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  • Female  (10)
  • Electronic structure and strongly correlated systems
  • 2015-2019  (9)
  • 2010-2014  (8)
  • 1
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    Spin-liquid ground state in the frustrated J_{1} −J_{2} zigzag chain system BaTb_{2} O_{4} (2015)
    American Physical Society (APS)
    Details
    Publication Date: 2015-07-14
    Description: Author(s): A. A. Aczel, L. Li, V. O. Garlea, J.-Q. Yan, F. Weickert, V. S. Zapf, R. Movshovich, M. Jaime, P. J. Baker, V. Keppens, and D. Mandrus We have investigated polycrystalline samples of the zigzag chain system BaTb 2 O 4 with magnetic susceptibility, heat capacity, neutron powder diffraction, and muon spin relaxation ( μ SR ) . No magnetic transitions are observed in the bulk measurements, while neutron diffraction reveals the presence of lo… [Phys. Rev. B 92, 041110(R)] Published Mon Jul 13, 2015
    Keywords: Electronic structure and strongly correlated systems
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 2
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    Fluid interactions with metafilms/metasurfaces for tuning, sensing, and microwave-assisted chemical processes (2011)
    American Physical Society (APS)
    Details
    Publication Date: 2011-05-26
    Description: Author(s): Joshua A. Gordon, Christopher L. Holloway, James Booth, Sung Kim, Yu Wang, James Baker-Jarvis, and David R. Novotny In this paper we demonstrate tunability of a metasurface, which is the two-dimensional equivalent of a metamaterial, also referred to as a metafilm, by changing the permittivity in a continuous flow channel that interacts with the metasurface. Numerical simulations and experimental results are prese... [Phys. Rev. B 83, 205130] Published Wed May 25, 2011
    Keywords: Electronic structure and strongly correlated systems
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 3
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    One-dimensional mimicking of electronic structure: The case for exponentials (2015)
    American Physical Society (APS)
    Details
    Publication Date: 2015-06-27
    Description: Author(s): Thomas E. Baker, E. Miles Stoudenmire, Lucas O. Wagner, Kieron Burke, and Steven R. White An exponential interaction is constructed so that one-dimensional atoms and chains of atoms mimic the general behavior of their three-dimensional counterparts. Relative to the more commonly used soft-Coulomb interaction, the exponential greatly diminishes the computational time needed for calculatin… [Phys. Rev. B 91, 235141] Published Wed Jun 24, 2015
    Keywords: Electronic structure and strongly correlated systems
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 4
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    Tumour angiogenesis is reduced in the Tc1 mouse model of Down's syndrome (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-06-11
    Description: Down's syndrome (DS) is a genetic disorder caused by full or partial trisomy of human chromosome 21 and presents with many clinical phenotypes including a reduced incidence of solid tumours. Recent work with the Ts65Dn model of DS, which has orthologues of about 50% of the genes on chromosome 21 (Hsa21), has indicated that three copies of the ETS2 (ref. 3) or DS candidate region 1 (DSCR1) genes (a previously known suppressor of angiogenesis) is sufficient to inhibit tumour growth. Here we use the Tc1 transchromosomic mouse model of DS to dissect the contribution of extra copies of genes on Hsa21 to tumour angiogenesis. This mouse expresses roughly 81% of Hsa21 genes but not the human DSCR1 region. We transplanted B16F0 and Lewis lung carcinoma tumour cells into Tc1 mice and showed that growth of these tumours was substantially reduced compared with wild-type littermate controls. Furthermore, tumour angiogenesis was significantly repressed in Tc1 mice. In particular, in vitro and in vivo angiogenic responses to vascular endothelial growth factor (VEGF) were inhibited. Examination of the genes on the segment of Hsa21 in Tc1 mice identified putative anti-angiogenic genes (ADAMTS1and ERG) and novel endothelial cell-specific genes, never previously shown to be involved in angiogenesis (JAM-B and PTTG1IP), that, when overexpressed, are responsible for inhibiting angiogenic responses to VEGF. Three copies of these genes within the stromal compartment reduced tumour angiogenesis, explaining the reduced tumour growth in DS. Furthermore, we expect that, in addition to the candidate genes that we show to be involved in the repression of angiogenesis, the Tc1 mouse model of DS will permit the identification of other endothelium-specific anti-angiogenic targets relevant to a broad spectrum of cancer patients.