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  • 1
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    Lightwave-driven quasiparticle collisions on a subcycle timescale (2016)
    Springer Nature
    In: Nature
    Details
    Publikationsdatum: 2016-05-12
    Beschreibung: Lightwave-driven quasiparticle collisions on a subcycle timescale Nature 533, 7602 (2016). doi:10.1038/nature17958 Authors: F. Langer, M. Hohenleutner, C. P. Schmid, C. Poellmann, P. Nagler, T. Korn, C. Schüller, M. S. Sherwin, U. Huttner, J. T. Steiner, S. W. Koch, M. Kira & R. Huber Ever since Ernest Rutherford scattered α-particles from gold foils, collision experiments have revealed insights into atoms, nuclei and elementary particles. In solids, many-body correlations lead to characteristic resonances—called quasiparticles—such as excitons, dropletons, polarons and Cooper pairs. The structure and dynamics of quasiparticles are important because they define macroscopic phenomena such as Mott insulating states, spontaneous spin- and charge-order, and high-temperature superconductivity. However, the extremely short lifetimes of these entities make practical implementations of a suitable collider challenging. Here we exploit lightwave-driven charge transport, the foundation of attosecond science, to explore ultrafast quasiparticle collisions directly in the time domain: a femtosecond optical pulse creates excitonic electron–hole pairs in the layered dichalcogenide tungsten diselenide while a strong terahertz field accelerates and collides the electrons with the holes. The underlying dynamics of the wave packets, including collision, pair annihilation, quantum interference and dephasing, are detected as light emission in high-order spectral sidebands of the optical excitation. A full quantum theory explains our observations microscopically. This approach enables collision experiments with various complex quasiparticles and suggests a promising new way of generating sub-femtosecond pulses.
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Springer Nature
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  • 2
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    Graded band gap GaInNAs solar cells (2015)
    American Institute of Physics (AIP)
    Details
    Publikationsdatum: 2015-06-09
    Beschreibung: Dilute nitride GaInN(Sb)As with a band gap (E g ) of 1.0 eV is a promising material for the integration in next generation multijunction solar cells. We have investigated the effect of a compositionally graded GaInNAs absorber layer on the spectral response of a GaInNAs sub cell. We produced band gap gradings (ΔE g ) of up to 39 meV across a 1  μ m thick GaInNAs layer. Thereby, the external quantum efficiency—compared to reference cells—was increased due to the improved extraction of photo-generated carriers from 34.0% to 36.7% for the wavelength range from 900 nm to 1150 nm. However, this device figure improvement is accompanied by a small decrease in the open circuit voltage of about 20 mV and the shift of the absorption edge to shorter wavelengths.
    Print ISSN: 0003-6951
    Digitale ISSN: 1077-3118
    Thema: Physik
    Publiziert von American Institute of Physics (AIP)
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  • 3
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    Del-1, an endogenous leukocyte-endothelial adhesion inhibitor, limits inflammatory cell recruitment (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-11-15
    Beschreibung: Leukocyte recruitment to sites of infection or inflammation requires multiple adhesive events. Although numerous players promoting leukocyte-endothelial interactions have been characterized, functionally important endogenous inhibitors of leukocyte adhesion have not been identified. Here we describe the endothelially derived secreted molecule Del-1 (developmental endothelial locus-1) as an anti-adhesive factor that interferes with the integrin LFA-1-dependent leukocyte-endothelial adhesion. Endothelial Del-1 deficiency increased LFA-1-dependent leukocyte adhesion in vitro and in vivo. Del-1-/- mice displayed significantly higher neutrophil accumulation in lipopolysaccharide-induced lung inflammation in vivo, which was reversed in Del-1/LFA-1 double-deficient mice. Thus, Del-1 is an endogenous inhibitor of inflammatory cell recruitment and could provide a basis for targeting leukocyte-endothelial interactions in disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2753175/" 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/PMC2753175/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, Eun Young -- Chavakis, Emmanouil -- Czabanka, Marcus A -- Langer, Harald F -- Fraemohs, Line -- Economopoulou, Matina -- Kundu, Ramendra K -- Orlandi, Alessia -- Zheng, Ying Yi -- Prieto, Darue A -- Ballantyne, Christie M -- Constant, Stephanie L -- Aird, William C -- Papayannopoulou, Thalia -- Gahmberg, Carl G -- Udey, Mark C -- Vajkoczy, Peter -- Quertermous, Thomas -- Dimmeler, Stefanie -- Weber, Christian -- Chavakis, Triantafyllos -- AI067254/AI/NIAID NIH HHS/ -- R01 HL082927/HL/NHLBI NIH HHS/ -- Z01 BC010790-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 14;322(5904):1101-4. doi: 10.1126/science.1165218.