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  • 1
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    Structural insights into the evolutionary paths of oxylipin biosynthetic enzymes (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-08-22
    Beschreibung: The oxylipin pathway generates not only prostaglandin-like jasmonates but also green leaf volatiles (GLVs), which confer characteristic aromas to fruits and vegetables. Although allene oxide synthase (AOS) and hydroperoxide lyase are atypical cytochrome P450 family members involved in the synthesis of jasmonates and GLVs, respectively, it is unknown how these enzymes rearrange their hydroperoxide substrates into different products. Here we present the crystal structures of Arabidopsis thaliana AOS, free and in complex with substrate or intermediate analogues. The structures reveal an unusual active site poised to control the reactivity of an epoxyallylic radical and its cation by means of interactions with an aromatic pi-system. Replacing the amino acid involved in these steps by a non-polar residue markedly reduces AOS activity and, unexpectedly, is both necessary and sufficient for converting AOS into a GLV biosynthetic enzyme. Furthermore, by combining our structural data with bioinformatic and biochemical analyses, we have discovered previously unknown hydroperoxide lyase in plant growth-promoting rhizobacteria, AOS in coral, and epoxyalcohol synthase in amphioxus. These results indicate that oxylipin biosynthetic genes were present in the last common ancestor of plants and animals, but were subsequently lost in all metazoan lineages except Placozoa, Cnidaria and Cephalochordata.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Dong-Sun -- Nioche, Pierre -- Hamberg, Mats -- Raman, C S -- R01 AI054444/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Sep 18;455(7211):363-8. doi: 10.1038/nature07307. Epub 2008 Aug 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Texas Medical School, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18716621" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Arabidopsis/enzymology/genetics ; Binding Sites ; Catalysis ; Cytochrome P-450 Enzyme System/chemistry/metabolism ; *Evolution, Molecular ; Intramolecular Oxidoreductases/*chemistry/genetics/*metabolism ; Models, Chemical ; Models, Molecular ; Molecular Sequence Data ; Oxylipins/*metabolism ; Point Mutation/genetics ; Protein Conformation
    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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  • 2
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    Cell biology: Stairway to the proteasome (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-12-04
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raman, Malavika -- Harper, J Wade -- R01 AG011085/AG/NIA NIH HHS/ -- R01 GM070565/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Dec 3;462(7273):585-6. doi: 10.1038/462585a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19956252" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Biology ; Cyclin E/metabolism ; Humans ; Models, Molecular ; Proteasome Endopeptidase Complex/*physiology ; Ubiquitin-Activating Enzymes/metabolism ; Ubiquitination/*physiology
    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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  • 3
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    Hemagglutinin receptor binding avidity drives influenza A virus antigenic drift (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2009-11-11
    Beschreibung: Rapid antigenic evolution in the influenza A virus hemagglutinin precludes effective vaccination with existing vaccines. To understand this phenomenon, we passaged virus in mice immunized with influenza vaccine. Neutralizing antibodies selected mutants with single-amino acid hemagglutinin substitutions that increased virus binding to cell surface glycan receptors. Passaging these high-avidity binding mutants in naive mice, but not immune mice, selected for additional hemagglutinin substitutions that decreased cellular receptor binding avidity. Analyzing a panel of monoclonal antibody hemagglutinin escape mutants revealed a positive correlation between receptor binding avidity and escape from polyclonal antibodies. We propose that in response to variation in neutralizing antibody pressure between individuals, influenza A virus evolves by adjusting receptor binding avidity via amino acid substitutions throughout the hemagglutinin globular domain, many of which simultaneously alter antigenicity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784927/" 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/PMC2784927/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hensley, Scott E -- Das, Suman R -- Bailey, Adam L -- Schmidt, Loren M -- Hickman, Heather D -- Jayaraman, Akila -- Viswanathan, Karthik -- Raman, Rahul -- Sasisekharan, Ram -- Bennink, Jack R -- Yewdell, Jonathan W -- GM 57073/GM/NIGMS NIH HHS/ -- U54 GM62116/GM/NIGMS NIH HHS/ -- Z01 AI001014-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 30;326(5953):734-6. doi: 10.1126/science.1178258.