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3479956/" 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/PMC3479956/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, Louise E -- Watson, Alan R -- Baker, Marianne -- Jones, Tania A -- D'Amico, Gabriela -- Robinson, Stephen D -- Joffre, Carine -- Garrido-Urbani, Sarah -- Rodriguez-Manzaneque, Juan Carlos -- Martino-Echarri, Estefania -- Aurrand-Lions, Michel -- Sheer, Denise -- Dagna-Bricarelli, Franca -- Nizetic, Dean -- McCabe, Christopher J -- Turnell, Andrew S -- Kermorgant, Stephanie -- Imhof, Beat A -- Adams, Ralf -- Fisher, Elizabeth M C -- Tybulewicz, Victor L J -- Hart, Ian R -- Hodivala-Dilke, Kairbaan M -- 080174/Wellcome Trust/United Kingdom -- 12007/Cancer Research UK/United Kingdom -- A12007/Cancer Research UK/United Kingdom -- A3585/Cancer Research UK/United Kingdom -- G0501003/Medical Research Council/United Kingdom -- G0501003(75694)/Medical Research Council/United Kingdom -- G0601056/Medical Research Council/United Kingdom -- G0901609/Medical Research Council/United Kingdom -- MC_U117527252/Medical Research Council/United Kingdom -- U.1175.02.001.00001(60485)/Medical Research Council/United Kingdom -- England -- Nature. 2010 Jun 10;465(7299):813-7. doi: 10.1038/nature09106.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Adhesion and Angiogenesis Laboratory, Barts Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK. l.reynolds@qmul.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20535211" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/genetics/metabolism ; Animals ; Carcinoma, Lewis Lung/*blood supply/complications/genetics/pathology ; Carrier Proteins/genetics/metabolism ; Cell Adhesion Molecules/antagonists & inhibitors/genetics/metabolism ; Chromosomes, Mammalian/genetics ; *Disease Models, Animal ; Down Syndrome/complications/*genetics/physiopathology ; Female ; Gene Dosage/*genetics ; Humans ; Immunoglobulins/genetics/metabolism ; Male ; Melanoma, Experimental/*blood supply/complications/genetics/pathology ; Mice ; Neoplasm Transplantation ; Neovascularization, Pathologic/*genetics/pathology ; Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Protein c-ets-2/genetics/metabolism ; Transcription Factors ; Trisomy/genetics ; Vascular Endothelial Growth Factor A/antagonists & ; inhibitors/metabolism/pharmacology ; Vascular Endothelial Growth Factor Receptor-2/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-11-04
    Description: Advanced age is the main risk factor for most chronic diseases and functional deficits in humans, but the fundamental mechanisms that drive ageing remain largely unknown, impeding the development of interventions that might delay or prevent age-related disorders and maximize healthy lifespan. Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells. Senescent cells accumulate in various tissues and organs with ageing and have been hypothesized to disrupt tissue structure and function because of the components they secrete. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16(Ink4a), to design a novel transgene, INK-ATTAC, for inducible elimination of p16(Ink4a)-positive senescent cells upon administration of a drug. Here we show that in the BubR1 progeroid mouse background, INK-ATTAC removes p16(Ink4a)-positive senescent cells upon drug treatment. In tissues--such as adipose tissue, skeletal muscle and eye--in which p16(Ink4a) contributes to the acquisition of age-related pathologies, life-long removal of p16(Ink4a)-expressing cells delayed onset of these phenotypes. Furthermore, late-life clearance attenuated progression of already established age-related disorders. These data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468323/" 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/PMC3468323/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, Darren J -- Wijshake, Tobias -- Tchkonia, Tamar -- LeBrasseur, Nathan K -- Childs, Bennett G -- van de Sluis, Bart -- Kirkland, James L -- van Deursen, Jan M -- AG13925/AG/NIA NIH HHS/ -- CA96985/CA/NCI NIH HHS/ -- P30 DK050456/DK/NIDDK NIH HHS/ -- R01 AG013925/AG/NIA NIH HHS/ -- R01 AG013925-14/AG/NIA NIH HHS/ -- R01 CA096985/CA/NCI NIH HHS/ -- R01 CA096985-10/CA/NCI NIH HHS/ -- England -- Nature. 