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  • 1
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    Tbx3 improves the germ-line competency of induced pluripotent stem cells (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-02-09
    Description: Induced pluripotent stem (iPS) cells can be obtained by the introduction of defined factors into somatic cells. The combination of Oct4 (also known as Pou5f1), Sox2 and Klf4 (which we term OSK) constitutes the minimal requirement for generating iPS cells from mouse embryonic fibroblasts. These cells are thought to resemble embryonic stem cells (ESCs) on the basis of global gene expression analyses; however, few studies have tested the ability and efficiency of iPS cells to contribute to chimaerism, colonization of germ tissues, and most importantly, germ-line transmission and live birth from iPS cells produced by tetraploid complementation. Using genomic analyses of ESC genes that have roles in pluripotency and fusion-mediated somatic cell reprogramming, here we show that the transcription factor Tbx3 significantly improves the quality of iPS cells. iPS cells generated with OSK and Tbx3 (OSKT) are superior in both germ-cell contribution to the gonads and germ-line transmission frequency. However, global gene expression profiling could not distinguish between OSK and OSKT iPS cells. Genome-wide chromatin immunoprecipitation sequencing analysis of Tbx3-binding sites in ESCs suggests that Tbx3 regulates pluripotency-associated and reprogramming factors, in addition to sharing many common downstream regulatory targets with Oct4, Sox2, Nanog and Smad1. This study underscores the intrinsic qualitative differences between iPS cells generated by different methods, and highlights the need to rigorously characterize iPS cells beyond in vitro studies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2901797/" 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/PMC2901797/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Jianyong -- Yuan, Ping -- Yang, Henry -- Zhang, Jinqiu -- Soh, Boon Seng -- Li, Pin -- Lim, Siew Lan -- Cao, Suying -- Tay, Junliang -- Orlov, Yuriy L -- Lufkin, Thomas -- Ng, Huck-Hui -- Tam, Wai-Leong -- Lim, Bing -- AI54973/AI/NIAID NIH HHS/ -- DK047636/DK/NIDDK NIH HHS/ -- R01 AI054973-05/AI/NIAID NIH HHS/ -- R01 DK047636-08/DK/NIDDK NIH HHS/ -- England -- Nature. 2010 Feb 25;463(7284):1096-100. doi: 10.1038/nature08735. Epub 2010 Feb 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell and Developmental Biology, Genome Institute of Singapore, 138672, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20139965" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Fusion ; Cellular Reprogramming ; Chimera/embryology/*metabolism ; Chromatin Immunoprecipitation ; Embryo, Mammalian/cytology ; Female ; Fibroblasts/cytology/metabolism ; Gene Expression Profiling ; Gene Expression Regulation/genetics ; Germ Cells/*cytology/*metabolism ; Gonads/*cytology ; Homeodomain Proteins/metabolism ; Induced Pluripotent Stem Cells/*cytology/*metabolism ; Kruppel-Like Transcription Factors/genetics/metabolism ; Male ; Mice ; Mice, Transgenic ; Octamer Transcription Factor-3/genetics/metabolism ; Regulatory Sequences, Nucleic Acid ; SOXB1 Transcription Factors/genetics/metabolism ; Smad1 Protein/metabolism ; T-Box Domain Proteins/genetics/*metabolism ; Transcription, Genetic/genetics ; Transduction, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Targeting Plasmodium PI(4)K to eliminate malaria (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-11-29
    Description: Achieving the goal of malaria elimination will depend on targeting Plasmodium pathways essential across all life stages. Here we identify a lipid kinase, phosphatidylinositol-4-OH kinase (PI(4)K), as the target of imidazopyrazines, a new antimalarial compound class that inhibits the intracellular development of multiple Plasmodium species at each stage of infection in the vertebrate host. Imidazopyrazines demonstrate potent preventive, therapeutic, and transmission-blocking activity in rodent malaria models, are active against blood-stage field isolates of the major human pathogens P. falciparum and P. vivax, and inhibit liver-stage hypnozoites in the simian parasite P. cynomolgi. We show that imidazopyrazines exert their effect through inhibitory interaction with the ATP-binding pocket of PI(4)K, altering the intracellular distribution of phosphatidylinositol-4-phosphate. Collectively, our data define PI(4)K as a key Plasmodium vulnerability, opening up new avenues of target-based discovery to identify drugs with an ideal activity profile for the prevention, treatment and elimination of malaria.