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19900932" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antibodies, Neutralizing/immunology ; Antibodies, Viral/immunology ; Antigenic Variation/genetics/*immunology ; Cell Line ; Hemagglutinin Glycoproteins, Influenza Virus/genetics/immunology/*metabolism ; Influenza A Virus, H1N1 Subtype/genetics/*immunology ; Influenza Vaccines/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Models, Immunological ; Mutation ; Receptors, Virus/*metabolism ; Serial Passage
    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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  • 4
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    Femtomolar sensitivity of a NO sensor from Clostridium botulinum (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-10-09
    Beschreibung: Nitric oxide (NO) is extremely toxic to Clostridium botulinum, but its molecular targets are unknown. Here, we identify a heme protein sensor (SONO) that displays femtomolar affinity for NO. The crystal structure of the SONO heme domain reveals a previously undescribed fold and a strategically placed tyrosine residue that modulates heme-nitrosyl coordination. Furthermore, the domain architecture of a SONO ortholog cloned from Chlamydomonas reinhardtii indicates that NO signaling through cyclic guanosine monophosphate arose before the origin of multicellular eukaryotes. Our findings have broad implications for understanding bacterial responses to NO, as well as for the activation of mammalian NO-sensitive guanylyl cyclase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nioche, Pierre -- Berka, Vladimir -- Vipond, Julia -- Minton, Nigel -- Tsai, Ah-Lim -- Raman, C S -- AY343540/PHS HHS/ -- R01 AI054444/AI/NIAID NIH HHS/ -- R01 AI054444-05/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1550-3. Epub 2004 Oct 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Structural Biology Research Center and Department of Biochemistry and Molecular Biology, University of Texas Medical School, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15472039" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aerobiosis ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Bacterial Proteins/chemistry/metabolism ; Biological Evolution ; Carrier Proteins/*chemistry/genetics/*metabolism ; Chemotaxis ; Chlamydomonas reinhardtii/chemistry/genetics/metabolism ; Cloning, Molecular ; Clostridium botulinum/*chemistry/genetics/*metabolism ; Crystallography, X-Ray ; Electron Spin Resonance Spectroscopy ; Escherichia coli/genetics/growth & development ; Guanylate Cyclase ; Heme/chemistry/metabolism ; Hemeproteins/*chemistry/genetics/*metabolism ; Humans ; Hydrogen Bonding ; Ligands ; Models, Molecular ; Molecular Sequence Data ; Nitric Oxide/*metabolism ; Protein Folding ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protoporphyrins/analysis/metabolism ; Receptors, Cytoplasmic and Nuclear/chemistry/metabolism ; Sequence Alignment ; Signal Transduction ; Static Electricity ; Thermoanaerobacter/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)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease (2005)
    American Association for the Advancement of Science (AAAS)
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    Publikationsdatum: 2005-02-26
    Beschreibung: We identified axonal defects in mouse models of Alzheimer's disease that preceded known disease-related pathology by more than a year; we observed similar axonal defects in the early stages of Alzheimer's disease in humans. Axonal defects consisted of swellings that accumulated abnormal amounts of microtubule-associated and molecular motor proteins, organelles, and vesicles. Impairing axonal transport by reducing the dosage of a kinesin molecular motor protein enhanced the frequency of axonal defects and increased amyloid-beta peptide levels and amyloid deposition. Reductions in microtubule-dependent transport may stimulate proteolytic processing of beta-amyloid precursor protein, resulting in the development of senile plaques and Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokin, Gorazd B -- Lillo, Concepcion -- Falzone, Tomas L -- Brusch, Richard G -- Rockenstein, Edward -- Mount, Stephanie L -- Raman, Rema -- Davies, Peter -- Masliah, Eliezer -- Williams, David S -- Goldstein, Lawrence S B -- EY12598/EY/NEI NIH HHS/ -- EY13408/EY/NEI NIH HHS/ -- P50 AG05131/AG/NIA NIH HHS/ -- R01 EY007042/EY/NEI NIH HHS/ -- R01 EY007042-19/EY/NEI NIH HHS/ -- R01 EY013408/EY/NEI NIH HHS/ -- R01 EY013408-02/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1282-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cellular and Molecular Medicine, School of Medicine, University of California San Diego (UCSD), 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731448" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aged ; Aged, 80 and over ; Alzheimer Disease/genetics/*metabolism/*pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Animals ; *Axonal Transport ; Axons/*pathology/physiology ; Basal Nucleus of Meynert/pathology ; Brain/*metabolism/*pathology ; Cells, Cultured ; Cytoplasmic Vesicles/ultrastructure ; Female ; Hippocampus ; Humans ; Kinesin/metabolism ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/genetics/metabolism ; Neurons/metabolism ; Organelles/ultrastructure ; Plaque, Amyloid/pathology ; Time Factors
    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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  • 6
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    A FOXO3-IRF7 gene regulatory circuit limits inflammatory sequelae of antiviral responses (2012)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2012-09-18
    Beschreibung: Antiviral responses must be tightly regulated to defend rapidly against infection while minimizing inflammatory damage. Type 1 interferons (IFN-I) are crucial mediators of antiviral responses and their transcription is regulated by a variety of transcription factors; principal among these is the family of interferon regulatory factors (IRFs). The IRF gene regulatory networks are complex and contain multiple feedback loops. The tools of systems biology are well suited to elucidate the complex interactions that give rise to precise coordination of the interferon response. Here we have used an unbiased systems approach to predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. Genome-wide location analysis combined with gene deletion studies identified the Irf7 gene as a critical target of FOXO3. FOXO3 was identified as a negative regulator of Irf7 transcription and we have further demonstrated that FOXO3, IRF7 and IFN-I form a coherent feed-forward regulatory circuit. Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechanism for establishing the requisite set points in the interferon pathway that balances the beneficial effects and deleterious sequelae of the antiviral response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556990/" 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/PMC3556990/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Litvak, Vladimir -- Ratushny, Alexander V -- Lampano, Aaron E -- Schmitz, Frank -- Huang, Albert C -- Raman, Ayush -- Rust, Alistair G -- Bergthaler, Andreas -- Aitchison, John D -- Aderem, Alan -- HHSN272200700038C/AI/NIAID NIH HHS/ -- HHSN272200700038C/PHS HHS/ -- HHSN272200800058C/AI/NIAID NIH HHS/ -- HSN272200800058C/PHS HHS/ -- R01 AI025032/AI/NIAID NIH HHS/ -- R01 AI032972/AI/NIAID NIH HHS/ -- R01AI025032/AI/NIAID NIH HHS/ -- R01AI032972/AI/NIAID NIH HHS/ -- U19 AI100627/AI/NIAID NIH HHS/ -- U54 GM103511/GM/NIGMS NIH HHS/ -- U54 RR022220/RR/NCRR NIH HHS/ -- U54GM103511/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Oct 18;490(7420):421-5. doi: 10.1038/nature11428. Epub 2012 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Seattle Biomedical Research Institute, Seattle, Washington 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22982991" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Female ; Forkhead Transcription Factors/deficiency/genetics/*metabolism ; Gene Deletion ; Gene Expression Regulation/*immunology ; Inflammation/genetics/*immunology/*pathology ; Interferon Regulatory Factor-7/deficiency/genetics/*metabolism ; Interferon Type I/immunology ; Lung/immunology/pathology/virology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Reproducibility of Results ; Vesiculovirus/*immunology
    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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    Landscape of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarization (2013)
    Nature Publishing Group (NPG)
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    Publikationsdatum: 2013-03-19
