Search Results - (Author, Cooperation:S. Dawson)
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1Staff View
Publication Date: 2018-02-01Publisher: American Physical Society (APS)Print ISSN: 0556-2821Electronic ISSN: 1089-4918Topics: PhysicsKeywords: Beyond the standard modelPublished by: -
2Staff View
Publication Date: 2018-05-16Publisher: American Physical Society (APS)Print ISSN: 0556-2821Electronic ISSN: 1089-4918Topics: PhysicsKeywords: Electroweak interactionsPublished by: -
3Kam, T.-I., Mao, X., Park, H., Chou, S.-C., Karuppagounder, S. S., Umanah, G. E., Yun, S. P., Brahmachari, S., Panicker, N., Chen, R., Andrabi, S. A., Qi, C., Poirier, G. G., Pletnikova, O., Troncoso, J. C., Bekris, L. M., Leverenz, J. B., Pantelyat, A., Ko, H. S., Rosenthal, L. S., Dawson, T. M., Dawson, V. L.
American Association for the Advancement of Science (AAAS)
Published 2018Staff ViewPublication Date: 2018-11-02Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyGeosciencesComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Medicine, Diseases, Online OnlyPublished by: -
4Staff View
Publication Date: 2018-11-06Publisher: American Physical Society (APS)Print ISSN: 0556-2821Electronic ISSN: 1089-4918Topics: PhysicsKeywords: Beyond the standard modelPublished by: -
5M. G. Prokopenko ; M. B. Hirst ; L. De Brabandere ; D. J. Lawrence ; W. M. Berelson ; J. Granger ; B. X. Chang ; S. Dawson ; E. J. Crane, 3rd ; L. Chong ; B. Thamdrup ; A. Townsend-Small ; D. M. Sigman
Nature Publishing Group (NPG)
Published 2013Staff ViewPublication Date: 2013-08-09Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Anaerobiosis ; Bacteria/classification/genetics/*metabolism ; Carbon/metabolism ; Geologic Sediments/*microbiology ; Molecular Sequence Data ; Nitrogen/*metabolism ; Oxidation-Reduction ; Pacific Ocean ; Phylogeny ; Sulfur/metabolism ; Thiotrichaceae/classification/genetics/*metabolismPublished by: -
6R. E. Meyer ; S. Kim ; D. Obeso ; P. D. Straight ; M. Winey ; D. S. Dawson
American Association for the Advancement of Science (AAAS)
Published 2013Staff ViewPublication Date: 2013-02-02Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Aurora Kinases ; Chromosome Segregation/genetics/*physiology ; Chromosomes, Fungal/*genetics ; Intracellular Signaling Peptides and Proteins/genetics/*physiology ; Kinetochores/enzymology ; Meiosis/genetics/*physiology ; Microtubules/enzymology ; Mutation ; Protein-Serine-Threonine Kinases/genetics/*physiology ; Saccharomyces cerevisiae/enzymology/genetics/*physiology ; Saccharomyces cerevisiae Proteins/genetics/*physiologyPublished by: -
7Staff View
Publication Date: 2018-06-14Publisher: Royal SocietyElectronic ISSN: 2054-5703Topics: Natural Sciences in GeneralKeywords: psychologyPublished by: -
8Ponce Dawson, S. ; Chen, S. ; Doolen, G. D.
