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  • 1
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    Immunology. CD8alphaalpha and T cell memory (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Sangwon V -- Flavell, Richard A -- New York, N.Y. -- Science. 2004 Apr 23;304(5670):529-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15105485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD8/*immunology/metabolism ; Arenaviridae Infections/immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cell Differentiation ; Cell Survival ; *Immunologic Memory ; Interleukin-7/metabolism ; *Lymphocyte Activation ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/immunology/metabolism ; Mice ; Mice, Knockout ; Models, Immunological ; Receptors, Interleukin-2/metabolism ; Receptors, Interleukin-7/metabolism ; Signal Transduction ; T-Lymphocyte Subsets/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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  • 2
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    DDX5 and its associated lncRNA Rmrp modulate TH17 cell effector functions (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-12-18
    Description: T helper 17 (TH17) lymphocytes protect mucosal barriers from infections, but also contribute to multiple chronic inflammatory diseases. Their differentiation is controlled by RORgammat, a ligand-regulated nuclear receptor. Here we identify the RNA helicase DEAD-box protein 5 (DDX5) as a RORgammat partner that coordinates transcription of selective TH17 genes, and is required for TH17-mediated inflammatory pathologies. Surprisingly, the ability of DDX5 to interact with RORgammat and coactivate its targets depends on intrinsic RNA helicase activity and binding of a conserved nuclear long noncoding RNA (lncRNA), Rmrp, which is mutated in patients with cartilage-hair hypoplasia. A targeted Rmrp gene mutation in mice, corresponding to a gene mutation in cartilage-hair hypoplasia patients, altered lncRNA chromatin occupancy, and reduced the DDX5-RORgammat interaction and RORgammat target gene transcription. Elucidation of the link between Rmrp and the DDX5-RORgammat complex reveals a role for RNA helicases and lncRNAs in tissue-specific transcriptional regulation, and provides new opportunities for therapeutic intervention in TH17-dependent diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762670/" 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/PMC4762670/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Wendy -- Thomas, Benjamin -- Flynn, Ryan A -- Gavzy, Samuel J -- Wu, Lin -- Kim, Sangwon V -- Hall, Jason A -- Miraldi, Emily R -- Ng, Charles P -- Rigo, Frank W -- Meadows, Sarah -- Montoya, Nina R -- Herrera, Natalia G -- Domingos, Ana I -- Rastinejad, Fraydoon -- Myers, Richard M -- Fuller-Pace, Frances V -- Bonneau, Richard -- Chang, Howard Y -- Acuto, Oreste -- Littman, Dan R -- 1F30CA189514-01/CA/NCI NIH HHS/ -- F30 CA189514/CA/NCI NIH HHS/ -- P50 HG007735/HG/NHGRI NIH HHS/ -- P50-HG007735/HG/NHGRI NIH HHS/ -- R01 AI080885/AI/NIAID NIH HHS/ -- R01 AI121436/AI/NIAID NIH HHS/ -- R01 DK103358/DK/NIDDK NIH HHS/ -- R01 HG004361/HG/NHGRI NIH HHS/ -- R01AI080885/AI/NIAID NIH HHS/ -- R01DK103358/DK/NIDDK NIH HHS/ -- R01HG004361/HG/NHGRI NIH HHS/ -- T32 AI100853/AI/NIAID NIH HHS/ -- T32 CA009161/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Dec 24;528(7583):517-22. doi: 10.1038/nature16193. Epub 2015 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA. ; Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK. ; Center for Personal Dynamic Regulomes, Stanford University, Stanford, California 94305, USA. ; Center for Genomics and Systems Biology, Department of Biology, New York University, New York, New York 10003, USA. ; Courant Institute of Mathematical Sciences, Computer Science Department, New York University, New York, New York 10012, USA. ; Simons Center for Data Analysis, Simons Foundation, New York, New York 10010, USA. ; Isis Pharmaceuticals, Carlsbad, California 92010, USA. ; HudsonAlpha Institute for Biotechnology, Huntsville, Alabama 35806, USA. ; Instituto Gulbenkian de Ciencia, Oeiras 2780-156, Portugal. ; Integrative Metabolism Program, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida 32827, USA. ; Division of Cancer Research, University of Dundee, Dundee DD1 9SY, UK. ; Howard Hughes Medical Institute, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26675721" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/genetics/metabolism ; DEAD-box RNA Helicases/genetics/*metabolism ; Female ; Gene Expression Regulation/genetics ; Hair/abnormalities ; Hirschsprung Disease/genetics ; Humans ; Immunologic Deficiency Syndromes/genetics ; Inflammation/immunology/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mutation/genetics ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Organ Specificity ; Osteochondrodysplasias/congenital/genetics ; Protein Binding ; RNA, Long Noncoding/genetics/*metabolism ; Th17 Cells/*immunology/*metabolism ; Transcription, Genetic/genetics