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3940870/" 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/PMC3940870/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNamara, Case W -- Lee, Marcus C S -- Lim, Chek Shik -- Lim, Siau Hoi -- Roland, Jason -- Nagle, Advait -- Simon, Oliver -- Yeung, Bryan K S -- Chatterjee, Arnab K -- McCormack, Susan L -- Manary, Micah J -- Zeeman, Anne-Marie -- Dechering, Koen J -- Kumar, T R Santha -- Henrich, Philipp P -- Gagaring, Kerstin -- Ibanez, Maureen -- Kato, Nobutaka -- Kuhen, Kelli L -- Fischli, Christoph -- Rottmann, Matthias -- Plouffe, David M -- Bursulaya, Badry -- Meister, Stephan -- Rameh, Lucia -- Trappe, Joerg -- Haasen, Dorothea -- Timmerman, Martijn -- Sauerwein, Robert W -- Suwanarusk, Rossarin -- Russell, Bruce -- Renia, Laurent -- Nosten, Francois -- Tully, David C -- Kocken, Clemens H M -- Glynne, Richard J -- Bodenreider, Christophe -- Fidock, David A -- Diagana, Thierry T -- Winzeler, Elizabeth A -- 078285/Wellcome Trust/United Kingdom -- 089275/Wellcome Trust/United Kingdom -- 090534/Wellcome Trust/United Kingdom -- 096157/Wellcome Trust/United Kingdom -- R01 AI079709/AI/NIAID NIH HHS/ -- R01 AI085584/AI/NIAID NIH HHS/ -- R01 AI090141/AI/NIAID NIH HHS/ -- R01 AI103058/AI/NIAID NIH HHS/ -- R01079709/PHS HHS/ -- R01085584/PHS HHS/ -- R01AI090141/AI/NIAID NIH HHS/ -- WT078285/Wellcome Trust/United Kingdom -- WT096157/Wellcome Trust/United Kingdom -- England -- Nature. 2013 Dec 12;504(7479):248-53. doi: 10.1038/nature12782. Epub 2013 Nov 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Genomics Institute of the Novartis Research Foundation, San Diego, California 92121, USA [2]. ; 1] Department of Microbiology & Immunology, Columbia University Medical Center, New York, New York 10032, USA [2]. ; Novartis Institutes for Tropical Disease, 138670 Singapore. ; Genomics Institute of the Novartis Research Foundation, San Diego, California 92121, USA. ; Department of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, California 92093, USA. ; Department of Parasitology, Biomedical Primate Research Centre, PO Box 3306, 2280 GH Rijswijk, The Netherlands. ; TropIQ Health Sciences, 6525 GA Nijmegen, The Netherlands. ; Department of Microbiology & Immunology, Columbia University Medical Center, New York, New York 10032, USA. ; Swiss Tropical and Public Health Institute, CH-4002 Basel, Switzerland. ; 1] Swiss Tropical and Public Health Institute, CH-4002 Basel, Switzerland [2] University of Basel, CH-4003 Basel, Switzerland. ; Department of Medicine, School of Medicine, Boston University, Boston, Massachusetts 02118, USA. ; Novartis Institutes for BioMedical Research, CH-4002 Basel, Switzerland. ; 1] TropIQ Health Sciences, 6525 GA Nijmegen, The Netherlands [2] Department of Medical Microbiology, Radboud University, Nijmegen Medical CentrePO Box 9101, 6500 HB Nijmegen, The Netherlands. ; Laboratory of Malaria Immunobiology, Singapore Immunology Network, Agency for Science Technology and Research (A*STAR), Biopolis, 138648 Singapore. ; 1] Laboratory of Malaria Immunobiology, Singapore Immunology Network, Agency for Science Technology and Research (A*STAR), Biopolis, 138648 Singapore [2] Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, National University Health System, 117545 Singapore. ; 1] Centre for Tropical Medicine, Nuffield Department of Medicine, University of Oxford, Oxford OX3 7BN, UK [2] Shoklo Malaria Research Unit, Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Mae Sot 63110, Thailand. ; 1] Department of Microbiology & Immunology, Columbia University Medical Center, New York, New York 10032, USA [2] Division of Infectious Diseases, Department of Medicine, Columbia University Medical Center, New York, New York 10032, USA. ; 1] Genomics Institute of the Novartis Research Foundation, San Diego, California 92121, USA [2] Department of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24284631" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Phosphatidylinositol 4-Kinase/*antagonists & ; inhibitors/chemistry/genetics/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; Cytokinesis/drug effects ; Drug Resistance/drug effects/genetics ; Fatty Acids/metabolism ; Female ; Hepatocytes/parasitology ; Humans ; Imidazoles/metabolism/pharmacology ; Life Cycle Stages/drug effects ; Macaca mulatta ; Malaria/*drug therapy/*parasitology ; Male ; Models, Biological ; Models, Molecular ; Phosphatidylinositol Phosphates/metabolism ; Plasmodium/classification/*drug effects/*enzymology/growth & development ; Pyrazoles/metabolism/pharmacology ; Quinoxalines/metabolism/pharmacology ; Reproducibility of Results ; Schizonts/cytology/drug effects ; rab GTP-Binding Proteins/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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  • 3
