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  • 1
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    Correction of sickle cell disease in transgenic mouse models by gene therapy (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2001-12-18
    Beschreibung: Sickle cell disease (SCD) is caused by a single point mutation in the human betaA globin gene that results in the formation of an abnormal hemoglobin [HbS (alpha2betaS2)]. We designed a betaA globin gene variant that prevents HbS polymerization and introduced it into a lentiviral vector we optimized for transfer to hematopoietic stem cells and gene expression in the adult red blood cell lineage. Long-term expression (up to 10 months) was achieved, without preselection, in all transplanted mice with erythroid-specific accumulation of the antisickling protein in up to 52% of total hemoglobin and 99% of circulating red blood cells. In two mouse SCD models, Berkeley and SAD, inhibition of red blood cell dehydration and sickling was achieved with correction of hematological parameters, splenomegaly, and prevention of the characteristic urine concentration defect.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pawliuk, R -- Westerman, K A -- Fabry, M E -- Payen, E -- Tighe, R -- Bouhassira, E E -- Acharya, S A -- Ellis, J -- London, I M -- Eaves, C J -- Humphries, R K -- Beuzard, Y -- Nagel, R L -- Leboulch, P -- HL554352/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2001 Dec 14;294(5550):2368-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard-MIT, Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11743206" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Anemia, Sickle Cell/genetics/*therapy ; Animals ; Disease Models, Animal ; Erythrocytes/metabolism ; Gene Expression ; *Genetic Therapy ; *Genetic Vectors ; Globins/*genetics/metabolism ; HIV-1/*genetics ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/metabolism ; Hemoglobin, Sickle/metabolism ; Humans ; Lentivirus/genetics ; Locus Control Region ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Oxyhemoglobins/metabolism ; RNA, Messenger/genetics/metabolism ; Thalassemia/genetics/therapy ; Transduction, Genetic ; Transgenes ; beta-Globins
    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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    Untangling dendrites with quantitative models (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-10-29
    Beschreibung: Our understanding of the function of dendrites has been greatly enriched by an inspiring dialogue between theory and experiments. Rather than functionally ignoring dendrites, representing neurons as single summing points, we have realized that dendrites are electrically and chemically distributed nonlinear units and that this has important consequences for interpreting experimental data and for the role of neurons in information processing. Here, we examine the route to unraveling some of the enigmas of dendrites and highlight the main insights that have been gained. Future directions are discussed that will enable theory and models to keep shedding light on dendrites, where the most fundamental input-output adaptive processes take place.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Segev, I -- London, M -- New York, N.Y. -- Science. 2000 Oct 27;290(5492):744-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Interdisciplinary Center for Neural Computation, The Hebrew University of Jerusalem, Jerusalem, 91904, Israel. idan@lobster.ls.huji.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11052930" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Dendrites/*physiology ; Electrophysiology ; Humans ; Information Theory ; Ion Channel Gating ; Ion Channels/physiology ; Learning ; Mathematics ; Mental Processes ; *Models, Neurological ; Neuronal Plasticity ; Neurons/*physiology ; Synapses/*physiology ; *Synaptic Transmission
    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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  • 3
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    Steroid binding at sigma receptors suggests a link between endocrine, nervous, and immune systems (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1988-04-08
    Beschreibung: Specific sigma binding sites have been identified in the mammalian brain and lymphoid tissue. In this study, certain gonadal and adrenal steroids, particularly progesterone, were found to inhibit sigma receptor binding in homogenates of brain and spleen. The findings suggest that steroids are naturally occurring ligands for sigma receptors and raise the possibility that these sites mediate some aspects of steroid-induced mental disturbances and alterations in immune functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, T P -- London, E D -- Jaffe, J H -- New York, N.Y. -- Science. 1988 Apr 8;240(4849):219-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2832949" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain/metabolism ; Endocrine Glands/*physiology ; Guinea Pigs ; Haloperidol/metabolism ; *Immunity ; Male ; *Nervous System Physiological Phenomena ; Phenazocine/analogs & derivatives/metabolism ; Receptors, Opioid/*metabolism ; Receptors, sigma ; Spleen/metabolism ; Steroids/*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)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Sensitivity to perturbations in vivo implies high noise and suggests rate coding in cortex (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-07-03