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19008446" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Bronchoalveolar Lavage Fluid/cytology/immunology ; Carrier Proteins/*physiology ; *Cell Adhesion ; Endothelial Cells/*physiology ; Intercellular Adhesion Molecule-1/metabolism ; Leukocyte Rolling ; Ligands ; Lipopolysaccharides/immunology ; Lung/blood supply/immunology ; Lymphocyte Function-Associated Antigen-1/metabolism ; Mice ; Monocytes/*physiology ; *Neutrophil Infiltration ; Neutrophils/*physiology ; Peritonitis/immunology ; Pneumonia/*immunology ; Recombinant Fusion Proteins/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)
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  • 4
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    Lipin1 deficiency causes sarcoplasmic reticulum stress and chaperone-responsive myopathy (2019)
    Springer Nature
    Details
    Publikationsdatum: 2019
    Beschreibung: 〈p〉As a consequence of impaired glucose or fatty acid metabolism, bioenergetic stress in skeletal muscles may trigger myopathy and rhabdomyolysis. Genetic mutations causing loss of function of the LPIN1 gene frequently lead to severe rhabdomyolysis bouts in children, though the metabolic alterations and possible therapeutic interventions remain elusive. Here, we show that lipin1 deficiency in mouse skeletal muscles is sufficient to trigger myopathy. Strikingly, muscle fibers display strong accumulation of both neutral and phospholipids. The metabolic lipid imbalance can be traced to an altered fatty acid synthesis and fatty acid oxidation, accompanied by a defect in acyl chain elongation and desaturation. As an underlying cause, we reveal a severe sarcoplasmic reticulum (SR) stress, leading to the activation of the lipogenic SREBP1c/SREBP2 factors, the accumulation of the Fgf21 cytokine, and alterations of SR–mitochondria morphology. Importantly, pharmacological treatments with the chaperone TUDCA and the fatty acid oxidation activator bezafibrate improve muscle histology and strength of lipin1 mutants. Our data reveal that SR stress and alterations in SR–mitochondria contacts are contributing factors and potential intervention targets of the myopathy associated with lipin1 deficiency.〈/p〉
    Print ISSN: 0261-4189
    Digitale ISSN: 1460-2075
    Thema: Biologie , Medizin
    Publiziert von Springer Nature im Namen von The European Molecular Biology Organization (EMBO).
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  • 5
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    Lipin1 deficiency causes sarcoplasmic reticulum stress and chaperone-responsive myopathy (2018)
    Springer Nature
    Details
    Publikationsdatum: 2018
    Beschreibung: 〈sec〉〈st〉Synopsis〈/st〉〈p〉〈textbox textbox-type="graphic"〉〈p〉〈inline-fig〉〈/inline-fig〉〈/p〉〈/textbox〉〈/p〉 〈p〉Loss-of-function mutations of ER-resident phosphatidate phosphatase lipin1 (〈i〉LPIN1〈/i〉) frequently lead to severe muscle injury in children, but the underlying cellular mechanism remains elusive. Here, genetic analysis identified sarcoplasmic reticulum (SR) stress response and altered mitochondrial morphology as primary causes for detrimental lipid accumulation, pointing to potential therapeutic interventions.〈/p〉 〈p〉 〈l type="unord"〉〈li〉〈p〉Skeletal muscle specific 〈i〉Lpin1〈/i〉 depletion in mice results in myopathy.〈/p〉〈/li〉 〈li〉〈p〉Lipin1 mutant muscles show increased fatty acid biosynthesis and lipid levels.〈/p〉〈/li〉 〈li〉〈p〉Lipin1 deficiency triggers unfolded stress response and SR fragmentation.〈/p〉〈/li〉 〈li〉〈p〉mtDNA levels and SR-mitochondria contacts are impaired at 〈i〉Lpin1〈/i〉 deletion.〈/p〉〈/li〉 〈li〉〈p〉Lipin1-dependent myopathy is rescued by treatment with the chaperone TUDCA or fatty acid oxidation agonist bezafibrate.〈/p〉〈/li〉〈/l〉 〈/p〉〈/sec〉
    Print ISSN: 0261-4189
    Digitale ISSN: 1460-2075
    Thema: Biologie , Medizin
    Publiziert von Springer Nature im Namen von The European Molecular Biology Organization (EMBO).
