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  • 1
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    Vitamin D receptor as an intestinal bile acid sensor (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-05-23
    Beschreibung: The vitamin D receptor (VDR) mediates the effects of the calcemic hormone 1alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3]. We show that VDR also functions as a receptor for the secondary bile acid lithocholic acid (LCA), which is hepatotoxic and a potential enteric carcinogen. VDR is an order of magnitude more sensitive to LCA and its metabolites than are other nuclear receptors. Activation of VDR by LCA or vitamin D induced expression in vivo of CYP3A, a cytochrome P450 enzyme that detoxifies LCA in the liver and intestine. These studies offer a mechanism that may explain the proposed protective effects of vitamin D and its receptor against colon cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makishima, Makoto -- Lu, Timothy T -- Xie, Wen -- Whitfield, G Kerr -- Domoto, Hideharu -- Evans, Ronald M -- Haussler, Mark R -- Mangelsdorf, David J -- New York, N.Y. -- Science. 2002 May 17;296(5571):1313-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12016314" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Aryl Hydrocarbon Hydroxylases ; Binding, Competitive ; COS Cells ; Cell Line ; Colonic Neoplasms/prevention & control ; Cytochrome P-450 CYP3A ; Cytochrome P-450 Enzyme System/genetics/metabolism ; DNA-Binding Proteins/metabolism ; Dimerization ; Gene Expression Regulation, Enzymologic ; Histone Acetyltransferases ; Humans ; Intestine, Small/*metabolism ; Ligands ; Lithocholic Acid/analogs & derivatives/*metabolism/pharmacology ; Male ; Mice ; Nuclear Receptor Coactivator 1 ; Oxidoreductases, N-Demethylating/genetics/metabolism ; Promoter Regions, Genetic ; Rats ; Receptors, Calcitriol/agonists/genetics/*metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Steroid/metabolism ; Transcription Factors/metabolism ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 2
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    Translational repression and eIF4A2 activity are critical for microRNA-mediated gene regulation (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2013-04-06
    Beschreibung: MicroRNAs (miRNAs) control gene expression through both translational repression and degradation of target messenger RNAs (mRNAs). However, the interplay between these processes and the precise molecular mechanisms involved remain unclear. Here, we show that translational inhibition is the primary event required for mRNA degradation. Translational inhibition depends on miRNAs impairing the function of the eIF4F initiation complex. We define the RNA helicase eIF4A2 as the key factor of eIF4F through which miRNAs function. We uncover a correlation between the presence of miRNA target sites in the 3' untranslated region (3'UTR) of mRNAs and secondary structure in the 5'UTR and show that mRNAs with unstructured 5'UTRs are refractory to miRNA repression. These data support a linear model for miRNA-mediated gene regulation in which translational repression via eIF4A2 is required first, followed by mRNA destabilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meijer, H A -- Kong, Y W -- Lu, W T -- Wilczynska, A -- Spriggs, R V -- Robinson, S W -- Godfrey, J D -- Willis, A E -- Bushell, M -- MC_UP_A600_1023/Medical Research Council/United Kingdom -- MC_UP_A600_1024/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Apr 5;340(6128):82-5. doi: 10.1126/science.1231197.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Toxicology Unit, Hodgkin Building, Lancaster Road, Leicester LE1 9HN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23559250" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Eukaryotic Initiation Factor-4A/*biosynthesis ; *Gene Expression Regulation ; HEK293 Cells ; HeLa Cells ; Humans ; MicroRNAs/*metabolism ; *Protein Biosynthesis ; *RNA Stability ; RNA, Messenger/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 3
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    Neural mechanisms of ageing and cognitive decline (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-03-26