    Beschreibung: It is well known that neural activity exhibits variability, in the sense that identical sensory stimuli produce different responses, but it has been difficult to determine what this variability means. Is it noise, or does it carry important information-about, for example, the internal state of the organism? Here we address this issue from the bottom up, by asking whether small perturbations to activity in cortical networks are amplified. Based on in vivo whole-cell patch-clamp recordings in rat barrel cortex, we find that a perturbation consisting of a single extra spike in one neuron produces approximately 28 additional spikes in its postsynaptic targets. We also show, using simultaneous intra- and extracellular recordings, that a single spike in a neuron produces a detectable increase in firing rate in the local network. Theoretical analysis indicates that this amplification leads to intrinsic, stimulus-independent variations in membrane potential of the order of +/-2.2-4.5 mV-variations that are pure noise, and so carry no information at all. Therefore, for the brain to perform reliable computations, it must either use a rate code, or generate very large, fast depolarizing events, such as those proposed by the theory of synfire chains. However, in our in vivo recordings, we found that such events were very rare. Our findings are thus consistent with the idea that cortex is likely to use primarily a rate code.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898896/" 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/PMC2898896/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉London, Michael -- Roth, Arnd -- Beeren, Lisa -- Hausser, Michael -- Latham, Peter E -- G0500244/Medical Research Council/United Kingdom -- R01 MH062447-08/MH/NIMH NIH HHS/ -- R01 MH62447/MH/NIMH NIH HHS/ -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Jul 1;466(7302):123-7. doi: 10.1038/nature09086.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wolfson Institute for Biomedical Research and Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20596024" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Action Potentials/physiology ; Animals ; Artifacts ; Cerebral Cortex/cytology/*physiology ; *Models, Neurological ; Neurons/metabolism ; Patch-Clamp Techniques ; Probability ; Rats ; Rats, Sprague-Dawley ; Stochastic Processes
    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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    Activating mutations in ALK provide a therapeutic target in neuroblastoma (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-10-17
    Beschreibung: Neuroblastoma, an embryonal tumour of the peripheral sympathetic nervous system, accounts for approximately 15% of all deaths due to childhood cancer. High-risk neuroblastomas are rapidly progressive; even with intensive myeloablative chemotherapy, relapse is common and almost uniformly fatal. Here we report the detection of previously unknown mutations in the ALK gene, which encodes a receptor tyrosine kinase, in 8% of primary neuroblastomas. Five non-synonymous sequence variations were identified in the kinase domain of ALK, of which three were somatic and two were germ line. The most frequent mutation, F1174L, was also identified in three different neuroblastoma cell lines. ALK complementary DNAs encoding the F1174L and R1275Q variants, but not the wild-type ALK cDNA, transformed interleukin-3-dependent murine haematopoietic Ba/F3 cells to cytokine-independent growth. Ba/F3 cells expressing these mutations were sensitive to the small-molecule inhibitor of ALK, TAE684 (ref. 4). Furthermore, two human neuroblastoma cell lines harbouring the F1174L mutation were also sensitive to the inhibitor. Cytotoxicity was associated with increased amounts of apoptosis as measured by TdT-mediated dUTP nick end labelling (TUNEL). Short hairpin RNA (shRNA)-mediated knockdown of ALK expression in neuroblastoma cell lines with the F1174L mutation also resulted in apoptosis and impaired cell proliferation. Thus, activating alleles of the ALK receptor tyrosine kinase are present in primary neuroblastoma tumours and in established neuroblastoma cell lines, and confer sensitivity to ALK inhibition with small molecules, providing a molecular rationale for targeted therapy of this disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587486/" 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/PMC2587486/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉George, Rani E -- Sanda, Takaomi -- Hanna, Megan -- Frohling, Stefan -- Luther, William 2nd -- Zhang, Jianming -- Ahn, Yebin -- Zhou, Wenjun -- London, Wendy B -- McGrady, Patrick -- Xue, Liquan -- Zozulya, Sergey -- Gregor, Vlad E -- Webb, Thomas R -- Gray, Nathanael S -- Gilliland, D Gary -- Diller, Lisa -- Greulich, Heidi -- Morris, Stephan W -- Meyerson, Matthew -- Look, A Thomas -- CA21765/CA/NCI NIH HHS/ -- CA69129/CA/NCI NIH HHS/ -- K08 NS047983/NS/NINDS NIH HHS/ -- K08 NS047983-03/NS/NINDS NIH HHS/ -- K08 NS047983-04/NS/NINDS NIH HHS/ -- K08 NS047983-05/NS/NINDS NIH HHS/ -- England -- Nature. 