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  • 6
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    Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells (2016)
    Springer Nature
    Details
    Publikationsdatum: 2016-05-20
    Beschreibung: Article Factor XII initiates the intrinsic blood coagulation cascade and the kinin system. Here the authors show that Factor XII is elevated in the blood of multiple sclerosis patients, activates dendritic cells via CD87 and cAMP, and its blockade inhibits immunopathology in a mouse model of the disease. Nature Communications doi: 10.1038/ncomms11626 Authors: Kerstin Göbel, Susann Pankratz, Chloi-Magdalini Asaridou, Alexander M. Herrmann, Stefan Bittner, Monika Merker, Tobias Ruck, Sarah Glumm, Friederike Langhauser, Peter Kraft, Thorsten F. Krug, Johanna Breuer, Martin Herold, Catharina C. Gross, Denise Beckmann, Adelheid Korb-Pap, Michael K. Schuhmann, Stefanie Kuerten, Ioannis Mitroulis, Clemens Ruppert, Marc W. Nolte, Con Panousis, Luisa Klotz, Beate Kehrel, Thomas Korn, Harald F. Langer, Thomas Pap, Bernhard Nieswandt, Heinz Wiendl, Triantafyllos Chavakis, Christoph Kleinschnitz, Sven G. Meuth
    Digitale ISSN: 2041-1723
    Thema: Biologie , Chemie und Pharmazie , Allgemeine Naturwissenschaft , Physik
    Publiziert von Springer Nature
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  • 7
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    Real-time observation of interfering crystal electrons in high-harmonic generation (2015)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2015-08-01
    Beschreibung: Acceleration and collision of particles has been a key strategy for exploring the texture of matter. Strong light waves can control and recollide electronic wavepackets, generating high-harmonic radiation that encodes the structure and dynamics of atoms and molecules and lays the foundations of attosecond science. The recent discovery of high-harmonic generation in bulk solids combines the idea of ultrafast acceleration with complex condensed matter systems, and provides hope for compact solid-state attosecond sources and electronics at optical frequencies. Yet the underlying quantum motion has not so far been observable in real time. Here we study high-harmonic generation in a bulk solid directly in the time domain, and reveal a new kind of strong-field excitation in the crystal. Unlike established atomic sources, our solid emits high-harmonic radiation as a sequence of subcycle bursts that coincide temporally with the field crests of one polarity of the driving terahertz waveform. We show that these features are characteristic of a non-perturbative quantum interference process that involves electrons from multiple valence bands. These results identify key mechanisms for future solid-state attosecond sources and next-generation light-wave electronics. The new quantum interference process justifies the hope for all-optical band-structure reconstruction and lays the foundation for possible quantum logic operations at optical clock rates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hohenleutner, M -- Langer, F -- Schubert, O -- Knorr, M -- Huttner, U -- Koch, S W -- Kira, M -- Huber, R -- England -- Nature. 2015 Jul 30;523(7562):572-5. doi: 10.1038/nature14652.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, University of Regensburg, 93040 Regensburg, Germany. ; Department of Physics, University of Marburg, 35032 Marburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26223624" target="_blank"〉PubMed〈/a〉
    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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    Dichloroacetate prevents restenosis in preclinical animal models of vessel injury (2014)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2014-04-22
