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  • American Association for the Advancement of Science (AAAS)  (219)
  • 2015-2019  (137)
  • 2000-2004  (82)
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  • 1
    Publication Date: 2019
    Description: 〈p〉Adding energy to a system through transient stirring usually leads to more disorder. In contrast, point-like vortices in a bounded two-dimensional fluid are predicted to reorder above a certain energy, forming persistent vortex clusters. In this study, we experimentally realize these vortex clusters in a planar superfluid: a 〈sup〉87〈/sup〉Rb Bose-Einstein condensate confined to an elliptical geometry. We demonstrate that the clusters persist for long time periods, maintaining the superfluid system in a high-energy state far from global equilibrium. Our experiments explore a regime of vortex matter at negative absolute temperatures and have relevance for the dynamics of topological defects, two-dimensional turbulence, and systems such as helium films, nonlinear optical materials, fermion superfluids, and quark-gluon plasmas.〈/p〉
    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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  • 2
    Publication Date: 2019
    Description: 〈p〉Chemical defense against predators is widespread in natural ecosystems. Occasionally, taxonomically distant organisms share the same defense chemical. Here, we describe an unusual tripartite marine symbiosis, in which an intracellular bacterial symbiont ("〈i〉Candidatus〈/i〉 Endobryopsis kahalalidefaciens") uses a diverse array of biosynthetic enzymes to convert simple substrates into a library of complex molecules (the kahalalides) for chemical defense of the host, the alga 〈i〉Bryopsis〈/i〉 sp., against predation. The kahalalides are subsequently hijacked by a third partner, the herbivorous mollusk 〈i〉Elysia rufescens〈/i〉, and employed similarly for defense. "〈i〉Ca〈/i〉. E. kahalalidefaciens" has lost many essential traits for free living and acts as a factory for kahalalide production. This interaction between a bacterium, an alga, and an animal highlights the importance of chemical defense in the evolution of complex symbioses.〈/p〉
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2019
    Description: 〈p〉High magnetic fields suppress cuprate superconductivity to reveal an unusual density wave (DW) state coexisting with unexplained quantum oscillations. Although routinely labeled a charge density wave (CDW), this DW state could actually be an electron-pair density wave (PDW). To search for evidence of a field-induced PDW, we visualized modulations in the density of electronic states 〈i〉N〈/i〉(〈i〉r〈/i〉) within the halo surrounding Bi〈sub〉2〈/sub〉Sr〈sub〉2〈/sub〉CaCu〈sub〉2〈/sub〉O〈sub〉8〈/sub〉 vortex cores. We detected numerous phenomena predicted for a field-induced PDW, including two sets of particle-hole symmetric 〈i〉N〈/i〉(〈i〉r〈/i〉) modulations with wave vectors 〈b〉〈i〉Q〈sub〉P〈/sub〉〈/i〉〈/b〉 and 〈b〉2〈i〉Q〈/i〉〈sub〉P〈/sub〉〈/b〉, with the latter decaying twice as rapidly from the core as the former. These data imply that the primary field-induced state in underdoped superconducting cuprates is a PDW, with approximately eight CuO〈sub〉2〈/sub〉 unit-cell periodicity and coexisting with its secondary CDWs.〈/p〉
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  • 4
    Publication Date: 2000-08-26
    Description: Whereas T helper cells recognize peptide-major histocompatibility complex (MHC) class II complexes through their T cell receptors (TCRs), CD4 binds to an antigen-independent region of the MHC. Using green fluorescent protein-tagged chimeras and three-dimensional video microscopy, we show that CD4 and TCR-associated CD3zeta cluster in the interface coincident with increases in intracellular calcium. Signaling-, costimulation-, and cytoskeleton-dependent processes then stabilize CD3zeta in a single cluster at the center of the interface, while CD4 moves to the periphery. Thus, the CD4 coreceptor may serve primarily to "boost" recognition of ligand by the TCR and may not be required once activation has been initiated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krummel, M F -- Sjaastad, M D -- Wulfing, C -- Davis, M M -- New York, N.Y. -- Science. 2000 Aug 25;289(5483):1349-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, and the Howard Hughes Medical Institute, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10958781" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD3/*metabolism ; Antigens, CD4/*metabolism ; Calcium Signaling ; Cell Line ; Cytoskeleton/physiology ; Histocompatibility Antigens Class II/immunology/metabolism ; Ligands ; *Lymphocyte Activation ; Microscopy, Video ; Phosphorylation ; Receptors, Antigen, T-Cell/immunology/metabolism ; Recombinant Fusion Proteins/metabolism ; T-Lymphocytes, Helper-Inducer/*immunology/metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2000-11-25