2008 Oct 16;455(7215):975-8. doi: 10.1038/nature07397.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18923525" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Animals ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Enzyme Activation/genetics ; Genome, Human/genetics ; Humans ; In Situ Hybridization, Fluorescence ; In Situ Nick-End Labeling ; Mice ; Mutation/*genetics ; Neuroblastoma/enzymology/*genetics/pathology/*therapy ; Polymorphism, Single Nucleotide/genetics ; Protein Structure, Tertiary/genetics ; Protein-Tyrosine Kinases/*antagonists & inhibitors/chemistry/*genetics/metabolism ; Receptor Protein-Tyrosine Kinases ; Sequence Analysis, DNA
    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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  • 6
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    Interleukin receptor activates a MYD88-ARNO-ARF6 cascade to disrupt vascular stability (2012)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2012-11-13
    Beschreibung: The innate immune response is essential for combating infectious disease. Macrophages and other cells respond to infection by releasing cytokines, such as interleukin-1beta (IL-1beta), which in turn activate a well-described, myeloid-differentiation factor 88 (MYD88)-mediated, nuclear factor-kappaB (NF-kappaB)-dependent transcriptional pathway that results in inflammatory-cell activation and recruitment. Endothelial cells, which usually serve as a barrier to the movement of inflammatory cells out of the blood and into tissue, are also critical mediators of the inflammatory response. Paradoxically, the cytokines vital to a successful immune defence also have disruptive effects on endothelial cell-cell interactions and can trigger degradation of barrier function and dissociation of tissue architecture. The mechanism of this barrier dissolution and its relationship to the canonical NF-kappaB pathway remain poorly defined. Here we show that the direct, immediate and disruptive effects of IL-1beta on endothelial stability in a human in vitro cell model are NF-kappaB independent and are instead the result of signalling through the small GTPase ADP-ribosylation factor 6 (ARF6) and its activator ARF nucleotide binding site opener (ARNO; also known as CYTH2). Moreover, we show that ARNO binds directly to the adaptor protein MYD88, and thus propose MYD88-ARNO-ARF6 as a proximal IL-1beta signalling pathway distinct from that mediated by NF-kappaB. Finally, we show that SecinH3, an inhibitor of ARF guanine nucleotide-exchange factors such as ARNO, enhances vascular stability and significantly improves outcomes in animal models of inflammatory arthritis and acute inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521847/" 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/PMC3521847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Weiquan -- London, Nyall R -- Gibson, Christopher C -- Davis, Chadwick T -- Tong, Zongzhong -- Sorensen, Lise K -- Shi, Dallas S -- Guo, Jinping -- Smith, Matthew C P -- Grossmann, Allie H -- Thomas, Kirk R -- Li, Dean Y -- R01 CA163970/CA/NCI NIH HHS/ -- R01 HL065648/HL/NHLBI NIH HHS/ -- R01 HL084516/HL/NHLBI NIH HHS/ -- U54 HL112311/HL/NHLBI NIH HHS/ -- England -- Nature. 2012 Dec 13;492(7428):252-5. doi: 10.1038/nature11603. Epub 2012 Nov 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Utah, Salt Lake City, Utah 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23143332" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ADP-Ribosylation Factors/*metabolism ; Adjuvants, Immunologic/pharmacology ; Animals ; Arthritis/pathology ; Cadherins/metabolism ; Capillary Permeability/drug effects ; Cell Line ; Endothelial Cells/drug effects ; Enzyme Activation/drug effects ; GTPase-Activating Proteins/*metabolism ; Humans ; Interleukin-1beta/pharmacology ; Myeloid Differentiation Factor 88/*metabolism ; NF-kappa B/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Transport/drug effects ; Purines/pharmacology ; Receptors, Interleukin/*metabolism ; Signal Transduction ; Thiophenes/pharmacology
    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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  • 7
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    Non-A, non-B hepatitis: ultrastructural evidence for two agents in experimentally infected chimpanzees (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1979-07-13