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    Control of autoimmune diabetes in NOD mice by GAD expression or suppression in beta cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: Glutamic acid decarboxylase (GAD) is a pancreatic beta cell autoantigen in humans and nonobese diabetic (NOD) mice. beta Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the beta cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of beta cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, beta cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoon, J W -- Yoon, C S -- Lim, H W -- Huang, Q Q -- Kang, Y -- Pyun, K H -- Hirasawa, K -- Sherwin, R S -- Jun, H S -- DK 45735/DK/NIDDK NIH HHS/ -- DK 53015-01/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 14;284(5417):1183-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral and Immunopathogenesis of Diabetes, Julia McFarlane Diabetes Research Centre, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada. yoon@ucalgary.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325232" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Autoantigens/genetics/*immunology/physiology ; Autoimmunity ; DNA, Antisense ; Diabetes Mellitus, Type 1/*enzymology/*immunology/pathology ; Female ; Gene Expression ; Glutamate Decarboxylase/genetics/*immunology/physiology ; Insulin/blood/metabolism ; Islets of Langerhans/*enzymology/immunology/metabolism/pathology ; Islets of Langerhans Transplantation ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; T-Lymphocytes/immunology ; Transgenes
    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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  • 4
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    Characterization of an avian influenza A (H5N1) virus isolated from a child with a fatal respiratory illness (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: An avian H5N1 influenza A virus (A/Hong Kong/156/97) was isolated from a tracheal aspirate obtained from a 3-year-old child in Hong Kong with a fatal illness consistent with influenza. Serologic analysis indicated the presence of an H5 hemagglutinin. All eight RNA segments were derived from an avian influenza A virus. The hemagglutinin contained multiple basic amino acids adjacent to the cleavage site, a feature characteristic of highly pathogenic avian influenza A viruses. The virus caused 87.5 to 100 percent mortality in experimentally inoculated White Plymouth Rock and White Leghorn chickens. These results may have implications for global influenza surveillance and planning for pandemic influenza.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Subbarao, K -- Klimov, A -- Katz, J -- Regnery, H -- Lim, W -- Hall, H -- Perdue, M -- Swayne, D -- Bender, C -- Huang, J -- Hemphill, M -- Rowe, T -- Shaw, M -- Xu, X -- Fukuda, K -- Cox, N -- New York, N.Y. -- Science. 1998 Jan 16;279(5349):393-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Influenza Branch, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9430591" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Chickens ; Child, Preschool ; Disease Outbreaks ; Fatal Outcome ; Female ; Genes, Viral ; Hemagglutinin Glycoproteins, Influenza Virus/chemistry/*genetics ; Hong Kong/epidemiology ; Humans ; *Influenza A Virus, H5N1 Subtype ; Influenza A virus/*genetics/isolation & purification/*pathogenicity ; Influenza in Birds/virology ; Influenza, Human/epidemiology/*virology ; Male ; Molecular Sequence Data ; Neuraminidase/genetics ; Phylogeny ; Virulence ; Virus Replication
    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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  • 5
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    CHD1 motor protein is required for deposition of histone variant H3.3 into chromatin in vivo (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-25