2011 Nov 2;479(7372):232-6. doi: 10.1038/nature10600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric and Adolescent Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22048312" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/cytology/drug effects/pathology ; Aging/drug effects/*physiology ; Animals ; Bone Marrow Cells/cytology/drug effects ; Cell Aging/drug effects/*physiology ; Cell Count ; Cell Cycle Proteins ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/*metabolism ; Eye/cytology/drug effects/pathology ; Female ; Gene Expression ; Genotype ; Longevity/drug effects/physiology ; Male ; Mice ; Mice, Transgenic ; Muscle, Skeletal/cytology/drug effects/pathology ; Phenotype ; Progeria/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Tacrolimus/analogs & derivatives/pharmacology ; Time Factors ; Weaning
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  • 6
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    A synthetic homing endonuclease-based gene drive system in the human malaria mosquito (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-04-22
    Description: Genetic methods of manipulating or eradicating disease vector populations have long been discussed as an attractive alternative to existing control measures because of their potential advantages in terms of effectiveness and species specificity. The development of genetically engineered malaria-resistant mosquitoes has shown, as a proof of principle, the possibility of targeting the mosquito's ability to serve as a disease vector. The translation of these achievements into control measures requires an effective technology to spread a genetic modification from laboratory mosquitoes to field populations. We have suggested previously that homing endonuclease genes (HEGs), a class of simple selfish genetic elements, could be exploited for this purpose. Here we demonstrate that a synthetic genetic element, consisting of mosquito regulatory regions and the homing endonuclease gene I-SceI, can substantially increase its transmission to the progeny in transgenic mosquitoes of the human malaria vector Anopheles gambiae. We show that the I-SceI element is able to invade receptive mosquito cage populations rapidly, validating mathematical models for the transmission dynamics of HEGs. Molecular analyses confirm that expression of I-SceI in the male germline induces high rates of site-specific chromosomal cleavage and gene conversion, which results in the gain of the I-SceI gene, and underlies the observed genetic drive. These findings demonstrate a new mechanism by which genetic control measures can be implemented. Our results also show in principle how sequence-specific genetic drive elements like HEGs could be used to take the step from the genetic engineering of individuals to the genetic engineering of populations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093433/" 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/PMC3093433/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Windbichler, Nikolai -- Menichelli, Miriam -- Papathanos, Philippos Aris -- Thyme, Summer B -- Li, Hui -- Ulge, Umut Y -- Hovde, Blake T -- Baker, David -- Monnat, Raymond J Jr -- Burt, Austin -- Crisanti, Andrea -- CA133831/CA/NCI NIH HHS/ -- RL1 CA133831/CA/NCI NIH HHS/ -- RL1 CA133831-01/CA/NCI NIH HHS/ -- RL1 CA133831-02/CA/NCI NIH HHS/ -- RL1 CA133831-03/CA/NCI NIH HHS/ -- RL1 CA133831-04/CA/NCI NIH HHS/ -- RL1 CA133831-05/CA/NCI NIH HHS/ -- RL1 GM084433/GM/NIGMS NIH HHS/ -- RL1 GM084433-01/GM/NIGMS NIH HHS/ -- RL1 GM084433-02/GM/NIGMS NIH HHS/ -- RL1 GM084433-03/GM/NIGMS NIH HHS/ -- RL1 GM084433-04/GM/NIGMS NIH HHS/ -- RL1 GM084433-05/GM/NIGMS NIH HHS/ -- T32 CA080416/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 May 12;473(7346):212-5. doi: 10.1038/nature09937. Epub 2011 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Imperial College London, Department of Life Sciences, South Kensington Campus, London, SW7 2AZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21508956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Anopheles gambiae/*genetics ; Deoxyribonucleases, Type II Site-Specific/genetics ; Female ; Genes, Reporter/genetics ; *Genetic Engineering ; Genotype ; Insect Vectors/*genetics ; Male ; Molecular Sequence Data ; Mosquito Control/*methods ; Saccharomyces cerevisiae Proteins/genetics