    Description: beta-Arrestins, originally discovered in the context of heterotrimeric guanine nucleotide binding protein-coupled receptor (GPCR) desensitization, also function in internalization and signaling of these receptors. We identified c-Jun amino-terminal kinase 3 (JNK3) as a binding partner of beta-arrestin 2 using a yeast two-hybrid screen and by coimmunoprecipitation from mouse brain extracts or cotransfected COS-7 cells. The upstream JNK activators apoptosis signal-regulating kinase 1 (ASK1) and mitogen-activated protein kinase (MAPK) kinase 4 were also found in complex with beta-arrestin 2. Cellular transfection of beta-arrestin 2 caused cytosolic retention of JNK3 and enhanced JNK3 phosphorylation stimulated by ASK1. Moreover, stimulation of the angiotensin II type 1A receptor activated JNK3 and triggered the colocalization of beta-arrestin 2 and active JNK3 to intracellular vesicles. Thus, beta-arrestin 2 acts as a scaffold protein, which brings the spatial distribution and activity of this MAPK module under the control of a GPCR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, P H -- Chow, C W -- Miller, W E -- Laporte, S A -- Field, M E -- Lin, F T -- Davis, R J -- Lefkowitz, R J -- CA65861/CA/NCI NIH HHS/ -- CA85422/CA/NCI NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Box 3821, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090355" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/metabolism/pharmacology ; Animals ; Arrestins/genetics/*metabolism ; COS Cells ; Cell Line ; Cell Nucleus/metabolism ; Cytosol/enzymology/metabolism ; Endosomes/enzymology/metabolism ; Enzyme Activation ; Humans ; *MAP Kinase Kinase 4 ; MAP Kinase Kinase Kinase 5 ; MAP Kinase Kinase Kinases/*metabolism ; *MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 10 ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mitogen-Activated Protein Kinases/*metabolism ; Mutation ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Rats ; Receptor, Angiotensin, Type 1 ; Receptors, Angiotensin/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Two-Hybrid System Techniques
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-11-04
    Description: Experiments, employing crossed molecular beams, with vibrational state resolution have been performed on the simplest four-atom reaction, OH + D2 --〉 HOD + D. In good agreement with the most recent quantum scattering predictions, mode-specific reaction dynamics is observed, with vibration in the newly formed oxygen-deuterium bond preferentially excited to v = 2. This demonstrates that quantum theoretical calculations, which in the past decade have achieved remarkable accuracy for three-atom reactions involving three dimensions, have progressed to the point where it is now possible to accurately predict energy disposal in four-atom reactions involving six dimensions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strazisar, B R -- Lin, C -- Davis, H F -- New York, N.Y. -- Science. 2000 Nov 3;290(5493):958-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY 14850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11062122" target="_blank"〉PubMed〈/a〉
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  • 7
    Publication Date: 2000-05-08
    Description: The c-Jun NH2-terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts. Fibroblasts with simultaneous targeted disruptions of all the functional Jnk genes were protected against UV-stimulated apoptosis. The absence of JNK caused a defect in the mitochondrial death signaling pathway, including the failure to release cytochrome c. These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tournier, C -- Hess, P -- Yang, D D -- Xu, J -- Turner, T K -- Nimnual, A -- Bar-Sagi, D -- Jones, S N -- Flavell, R A -- Davis, R J -- New York, N.Y. -- Science. 2000 May 5;288(5467):870-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry & Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10797012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 3 ; Caspase 9 ; Caspases/metabolism ; Cell Count ; Cell Division ; Cells, Cultured ; Cytochrome c Group/*metabolism ; DNA Fragmentation ; Enzyme Activation ; Fibroblasts ; Gene Targeting ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Methyl Methanesulfonate/pharmacology ; Mice ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinases/genetics/*metabolism ; NF-kappa B/metabolism ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Tumor Suppressor Protein p53/metabolism ; Ultraviolet Rays
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  • 8
    Publication Date: 2000-04-15
