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  • 1
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    Ground-Motion Observations at Hotel Montana during the M 7.0 2010 Haiti Earthquake: Topography or Soil Amplification? (2013)
    Seismological Society of America (SSA)
    Details
    Publikationsdatum: 2013-10-01
    Beschreibung: Unusually severe structural damage was reported during the 2010 M  7.0 Haiti earthquake in the vicinity of Hotel Montana, located on top of a ridge in the district of Pétionville. Prompted by the observations, U.S. Geological Survey seismic stations were deployed, and aftershock recordings indicated ground-motion amplification on the top of the hill compared to adjacent stations on reference site conditions. The presence of topographic relief has been shown to significantly aggravate the consequences of strong ground motion during past events, and topographic effects were brought forward to explain the observations. In this paper, we test the hypothesis of topographic amplification as the dominant factor that contributed to the damage concentration in the vicinity of Hotel Montana. We initially conduct numerical simulations of the ridge seismic response assuming elastic homogeneous site conditions, and show that numerical predictions of topographic amplification disagree with the field data both in amplitude and in frequency. Conversely, while 1D ground-response analyses for the site conditions at the hilltop predict amplification in the same frequency range as the field data, they significantly underestimate the recorded amplitude. We then conduct numerical simulations of the foothill ridge response to seismic motion while accounting for soil layering, and qualitatively demonstrate that the recorded amplification is most likely attributed to coupled site–topographic amplification effects, namely to seismic waves trapped in the soft soil layers of the near surface, amplified as a consequence of reverberations, and further modified due to diffraction and scattering upon incidence on the irregular ground surface. Parametric investigations of the topography–soil amplification coupling effects are then conducted, and our results show that when accounting for a hypothetical soil–bedrock interface at 100 m depth, predictions are in excellent agreement with the observed motion.
    Print ISSN: 0037-1106
    Digitale ISSN: 1943-3573
    Thema: Geologie und Paläontologie , Physik
    Publiziert von Seismological Society of America (SSA)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Inhibition of stemness factors for differentiation [Biochemistry] (2014)
    National Academy of Sciences
    Details
    Publikationsdatum: 2014-02-05
    Beschreibung: The potential for pluripotent cells to differentiate into diverse specialized cell types has given much hope to the field of regenerative medicine. Nevertheless, the low efficiency of cell commitment has been a major bottleneck in this field. Here we provide a strategy to enhance the efficiency of early differentiation of...
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Publiziert von National Academy of Sciences
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  • 3
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    SUMO1-dependent modulation of SERCA2a in heart failure (2011)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2011-09-09
    Beschreibung: The calcium-transporting ATPase ATP2A2, also known as SERCA2a, is a critical ATPase responsible for Ca(2+) re-uptake during excitation-contraction coupling. Impaired Ca(2+) uptake resulting from decreased expression and reduced activity of SERCA2a is a hallmark of heart failure. Accordingly, restoration of SERCA2a expression by gene transfer has proved to be effective in improving cardiac function in heart-failure patients, as well as in animal models. The small ubiquitin-related modifier (SUMO) can be conjugated to lysine residues of target proteins, and is involved in many cellular processes. Here we show that SERCA2a is SUMOylated at lysines 480 and 585 and that this SUMOylation is essential for preserving SERCA2a ATPase activity and stability in mouse and human cells. The levels of SUMO1 and the SUMOylation of SERCA2a itself were greatly reduced in failing hearts. SUMO1 restitution by adeno-associated-virus-mediated gene delivery