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  • 7
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    Protective mucosal immunity mediated by epithelial CD1d and IL-10 (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-04-11
    Description: The mechanisms by which mucosal homeostasis is maintained are of central importance to inflammatory bowel disease. Critical to these processes is the intestinal epithelial cell (IEC), which regulates immune responses at the interface between the commensal microbiota and the host. CD1d presents self and microbial lipid antigens to natural killer T (NKT) cells, which are involved in the pathogenesis of colitis in animal models and human inflammatory bowel disease. As CD1d crosslinking on model IECs results in the production of the important regulatory cytokine interleukin (IL)-10 (ref. 9), decreased epithelial CD1d expression--as observed in inflammatory bowel disease--may contribute substantially to intestinal inflammation. Here we show in mice that whereas bone-marrow-derived CD1d signals contribute to NKT-cell-mediated intestinal inflammation, engagement of epithelial CD1d elicits protective effects through the activation of STAT3 and STAT3-dependent transcription of IL-10, heat shock protein 110 (HSP110; also known as HSP105), and CD1d itself. All of these epithelial elements are critically involved in controlling CD1d-mediated intestinal inflammation. This is demonstrated by severe NKT-cell-mediated colitis upon IEC-specific deletion of IL-10, CD1d, and its critical regulator microsomal triglyceride transfer protein (MTP), as well as deletion of HSP110 in the radioresistant compartment. Our studies thus uncover a novel pathway of IEC-dependent regulation of mucosal homeostasis and highlight a critical role of IL-10 in the intestinal epithelium, with broad implications for diseases such as inflammatory bowel disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4132962/" 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/PMC4132962/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olszak, Torsten -- Neves, Joana F -- Dowds, C Marie -- Baker, Kristi -- Glickman, Jonathan -- Davidson, Nicholas O -- Lin, Chyuan-Sheng -- Jobin, Christian -- Brand, Stephan -- Sotlar, Karl -- Wada, Koichiro -- Katayama, Kazufumi -- Nakajima, Atsushi -- Mizuguchi, Hiroyuki -- Kawasaki, Kunito -- Nagata, Kazuhiro -- Muller, Werner -- Snapper, Scott B -- Schreiber, Stefan -- Kaser, Arthur -- Zeissig, Sebastian -- Blumberg, Richard S -- 260961/European Research Council/International -- AI50950/AI/NIAID NIH HHS/ -- DK0034854/DK/NIDDK NIH HHS/ -- DK034854/DK/NIDDK NIH HHS/ -- DK044319/DK/NIDDK NIH HHS/ -- DK051362/DK/NIDDK NIH HHS/ -- DK053056/DK/NIDDK NIH HHS/ -- DK088199/DK/NIDDK NIH HHS/ -- DK56260/DK/NIDDK NIH HHS/ -- HL38180/HL/NHLBI NIH HHS/ -- HL59561/HL/NHLBI NIH HHS/ -- P30 DK034854/DK/NIDDK NIH HHS/ -- P30 DK052574/DK/NIDDK NIH HHS/ -- P30CA013696/CA/NCI NIH HHS/ -- P30DK52574/DK/NIDDK NIH HHS/ -- R01 DK044319/DK/NIDDK NIH HHS/ -- England -- Nature. 2014 May 22;509(7501):497-502. doi: 10.1038/nature13150. Epub 2014 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Division of Gastroenterology, Hepatology, and Endoscopy, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA [2]. ; 1] Department of Internal Medicine I, University Medical Center Schleswig-Holstein, 24105 Kiel, Germany [2]. ; Division of Gastroenterology, Hepatology, and Endoscopy, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. ; GI Pathology, Miraca Life Sciences, Newton, Massachusetts 02464, USA. ; Division of Gastroenterology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York 10032, USA. ; Department of Medicine, Department of Infectious Diseases & Pathology, University of Florida, Gainesville, Florida 32611, USA. ; Department of Medicine II-Grosshadern, Ludwig Maximilians University, Munich 81377, Germany. ; Institute of Pathology, Ludwig Maximilians University, Munich 80337, Germany. ; Department of Pharmacology, Graduate School of Dentistry, Osaka University, Osaka 565-0871, Japan. ; Gastroenterology Division, Yokohama City University School of Medicine, Yokohama, Kanagawa 236-0027, Japan. ; Laboratory of Biochemistry and Molecular Biology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka 565-0871, Japan. ; Department of Molecular Biosciences, Faculty of Life Sciences, Kyoto Sangyo University, Motoyama, Kamigamo, Kita-ku, Kyoto 