    Beschreibung: Despite the introduction of antiproliferative drug-eluting stents, coronary heart disease remains the leading cause of death in the United States. In-stent restenosis and bypass graft failure are characterized by excessive smooth muscle cell (SMC) proliferation and concomitant myointima formation with luminal obliteration. Here we show that during the development of myointimal hyperplasia in human arteries, SMCs show hyperpolarization of their mitochondrial membrane potential (DeltaPsim) and acquire a temporary state with a high proliferative rate and resistance to apoptosis. Pyruvate dehydrogenase kinase isoform 2 (PDK2) was identified as a key regulatory protein, and its activation proved necessary for relevant myointima formation. Pharmacologic PDK2 blockade with dichloroacetate or lentiviral PDK2 knockdown prevented DeltaPsim hyperpolarization, facilitated apoptosis and reduced myointima formation in injured human mammary and coronary arteries, rat aortas, rabbit iliac arteries and swine (pig) coronary arteries. In contrast to several commonly used antiproliferative drugs, dichloroacetate did not prevent vessel re-endothelialization. Targeting myointimal DeltaPsim and alleviating apoptosis resistance is a novel strategy for the prevention of proliferative vascular diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4323184/" 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/PMC4323184/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deuse, Tobias -- Hua, Xiaoqin -- Wang, Dong -- Maegdefessel, Lars -- Heeren, Joerg -- Scheja, Ludger -- Bolanos, Juan P -- Rakovic, Aleksandar -- Spin, Joshua M -- Stubbendorff, Mandy -- Ikeno, Fumiaki -- Langer, Florian -- Zeller, Tanja -- Schulte-Uentrop, Leonie -- Stoehr, Andrea -- Itagaki, Ryo -- Haddad, Francois -- Eschenhagen, Thomas -- Blankenberg, Stefan -- Kiefmann, Rainer -- Reichenspurner, Hermann -- Velden, Joachim -- Klein, Christine -- Yeung, Alan -- Robbins, Robert C -- Tsao, Philip S -- Schrepfer, Sonja -- 1R01HL105299/HL/NHLBI NIH HHS/ -- R01 HL105299/HL/NHLBI NIH HHS/ -- England -- Nature. 2014 May 29;509(7502):641-4. doi: 10.1038/nature13232. Epub 2014 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] TSI-laboratory, University Heart Center Hamburg, Martinistrasse 52, 20246 Hamburg, Germany [2] Cardiovascular Research Center Hamburg (CVRC) and DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Luebeck, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany [3] Cardiovascular Surgery, University Heart Center Hamburg, Martinistrasse 52, 20246 Hamburg, Germany. ; 1] TSI-laboratory, University Heart Center Hamburg, Martinistrasse 52, 20246 Hamburg, Germany [2] Cardiovascular Research Center Hamburg (CVRC) and DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Luebeck, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. ; Department of Medicine, Atherosclerosis Research Unit, Karolinska Institute, CMM L8:03, 17176 Stockholm, Sweden. ; Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. ; Institute of Functional Biology and Genomics, University of Salamanca-CSIC, Zacarias Gonzalez 2, 37007 Salamanca, Spain. ; Institute of Neurogenetics, University of Lubeck, Maria-Goeppert-Strasse 1, 23562 Lubeck, Germany. ; Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, 300 Pasteur Drive, Stanford, California 94305, USA. ; Institute of Pathology, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. ; 1] Cardiovascular Research Center Hamburg (CVRC) and DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Luebeck, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany [2] Department of General and Interventional Cardiology, University Heart Center Hamburg, Martinistrasse 52, 20246 Hamburg, Germany. ; 1] Cardiovascular Research Center Hamburg (CVRC) and DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Luebeck, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany [2] Department of Anaesthesiology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. ; 1] Cardiovascular Research Center Hamburg (CVRC) and DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Luebeck, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany [2] Institute of Experimental Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. ; 1] Cardiovascular Research Center Hamburg (CVRC) and DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Luebeck, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany [2] Cardiovascular Surgery, University Heart Center Hamburg, Martinistrasse 52, 20246 Hamburg, Germany. ; Department of Nephropathology, Institute of Pathology, University Hospital Erlangen, Krankenhausstrasse 8-10, 91054 Erlangen, Germany. ; Department of Cardiothoracic Surgery and Stanford Cardiovascular Institute, Stanford University, 300 Pasteur Drive, Stanford, California 94305, USA. ; 1] Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University, 300 Pasteur Drive, Stanford, California 94305, USA [2] Veterans Affairs Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, California 94304, USA. ; 1] TSI-laboratory, University