    Description: The organization of chromatin affects all aspects of nuclear DNA metabolism in eukaryotes. H3.3 is an evolutionarily conserved histone variant and a key substrate for replication-independent chromatin assembly. Elimination of chromatin remodeling factor CHD1 in Drosophila embryos abolishes incorporation of H3.3 into the male pronucleus, renders the paternal genome unable to participate in zygotic mitoses, and leads to the development of haploid embryos. Furthermore, CHD1, but not ISWI, interacts with HIRA in cytoplasmic extracts. Our findings establish CHD1 as a major factor in replacement histone metabolism in the nucleus and reveal a critical role for CHD1 in the earliest developmental instances of genome-scale, replication-independent nucleosome assembly. Furthermore, our results point to the general requirement of adenosine triphosphate (ATP)-utilizing motor proteins for histone deposition in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014568/" 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/PMC3014568/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Konev, Alexander Y -- Tribus, Martin -- Park, Sung Yeon -- Podhraski, Valerie -- Lim, Chin Yan -- Emelyanov, Alexander V -- Vershilova, Elena -- Pirrotta, Vincenzo -- Kadonaga, James T -- Lusser, Alexandra -- Fyodorov, Dmitry V -- GM58272/GM/NIGMS NIH HHS/ -- GM74233/GM/NIGMS NIH HHS/ -- R01 GM074233/GM/NIGMS NIH HHS/ -- Y 275/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2007 Aug 24;317(5841):1087-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717186" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Cell Cycle Proteins/metabolism ; Chromatin/*metabolism ; *Chromatin Assembly and Disassembly ; DNA-Binding Proteins/genetics/*metabolism ; Drosophila/embryology/genetics/metabolism/*physiology ; Drosophila Proteins/genetics/*metabolism ; Embryo, Nonmammalian/physiology ; Embryonic Development ; Female ; Haploidy ; Histone Chaperones ; Histones/*metabolism ; Male ; Mutation ; Nucleosomes/metabolism ; Protamines/metabolism ; Spermatozoa/physiology ; Transcription Factors/genetics/*metabolism ; Transgenes
    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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  • 6
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    Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-26
    Description: Amyloid-beta (Abeta) accumulation in the brain extracellular space is a hallmark of Alzheimer's disease. The factors regulating this process are only partly understood. Abeta aggregation is a concentration-dependent process that is likely responsive to changes in brain interstitial fluid (ISF) levels of Abeta. Using in vivo microdialysis in mice, we found that the amount of ISF Abeta correlated with wakefulness. The amount of ISF Abeta also significantly increased during acute sleep deprivation and during orexin infusion, but decreased with infusion of a dual orexin receptor antagonist. Chronic sleep restriction significantly increased, and a dual orexin receptor antagonist decreased, Abeta plaque formation in amyloid precursor protein transgenic mice. Thus, the sleep-wake cycle and orexin may play a role in the pathogenesis of Alzheimer's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789838/" 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/PMC2789838/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Jae-Eun -- Lim, Miranda M -- Bateman, Randall J -- Lee, James J -- Smyth, Liam P -- Cirrito, John R -- Fujiki, Nobuhiro -- Nishino, Seiji -- Holtzman, David M -- AG025824/AG/NIA NIH HHS/ -- AG029524/AG/NIA NIH HHS/ -- AG030946/AG/NIA NIH HHS/ -- K01 AG029524/AG/NIA NIH HHS/ -- K01 AG029524-03/AG/NIA NIH HHS/ -- K23 AG030946/AG/NIA NIH HHS/ -- K23 AG030946-03/AG/NIA NIH HHS/ -- MH072525/MH/NIMH NIH HHS/ -- NS065667/NS/NINDS NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30 DK056341-09/DK/NIDDK NIH HHS/ -- P30 NS057105/NS/NINDS NIH HHS/ -- P30 NS057105-04/NS/NINDS NIH HHS/ -- P50 AG005681/AG/NIA NIH HHS/ -- R01 AG025824/AG/NIA NIH HHS/ -- R01 AG025824-03/AG/NIA NIH HHS/ -- R01 MH072525/MH/NIMH NIH HHS/ -- R01 MH072525-04/MH/NIMH NIH HHS/ -- R01 NS065667/NS/NINDS NIH HHS/ -- R01 NS065667-02/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):1005-7. doi: 10.1126/science.1180962. Epub 2009 Sep 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Washington University, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19779148" target="_blank"〉PubMed〈/a〉