603-8555, Japan. ; Faculty of Life Sciences, University of Manchester, Manchester M13 9PL, UK. ; 1] Division of Gastroenterology, Hepatology, and Endoscopy, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Children's Hospital Boston, Boston, Massachusetts 02115, USA. ; Department of Internal Medicine I, University Medical Center Schleswig-Holstein, 24105 Kiel, Germany. ; Division of Gastroenterology, Addenbrooke Hospital, University of Cambridge, Cambridge CB2 0QQ, UK. ; 1] Division of Gastroenterology, Hepatology, and Endoscopy, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Department of Internal Medicine I, University Medical Center Schleswig-Holstein, 24105 Kiel, Germany [3].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24717441" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD1d/*immunology ; Carrier Proteins/metabolism ; Colitis/immunology/pathology ; Disease Models, Animal ; Epithelial Cells/*immunology/metabolism ; Female ; HSP110 Heat-Shock Proteins/genetics/metabolism ; Humans ; Immunity, Mucosal/*immunology ; Inflammation/immunology/pathology ; Inflammatory Bowel Diseases/immunology/pathology ; Interleukin-10/genetics/*immunology ; Intestinal Mucosa/*cytology/*immunology ; Male ; Mice ; Natural Killer T-Cells/immunology/metabolism ; Oxazolone ; STAT3 Transcription Factor/metabolism
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  • 8
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    Distinct physiological and behavioural functions for parental alleles of imprinted Grb10 (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-01-29
    Description: Imprinted genes, defined by their preferential expression of a single parental allele, represent a subset of the mammalian genome and often have key roles in embryonic development, but also postnatal functions including energy homeostasis and behaviour. When the two parental alleles are unequally represented within a social group (when there is sex bias in dispersal and/or variance in reproductive success), imprinted genes may evolve to modulate social behaviour, although so far no such instance is known. Predominantly expressed from the maternal allele during embryogenesis, Grb10 encodes an intracellular adaptor protein that can interact with several receptor tyrosine kinases and downstream signalling molecules. Here we demonstrate that within the brain Grb10 is expressed from the paternal allele from fetal life into adulthood and that ablation of this expression engenders increased social dominance specifically among other aspects of social behaviour, a finding supported by the observed increase in allogrooming by paternal Grb10-deficient animals. Grb10 is, therefore, the first example of an imprinted gene that regulates social behaviour. It is also currently alone in exhibiting imprinted expression from each of the parental alleles in a tissue-specific manner, as loss of the peripherally expressed maternal allele leads to significant fetal and placental overgrowth. Thus Grb10 is, so far, a unique imprinted gene, able to influence distinct physiological processes, fetal growth and adult behaviour, owing to actions of the two parental alleles in different tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031026/" 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/PMC3031026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garfield, Alastair S -- Cowley, Michael -- Smith, Florentia M -- Moorwood, Kim -- Stewart-Cox, Joanne E -- Gilroy, Kerry -- Baker, Sian -- Xia, Jing -- Dalley, Jeffrey W -- Hurst, Laurence D -- Wilkinson, Lawrence S -- Isles, Anthony R -- Ward, Andrew -- 093875/Wellcome Trust/United Kingdom -- G0300415/Medical Research Council/United Kingdom -- G0300415(66812)/Medical Research Council/United Kingdom -- G11786/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2011 Jan 27;469(7331):534-8. doi: 10.1038/nature09651.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology & Biochemistry and Centre for Regenerative Medicine, University of Bath, Claverton Down, Bath BA2 7AY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21270893" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Behavior, Animal/*physiology ; Central Nervous System/embryology ; Female ; GRB10 Adaptor Protein/*genetics/*metabolism ; Gene Expression Regulation, Developmental ; Genomic Imprinting/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Social Dominance
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  • 9
