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  • 1
    Publication Date: 2016-04-08
    Description: A novel radially local approximation of the drift kinetic equation is presented. The new drift kinetic equation that includes both E × B and tangential magnetic drift terms is written in the conservative form and it has favorable properties for numerical simulation that any additional terms for particle and energy sources are unnecessary for obtaining stationary solutions under the radially local approximation. These solutions satisfy the intrinsic ambipolarity condition for neoclassical particle fluxes in the presence of quasisymmetry of the magnetic field strength. Also, another radially local drift kinetic equation is presented, from which the positive definiteness of entropy production due to neoclassical transport and Onsager symmetry of neoclassical transport coefficients are derived while it sacrifices the ambipolarity condition for neoclassical particle fluxes in axisymmetric and quasi-symmetric systems.
    Print ISSN: 1070-664X
    Electronic ISSN: 1089-7674
    Topics: Physics
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  • 2
    Publication Date: 2016-08-03
    Description: Recent large-scale infrared surveys have been revealing stellar populations in the inner Galaxy seen through strong interstellar extinction in the disc. In particular, classical Cepheids with their period–luminosity and period–age relations are useful tracers of Galactic structure and evolution. Interesting groups of Cepheids reported recently include four Cepheids in the nuclear stellar disc (NSD), about 200 pc around the Galactic Centre, found by Matsunaga et al. and those spread across the inner part of the disc reported by Dékány and collaborators. We here report our discovery of nearly 30 classical Cepheids towards the bulge region, some of which are common with Dékány et al., and discuss the large impact of the reddening correction on distance estimates for these objects. Assuming that the four Cepheids in the NSD are located at the distance of the Galactic Centre and that the near-infrared extinction law, i.e. wavelength dependency of the interstellar extinction, is not systematically different between the NSD and other bulge lines of sight, most of the other Cepheids presented here are located significantly further than the Galactic Centre. This suggests a lack of Cepheids in the inner 2.5 kpc region of the Galactic disc except the NSD. Recent radio observations show a similar distribution of star-forming regions.
    Print ISSN: 0035-8711
    Electronic ISSN: 1365-2966
    Topics: Physics
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  • 3
    Publication Date: 2015-04-12
    Description: We estimated spatiotemporal slip distributions from three long-term slow slip events (L-SSEs) that occurred beneath the Bungo Channel at the convergent plate boundary between the subducting oceanic Philippine Sea plate and the continental Amurian plate in southwest Japan between 1997 and 1998, 2002 and 2004 and 2009 and 2011. For this purpose, we employed an inversion method using a Bayesian Information Criterion (ABIC), which included the following three prior constraints: the spatial slip distribution was smooth to some extent, slip directions were mostly oriented in the direction of plate convergence and the temporal change in slip was smooth to some extent. Our results revealed that the three L-SSEs had a common feature: slipped regions expanded southwestward at accelerating slip velocities. We also found that major slipped regions migrated southwestward by approximately 50–100 km yr –1 . In contrast, southwestward and northeastward migration of the slipped regions, whose direction differed from event to event, was also identified before or after the periods when the slip velocities were at their greatest. Comparing the obtained spatiotemporal slip distributions of the three L-SSEs with slip-deficit rate distributions obtained in our previous study, we investigated the accumulation process of the slip deficit caused by slip-deficit rate distributions and the release processes of the slip deficit caused by the obtained spatiotemporal slip distributions of the three L-SSEs. At the western plate interface of the Bungo Channel, as the slip-deficit rate was small and the amounts of slips associated with the three L-SSEs were large, most of the accumulated slip deficit was estimated to have been released. In contrast, at the eastern plate interface, as the slip-deficit rate was large and the amounts of slips associated with the three L-SSEs were small, the slip deficit was estimated to have accumulated effectively. These results suggest that the slipped regions of the three L-SSEs and the strongly coupled region are not spatially complementary; the accumulated slip deficit showed spatial variation even at approximately the same depth range along the arc.
    Keywords: Seismology
    Print ISSN: 0956-540X
    Electronic ISSN: 1365-246X
    Topics: Geosciences
    Published by Oxford University Press on behalf of The Deutsche Geophysikalische Gesellschaft (DGG) and the Royal Astronomical Society (RAS).
