiology of vascular dementia and stroke, but the underlying mechanisms remain to be fully defined. Here, we test the hypothesis that oxidative stress interferes with endogenous white matter repair by disrupting renewal processes mediated by oligodendrocyte precursor cells (OPCs).</P><P><B>Methods—</B></P><P>In vitro, primary rat OPCs were exposed to sublethal CoCl<SUB>2</SUB> for 7 days to induce prolonged chemical hypoxic stress. Then, OPC proliferation/differentiation was assessed. In vivo, prolonged cerebral hypoperfusion was induced by bilateral common carotid artery stenosis in mice. Then, reactive oxygen species production, myelin density, oligodendrocyte versus OPC counts, and cognitive function were evaluated. To block oxidative stress, OPCs and mice were treated with the radical scavenger edaravone.</P><P><B>Results—</B></P><P>Prolonged chemical hypoxic stress suppressed OPC differentiation in vitro. Radical scavenging with edaravone ameliorated these effects. After 28 days of cerebral hypoperfusion in vivo, reactive oxygen species levels were increased in damaged white matter, along with the suppression of OPC-to-oligodendrocyte differentiation and loss of myelin staining. Concomitantly, mice showed functional deficits in working memory. Radical scavenging with edaravone rescued OPC differentiation, ameliorated myelin loss, and restored working memory function.</P><P><B>Conclusions—</B></P><P>Our proof-of-concept study demonstrates that after prolonged cerebral hypoperfusion, oxidative stress interferes with white matter repair by disrupting OPC renewal mechanisms. Radical scavengers may provide a potential therapeutic approach for white matter injury in vascular dementia and stroke.</P>
A single particle Hamiltonian for electro-magnetic properties of graphene nanoribbons
Lee, H.,Wakabayashi, K.,Son, Y.W.,Miyamoto, Y. Pergamon Press ; Elsevier Science Ltd 2012 Carbon Vol.50 No.10
Graphene zigzag edges are known to show the spin polarized ferromagnetic states, which are well described by the mean field treatment of Hubbard model. The parameter of onsite Coulomb interaction U is estimated to be comparable to the kinetic hopping parameter t so as to fit the electronic band structures obtained by the spin-polarized density functional theory (DFT). In this paper, we propose a simple way to transfer the electronic band structures obtained by DFT onto the mean-field Hubbard Hamiltonian by adopting site-dependent U parameter, which is taken as the decaying function from the edge. This approach is applicable to both anti-ferromagnetic and ferromagnetic states between two edges of graphene nanoribbons and will serve to perform the further large-scale simulation of electro-magnetic transport properties of graphene-based nanodevices.
MOSFET Model HiSIM Based on Surface-Potential Description for Enabling Accurate RF-CMOS Design
M. Miura-Mattausch,H. J. Mattausch,T. Ohguro,T. Iizuka,M. Taguchi,S. Kumashiro,S. Miyamoto 대한전자공학회 2004 Journal of semiconductor technology and science Vol.4 No.3
The origin of the phenomena, obstructing circuit performance in the RF operating regime, as well as their modeling will be discussed. The applied surface-potential-based modeling allows self-consistent description of all phenomena important for accurate circuit simulation, as demonstrated with the MOSFET model HiSIM.<br/>