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    Electronic and magnetic properties of the candidate magnetocaloric-material double perovskites ${\mathrm{La}}_{2}{\mathrm{MnCoO}}_{6}$, ${\mathrm{La}}_{2}{\mathrm{MnNiO}}_{6}$, and ${\mathrm{La}}_{2}{\mathrm{MnFeO}}_{6}$ (2018)
    American Physical Society (APS)
    Details
    Publication Date: 2018-09-18
    Description: Author(s): C. Gauvin-Ndiaye, T. E. Baker, P. Karan, É. Massé, M. Balli, N. Brahiti, M. A. Eskandari, P. Fournier, A.-M. S. Tremblay, and R. Nourafkan The search for room-temperature magnetocaloric materials for refrigeration has led to investigations of double perovskites. In particular, a puzzle has appeared in the La 2 MnNiO 6 , La 2 MnCoO 6 , and La 2 MnFeO 6 family of compounds. They share the same crystal structure, but while La 2 MnNiO 6 and La 2 MnCoO 6 ar... [Phys. Rev. B 98, 125132] Published Mon Sep 17, 2018
    Keywords: Electronic structure and strongly correlated systems
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  • 10
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    Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice (2016)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2016-01-20
    Description: Mitochondrial morphology is shaped by fusion and division of their membranes. Here, we found that adult myocardial function depends on balanced mitochondrial fusion and fission, maintained by processing of the dynamin-like guanosine triphosphatase OPA1 by the mitochondrial peptidases YME1L and OMA1. Cardiac-specific ablation of Yme1l in mice activated OMA1 and accelerated OPA1 proteolysis, which triggered mitochondrial fragmentation and altered cardiac metabolism. This caused dilated cardiomyopathy and heart failure. Cardiac function and mitochondrial morphology were rescued by Oma1 deletion, which prevented OPA1 cleavage. Feeding mice a high-fat diet or ablating Yme1l in skeletal muscle restored cardiac metabolism and preserved heart function without suppressing mitochondrial fragmentation. Thus, unprocessed OPA1 is sufficient to maintain heart function, OMA1 is a critical regulator of cardiomyocyte survival, and mitochondrial morphology and cardiac metabolism are intimately linked.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wai, Timothy -- Garcia-Prieto, Jaime -- Baker, Michael J -- Merkwirth, Carsten -- Benit, Paule -- Rustin, Pierre -- Ruperez, Francisco Javier -- Barbas, Coral -- Ibanez, Borja -- Langer, Thomas -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):aad0116. doi: 10.1126/science.aad0116.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, 50674 Cologne, Germany. Max-Planck-Institute for Biology of Aging, Cologne, Germany. ; Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain. ; Institute for Genetics, University of Cologne, 50674 Cologne, Germany. ; INSERM UMR 1141, Hopital Robert Debre, Paris, France. Universite Paris 7, Faculte de Medecine Denis Diderot, Paris, France. ; Centre for Metabolomics and Bioanalysis (CEMBIO), Faculty of Pharmacy, Universidad San Pablo CEU, Campus Monteprincipe, Boadilla del Monte, 28668 Madrid, Spain. ; Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain. Department of Cardiology, Instituto de Investigacion Sanitaria (IIS), Fundacion Jimenez Diaz Hospital, Madrid, Spain. thomas.langer@uni-koeln.de bibanez@cnic.es. ; Institute for Genetics, University of Cologne, 50674 Cologne, Germany. Max-Planck-Institute for Biology of Aging, Cologne, Germany. Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany. Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany. thomas.langer@uni-koeln.de bibanez@cnic.es.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785494" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomyopathy, Dilated/genetics/metabolism/pathology ; Diet, High-Fat ; Embryonic Development ; Female ; GTP Phosphohydrolases ; Gene Deletion ; Heart/embryology ; Heart Failure/genetics/*metabolism/pathology ; Male ; Metalloendopeptidases/genetics ; Metalloproteases/genetics/metabolism ; Mice ; Mice, Knockout ; Mitochondria, Heart/*metabolism/ultrastructure ; *Mitochondrial Degradation ; *Mitochondrial Dynamics ; Mitochondrial Proteins/genetics/metabolism ; Muscle, Skeletal/enzymology ; Myocardium/*metabolism/pathology ; Myocytes, Cardiac/enzymology/pathology ; Proteolysis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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