    Beschreibung: During the past century, treatments for the diseases of youth and middle age have helped raise life expectancy significantly. However, cognitive decline has emerged as one of the greatest health threats of old age, with nearly 50% of adults over the age of 85 afflicted with Alzheimer's disease. Developing therapeutic interventions for such conditions demands a greater understanding of the processes underlying normal and pathological brain ageing. Recent advances in the biology of ageing in model organisms, together with molecular and systems-level studies of the brain, are beginning to shed light on these mechanisms and their potential roles in cognitive decline.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927852/" 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/PMC2927852/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, Nicholas A -- Lu, Tao -- Yankner, Bruce A -- DP1 AG044161/AG/NIA NIH HHS/ -- P01 AG027916/AG/NIA NIH HHS/ -- P01 AG027916-05/AG/NIA NIH HHS/ -- R01 AG026651/AG/NIA NIH HHS/ -- R01 AG026651-05/AG/NIA NIH HHS/ -- R01 AG027040/AG/NIA NIH HHS/ -- R01 AG027040-04/AG/NIA NIH HHS/ -- RC1 AG036106/AG/NIA NIH HHS/ -- RC1 AG036106-02/AG/NIA NIH HHS/ -- England -- Nature. 2010 Mar 25;464(7288):529-35. doi: 10.1038/nature08983.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20336135" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aging/*pathology ; Animals ; Autophagy ; Brain/physiology/*physiopathology ; Cognition Disorders/*physiopathology ; Epigenesis, Genetic/physiology ; Humans ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; Mitochondria/pathology ; Oxidative Stress/physiology ; Signal Transduction
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
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  • 4
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    REST and stress resistance in ageing and Alzheimer's disease (2014)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2014-03-29
    Beschreibung: Human neurons are functional over an entire lifetime, yet the mechanisms that preserve function and protect against neurodegeneration during ageing are unknown. Here we show that induction of the repressor element 1-silencing transcription factor (REST; also known as neuron-restrictive silencer factor, NRSF) is a universal feature of normal ageing in human cortical and hippocampal neurons. REST is lost, however, in mild cognitive impairment and Alzheimer's disease. Chromatin immunoprecipitation with deep sequencing and expression analysis show that REST represses genes that promote cell death and Alzheimer's disease pathology, and induces the expression of stress response genes. Moreover, REST potently protects neurons from oxidative stress and amyloid beta-protein toxicity, and conditional deletion of REST in the mouse brain leads to age-related neurodegeneration. A functional orthologue of REST, Caenorhabditis elegans SPR-4, also protects against oxidative stress and amyloid beta-protein toxicity. During normal ageing, REST is induced in part by cell non-autonomous Wnt signalling. However, in Alzheimer's disease, frontotemporal dementia and dementia with Lewy bodies, REST is lost from the nucleus and appears in autophagosomes together with pathological misfolded proteins. Finally, REST levels during ageing are closely correlated with cognitive preservation and longevity. Thus, the activation state of REST may distinguish neuroprotection from neurodegeneration in the ageing brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110979/" 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/PMC4110979/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Tao -- Aron, Liviu -- Zullo, Joseph -- Pan, Ying -- Kim, Haeyoung -- Chen, Yiwen -- Yang, Tun-Hsiang -- Kim, Hyun-Min -- Drake, Derek -- Liu, X Shirley -- Bennett, David A -- Colaiacovo, Monica P -- Yankner, Bruce A -- DP1 AG044161/AG/NIA NIH HHS/ -- DP1 OD006849/OD/NIH HHS/ -- DP1OD006849/OD/NIH HHS/ -- P01 AG027916/AG/NIA NIH HHS/ -- P01AG27916/AG/NIA NIH HHS/ -- P30 AG010161/AG/NIA NIH HHS/ -- P30AG10161/AG/NIA NIH HHS/ -- R01 AG015819/AG/NIA NIH HHS/ -- R01 AG017917/AG/NIA NIH HHS/ -- R01 AG026651/AG/NIA NIH HHS/ -- R01 GM105853/GM/NIGMS NIH HHS/ -- R01AG15819/AG/NIA NIH HHS/ -- R01AG17917/AG/NIA NIH HHS/ -- R01AG26651/AG/NIA NIH HHS/ -- R01GM072551/GM/NIGMS NIH HHS/ -- T32 AG000222/AG/NIA NIH HHS/ -- England -- Nature. 2014 Mar 27;507(7493):448-54. doi: 10.1038/nature13163. Epub 2014 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Department of Biostatistics and Computational Biology, Dana-Faber Cancer Institute and Harvard School of Public Health, Boston, Massachusetts 02115, USA. ; Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, Illinois 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670762" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aged ; Aged, 80 and over ; Aging/genetics/*metabolism/pathology ; Alzheimer Disease/genetics/*metabolism/pathology ; Amyloid beta-Peptides/antagonists & inhibitors/toxicity ; Animals ; Autophagy ; Brain/cytology/metabolism/pathology ; Caenorhabditis elegans Proteins/metabolism ; Cell Death/genetics ; Cell Nucleus/metabolism ; Chromatin Immunoprecipitation ; Cognition ; DNA-Binding Proteins/metabolism ; Down-Regulation ; Frontotemporal Dementia/metabolism/pathology ; Gene Expression Regulation ; Humans ; Lewy Body Disease/metabolism/pathology ; Longevity ; Mice ; Mild Cognitive Impairment/metabolism ; Neurons/cytology/metabolism/pathology ; Neuroprotective Agents/metabolism ; *Oxidative Stress/genetics/physiology ; Phagosomes ; Repressor Proteins/deficiency/genetics/*metabolism ; Transcription Factors/metabolism ; Up-Regulation ; Wnt Signaling Pathway ; Young Adult