    Beschreibung: The PARKIN ubiquitin ligase (also known as PARK2) and its regulatory kinase PINK1 (also known as PARK6), often mutated in familial early-onset Parkinson's disease, have central roles in mitochondrial homeostasis and mitophagy. Whereas PARKIN is recruited to the mitochondrial outer membrane (MOM) upon depolarization via PINK1 action and can ubiquitylate porin, mitofusin and Miro proteins on the MOM, the full repertoire of PARKIN substrates--the PARKIN-dependent ubiquitylome--remains poorly defined. Here we use quantitative diGly capture proteomics (diGly) to elucidate the ubiquitylation site specificity and topology of PARKIN-dependent target modification in response to mitochondrial depolarization. Hundreds of dynamically regulated ubiquitylation sites in dozens of proteins were identified, with strong enrichment for MOM proteins, indicating that PARKIN dramatically alters the ubiquitylation status of the mitochondrial proteome. Using complementary interaction proteomics, we found depolarization-dependent PARKIN association with numerous MOM targets, autophagy receptors, and the proteasome. Mutation of the PARKIN active site residue C431, which has been found mutated in Parkinson's disease patients, largely disrupts these associations. Structural and topological analysis revealed extensive conservation of PARKIN-dependent ubiquitylation sites on cytoplasmic domains in vertebrate and Drosophila melanogaster MOM proteins. These studies provide a resource for understanding how the PINK1-PARKIN pathway re-sculpts the proteome to support mitochondrial homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3641819/" 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/PMC3641819/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sarraf, Shireen A -- Raman, Malavika -- Guarani-Pereira, Virginia -- Sowa, Mathew E -- Huttlin, Edward L -- Gygi, Steven P -- Harper, J Wade -- CA139885/CA/NCI NIH HHS/ -- GM067945/GM/NIGMS NIH HHS/ -- GM070565/GM/NIGMS NIH HHS/ -- GM095567/GM/NIGMS NIH HHS/ -- R01 GM067945/GM/NIGMS NIH HHS/ -- R01 GM070565/GM/NIGMS NIH HHS/ -- R01 GM095567/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 Apr 18;496(7445):372-6. doi: 10.1038/nature12043. Epub 2013 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23503661" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Drosophila Proteins/metabolism ; Drosophila melanogaster/metabolism ; Humans ; *Membrane Potential, Mitochondrial ; Mice ; Mitochondria/chemistry/*metabolism ; Mitochondrial Membranes/*metabolism ; Mitochondrial Proteins/*metabolism ; Protein Kinases/metabolism ; Proteome/*metabolism ; Proteomics ; Ubiquitin-Protein Ligases/*metabolism ; *Ubiquitination
    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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  • 8
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    Purkinje neuron synchrony elicits time-locked spiking in the cerebellar nuclei (2011)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2011-12-27
    Beschreibung: An unusual feature of the cerebellar cortex is that its output neurons, Purkinje cells, release GABA (gamma-aminobutyric acid). Their high intrinsic firing rates (50 Hz) and extensive convergence predict that their target neurons in the cerebellar nuclei would be largely inhibited unless Purkinje cells pause their spiking, yet Purkinje and nuclear neuron firing rates do not always vary inversely. One indication of how these synapses transmit information is that populations of Purkinje neurons synchronize their spikes during cerebellar behaviours. If nuclear neurons respond to Purkinje synchrony, they may encode signals from subsets of inhibitory inputs. Here we show in weanling and adult mice that nuclear neurons transmit the timing of synchronous Purkinje afferent spikes, owing to modest Purkinje-to-nuclear convergence ratios ( approximately 40:1), fast inhibitory postsynaptic current kinetics (tau(decay) = 2.5 ms) and high intrinsic firing rates ( approximately 90 Hz). In vitro, dynamically clamped asynchronous inhibitory postsynaptic potentials mimicking Purkinje afferents suppress nuclear cell spiking, whereas synchronous inhibitory postsynaptic potentials entrain nuclear cell spiking. With partial synchrony, nuclear neurons time-lock their spikes to the synchronous subpopulation of inputs, even when only 2 out of 40 afferents synchronize. In vivo, nuclear neurons reliably phase-lock to regular trains of molecular layer stimulation. Thus, cerebellar nuclear neurons can preferentially relay the spike timing of synchronized Purkinje cells to downstream premotor areas.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3268051/" 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/PMC3268051/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Person, Abigail L -- Raman, Indira M -- F32 NS067831/NS/NINDS NIH HHS/ -- F32 NS067831-02/NS/NINDS NIH HHS/ -- F32-NS067831/NS/NINDS NIH HHS/ -- R01 NS039395/NS/NINDS NIH HHS/ -- R01 NS039395-13/NS/NINDS NIH HHS/ -- R01-NS39395/NS/NINDS NIH HHS/ -- England -- Nature. 2011 Dec 25;481(7382):502-5. doi: 10.1038/nature10732.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Northwestern University, Evanston, Illinois 60208, USA. a-person@northwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22198670" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Action Potentials/physiology ; Animals ; Cerebellar Cortex/cytology ; Cerebellar Nuclei/*physiology ; Inhibitory Postsynaptic Potentials/*physiology ; Kinetics ; Mice ; Mice, Inbred C57BL ; Purkinje Cells/*physiology ; Time Factors ; Weaning