    Description: Virulence of Vibrio cholerae depends on secretion of cholera toxin (CT), which is encoded within the genome of a filamentous phage, CTXphi. Release of CT is mediated by the extracellular protein secretion (eps) type II secretion system. Here, the outer membrane component of this system, EpsD, was shown to be required for secretion of the phage as well. Thus, EpsD plays a role both in pathogenicity and in horizontal transfer of a key virulence gene. Genomic analysis suggests that additional filamentous phages also exploit chromosome-encoded outer membrane channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, B M -- Lawson, E H -- Sandkvist, M -- Ali, A -- Sozhamannan, S -- Waldor, M K -- AI-42347/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):333-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Geographic Medicine and Infectious Diseases, Tufts University School of Medicine, Boston, MA 02111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10764646" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Outer Membrane Proteins/genetics/*metabolism ; Bacteriophages/genetics/growth & development/*metabolism ; Cholera Toxin/*metabolism ; Genes, Bacterial ; Genetic Complementation Test ; Metalloendopeptidases/metabolism ; Mutagenesis, Insertional ; Plasmids ; Transduction, Genetic ; Vibrio cholerae/genetics/*metabolism/pathogenicity ; Virulence
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  • 9
    Publication Date: 2001-12-26
    Description: The circadian clock in the suprachiasmatic nucleus (SCN) is thought to drive daily rhythms of behavior by secreting factors that act locally within the hypothalamus. In a systematic screen, we identified transforming growth factor-alpha (TGF-alpha) as a likely SCN inhibitor of locomotion. TGF-alpha is expressed rhythmically in the SCN, and when infused into the third ventricle it reversibly inhibited locomotor activity and disrupted circadian sleep-wake cycles. These actions are mediated by epidermal growth factor (EGF) receptors on neurons in the hypothalamic subparaventricular zone. Mice with a hypomorphic EGF receptor mutation exhibited excessive daytime locomotor activity and failed to suppress activity when exposed to light. These results implicate EGF receptor signaling in the daily control of locomotor activity, and identify a neural circuit in the hypothalamus that likely mediates the regulation of behavior both by the SCN and the retina.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kramer, A -- Yang, F C -- Snodgrass, P -- Li, X -- Scammell, T E -- Davis, F C -- Weitz, C J -- HD-18686/HD/NICHD NIH HHS/ -- MH62589/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2001 Dec 21;294(5551):2511-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11752569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/drug effects/physiology ; Body Temperature/drug effects ; Cerebral Ventricles/metabolism ; Circadian Rhythm/drug effects/*physiology ; Cricetinae ; Darkness ; Epidermal Growth Factor/pharmacology ; Female ; Hypothalamus/*metabolism ; Ligands ; Light ; Male ; Mesocricetus ; Mice ; *Motor Activity/drug effects ; Neural Pathways/physiology ; Neurons/metabolism ; Point Mutation ; Receptor, Epidermal Growth Factor/genetics/*metabolism ; Retina/metabolism ; Retinal Ganglion Cells/metabolism ; Signal Transduction ; Sleep/drug effects/*physiology ; Suprachiasmatic Nucleus/*metabolism ; Transforming Growth Factor alpha/administration & ; dosage/genetics/metabolism/pharmacology
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  • 10
    Publication Date: 2001-09-15
    Description: Throughout the past four decades, silicon semiconductor technology has advanced at exponential rates in both performance and productivity. Concerns have been raised, however, that the limits of silicon technology may soon be reached. Analysis of fundamental, material, device, circuit, and system limits reveals that silicon technology has an enormous remaining potential to achieve terascale integration (TSI) of more than 1 trillion transistors per chip. Such massive-scale integration is feasible assuming the development and economical mass production of double-gate metal-oxide-semiconductor field effect transistors with gate oxide thickness of about 1 nanometer, silicon channel thickness of about 3 nanometers, and channel length of about 10 nanometers. The development of interconnecting wires for these transistors presents a major challenge to the achievement of nanoelectronics for TSI.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meindl, J D -- Chen, Q -- Davis, J A -- New York, N.Y. -- Science. 2001 Sep 14;293(5537):2044-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Electrical and Computer Engineering, Microelectronics Research Center, Georgia Institute of Technology, Atlanta, GA 30332-0269, USA. james.meindl@mirc.gatech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11557881" target="_blank"〉PubMed〈/a〉
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