    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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  • 3
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    Digoxin and its derivatives suppress TH17 cell differentiation by antagonizing RORgammat activity (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-03-29
    Description: CD4(+) T helper lymphocytes that express interleukin-17 (T(H)17 cells) have critical roles in mouse models of autoimmunity, and there is mounting evidence that they also influence inflammatory processes in humans. Genome-wide association studies in humans have linked genes involved in T(H)17 cell differentiation and function with susceptibility to Crohn's disease, rheumatoid arthritis and psoriasis. Thus, the pathway towards differentiation of T(H)17 cells and, perhaps, of related innate lymphoid cells with similar effector functions, is an attractive target for therapeutic applications. Mouse and human T(H)17 cells are distinguished by expression of the retinoic acid receptor-related orphan nuclear receptor RORgammat, which is required for induction of IL-17 transcription and for the manifestation of T(H)17-dependent autoimmune disease in mice. By performing a chemical screen with an insect cell-based reporter system, we identified the cardiac glycoside digoxin as a specific inhibitor of RORgammat transcriptional activity. Digoxin inhibited murine T(H)17 cell differentiation without affecting differentiation of other T cell lineages and was effective in delaying the onset and reducing the severity of autoimmune disease in mice. At high concentrations, digoxin is toxic for human cells, but non-toxic synthetic derivatives 20,22-dihydrodigoxin-21,23-diol and digoxin-21-salicylidene specifically inhibited induction of IL-17 in human CD4(+) T cells. Using these small-molecule compounds, we demonstrate that RORgammat is important for the maintenance of IL-17 expression in mouse and human effector T cells. These data indicate that derivatives of digoxin can be used as chemical templates for the development of RORgammat-targeted therapeutic agents that attenuate inflammatory lymphocyte function and autoimmune disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3172133/" 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/PMC3172133/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huh, Jun R -- Leung, Monica W L -- Huang, Pengxiang -- Ryan, Daniel A -- Krout, Michael R -- Malapaka, Raghu R V -- Chow, Jonathan -- Manel, Nicolas -- Ciofani, Maria -- Kim, Sangwon V -- Cuesta, Adolfo -- Santori, Fabio R -- Lafaille, Juan J -- Xu, H Eric -- Gin, David Y -- Rastinejad, Fraydoon -- Littman, Dan R -- 2R01GM55217/GM/NIGMS NIH HHS/ -- F32GM0860552/GM/NIGMS NIH HHS/ -- R01 AI080885/AI/NIAID NIH HHS/ -- R01AI080885/AI/NIAID NIH HHS/ -- R01GM058833/GM/NIGMS NIH HHS/ -- R01GM067659/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Apr 28;472(7344):486-90. doi: 10.1038/nature09978. Epub 2011 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21441909" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/drug therapy/immunology/pathology ; Autoimmunity/drug effects/immunology ; Cell Differentiation/*drug effects ; Cell Line ; Digoxin/*analogs & derivatives/chemistry/metabolism/*pharmacology/therapeutic use ; Drosophila/cytology ; Humans ; Interleukin-17/biosynthesis/immunology ; Mice ; Nuclear Receptor Subfamily 1, Group F, Member 3/*antagonists & ; inhibitors/metabolism ; Th17 Cells/*cytology/*drug effects/immunology ; Transcription, Genetic/drug effects/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Modulation of cell adhesion and motility in the immune system by Myo1f (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: Although class I myosins are known to play a wide range of roles, the physiological function of long-tailed class I myosins in vertebrates remains elusive. We demonstrated that one of these proteins, Myo1f, is expressed predominantly in the mammalian immune system. Cells from Myo1f-deficient mice exhibited abnormally increased adhesion and reduced motility, resulting from augmented exocytosis of beta2 integrin-containing granules. Also, the cortical actin that co-localizes with Myo1f was reduced in Myo1f-deficient cells. In vivo, Myo1f-deficient mice showed