    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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  • 9
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    Transmission and pathogenesis of swine-origin 2009 A(H1N1) influenza viruses in ferrets and mice (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2009-07-04
    Beschreibung: Recent reports of mild to severe influenza-like illness in humans caused by a novel swine-origin 2009 A(H1N1) influenza virus underscore the need to better understand the pathogenesis and transmission of these viruses in mammals. In this study, selected 2009 A(H1N1) influenza isolates were assessed for their ability to cause disease in mice and ferrets and compared with a contemporary seasonal H1N1 virus for their ability to transmit to naive ferrets through respiratory droplets. In contrast to seasonal influenza H1N1 virus, 2009 A(H1N1) influenza viruses caused increased morbidity, replicated to higher titers in lung tissue, and were recovered from the intestinal tract of intranasally inoculated ferrets. The 2009 A(H1N1) influenza viruses exhibited less efficient respiratory droplet transmission in ferrets in comparison with the highly transmissible phenotype of a seasonal H1N1 virus. Transmission of the 2009 A(H1N1) influenza viruses was further corroborated by characterizing the binding specificity of the viral hemagglutinin to the sialylated glycan receptors (in the human host) by use of dose-dependent direct receptor-binding and human lung tissue-binding assays.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2953552/" 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/PMC2953552/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maines, Taronna R -- Jayaraman, Akila -- Belser, Jessica A -- Wadford, Debra A -- Pappas, Claudia -- Zeng, Hui -- Gustin, Kortney M -- Pearce, Melissa B -- Viswanathan, Karthik -- Shriver, Zachary H -- Raman, Rahul -- Cox, Nancy J -- Sasisekharan, Ram -- Katz, Jacqueline M -- Tumpey, Terrence M -- GM 57073/GM/NIGMS NIH HHS/ -- R01 GM057073/GM/NIGMS NIH HHS/ -- R01 GM057073-09/GM/NIGMS NIH HHS/ -- R37 GM057073/GM/NIGMS NIH HHS/ -- U54 GM062116/GM/NIGMS NIH HHS/ -- U54 GM062116-09/GM/NIGMS NIH HHS/ -- U54 GM62116/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):484-7. doi: 10.1126/science.1177238. Epub 2009 Jul 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Influenza Division, National Center for Immunization and Respiratory Diseases, 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/19574347" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Animals ; Disease Models, Animal ; Female ; Ferrets ; Hemagglutinin Glycoproteins, Influenza Virus/chemistry/metabolism ; Humans ; Influenza A Virus, H1N1 Subtype/*pathogenicity ; Influenza, Human/transmission/*virology ; Intestines/virology ; Male ; Mice ; Mice, Inbred BALB C ; Models, Molecular ; Orthomyxoviridae Infections/*transmission/*virology ; Protein Binding ; Receptors, Virus/metabolism ; Respiratory System/virology ; Swine ; Virus Replication
    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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    Investigations of High Pressure Acoustic Waves in Resonators with Seal-Like Features (2004)
    In:  CASI
    Details
    Publikationsdatum: 2018-06-06
    Beschreibung: 1) Standing waves with maximum pressures of 188 kPa have been produced in resonators containing ambient pressure air; 2) Addition of structures inside the resonator shifts the fundamental frequency and decreases the amplitude of the generated pressure waves; 3) Addition of holes to the resonator does reduce the magnitude of the acoustic waves produced, but their addition does not prohibit the generation of large magnitude non-linear standing waves; 4) The feasibility of reducing leakage using non-linear acoustics has been confirmed.
    Schlagwort(e): Acoustics
    Materialart: 2003 NASA Seal/Secondary Air System Workshop, Volume 1; 239-271; NASA/CP-2004-212963/VOL1
    Format: application/pdf
    Standort Signatur Erwartet Verfügbarkeit
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