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Synthetic biology moving into the clinic (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2011-09-03
    Beschreibung: Synthetic biology is an emerging field focused on engineering biomolecular systems and cellular capabilities for a variety of applications. Substantial progress began a little over a decade ago with the creation of synthetic gene networks inspired by electrical engineering. Since then, the field has designed and built increasingly complex circuits and constructs and begun to use these systems in a variety of settings, including the clinic. These efforts include the development of synthetic biology therapies for the treatment of infectious diseases and cancer, as well as approaches in vaccine development, microbiome engineering, cell therapy, and regenerative medicine. Here, we highlight advances in the biomedical application of synthetic biology and discuss the field's clinical potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruder, Warren C -- Lu, Ting -- Collins, James J -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1248-52. doi: 10.1126/science.1206843.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biomedical Engineering, and Center for BioDynamics, Boston University, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885773" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Bacterial Infections/prevention & control/*therapy ; Cell Transplantation ; Culicidae/genetics ; *Gene Regulatory Networks ; *Genetic Engineering ; Humans ; Insect Vectors/genetics ; Malaria/prevention & control/transmission ; Metagenome/genetics ; Neoplasms/*therapy ; Regenerative Medicine/methods ; Synthetic Biology/*methods ; *Vaccines, Synthetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4 (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2015-09-26
    Beschreibung: Cellular senescence is a terminal stress-activated program controlled by the p53 and p16(INK4a) tumor suppressor proteins. A striking feature of senescence is the senescence-associated secretory phenotype (SASP), a pro-inflammatory response linked to tumor promotion and aging. We have identified the transcription factor GATA4 as a senescence and SASP regulator. GATA4 is stabilized in cells undergoing senescence and is required for the SASP. Normally, GATA4 is degraded by p62-mediated selective autophagy, but this regulation is suppressed during senescence, thereby stabilizing GATA4. GATA4 in turn activates the transcription factor NF-kappaB to initiate the SASP and facilitate senescence. GATA4 activation depends on the DNA damage response regulators ATM and ATR, but not on p53 or p16(INK4a). GATA4 accumulates in multiple tissues, including the aging brain, and could contribute to aging and its associated inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Chanhee -- Xu, Qikai -- Martin, Timothy D -- Li, Mamie Z -- Demaria, Marco -- Aron, Liviu -- Lu, Tao -- Yankner, Bruce A -- Campisi, Judith -- Elledge, Stephen J -- AG009909/AG/NIA NIH HHS/ -- AG017242/AG/NIA NIH HHS/ -- AG046174/AG/NIA NIH HHS/ -- DP1 OD006849/OD/NIH HHS/ -- DP1OD006849/OD/NIH HHS/ -- GM44664/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Sep 25;349(6255):aaa5612. doi: 10.1126/science.aaa5612.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Buck Institute for Research on Aging, Novato, CA 94945, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. selledge@genetics.med.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26404840" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aging/*genetics/metabolism ; Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Autophagy/*genetics ; Brain/metabolism ; Cell Aging/*genetics ; Cell Cycle/genetics ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16 ; *DNA Damage ; Fibroblasts ; GATA4 Transcription Factor/genetics/*metabolism ; Gene Expression Profiling ; Humans ; Inflammation/*genetics ; Interleukin-1alpha/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/metabolism ; NF-kappa B/metabolism ; Phenotype ; Promoter Regions, Genetic ; Tumor Necrosis Factor Receptor-Associated Peptides and ; Proteins/genetics/metabolism ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 7