College Park, Md. : American Institute of Physics (AIP)
Published 1993Staff ViewISSN: 1089-7690Source: AIP Digital ArchiveTopics: PhysicsChemistry and PharmacologyNotes: A lattice Boltzmann model for reaction-diffusion systems is developed. The method provides an efficient computational scheme for simulating a variety of problems described by the reaction-diffusion equations. Diffusion phenomena, the decay to a limit cycle, and the formation of Turing patterns are studied. The results of lattice Boltzmann calculations are compared with the lattice gas method and with theoretical predictions, showing quantitative agreement. The model is extended to include velocity convection in chemically reacting fluid flows.Type of Medium: Electronic ResourceURL: -
9Staff View
ISSN: 1471-4159Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Abstract: The mechanism by which opiates affect fetal development is unknown, but one potential target is the programmed cell death (apoptosis) pathway of neurons. Apoptosis was induced in both primary neuronal cultures from embryonic day 7 cerebral hemispheres of chick brain (E7CH) and the F-11κ7 cell line (an immortalized mouse neuroblastoma × dorsal root ganglion hybrid stably transfected to overexpress κ-opioid receptors) by either staurosporine or the phosphatidylinositol 3-kinase inhibitors wortmannin and LY294002. Cells pretreated with either the μ-specific opioid agonist morphiceptin (E7CH) or the κ-specific opioid agonist U69,593 (F-11κ7) for 24 h showed increased apoptosis in response to staurosporine or wortmannin when compared with nonpretreated cells. The effects of morphiceptin and U69,593 were time- and dose-dependent and antagonist-reversible, suggesting that they were receptor-mediated. Neither morphiceptin nor U69,593 by themselves had any measurable effect on cell viability or DNA fragmentation, and coaddition of opiates at the same time as staurosporine, wortmannin, or LY294002 did not enhance apoptosis. Time course studies indicated a maximal opioid effect at a time (16–24 h) when inhibition of adenylate cyclase had been maximal for many hours. Addition of dibutyryl cyclic AMP either before or at the time of opioid addition protected against apoptosis and reduced fragmentation to levels seen for staurosporine plus dibutyryl cyclic AMP alone. The specificity for cyclic AMP was confirmed by showing protection with the specific agonist Sp-adenosine 3′,5′-cyclic monophosphothioate and increased killing with the antagonist Rp-adenosine 3′,5′-cyclic monophosphothioate. We conclude that the opioid enhancement of apoptosis is based on the inhibition of adenylate cyclase and that the effect is time-dependent.Type of Medium: Electronic ResourceURL: -
10Staff View
ISSN: 1471-4159Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Abstract: Chronic exposure of embryonic brain to opioids leads to microcephaly and developmental abnormalities. An immortalized mouse neuroblastoma × dorsal root ganglion hybrid cell line stably transfected to overexpress κ-opioid receptors (F-11κ7) showed complete loss of κ-receptor binding to [3H]U69,593 after exposure to the κ-agonist U69,593 for 24 h. U69,593 had no measurable effect on cell viability as determined by either cell viability or DNA fragmentation assays. However, when cell death (apoptosis) was induced by either staurosporine or the phosphatidylinositol 3-kinase inhibitors wortmannin and LY294002, cells pretreated with U69,593 for 24 h showed increased apoptosis compared with untreated cells. Thus, staurosporine (50 nM), wortmannin (4 µM), and LY294002 (30 µM) treatment for 24 h induced a 50% loss of cell viability and DNA fragmentation in 24 h. U69,593 pretreatment produced the same killing at lower concentrations, namely, 20 nM staurosporine, 2 µM wortmannin, and 14 µM LY294002, respectively. The effects of U69,593 were time-, dose-, and naloxone-reversible, suggesting that they are receptor-mediated. However, coaddition of U69,593 at the same time as staurosporine, wortmannin, or LY294002 did not enhance apoptosis. All three drugs that induced apoptosis were found to increase the level of ceramide, and pretreatment with U69,593 further increased the rate of formation of ceramide, a lipid that induces apoptosis in cells. We propose that chronic exposure to κ-receptor agonists promotes increased vulnerability of neurons to apoptosis.Type of Medium: Electronic ResourceURL: -
11Staff View