increased susceptibility to infection by Listeria monocytogenes and an impaired neutrophil response. Thus, Myo1f directs immune cell motility and innate host defense against infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Sangwon V -- Mehal, Wajahat Z -- Dong, Xuemei -- Heinrich, Volkmar -- Pypaert, Marc -- Mellman, Ira -- Dembo, Micah -- Mooseker, Mark S -- Wu, Dianqing -- Flavell, Richard A -- K08 DK02965/DK/NIDDK NIH HHS/ -- R01 DK25387/DK/NIDDK NIH HHS/ -- R01 GM054597/GM/NIGMS NIH HHS/ -- R01 GM073823/GM/NIGMS NIH HHS/ -- R01 GM72002/GM/NIGMS NIH HHS/ -- R01 HL080706/HL/NHLBI NIH HHS/ -- R01 HL080706-10/HL/NHLBI NIH HHS/ -- R01 HL080706-11/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):136-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023661" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Antigens, CD18/metabolism ; *Cell Adhesion ; Cell Degranulation ; *Cell Movement ; Chemotaxis, Leukocyte ; Colony Count, Microbial ; Cytoplasmic Granules/metabolism ; Exocytosis ; *Immunity, Innate ; Ligands ; Listeria monocytogenes/growth & development ; Listeriosis/*immunology/microbiology ; Mice ; Mice, Knockout ; Myosin Type I/deficiency/genetics/*physiology ; N-Formylmethionine Leucyl-Phenylalanine ; Neutrophil Activation ; Neutrophils/immunology/*physiology
    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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    GPR15-mediated homing controls immune homeostasis in the large intestine mucosa (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-05-11
    Description: Lymphocyte homing, which contributes to inflammation, has been studied extensively in the small intestine, but there is little known about homing to the large intestine, the site most commonly affected in inflammatory bowel disease. GPR15, an orphan heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptor, controlled the specific homing of T cells, particularly FOXP3(+) regulatory T cells (Tregs), to the large intestine lamina propria (LILP). GPR15 expression was modulated by gut microbiota and transforming growth factor-beta1, but not by retinoic acid. GPR15-deficient mice were prone to develop more severe large intestine inflammation, which was rescued by the transfer of GPR15-sufficient Tregs. Our findings thus describe a T cell-homing receptor for LILP and indicate that GPR15 plays a role in mucosal immune tolerance largely by regulating the influx of Tregs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762262/" 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/PMC3762262/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Sangwon V -- Xiang, Wenkai V -- Kwak, Changsoo -- Yang, Yi -- Lin, Xiyao W -- Ota, Mitsuhiko -- Sarpel, Umut -- Rifkin, Daniel B -- Xu, Ruliang -- Littman, Dan R -- 1T32AI100853-01./AI/NIAID NIH HHS/ -- 5P30CA016087-32/CA/NCI NIH HHS/ -- 5P30CA016087-33/CA/NCI NIH HHS/ -- P30 CA016087/CA/NCI NIH HHS/ -- P30 CA016087-30/CA/NCI NIH HHS/ -- T32 AI100853/AI/NIAID NIH HHS/ -- UL1 RR029893/RR/NCRR NIH HHS/ -- UL1RR029893/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Jun 21;340(6139):1456-9. doi: 10.1126/science.1237013. Epub 2013 May 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23661644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Citrobacter rodentium ; Colitis/immunology ; Colon/immunology ; Enterobacteriaceae Infections/immunology ; Helicobacter Infections/immunology ; Homeostasis ; Humans ; Immune Tolerance ; Intestinal Mucosa/*immunology ; Intestine, Large/*immunology/microbiology ; Intestine, Small/immunology ; Metagenome/physiology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Receptors, Lymphocyte Homing/*metabolism ; Receptors, Peptide/genetics/*metabolism ; T-Lymphocytes, Regulatory/*immunology/*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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  • 6
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    The maternal interleukin-17a pathway in mice promotes autism-like phenotypes in offspring (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-01-30