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    Nuclear pores. Architecture of the nuclear pore complex coat (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2015-03-07
    Beschreibung: The nuclear pore complex (NPC) constitutes the sole gateway for bidirectional nucleocytoplasmic transport. Despite half a century of structural characterization, the architecture of the NPC remains unknown. Here we present the crystal structure of a reconstituted ~400-kilodalton coat nucleoporin complex (CNC) from Saccharomyces cerevisiae at a 7.4 angstrom resolution. The crystal structure revealed a curved Y-shaped architecture and the molecular details of the coat nucleoporin interactions forming the central "triskelion" of the Y. A structural comparison of the yeast CNC with an electron microscopy reconstruction of its human counterpart suggested the evolutionary conservation of the elucidated architecture. Moreover, 32 copies of the CNC crystal structure docked readily into a cryoelectron tomographic reconstruction of the fully assembled human NPC, thereby accounting for ~16 megadalton of its mass.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stuwe, Tobias -- Correia, Ana R -- Lin, Daniel H -- Paduch, Marcin -- Lu, Vincent T -- Kossiakoff, Anthony A -- Hoelz, Andre -- 5 T32 GM07616/GM/NIGMS NIH HHS/ -- ACB-12002/PHS HHS/ -- AGM-12006/PHS HHS/ -- U01 GM094588/GM/NIGMS NIH HHS/ -- U54 GM087519/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Mar 6;347(6226):1148-52. doi: 10.1126/science.aaa4136. Epub 2015 Feb 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Chemistry and Chemical Engineering, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA. These authors contributed equally to this work. ; Division of Chemistry and Chemical Engineering, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA. ; Department of Biochemistry and Molecular Biology, University of Chicago, Chicago, IL 60637, USA. ; Division of Chemistry and Chemical Engineering, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA. hoelz@caltech.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25745173" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Crystallography, X-Ray ; Humans ; Nuclear Pore/*ultrastructure ; Nuclear Pore Complex Proteins/*chemistry ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Saccharomyces cerevisiae/*ultrastructure ; Saccharomyces cerevisiae Proteins/*chemistry
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 8
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    Human leukocyte functions and the U.S. safety standard for exposure to radio-frequency radiation (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1983-04-15
    Beschreibung: Human mononuclear leukocytes were exposed to microwaves at energies relevant to current public safety recommendations. No detectable effects on viability or function of the leukocytes resulted from exposure to microwaves at specific absorption rates up to 4 milliwatts per milliliter. The results were highly reproducible and provided no evidence that current safety standard recommendations are inappropriate insofar as leukocyte function is concerned.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, N J Jr -- Lu, S T -- Michaelson, S M -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):318-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6188214" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): DNA/biosynthesis ; Environmental Exposure ; Humans ; Leukocytes/*radiation effects ; Maximum Allowable Concentration ; Protein Biosynthesis ; RNA/biosynthesis ; Radio Waves/*adverse effects ; United States
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 9
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    Q&A: Cocktail maker (2015)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2015-12-03
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Tim -- Tauxe, Will -- England -- Nature. 2015 Dec 3;528(7580):S14. doi: 10.1038/528S14a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26630593" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Bacteriophages/physiology ; CRISPR-Cas Systems/genetics ; Feces/microbiology ; Genetic Engineering/*methods ; Genome, Human/genetics ; Humans ; Microbiota/drug effects/physiology ; *Quantum Dots ; Synthetic Biology/*methods
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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