maintained the protein abundance of SERCA2a and markedly improved cardiac function in mice with heart failure. This effect was comparable to SERCA2A gene delivery. Moreover, SUMO1 overexpression in isolated cardiomyocytes augmented contractility and accelerated Ca(2+) decay. Transgene-mediated SUMO1 overexpression rescued cardiac dysfunction induced by pressure overload concomitantly with increased SERCA2a function. By contrast, downregulation of SUMO1 using small hairpin RNA (shRNA) accelerated pressure-overload-induced deterioration of cardiac function and was accompanied by decreased SERCA2a function. However, knockdown of SERCA2a resulted in severe contractile dysfunction both in vitro and in vivo, which was not rescued by overexpression of SUMO1. Taken together, our data show that SUMOylation is a critical post-translational modification that regulates SERCA2a function, and provide a platform for the design of novel therapeutic strategies for heart failure.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3443490/" 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/PMC3443490/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kho, Changwon -- Lee, Ahyoung -- Jeong, Dongtak -- Oh, Jae Gyun -- Chaanine, Antoine H -- Kizana, Eddy -- Park, Woo Jin -- Hajjar, Roger J -- HL080498/HL/NHLBI NIH HHS/ -- HL093183/HL/NHLBI NIH HHS/ -- P20 HL100396/HL/NHLBI NIH HHS/ -- P20 HL100396-02/HL/NHLBI NIH HHS/ -- P20HL100396/HL/NHLBI NIH HHS/ -- R01 HL078731/HL/NHLBI NIH HHS/ -- R01 HL078731-04/HL/NHLBI NIH HHS/ -- R01 HL080498/HL/NHLBI NIH HHS/ -- R01 HL080498-05/HL/NHLBI NIH HHS/ -- R01 HL083156/HL/NHLBI NIH HHS/ -- R01 HL083156-05/HL/NHLBI NIH HHS/ -- R01 HL088434/HL/NHLBI NIH HHS/ -- R01 HL088434-02/HL/NHLBI NIH HHS/ -- England -- Nature. 2011 Sep 7;477(7366):601-5. doi: 10.1038/nature10407.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, Box 1030, New York, New York 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21900893" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; HEK293 Cells ; Heart Failure/*metabolism/physiopathology ; Humans ; Lysine/metabolism ; Mice ; Rats ; Rats, Sprague-Dawley ; SUMO-1 Protein/genetics/*metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/*metabolism ; *Sumoylation ; Sus scrofa
    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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  • 4
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    Inhibition of miR-25 improves cardiac contractility in the failing heart (2014)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2014-03-29
    Beschreibung: Heart failure is characterized by a debilitating decline in cardiac function, and recent clinical trial results indicate that improving the contractility of heart muscle cells by boosting intracellular calcium handling might be an effective therapy. MicroRNAs (miRNAs) are dysregulated in heart failure but whether they control contractility or constitute therapeutic targets remains speculative. Using high-throughput functional screening of the human microRNAome, here we identify miRNAs that suppress intracellular calcium handling in heart muscle by interacting with messenger RNA encoding the sarcoplasmic reticulum calcium uptake pump SERCA2a (also known as ATP2A2). Of 875 miRNAs tested, miR-25 potently delayed calcium uptake kinetics in cardiomyocytes in vitro and was upregulated in heart failure, both in mice and humans. Whereas adeno-associated virus 9 (AAV9)-mediated overexpression of miR-25 in vivo resulted in a significant loss of contractile function, injection of an antisense oligonucleotide (antagomiR) against miR-25 markedly halted established heart failure in a mouse model, improving cardiac function and survival relative to a control antagomiR oligonucleotide. These data reveal that increased expression of endogenous miR-25 contributes to declining cardiac function during heart failure and suggest that it might be targeted therapeutically to restore function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4131725/" 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/PMC4131725/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wahlquist, Christine -- Jeong, Dongtak -- Rojas-Munoz, Agustin -- Kho, Changwon -- Lee, Ahyoung -- Mitsuyama, Shinichi -- van Mil, Alain -- Park, Woo Jin -- Sluijter, Joost P G -- Doevendans, Pieter A F -- Hajjar, Roger J -- Mercola, Mark -- HHSN268201000045C/HL/NHLBI NIH HHS/ -- HHSN26820100045C/PHS HHS/ -- P01 HL098053/HL/NHLBI NIH HHS/ -- P01HL098053/HL/NHLBI NIH HHS/ -- P20 HL100396/HL/NHLBI NIH HHS/ -- P20HL100396/HL/NHLBI NIH HHS/ -- P30 AR061303/AR/NIAMS NIH HHS/ -- P30 CA030199/CA/NCI NIH HHS/ -- P30AR061303/AR/NIAMS NIH HHS/ -- P30CA030199/CA/NCI NIH HHS/ -- P50 HL112324/HL/NHLBI NIH HHS/ -- P50HL112324/HL/NHLBI NIH HHS/ -- R01 HL088434/HL/NHLBI NIH HHS/ -- R01 HL093183/HL/NHLBI NIH HHS/ -- R01 HL108176/HL/NHLBI NIH HHS/ -- R01 HL113601/HL/NHLBI NIH HHS/ -- R01HL088434/HL/NHLBI NIH HHS/ -- R01HL093183/HL/NHLBI NIH HHS/ -- R01HL108176/HL/NHLBI NIH HHS/ -- R01HL113601/HL/NHLBI NIH HHS/ -- S10 RR021084/RR/NCRR NIH HHS/ -- England -- Nature. 2014 Apr 24;508(7497):531-5. doi: 10.1038/nature13073. Epub 2014 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Bioengineering, University of California, San Diego, and the Muscle Development and Regeneration Program, Sanford-Burnham Medical Research Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA [2]. ; 1] The Cardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [2]. ; Department of Bioengineering, University of California, San Diego, and the Muscle Development and Regeneration Program, Sanford-Burnham Medical Research Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA. ; The Cardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA. ; 1] Department of Bioengineering, University of California, San Diego, and the Muscle Development and Regeneration Program, Sanford-Burnham Medical Research Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA [2] Department of Cardiology, University Medical Center Utrecht and ICIN Netherlands Heart Institute, Heidelberglaan 100, room G02.523, 3584 CX Utrecht, The Netherlands. ; Global Research Laboratory, Gwangju Institute of Science and Technology, 123 Cheomdan-gwagiro, Buk-gu, Gwangju 500-712, South Korea. ; Department of Cardiology, University Medical Center Utrecht and ICIN Netherlands Heart Institute, Heidelberglaan 100, room G02.523, 3584 CX Utrecht, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670661" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcium/metabolism ; Dependovirus/genetics ; Disease Models, Animal ; HEK293 Cells ; Heart/drug effects/physiology/physiopathology ; Heart Failure/*genetics/*therapy ; Humans ; Kinetics ; Male ; Mice ; MicroRNAs/analysis/*antagonists & inhibitors/genetics/metabolism ; Myocardial Contraction/*drug effects ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Oligonucleotides, Antisense/genetics/metabolism/pharmacology ; RNA, Messenger/genetics/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/genetics/metabolism ; Survival Analysis ; Up-Regulation/genetics
    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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    Increasing N abundance in the northwestern Pacific Ocean due to atmospheric nitrogen deposition (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2011-09-24
    Beschreibung: The relative abundance of nitrate (N) over phosphorus (P) has increased over the period since 1980 in the marginal seas bordering the northwestern Pacific Ocean, located downstream of the populated and industrialized Asian continent. The increase in N availability within the study area was mainly driven by increasing N concentrations and was most likely due to deposition of pollutant nitrogen from atmospheric sources. Atmospheric nitrogen deposition had a high temporal correlation with N availability in the study area (r = 0.74 to 0.88), except in selected areas wherein riverine nitrogen load may be of equal importance. The increase in N availability caused by atmospheric deposition and riverine input has switched extensive parts of the study area from being N-limited to P-limited.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Tae-Wook -- Lee, Kitack -- Najjar, Raymond G -- Jeong, Hee-Dong -- Jeong, Hae Jin -- New York, N.Y. -- Science. 2011 Oct 28;334(6055):505-9. doi: 10.1126/science.1206583. Epub 2011 Sep 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Environmental Science and Engineering, Pohang University of Science and Technology, Pohang, 790-784, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21940860" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Air Pollutants ; Atmosphere/*chemistry ; Ecosystem ; Nitrates/*analysis ; Nitrogen/*analysis ; Pacific Ocean ; Phosphorus/analysis ; Seawater/*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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  • 6