    Description: Viral infection during pregnancy has been correlated with increased frequency of autism spectrum disorder (ASD) in offspring. This observation has been modeled in rodents subjected to maternal immune activation (MIA). The immune cell populations critical in the MIA model have not been identified. Using both genetic mutants and blocking antibodies in mice, we show that retinoic acid receptor-related orphan nuclear receptor gamma t (RORgammat)-dependent effector T lymphocytes [for example, T helper 17 (TH17) cells] and the effector cytokine interleukin-17a (IL-17a) are required in mothers for MIA-induced behavioral abnormalities in offspring. We find that MIA induces an abnormal cortical phenotype, which is also dependent on maternal IL-17a, in the fetal brain. Our data suggest that therapeutic targeting of TH17 cells in susceptible pregnant mothers may reduce the likelihood of bearing children with inflammation-induced ASD-like phenotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, Gloria B -- Yim, Yeong S -- Wong, Helen -- Kim, Sangdoo -- Kim, Hyunju -- Kim, Sangwon V -- Hoeffer, Charles A -- Littman, Dan R -- Huh, Jun R -- F31 NS083277/NS/NINDS NIH HHS/ -- F31NS083277/NS/NINDS NIH HHS/ -- R00 DK091508/DK/NIDDK NIH HHS/ -- R00DK091508/DK/NIDDK NIH HHS/ -- R01 NS086933/NS/NINDS NIH HHS/ -- R01NS086933/NS/NINDS NIH HHS/ -- T32 AI100853/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Feb 26;351(6276):933-9. doi: 10.1126/science.aad0314. Epub 2016 Jan 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Center for Neural Science, New York University, New York, NY 10003, USA. Institute for Behavioral Genetics, Department of Integrated Physiology, University of Colorado, Boulder, CO 80303, USA. ; Division of Infectious Diseases and Immunology and Program in Innate Immunity, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA. ; Center for Neural Science, New York University, New York, NY 10003, USA. Institute for Behavioral Genetics, Department of Integrated Physiology, University of Colorado, Boulder, CO 80303, USA. charles.hoeffer@colorado.edu dan.littman@med.nyu.edu jun.huh@umassmed.edu. ; The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA. Howard Hughes Medical Institute, New York, NY 10016, USA. charles.hoeffer@colorado.edu dan.littman@med.nyu.edu jun.huh@umassmed.edu. ; Division of Infectious Diseases and Immunology and Program in Innate Immunity, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA. charles.hoeffer@colorado.edu dan.littman@med.nyu.edu jun.huh@umassmed.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26822608" target="_blank"〉PubMed〈/a〉
    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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    Corrigendum: DDX5 and its associated lncRNA Rmrp modulate TH17 cell effector functions (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-01-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Wendy -- Thomas, Benjamin -- Flynn, Ryan A -- Gavzy, Samuel J -- Wu, Lin -- Kim, Sangwon V -- Hall, Jason A -- Miraldi, Emily R -- Ng, Charles P -- Rigo, Frank -- Meadows, Sarah -- Montoya, Nina R -- Herrera, Natalia G -- Domingos, Ana I -- Rastinejad, Fraydoon -- Myers, Richard M -- Fuller-Pace, Frances V -- Bonneau, Richard -- Chang, Howard Y -- Acuto, Oreste -- Littman, Dan R -- England -- Nature. 2016 May 5;533(7601):130. doi: 10.1038/nature16968. Epub 2016 Jan 20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26789242" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Electronic Resource
    Electronic Resource
    Taking account of geometric factors and secondary interactions of fast neutrons with matter in elementary analysis (1987)
    Springer
    Atomic energy 62 (1987), S. 74-78 
    Details
    ISSN: 1573-8205
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01127420
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  • 9
    Electronic Resource
    Electronic Resource
    Polarization effects in pulsed electrical breakdown of suspensions (1972)
    Springer
    Russian physics journal 15 (1972), S. 355-358 
    Details
    ISSN: 1573-9228
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract The effect of conductivity and polarization of the solid and liquid phases on the pulsed electrical breakdown of suspensions was investigated. The variation of the suspension breakdown voltage with concentration of the disperse phase is attributed to distortion of the internal field due to impurity polarization and space-charge formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00834595
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  • 10
    Electronic Resource
    Electronic Resource
    Electric field distribution in a spherically symmetric two-component system at the front of a unit voltage pulse (1970)
    Springer
    Russian physics journal 13 (1970), S. 1431-1434 
    Details
    ISSN: 1573-9228
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract A solution is found for the electric field in the boundary layer of a spherically symmetric two-component (solid-liquid) system. The establishment of polarization is taken into account.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00818354
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