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  • 4
  • 5
    Publication Date: 2015-10-11
    Description: Contrary to the empirical Miedema and Hume-Rothery rules and a recent theoretical prediction, we report experimental evidence on the formation of Li-Cs alloys at very low pressure (〉0.1 GPa). We also succeeded in synthesizing a pure nonstoichiometric and ordered crystalline phase from an approximately equimolar mixture and resolved its structure using the maximum entropy method. The new alloy has a primitive cubic cell with the Li atom situated in the center and the Cs at the corners. This structure is stable to at least 10 GPa and has an anomalously high coefficient of thermal expansion at low pressure. Analysis of the valence charge density shows that electrons are donated from Cs to the Li " p "-orbitals, resulting in a rare formal oxidation state of –1 for Li. The observation indicates the diversity in the bonding of the seeming simple group I Li element.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 6
    Publication Date: 2015-02-04
    Description: Cytochrome c oxidase (CcO) is the only enzyme that uses oxygen to produce a proton gradient for ATP production during mitochondrial oxidative phosphorylation. Although CcO activity increases in response to hypoxia, the underlying regulatory mechanism remains elusive. By screening for hypoxia-inducible genes in cardiomyocytes, we identified hypoxia inducible domain family,...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 7
    Publication Date: 2011-04-20
    Description: UV radiation induces systemic immunosuppression. Because nonsteroidal anti-inflammatory drugs suppress UV-induced immunosuppression, prostanoids have been suspected as a crucial mediator of this UV effect. However, the identity of the prostanoid involved and its mechanism of action remain unclear. Here, we addressed this issue by subjecting mice deficient in each prostanoid receptor individually or mice treated with a subtype-specific antagonist to UV irradiation. Mice treated with an antagonist for prostaglandin E receptor subtype 4 (EP4), but not those deficient in other prostanoid receptors, show impaired UV-induced immunosuppression, whereas administration of an EP4 agonist rescues the impairment of the UV-induced immunosuppression in indomethacin-treated mice. The EP4 antagonist treatment suppresses an increase in the number of CD4+/forkhead box P3-positive (Foxp3+) regulatory T cells (Treg cells) in the peripheral lymph nodes (LNs) and dendritic cells expressing DEC205 in the LNs and the skin after UV irradiation. Furthermore, the EP4 antagonist treatment down-regulates UV-induced expression of receptor activator of NF-κB ligand (RANKL) in skin keratinocytes. Finally, administration of anti-RANKL antibody abolishes the restoration of UV-induced immunosuppression by EP4 agonism in indomethacin-treated mice. Thus, prostaglandin E2 (PGE2)–EP4 signaling mediates UV-induced immunosuppression by elevating the number of Treg cells through regulation of RANKL expression in the epidermis.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 8
    Publication Date: 2000-03-10
    Description: Chk2 is a protein kinase that is activated in response to DNA damage and may regulate cell cycle arrest. We generated Chk2-deficient mouse cells by gene targeting. Chk2-/- embryonic stem cells failed to maintain gamma-irradiation-induced arrest in the G2 phase of the cell cycle. Chk2-/- thymocytes were resistant to DNA damage-induced apoptosis. Chk2-/- cells were defective for p53 stabilization and for induction of p53-dependent transcripts such as p21 in response to gamma irradiation. Reintroduction of the Chk2 gene restored p53-dependent transcription in response to gamma irradiation. Chk2 directly phosphorylated p53 on serine 20, which is known to interfere with Mdm2 binding. This provides a mechanism for increased stability of p53 by prevention of ubiquitination in response to DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirao, A -- Kong, Y Y -- Matsuoka, S -- Wakeham, A -- Ruland, J -- Yoshida, H -- Liu, D -- Elledge, S J -- Mak, T W -- GM44664/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1824-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Amgen Institute, Ontario Cancer Institute, and Departments of Medical Biophysics and Immunology, University of Toronto, 620 University Avenue, Suite 706, Toronto, Ontario, M5G 2C1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins ; Checkpoint Kinase 2 ; *DNA Damage ; DNA-Binding Proteins ; G1 Phase ; G2 Phase ; Gamma Rays ; Gene Expression Regulation ; Gene Targeting ; Genes, Tumor Suppressor ; Genes, p53 ; Humans ; *Interphase ; Mice ; *Nuclear Proteins ; Phosphorylation ; Phosphoserine/metabolism ; *Protein Kinases ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-mdm2 ; Stem Cells/cytology/metabolism ; T-Lymphocytes/cytology ; Transcription, Genetic ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2002-10-05