    Keywords: Acetamides/pharmacology ; Alzheimer Disease/metabolism/*physiopathology ; Amyloid beta-Peptides/cerebrospinal fluid/*metabolism ; Animals ; Antigens, Surface/metabolism ; Circadian Rhythm ; Disease Models, Animal ; Extracellular Fluid/*metabolism ; Female ; Hippocampus/*metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/administration & dosage/*metabolism ; Isoquinolines/pharmacology ; Light ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuropeptides/administration & dosage/*metabolism ; Orexin Receptors ; Orexins ; Receptors, Cell Surface/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Neuropeptide/metabolism ; Signal Transduction ; *Sleep ; Sleep Deprivation ; *Wakefulness
    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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  • 7
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    Differences between tight and loose cultures: a 33-nation study (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-28
    Description: With data from 33 nations, we illustrate the differences between cultures that are tight (have many strong norms and a low tolerance of deviant behavior) versus loose (have weak social norms and a high tolerance of deviant behavior). Tightness-looseness is part of a complex, loosely integrated multilevel system that comprises distal ecological and historical threats (e.g., high population density, resource scarcity, a history of territorial conflict, and disease and environmental threats), broad versus narrow socialization in societal institutions (e.g., autocracy, media regulations), the strength of everyday recurring situations, and micro-level psychological affordances (e.g., prevention self-guides, high regulatory strength, need for structure). This research advances knowledge that can foster cross-cultural understanding in a world of increasing global interdependence and has implications for modeling cultural change.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gelfand, Michele J -- Raver, Jana L -- Nishii, Lisa -- Leslie, Lisa M -- Lun, Janetta -- Lim, Beng Chong -- Duan, Lili -- Almaliach, Assaf -- Ang, Soon -- Arnadottir, Jakobina -- Aycan, Zeynep -- Boehnke, Klaus -- Boski, Pawel -- Cabecinhas, Rosa -- Chan, Darius -- Chhokar, Jagdeep -- D'Amato, Alessia -- Ferrer, Montse -- Fischlmayr, Iris C -- Fischer, Ronald -- Fulop, Marta -- Georgas, James -- Kashima, Emiko S -- Kashima, Yoshishima -- Kim, Kibum -- Lempereur, Alain -- Marquez, Patricia -- Othman, Rozhan -- Overlaet, Bert -- Panagiotopoulou, Penny -- Peltzer, Karl -- Perez-Florizno, Lorena R -- Ponomarenko, Larisa -- Realo, Anu -- Schei, Vidar -- Schmitt, Manfred -- Smith, Peter B -- Soomro, Nazar -- Szabo, Erna -- Taveesin, Nalinee -- Toyama, Midori -- Van de Vliert, Evert -- Vohra, Naharika -- Ward, Colleen -- Yamaguchi, Susumu -- New York, N.Y. -- Science. 2011 May 27;332(6033):1100-4. doi: 10.1126/science.1197754.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Maryland, College Park, MD 20742, USA. mgelfand@psyc.umd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21617077" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Behavior ; *Cross-Cultural Comparison ; *Cultural Characteristics ; Female ; Government ; Humans ; Male ; Permissiveness ; Political Systems ; Population Density ; *Social Behavior ; *Social Conformity ; Social Control, Formal ; *Social Values ; Young Adult
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  • 8
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    Chronic mucocutaneous candidiasis in humans with inborn errors of interleukin-17 immunity (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-26
    Description: Chronic mucocutaneous candidiasis disease (CMCD) is characterized by recurrent or persistent infections of the skin, nails, and oral and genital mucosae caused by Candida albicans and, to a lesser extent, Staphylococcus aureus, in patients with no other infectious or autoimmune manifestations. We report two genetic etiologies of CMCD: autosomal recessive deficiency in the cytokine receptor, interleukin-17 receptor A (IL-17RA), and autosomal dominant deficiency of the cytokine interleukin-17F (IL-17F). IL-17RA deficiency is complete, abolishing cellular responses to IL-17A and IL-17F homo- and heterodimers. By contrast, IL-17F deficiency is partial, with mutant IL-17F-containing homo- and heterodimers displaying impaired, but not abolished, activity. These experiments of nature indicate that human IL-17A and IL-17F are essential for mucocutaneous immunity against C. albicans, but otherwise largely redundant.