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    Self-organization, condensation, and annihilation of topological vortices and antivortices in a multiferroic (2010)
    National Academy of Sciences
    Details
    Publikationsdatum: 2010-11-29
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Publiziert von National Academy of Sciences
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Temperature Evolution of Itinerant Ferromagnetism inSrRuO3Probed by Optical Spectroscopy (2013)
    American Physical Society
    Details
    Publikationsdatum: 2013-06-11
    Print ISSN: 0031-9007
    Digitale ISSN: 1079-7114
    Thema: Physik
    Publiziert von American Physical Society
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Evolution of the Domain Topology in a Ferroelectric (2013)
    American Physical Society
    Details
    Publikationsdatum: 2013-04-15
    Print ISSN: 0031-9007
    Digitale ISSN: 1079-7114
    Thema: Physik
    Publiziert von American Physical Society
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  • 9
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    A halo bias function measured deeply into voids without stochasticity (2014)
    Oxford University Press
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    Publikationsdatum: 2014-05-04
    Beschreibung: We study the relationship between dark-matter haloes and matter in the MIP (multum in parvo) N -body simulation ensemble, which allows precision measurements of this relationship, even deeply into voids. What enables this is a lack of discreteness, stochasticity, and exclusion, achieved by averaging over hundreds of possible sets of initial small-scale modes, while holding fixed large-scale modes that give the cosmic web. We find (i) that dark-matter-halo formation is greatly suppressed in voids; there is an exponential downturn at low densities in the otherwise power-law matter-to-halo density bias function. Thus, the rarity of haloes in voids is akin to the rarity of the largest clusters, and their abundance is quite sensitive to cosmological parameters. The exponential downturn appears both in an excursion-set model, and in a model in which fluctuations evolve in voids as in an open universe with an effective m proportional to a large-scale density. We also find that (ii) haloes typically populate the average halo-density field in a super-Poisson way, i.e. with a variance exceeding the mean; and (iii) the rank-order-Gaussianized halo and dark-matter fields are impressively similar in Fourier space. We compare both their power spectra and cross-correlation, supporting the conclusion that one is roughly a strictly increasing mapping of the other. The MIP ensemble especially reveals how halo abundance varies with ‘environmental’ quantities beyond the local matter density; (iv) we find a visual suggestion that at fixed matter density, filaments are more populated by haloes than clusters.
    Print ISSN: 0035-8711
    Digitale ISSN: 1365-2966
    Thema: Physik
    Publiziert von Oxford University Press
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Isobaric analog resonances of the N=21 nucleus ^{35}Si (2012)
    American Physical Society (APS)
    Details
    Publikationsdatum: 2012-03-16
    Beschreibung: Author(s): N. Imai, Y. Hirayama, Y. X. Watanabe, T. Teranishi, T. Hashimoto, S. Hayakawa, Y. Ichikawa, H. Ishiyama, S. C. Jeong, D. Kahl, S. Kubono, H. Miyatake, H. Ueno, H. Yamaguchi, K. Yoneda, and A. Yoshimi Neutron single-particle states in the neutron-rich nucleus 35 Si, which is located beside the N =20 shell breaking nucleus 32 Mg, were investigated through their isobaric analog resonances. The excitation function for 34 Si + p elastic scattering was measured around 0 ∘ in the laboratory frame by the thick... [Phys. Rev. C 85, 034313] Published Thu Mar 15, 2012
    Schlagwort(e): Nuclear Structure
    Print ISSN: 0556-2813
    Digitale ISSN: 1089-490X
    Thema: Physik
    Publiziert von American Physical Society (APS)
    Standort Signatur Erwartet Verfügbarkeit
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