Heart Center Hamburg, Martinistrasse 52, 20246 Hamburg, Germany [2] Cardiovascular Research Center Hamburg (CVRC) and DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Luebeck, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany [3] Cardiovascular Surgery, University Heart Center Hamburg, Martinistrasse 52, 20246 Hamburg, Germany [4] Department of Cardiothoracic Surgery and Stanford Cardiovascular Institute, Stanford University, 300 Pasteur Drive, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24747400" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Angioplasty, Balloon/adverse effects ; Animals ; Aorta/drug effects/*injuries/pathology ; Apoptosis/drug effects ; Arteries/drug effects/*injuries/pathology ; Cell Proliferation/drug effects ; Constriction, Pathologic/pathology/*prevention & control ; Coronary Vessels/drug effects/injuries/pathology ; Dichloroacetic Acid/*pharmacology/*therapeutic use ; Disease Models, Animal ; Enzyme Activation/drug effects ; Gene Knockdown Techniques ; Humans ; Hyperplasia/drug therapy/pathology ; Iliac Artery/drug effects/injuries/pathology ; Mammary Arteries/drug effects/injuries/pathology ; Membrane Potential, Mitochondrial/drug effects ; Mitochondria, Heart/drug effects/metabolism ; Myocytes, Smooth Muscle/drug effects/pathology ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/deficiency/genetics ; Rabbits ; Rats ; Secondary Prevention ; Stents/adverse effects ; Swine ; Tunica Intima/*drug effects/injuries/*pathology
    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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    Lightwave-driven quasiparticle collisions on a subcycle timescale (2016)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2016-05-14
    Beschreibung: Ever since Ernest Rutherford scattered alpha-particles from gold foils, collision experiments have revealed insights into atoms, nuclei and elementary particles. In solids, many-body correlations lead to characteristic resonances--called quasiparticles--such as excitons, dropletons, polarons and Cooper pairs. The structure and dynamics of quasiparticles are important because they define macroscopic phenomena such as Mott insulating states, spontaneous spin- and charge-order, and high-temperature superconductivity. However, the extremely short lifetimes of these entities make practical implementations of a suitable collider challenging. Here we exploit lightwave-driven charge transport, the foundation of attosecond science, to explore ultrafast quasiparticle collisions directly in the time domain: a femtosecond optical pulse creates excitonic electron-hole pairs in the layered dichalcogenide tungsten diselenide while a strong terahertz field accelerates and collides the electrons with the holes. The underlying dynamics of the wave packets, including collision, pair annihilation, quantum interference and dephasing, are detected as light emission in high-order spectral sidebands of the optical excitation. A full quantum theory explains our observations microscopically. This approach enables collision experiments with various complex quasiparticles and suggests a promising new way of generating sub-femtosecond pulses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langer, F -- Hohenleutner, M -- Schmid, C P -- Poellmann, C -- Nagler, P -- Korn, T -- Schuller, C -- Sherwin, M S -- Huttner, U -- Steiner, J T -- Koch, S W -- Kira, M -- Huber, R -- England -- Nature. 2016 May 11;533(7602):225-9. doi: 10.1038/nature17958.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, University of Regensburg, 93040 Regensburg, Germany. ; Department of Physics and the Institute for Terahertz Science and Technology, University of California at Santa Barbara, Santa Barbara, California 93106, USA. ; Department of Physics, University of Marburg, 35032 Marburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27172045" target="_blank"〉PubMed〈/a〉
    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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  • 10
    Digitale Medien
    Digitale Medien
    The antigenic profile of the mouse skeletal system
    Amsterdam : Elsevier
    Cryobiology 16 (1979), S. 603-604 
    Details
    ISSN: 0011-2240
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Biologie , Medizin
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1016/0011-2240(79)90145-7
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