    Beschreibung: Two different ultrastructural alterations were observed in liver cells of chimpanzees inoculated with plasma derived from two different patients with non-A, non-B hepatitis. During the acute phase of illness in one group of four chimpanzees, peculiar tubular structures, composed of two unit membranes with electron-opaque material in between, were observed in the cytoplasm of hepatocytes. In contrast, these structures were never detected in the liver cells of the second group of five chimpanzees that received the second inoculum, However, nuclear changes, usually associated with aggregates of 20- to 27-nanometer particles, were found in hepatocytes of the latter animals. Although these particles resembled viruses, they were not as uniform as small virus particles often appear. In five other chimpanzees inoculated with non-A, non-B hepatitis material not known to be related to the first two inocula, cytoplasmic structures were found in four, and nuclear structures were found in the remaining one. Thus, all 14 chimpanzees inoculated with transmissible non-A, non-B hepatitis agents could be classified as having either nuclear or cytoplasmic changes. These observations add support to epidemiologic data suggesting that there may be more than one agent of non-A, non-B hepatitis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimizu, Y K -- Feinstone, S M -- Purcell, R H -- Alter, H J -- London, W T -- New York, N.Y. -- Science. 1979 Jul 13;205(4402):197-200.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/451589" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Nucleus/ultrastructure ; Cytoplasm/ultrastructure ; Hepatitis, Viral, Animal/*microbiology ; Hepatitis, Viral, Human/*microbiology ; Inclusion Bodies, Viral/ultrastructure ; Liver/microbiology/ultrastructure ; Microscopy, Electron ; Pan troglodytes
    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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    Transmission of simian acquired immunodeficiency syndrome (SAIDS) with blood or filtered plasma (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1984-01-06
    Beschreibung: Simian acquired immunodeficiency syndrome (SAIDS), a disease clinically and pathologically similar to acquired immunodeficiency syndrome in humans, was transmitted from diseased rhesus monkeys (Macaca mulatta) to normal monkeys by inoculation with heparinized whole blood or plasma that had been passed through filters of 0.45 micrometer pore size. This suggests that the causative agent is small and most probably a virus. No viruses, however, were isolated by standard cell culture techniques from the blood or filtered plasma which caused SAIDS. Both cellular and humoral immunity were markedly depressed in animals with advanced SAIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gravell, M -- London, W T -- Houff, S A -- Madden, D L -- Dalakas, M C -- Sever, J L -- Osborn, K G -- Maul, D H -- Henrickson, R V -- Marx, P A -- RR00169/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 6;223(4631):74-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6318315" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acquired Immunodeficiency Syndrome/blood/immunology/*transmission ; Animals ; Blood/microbiology ; Cytomegalovirus/isolation & purification ; Filtration ; Immunoglobulins/analysis ; Lymphatic System/pathology ; Lymphocyte Activation ; Macaca mulatta ; *Plasma/microbiology ; Retroviridae/isolation & purification ; Viruses/isolation & purification
    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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  • 9
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    Reassortant virus derived from avian and human influenza A viruses is attenuated and immunogenic in monkeys (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1982-12-24
    Beschreibung: An influenza A reassortant virus that contained the hemagglutinin and neuraminidase genes of a virulent human virus, A/Udorn/72 (H3N2), and the six other influenza A virus genome segments from an avirulent avian virus, A/Mallard/New York/6750/78 (H2N2), was evaluated for its level of replication is squirrel monkeys and hamsters. In monkeys, the reassortant virus was as attenuated and as restricted in its level of replication in the upper and lower respiratory tract as its avian influenza virus parent. Nonetheless, infection with the reassortant induced significant resistant to challenge with virulent human influenza virus. In hamsters, the reassortant virus replicated to a level intermediate between that of its parents. These findings suggest that the nonsurface antigen genes of the avian parental virus are the primary determinants of restriction of replication of the reassortant virus in monkeys. Attenuation of the reassortant virus for primates is achieved by inefficient functioning of the avian influenza genes in primate cells, while antigenic specificity of the human influenza virus is provided by the neuraminidase and hemagglutinin genes derived from the human virus. This approach could lead to the development of a live influenza A virus vaccine that is attenuated for man if the avian influenza genes are similarly restricted in human cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, B R -- Sly, D L -- Tierney, E L -- Hosier, N T -- Massicot, J G -- London, W T -- Chanock, R M -- Webster, R G -- Hinshaw, V S -- CA 21765/CA/NCI NIH HHS/ -- N01-AI-02649/AI/NIAID NIH HHS/ -- N01-NS-7-2375/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1982 Dec 24;218(4579):1330-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6183749" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, Surface/genetics ; Cricetinae ; Epitopes/genetics/immunology ; Hemagglutinins/genetics/immunology ; Influenza A virus/*genetics ; Influenza Vaccines/*immunology ; Neuraminidase/genetics/immunology ; Saimiri ; Vaccines, Attenuated/immunology