    Description: 53BP1 binds to the tumor suppressor protein p53 and has a potential role in DNA damage responses. We used small interfering RNA (siRNA) directed against 53BP1 in mammalian cells to demonstrate that 53BP1 is a key transducer of the DNA damage checkpoint signal. 53BP1 was required for p53 accumulation, G2-M checkpoint arrest, and the intra-S-phase checkpoint in response to ionizing radiation. 53BP1 played a partially redundant role in phosphorylation of the downstream checkpoint effector proteins Brca1 and Chk2 but was required for the formation of Brca1 foci in a hierarchical branched pathway for the recruitment of repair and signaling proteins to sites of DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Bin -- Matsuoka, Shuhei -- Carpenter, Phillip B -- Elledge, Stephen J -- New York, N.Y. -- Science. 2002 Nov 15;298(5597):1435-8. Epub 2002 Oct 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Verna and Mars McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12364621" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/metabolism ; Carrier Proteins/genetics/*metabolism ; Cell Cycle Proteins/metabolism ; Checkpoint Kinase 2 ; DNA/biosynthesis ; *DNA Damage ; *G2 Phase ; Histones/metabolism ; Humans ; *Intracellular Signaling Peptides and Proteins ; *Mitosis ; Nuclear Proteins/metabolism ; *Phosphoproteins ; Phosphorylation ; Protein Kinases/metabolism ; *Protein-Serine-Threonine Kinases ; RNA, Small Interfering ; Radiation, Ionizing ; *S Phase ; Signal Transduction ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2008-05-13
    Description: The existence of a small population of 'cancer-initiating cells' responsible for tumour maintenance has been firmly demonstrated in leukaemia. This concept is currently being tested in solid tumours. Leukaemia-initiating cells, particularly those that are in a quiescent state, are thought to be resistant to chemotherapy and targeted therapies, resulting in disease relapse. Chronic myeloid leukaemia is a paradigmatic haematopoietic stem cell disease in which the leukaemia-initiating-cell pool is not eradicated by current therapy, leading to disease relapse on drug discontinuation. Here we define the critical role of the promyelocytic leukaemia protein (PML) tumour suppressor in haematopoietic stem cell maintenance, and present a new therapeutic approach for targeting quiescent leukaemia-initiating cells and possibly cancer-initiating cells by pharmacological inhibition of PML.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712082/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712082/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Keisuke -- Bernardi, Rosa -- Morotti, Alessandro -- Matsuoka, Sahoko -- Saglio, Giuseppe -- Ikeda, Yasuo -- Rosenblatt, Jacalyn -- Avigan, David E -- Teruya-Feldstein, Julie -- Pandolfi, Pier Paolo -- K99 CA139009/CA/NCI NIH HHS/ -- R00 CA139009/CA/NCI NIH HHS/ -- R37 CA071692/CA/NCI NIH HHS/ -- R37 CA071692-12/CA/NCI NIH HHS/ -- England -- Nature. 2008 Jun 19;453(7198):1072-8. doi: 10.1038/nature07016. Epub 2008 May 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genetics Program, Beth Israel Deaconess Cancer Center, Department of Medicine, Harvard Medical School, New Research Building, 330 Brookline Avenue, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18469801" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Arsenicals/pharmacology/therapeutic use ; Cell Line ; Coculture Techniques ; Female ; Gene Expression Regulation, Neoplastic ; Hematopoietic Stem Cells/pathology ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism/*pathology ; Male ; Mice ; Mice, Inbred C57BL ; Neoplastic Stem Cells/metabolism/*pathology ; Nuclear Proteins/antagonists & inhibitors/deficiency/genetics/*metabolism ; Oxides/pharmacology/therapeutic use ; Recurrence ; Regeneration ; Transcription Factors/antagonists & inhibitors/deficiency/genetics/*metabolism ; Tumor Suppressor Proteins/antagonists & ; inhibitors/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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