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3070042/" 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/PMC3070042/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Puel, Anne -- Cypowyj, Sophie -- Bustamante, Jacinta -- Wright, Jill F -- Liu, Luyan -- Lim, Hye Kyung -- Migaud, Melanie -- Israel, Laura -- Chrabieh, Maya -- Audry, Magali -- Gumbleton, Matthew -- Toulon, Antoine -- Bodemer, Christine -- El-Baghdadi, Jamila -- Whitters, Matthew -- Paradis, Theresa -- Brooks, Jonathan -- Collins, Mary -- Wolfman, Neil M -- Al-Muhsen, Saleh -- Galicchio, Miguel -- Abel, Laurent -- Picard, Capucine -- Casanova, Jean-Laurent -- 5UL1RR024143-04/RR/NCRR NIH HHS/ -- UL1 RR024143/RR/NCRR NIH HHS/ -- UL1 RR024143-04/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 1;332(6025):65-8. doi: 10.1126/science.1200439. Epub 2011 Feb 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Human Genetics of Infectious Diseases, Necker Branch, Institut National de la Sante et de la Recherche Medicale, U980, and University Paris Descartes, Necker Medical School, 75015 Paris, France. anne.puel@inserm.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350122" target="_blank"〉PubMed〈/a〉
    Keywords: Candida albicans ; Candidiasis, Chronic Mucocutaneous/*genetics/*immunology ; Child ; Child, Preschool ; Female ; Genes, Dominant ; Genes, Recessive ; Humans ; Interleukin-17/*immunology ; Male ; Molecular Sequence Data ; Mutation ; Pedigree ; Receptors, Interleukin-17/genetics ; Signal Transduction/genetics ; Th17 Cells/immunology
    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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    Asymmetric division of Drosophila male germline stem cell shows asymmetric histone distribution (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-03
    Description: Stem cells can self-renew and generate differentiating daughter cells. It is not known whether these cells maintain their epigenetic information during asymmetric division. Using a dual-color method to differentially label "old" versus "new" histones in Drosophila male germline stem cells (GSCs), we show that preexisting canonical H3, but not variant H3.3, histones are selectively segregated to the GSC, whereas newly synthesized histones incorporated during DNA replication are enriched in the differentiating daughter cell. The asymmetric histone distribution occurs in GSCs but not in symmetrically dividing progenitor cells. Furthermore, if GSCs are genetically manipulated to divide symmetrically, this asymmetric mode is lost. This work suggests that stem cells retain preexisting canonical histones during asymmetric cell divisions, probably as a mechanism to maintain their unique molecular properties.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3532436/" 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/PMC3532436/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tran, Vuong -- Lim, Cindy -- Xie, Jing -- Chen, Xin -- R01 HD065816/HD/NICHD NIH HHS/ -- R01HD065816/HD/NICHD NIH HHS/ -- R21 HD065089/HD/NICHD NIH HHS/ -- R21HD065089/HD/NICHD NIH HHS/ -- T32 GM007231/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 2;338(6107):679-82. doi: 10.1126/science.1226028.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Johns Hopkins University, Baltimore, MD 21218, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23118191" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; *Asymmetric Cell Division ; Cell Differentiation ; Drosophila ; Drosophila Proteins/*metabolism ; Epigenesis, Genetic ; Germ Cells/*cytology/*metabolism ; Histones/*metabolism ; Male ; Stem Cells/*cytology/*metabolism
    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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    Global health. The global prevalence of intimate partner violence against women (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-06-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Devries, K M -- Mak, J Y T -- Garcia-Moreno, C -- Petzold, M -- Child, J C -- Falder, G -- Lim, S -- Bacchus, L J -- Engell, R E -- Rosenfeld, L -- Pallitto, C -- Vos, T -- Abrahams, N -- Watts, C H -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1527-8. doi: 10.1126/science.1240937. Epub 2013 Jun 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gender Violence and Health Centre, London School of Hygiene and Tropical Medicine, London WC1E 7HT, UK. karen.devries@lshtm.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23788730" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Global Health ; Humans ; Male ; Prevalence ; Primary Prevention/methods ; Spouse Abuse/*prevention & control/*statistics & numerical data
    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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