    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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  • 10
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    The genome of a songbird (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-04-03
    Beschreibung: The zebra finch is an important model organism in several fields with unique relevance to human neuroscience. Like other songbirds, the zebra finch communicates through learned vocalizations, an ability otherwise documented only in humans and a few other animals and lacking in the chicken-the only bird with a sequenced genome until now. Here we present a structural, functional and comparative analysis of the genome sequence of the zebra finch (Taeniopygia guttata), which is a songbird belonging to the large avian order Passeriformes. We find that the overall structures of the genomes are similar in zebra finch and chicken, but they differ in many intrachromosomal rearrangements, lineage-specific gene family expansions, the number of long-terminal-repeat-based retrotransposons, and mechanisms of sex chromosome dosage compensation. We show that song behaviour engages gene regulatory networks in the zebra finch brain, altering the expression of long non-coding RNAs, microRNAs, transcription factors and their targets. We also show evidence for rapid molecular evolution in the songbird lineage of genes that are regulated during song experience. These results indicate an active involvement of the genome in neural processes underlying vocal communication and identify potential genetic substrates for the evolution and regulation of this behaviour.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187626/" 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/PMC3187626/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warren, Wesley C -- Clayton, David F -- Ellegren, Hans -- Arnold, Arthur P -- Hillier, Ladeana W -- Kunstner, Axel -- Searle, Steve -- White, Simon -- Vilella, Albert J -- Fairley, Susan -- Heger, Andreas -- Kong, Lesheng -- Ponting, Chris P -- Jarvis, Erich D -- Mello, Claudio V -- Minx, Pat -- Lovell, Peter -- Velho, Tarciso A F -- Ferris, Margaret -- Balakrishnan, Christopher N -- Sinha, Saurabh -- Blatti, Charles -- London, Sarah E -- Li, Yun -- Lin, Ya-Chi -- George, Julia -- Sweedler, Jonathan -- Southey, Bruce -- Gunaratne, Preethi -- Watson, Michael -- Nam, Kiwoong -- Backstrom, Niclas -- Smeds, Linnea -- Nabholz, Benoit -- Itoh, Yuichiro -- Whitney, Osceola -- Pfenning, Andreas R -- Howard, Jason -- Volker, Martin -- Skinner, Bejamin M -- Griffin, Darren K -- Ye, Liang -- McLaren, William M -- Flicek, Paul -- Quesada, Victor -- Velasco, Gloria -- Lopez-Otin, Carlos -- Puente, Xose S -- Olender, Tsviya -- Lancet, Doron -- Smit, Arian F A -- Hubley, Robert -- Konkel, Miriam K -- Walker, Jerilyn A -- Batzer, Mark A -- Gu, Wanjun -- Pollock, David D -- Chen, Lin -- Cheng, Ze -- Eichler, Evan E -- Stapley, Jessica -- Slate, Jon -- Ekblom, Robert -- Birkhead, Tim -- Burke, Terry -- Burt, David -- Scharff, Constance -- Adam, Iris -- Richard, Hugues -- Sultan, Marc -- Soldatov, Alexey -- Lehrach, Hans -- Edwards, Scott V -- Yang, Shiaw-Pyng -- Li, Xiaoching -- Graves, Tina -- Fulton, Lucinda -- Nelson, Joanne -- Chinwalla, Asif -- Hou, Shunfeng -- Mardis, Elaine R -- Wilson, Richard K -- BB/D013704/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E010652/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F007590/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBE0175091/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/E/I/00001425/Biotechnology and Biological Sciences Research Council/United Kingdom -- MC_U137761446/Medical Research Council/United Kingdom -- P30 DA018310/DA/NIDA NIH HHS/ -- R01 DC007218/DC/NIDCD NIH HHS/ -- R01 GM059290/GM/NIGMS NIH HHS/ -- R01 GM085233/GM/NIGMS NIH HHS/ -- R01 GM59290/GM/NIGMS NIH HHS/ -- R01 HG002939/HG/NHGRI NIH HHS/ -- R01 NS045264/NS/NINDS NIH HHS/ -- R01NS051820/NS/NINDS NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Apr 1;464(7289):757-62. doi: 10.1038/nature08819.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Genome Center, Washington University School of Medicine, Campus Box 8501, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA. wwarren@watson.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360741" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3' Untranslated Regions/genetics ; Animals ; Auditory Perception/genetics ; Brain/physiology ; Chickens/genetics ; Evolution, Molecular ; Female ; Finches/*genetics/physiology ; Gene Duplication ; Gene Regulatory Networks/genetics ; Genome/*genetics ; Male ; MicroRNAs/genetics ; Models, Animal ; Multigene Family/genetics ; Retroelements/genetics ; Sex Chromosomes/genetics ; Terminal Repeat Sequences/genetics ; Transcription, Genetic/genetics ; Vocalization, Animal/physiology
    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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