ISSN: 1471-4159Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Human glioma cell line U-373 MG expresses CMP-NeuAc : Galβ1,3GlcNAc α2,3-sialyltransferase [EC No. 2.4.99.6] (α2,3ST), UDP-GlcNAc : β-d-mannoside β1,6-N-acetylglucosaminyltransferase V [EC 2.4.1.155] (GnT-V) and UDP-GlcNAc3: β-d-mannoside β1,4-N-acetylglucosaminyltransferase III [EC 2.4.1.144] (GnT-III) but not CMP-NeuAc : Galβ1,4GlcNAc α2,6-sialyltransferase [EC 2.4.99.1] (α2,6ST) under normal culture conditions. We have previously shown that transfection of the α2,6ST gene into U-373 cells replaced α2,3-linked sialic acids with α2,6 sialic acids, resulting in a marked inhibition of glioma cell invasivity and a significant reduction in adhesivity. We now show that U-373 cells, which are typically highly resistant to cell death induced by chemotherapeutic agents (〈 10% death in 18 h), become more sensitive to apoptosis following overexpression of these four glycoprotein glycosyltransferases. U-373 cell viability showed a three-fold decrease (from 20 to 60% cell death) following treatment with staurosporine, C2-ceramide or etoposide, when either α2,6ST and GnT-V genes were stably overexpressed. Even glycosyltransferases typically raised in cancer cells, such as α2,3ST and GnT-III, were able to decrease viability two-fold (from 20 to 40% cell death) following stable overexpression. The increased susceptibility of glycosyltransferase-transfected U-373 cells to pro-apoptotic drugs was associated with increased ceramide levels in Rafts, increased caspase-3 activity and increased DNA fragmentation. In contrast, the same glycosyltransferase overexpression protected U-373 cells against a different class of apoptotic drugs, namely the phosphatidylinositol 3-kinase inhibitor LY294002. Thus altered surface protein glycosylation of a human glioblastoma cell line can lead to lowered resistance to chemotherapeutic agents.Type of Medium: Electronic ResourceURL: -
12Dawson, S. Ponce ; Lawniczak, A. ; Kapral, R.
College Park, Md. : American Institute of Physics (AIP)
Published 1994Staff ViewISSN: 1089-7690Source: AIP Digital ArchiveTopics: PhysicsChemistry and PharmacologyNotes: The interaction between the Turing instability and the instability induced by a differential flow is studied in the Selkov model. Both instabilities give rise to the formation of spatial patterns, and for a range of parameter values, these patterns can compete. The effect of anisotropic diffusion on the pattern formation process is investigated. Stripes with different orientations that travel with time and the suppression of patterns due to a competition of both instabilities are observed.Type of Medium: Electronic ResourceURL: -
13Bessant, J. ; Birley, S. ; Cooper, C. ; Dawson, S. ; Gennard, J. ; Gardiner, M. ; Gray, A. ; Jones, P. ; Mayer, C. ; McGee, J. ; Pidd, M. ; Rowley, G. ; Saunders, J. ; Stark, A.
Oxford, UK and Boston, USA : Blackwell Publishing Ltd
Published 2003Staff ViewISSN: 1467-8551Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: EconomicsNotes: This paper reviews the state of the field of the sub-disciplines within UK management research, based upon the submissions of 94 UK higher education institutions to the Business and Management Studies Panel in the UK's 2001 Research Assessment Exercise (RAE). It offers observations on the UK model of the assessment of quality in, and funding of, research conducted in publicly funded higher education institutions.Type of Medium: Electronic ResourceURL: -
14Childerhouse, S. J. ; Dawson, S. M. ; Slooten, E.
Oxford, UK : Blackwell Publishing Ltd
Published 1996Staff ViewISSN: 1748-7692Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: BiologyType of Medium: Electronic ResourceURL: -
15THOMAS, A. E. ; GREEN, F. R. ; DAWSON, S. J. ; LANE, A. ; HENNEY, A. M. ; KELLEHER, C. H. ; WILKES, H. C. ; BRENNAN, P. J. ; CRUICKSHANK, J. K. ; HAMSTEN, A. ; WIMAN, B. ; MEADE, T. W. ; HUMPHRIES, S. E.
Oxford, UK : Blackwell Publishing Ltd
Published 1992Staff ViewISSN: 1749-6632Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: Natural Sciences in GeneralType of Medium: Electronic ResourceURL: -
16Staff View
ISSN: 0003-4916Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: PhysicsType of Medium: Electronic ResourceURL: -
17Staff View
ISSN: 0003-4916Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: PhysicsType of Medium: Electronic ResourceURL: -
18Staff View
ISSN: 0925-7535Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: TechnologyType of Medium: Electronic ResourceURL: -
19Staff View
ISSN: 0007-1269Topics: PsychologyURL: -
20Staff View
ISSN: 0007-1269Topics: PsychologyURL: