ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Articles  (279)
  • Nature  (7)
  • 328
  • Natural Sciences in General  (279)
  • Electrical Engineering, Measurement and Control Technology
Collection
  • Articles  (279)
Journal
Topic
  • 1
    Publication Date: 1898-10-01
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2016-07-14
    Description: Cloche is a bHLH-PAS transcription factor that drives haemato-vascular specification Nature 535, 7611 (2016). doi:10.1038/nature18614 Authors: Sven Reischauer, Oliver A. Stone, Alethia Villasenor, Neil Chi, Suk-Won Jin, Marcel Martin, Miler T. Lee, Nana Fukuda, Michele Marass, Alec Witty, Ian Fiddes, Taiyi Kuo, Won-Suk Chung, Sherveen Salek, Robert Lerrigo, Jessica Alsiö, Shujun Luo, Dominika Tworus, Sruthy M. Augustine, Sophie Mucenieks, Björn Nystedt, Antonio J. Giraldez, Gary P. Schroth, Olov Andersson & Didier Y. R. Stainier Vascular and haematopoietic cells organize into specialized tissues during early embryogenesis to supply essential nutrients to all organs and thus play critical roles in development and disease. At the top of the haemato-vascular specification cascade lies cloche, a gene that when mutated in zebrafish leads to the striking phenotype of loss of most endothelial and haematopoietic cells and a significant increase in cardiomyocyte numbers. Although this mutant has been analysed extensively to investigate mesoderm diversification and differentiation and continues to be broadly used as a unique avascular model, the isolation of the cloche gene has been challenging due to its telomeric location. Here we used a deletion allele of cloche to identify several new cloche candidate genes within this genomic region, and systematically genome-edited each candidate. Through this comprehensive interrogation, we succeeded in isolating the cloche gene and discovered that it encodes a PAS-domain-containing bHLH transcription factor, and that it is expressed in a highly specific spatiotemporal pattern starting during late gastrulation. Gain-of-function experiments show that it can potently induce endothelial gene expression. Epistasis experiments reveal that it functions upstream of etv2 and tal1, the earliest expressed endothelial and haematopoietic transcription factor genes identified to date. A mammalian cloche orthologue can also rescue blood vessel formation in zebrafish cloche mutants, indicating a highly conserved role in vertebrate vasculogenesis and haematopoiesis. The identification of this master regulator of endothelial and haematopoietic fate enhances our understanding of early mesoderm diversification and may lead to improved protocols for the generation of endothelial and haematopoietic cells in vivo and in vitro.
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2019
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2016-08-11
    Description: SAR11 bacteria linked to ocean anoxia and nitrogen loss Nature 536, 7615 (2016). doi:10.1038/nature19068 Authors: Despina Tsementzi, Jieying Wu, Samuel Deutsch, Sangeeta Nath, Luis M. Rodriguez-R, Andrew S. Burns, Piyush Ranjan, Neha Sarode, Rex R. Malmstrom, Cory C. Padilla, Benjamin K. Stone, Laura A. Bristow, Morten Larsen, Jennifer B. Glass, Bo Thamdrup, Tanja Woyke, Konstantinos T. Konstantinidis & Frank J. Stewart Bacteria of the SAR11 clade constitute up to one half of all microbial cells in the oxygen-rich surface ocean. SAR11 bacteria are also abundant in oxygen minimum zones (OMZs), where oxygen falls below detection and anaerobic microbes have vital roles in converting bioavailable nitrogen to
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2008-08-30
    Description: It is thought that the Northern Hemisphere experienced only ephemeral glaciations from the Late Eocene to the Early Pliocene epochs (about 38 to 4 million years ago), and that the onset of extensive glaciations did not occur until about 3 million years ago. Several hypotheses have been proposed to explain this increase in Northern Hemisphere glaciation during the Late Pliocene. Here we use a fully coupled atmosphere-ocean general circulation model and an ice-sheet model to assess the impact of the proposed driving mechanisms for glaciation and the influence of orbital variations on the development of the Greenland ice sheet in particular. We find that Greenland glaciation is mainly controlled by a decrease in atmospheric carbon dioxide during the Late Pliocene. By contrast, our model results suggest that climatic shifts associated with the tectonically driven closure of the Panama seaway, with the termination of a permanent El Nino state or with tectonic uplift are not large enough to contribute significantly to the growth of the Greenland ice sheet; moreover, we find that none of these processes acted as a priming mechanism for glacial inception triggered by variations in the Earth's orbit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lunt, Daniel J -- Foster, Gavin L -- Haywood, Alan M -- Stone, Emma J -- England -- Nature. 2008 Aug 28;454(7208):1102-5. doi: 10.1038/nature07223.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BRIDGE, School of Geographical Sciences, University of Bristol, University Road, Bristol BS8 1SS, UK. d.j.lunt@bristol.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18756254" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/*chemistry ; Carbon Dioxide/analysis/*metabolism ; Climate ; Greenland ; History, Ancient ; *Ice Cover ; North America ; Rain ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 2008-07-04
    Description: Voyager 2 crossed the solar wind termination shock at 83.7 au in the southern hemisphere, approximately 10 au closer to the Sun than found by Voyager 1 in the north. This asymmetry could indicate an asymmetric pressure from an interstellar magnetic field, from transient-induced shock motion, or from the solar wind dynamic pressure. Here we report that the intensity of 4-5 MeV protons accelerated by the shock near Voyager 2 was three times that observed concurrently by Voyager 1, indicating differences in the shock at the two locations. (Companion papers report on the plasma, magnetic field, plasma-wave and lower energy particle observations at the shock.) Voyager 2 did not find the source of anomalous cosmic rays at the shock, suggesting that the source is elsewhere on the shock or in the heliosheath. The small intensity gradient of Galactic cosmic ray helium indicates that either the gradient is further out in the heliosheath or the local interstellar Galactic cosmic ray intensity is lower than expected.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Edward C -- Cummings, Alan C -- McDonald, Frank B -- Heikkila, Bryant C -- Lal, Nand -- Webber, William R -- England -- Nature. 2008 Jul 3;454(7200):71-4. doi: 10.1038/nature07022.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉California Institute of Technology, Pasadena, California 91125, USA. ecs@srl.caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18596802" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 7
    Publication Date: 2008-10-14
    Description: Susceptibility to Crohn's disease, a complex inflammatory disease involving the small intestine, is controlled by over 30 loci. One Crohn's disease risk allele is in ATG16L1, a gene homologous to the essential yeast autophagy gene ATG16 (ref. 2). It is not known how ATG16L1 or autophagy contributes to intestinal biology or Crohn's disease pathogenesis. To address these questions, we generated and characterized mice that are hypomorphic for ATG16L1 protein expression, and validated conclusions on the basis of studies in these mice by analysing intestinal tissues that we collected from Crohn's disease patients carrying the Crohn's disease risk allele of ATG16L1. Here we show that ATG16L1 is a bona fide autophagy protein. Within the ileal epithelium, both ATG16L1 and a second essential autophagy protein ATG5 are selectively important for the biology of the Paneth cell, a specialized epithelial cell that functions in part by secretion of granule contents containing antimicrobial peptides and other proteins that alter the intestinal environment. ATG16L1- and ATG5-deficient Paneth cells exhibited notable abnormalities in the granule exocytosis pathway. In addition, transcriptional analysis revealed an unexpected gain of function specific to ATG16L1-deficient Paneth cells including increased expression of genes involved in peroxisome proliferator-activated receptor (PPAR) signalling and lipid metabolism, of acute phase reactants and of two adipocytokines, leptin and adiponectin, known to directly influence intestinal injury responses. Importantly, Crohn's disease patients homozygous for the ATG16L1 Crohn's disease risk allele displayed Paneth cell granule abnormalities similar to those observed in autophagy-protein-deficient mice and expressed increased levels of leptin protein. Thus, ATG16L1, and probably the process of autophagy, have a role within the intestinal epithelium of mice and Crohn's disease patients by selective effects on the cell biology and specialized regulatory properties of Paneth cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695978/" 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/PMC2695978/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cadwell, Ken -- Liu, John Y -- Brown, Sarah L -- Miyoshi, Hiroyuki -- Loh, Joy -- Lennerz, Jochen K -- Kishi, Chieko -- Kc, Wumesh -- Carrero, Javier A -- Hunt, Steven -- Stone, Christian D -- Brunt, Elizabeth M -- Xavier, Ramnik J -- Sleckman, Barry P -- Li, Ellen -- Mizushima, Noboru -- Stappenbeck, Thaddeus S -- Virgin, Herbert W 4th -- AI062773/AI/NIAID NIH HHS/ -- DK43351/DK/NIDDK NIH HHS/ -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK040561-13/DK/NIDDK NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P30 DK043351-18/DK/NIDDK NIH HHS/ -- P30 DK052574-09/DK/NIDDK NIH HHS/ -- P30 DK52574/DK/NIDDK NIH HHS/ -- R01 AI062773/AI/NIAID NIH HHS/ -- R01 AI062773-01A1/AI/NIAID NIH HHS/ -- R01 AI062832/AI/NIAID NIH HHS/ -- R01 AI062832-04/AI/NIAID NIH HHS/ -- T32 AR007279/AR/NIAMS NIH HHS/ -- T32 AR007279-30/AR/NIAMS NIH HHS/ -- T32 AR07279/AR/NIAMS NIH HHS/ -- U54 AI057160/AI/NIAID NIH HHS/ -- U54 AI057160-010005/AI/NIAID NIH HHS/ -- U54 AI057160-05S10018/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Nov 13;456(7219):259-63. doi: 10.1038/nature07416. Epub 2008 Oct 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18849966" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Autophagy/*genetics ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Crohn Disease/genetics/pathology ; Exocytosis/genetics ; Homozygote ; Humans ; Mice ; Mice, Inbred C57BL ; Mutation ; Paneth Cells/*metabolism/pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 8
    Publication Date: 2009-09-18
    Description: Electric fields induce motion in many fluid systems, including polymer melts, surfactant micelles and colloidal suspensions. Likewise, electric fields can be used to move liquid drops. Electrically induced droplet motion manifests itself in processes as diverse as storm cloud formation, commercial ink-jet printing, petroleum and vegetable oil dehydration, electrospray ionization for use in mass spectrometry, electrowetting and lab-on-a-chip manipulations. An important issue in practical applications is the tendency for adjacent drops to coalesce, and oppositely charged drops have long been assumed to experience an attractive force that favours their coalescence. Here we report the existence of a critical field strength above which oppositely charged drops do not coalesce. We observe that appropriately positioned and oppositely charged drops migrate towards one another in an applied electric field; but whereas the drops coalesce as expected at low field strengths, they are repelled from one another after contact at higher field strengths. Qualitatively, the drops appear to 'bounce' off one another. We directly image the transient formation of a meniscus bridge between the bouncing drops, and propose that this temporary bridge is unstable with respect to capillary pressure when it forms in an electric field exceeding a critical strength. The observation of oppositely charged drops bouncing rather than coalescing in strong electric fields should affect our understanding of any process involving charged liquid drops, including de-emulsification, electrospray ionization and atmospheric conduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ristenpart, W D -- Bird, J C -- Belmonte, A -- Dollar, F -- Stone, H A -- England -- Nature. 2009 Sep 17;461(7262):377-80. doi: 10.1038/nature08294.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Engineering and Materials Science, University of California at Davis, 1 Shields Drive, Davis, California 95616, USA. wdristenpart@ucdavis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19759616" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 9
    Publication Date: 2009-10-23
    Description: The tumour stroma is believed to contribute to some of the most malignant characteristics of epithelial tumours. However, signalling between stromal and tumour cells is complex and remains poorly understood. Here we show that the genetic inactivation of Pten in stromal fibroblasts of mouse mammary glands accelerated the initiation, progression and malignant transformation of mammary epithelial tumours. This was associated with the massive remodelling of the extracellular matrix (ECM), innate immune cell infiltration and increased angiogenesis. Loss of Pten in stromal fibroblasts led to increased expression, phosphorylation (T72) and recruitment of Ets2 to target promoters known to be involved in these processes. Remarkably, Ets2 inactivation in Pten stroma-deleted tumours ameliorated disruption of the tumour microenvironment and was sufficient to decrease tumour growth and progression. Global gene expression profiling of mammary stromal cells identified a Pten-specific signature that was highly represented in the tumour stroma of patients with breast cancer. These findings identify the Pten-Ets2 axis as a critical stroma-specific signalling pathway that suppresses mammary epithelial tumours.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2767301/" 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/PMC2767301/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trimboli, Anthony J -- Cantemir-Stone, Carmen Z -- Li, Fu -- Wallace, Julie A -- Merchant, Anand -- Creasap, Nicholas -- Thompson, John C -- Caserta, Enrico -- Wang, Hui -- Chong, Jean-Leon -- Naidu, Shan -- Wei, Guo -- Sharma, Sudarshana M -- Stephens, Julie A -- Fernandez, Soledad A -- Gurcan, Metin N -- Weinstein, Michael B -- Barsky, Sanford H -- Yee, Lisa -- Rosol, Thomas J -- Stromberg, Paul C -- Robinson, Michael L -- Pepin, Francois -- Hallett, Michael -- Park, Morag -- Ostrowski, Michael C -- Leone, Gustavo -- P01 CA097189/CA/NCI NIH HHS/ -- P01 CA097189-050002/CA/NCI NIH HHS/ -- P01CA097189/CA/NCI NIH HHS/ -- R01 CA053271/CA/NCI NIH HHS/ -- R01 CA085619/CA/NCI NIH HHS/ -- R01 CA085619-05/CA/NCI NIH HHS/ -- R01 CA121275/CA/NCI NIH HHS/ -- R01 CA121275-02/CA/NCI NIH HHS/ -- R01 HD047470/HD/NICHD NIH HHS/ -- R01 HD047470-05/HD/NICHD NIH HHS/ -- R01CA053271/CA/NCI NIH HHS/ -- R01CA85619/CA/NCI NIH HHS/ -- R01HD47470/HD/NICHD NIH HHS/ -- England -- Nature. 2009 Oct 22;461(7267):1084-91. doi: 10.1038/nature08486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, College of Biological Sciences, The Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19847259" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*metabolism/*pathology ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic ; Extracellular Matrix/metabolism ; Fibroblasts/*metabolism ; Gene Deletion ; Gene Expression Regulation, Neoplastic ; Humans ; Immunity, Innate ; Mammary Neoplasms, Experimental/metabolism/pathology ; Mice ; Mice, Transgenic ; Neoplasms, Glandular and Epithelial/*metabolism/*pathology ; PTEN Phosphohydrolase/deficiency/genetics/*metabolism ; Proto-Oncogene Protein c-ets-2/deficiency/metabolism ; Stromal Cells/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 10
    Publication Date: 2009-08-21
    Description: A stochastic background of gravitational waves is expected to arise from a superposition of a large number of unresolved gravitational-wave sources of astrophysical and cosmological origin. It should carry unique signatures from the earliest epochs in the evolution of the Universe, inaccessible to standard astrophysical observations. Direct measurements of the amplitude of this background are therefore of fundamental importance for understanding the evolution of the Universe when it was younger than one minute. Here we report limits on the amplitude of the stochastic gravitational-wave background using the data from a two-year science run of the Laser Interferometer Gravitational-wave Observatory (LIGO). Our result constrains the energy density of the stochastic gravitational-wave background normalized by the critical energy density of the Universe, in the frequency band around 100 Hz, to be 〈6.9 x 10(-6) at 95% confidence. The data rule out models of early Universe evolution with relatively large equation-of-state parameter, as well as cosmic (super)string models with relatively small string tension that are favoured in some string theory models. This search for the stochastic background improves on the indirect limits from Big Bang nucleosynthesis and cosmic microwave background at 100 Hz.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LIGO Scientific Collaboration & Virgo Collaboration -- Abbott, B P -- Abbott, R -- Acernese, F -- Adhikari, R -- Ajith, P -- Allen, B -- Allen, G -- Alshourbagy, M -- Amin, R S -- Anderson, S B -- Anderson, W G -- Antonucci, F -- Aoudia, S -- Arain, M A -- Araya, M -- Armandula, H -- Armor, P -- Arun, K G -- Aso, Y -- Aston, S -- Astone, P -- Aufmuth, P -- Aulbert, C -- Babak, S -- Baker, P -- Ballardin, G -- Ballmer, S -- Barker, C -- Barker, D -- Barone, F -- Barr, B -- Barriga, P -- Barsotti, L -- Barsuglia, M -- Barton, M A -- Bartos, I -- Bassiri, R -- Bastarrika, M -- Bauer, Th S -- Behnke, B -- Beker, M -- Benacquista, M -- Betzwieser, J -- Beyersdorf, P T -- Bigotta, S -- Bilenko, I A -- Billingsley, G -- Birindelli, S -- Biswas, R -- Bizouard, M A -- Black, E -- Blackburn, J K -- Blackburn, L -- Blair, D -- Bland, B -- Boccara, C -- Bodiya, T P -- Bogue, L -- Bondu, F -- Bonelli, L -- Bork, R -- Boschi, V -- Bose, S -- Bosi, L -- Braccini, S -- Bradaschia, C -- Brady, P R -- Braginsky, V B -- Brand, J F J van den -- Brau, J E -- Bridges, D O -- Brillet, A -- Brinkmann, M -- Brisson, V -- Van Den Broeck, C -- Brooks, A F -- Brown, D A -- Brummit, A -- Brunet, G -- Bullington, A -- Bulten, H J -- Buonanno, A -- Burmeister, O -- Buskulic, D -- Byer, R L -- Cadonati, L -- Cagnoli, G -- Calloni, E -- Camp, J B -- Campagna, E -- Cannizzo, J -- Cannon, K C -- Canuel, B -- Cao, J -- Carbognani, F -- Cardenas, L -- Caride, S -- Castaldi, G -- Caudill, S -- Cavaglia, M -- Cavalier, F -- Cavalieri, R -- Cella, G -- Cepeda, C -- Cesarini, E -- Chalermsongsak, T -- Chalkley, E -- Charlton, P -- Chassande-Mottin, E -- Chatterji, S -- Chelkowski, S -- Chen, Y -- Christensen, N -- Chung, C T Y -- Clark, D -- Clark, J -- Clayton, J H -- Cleva, F -- Coccia, E -- Cokelaer, T -- Colacino, C N -- Colas, J -- Colla, A -- Colombini, M -- Conte, R -- Cook, D -- Corbitt, T R C -- Corda, C -- Cornish, N -- Corsi, A -- Coulon, J-P -- Coward, D -- Coyne, D C -- Creighton, J D E -- Creighton, T D -- Cruise, A M -- Culter, R M -- Cumming, A -- Cunningham, L -- Cuoco, E -- Danilishin, S L -- D'Antonio, S -- Danzmann, K -- Dari, A -- Dattilo, V -- Daudert, B -- Davier, M -- Davies, G -- Daw, E J -- Day, R -- De Rosa, R -- Debra, D -- Degallaix, J -- Del Prete, M -- Dergachev, V -- Desai, S -- Desalvo, R -- Dhurandhar, S -- Di Fiore, L -- Di Lieto, A -- Di Paolo Emilio, M -- Di Virgilio, A -- Diaz, M -- Dietz, A -- Donovan, F -- Dooley, K L -- Doomes, E E -- Drago, M -- Drever, R W P -- Dueck, J -- Duke, I -- Dumas, J-C -- Dwyer, J G -- Echols, C -- Edgar, M -- Effler, A -- Ehrens, P -- Ely, G -- Espinoza, E -- Etzel, T -- Evans, M -- Evans, T -- Fafone, V -- Fairhurst, S -- Faltas, Y -- Fan, Y -- Fazi, D -- Fehrmann, H -- Ferrante, I -- Fidecaro, F -- Finn, L S -- Fiori, I -- Flaminio, R -- Flasch, K -- Foley, S -- Forrest, C -- Fotopoulos, N -- Fournier, J-D -- Franc, J -- Franzen, A -- Frasca, S -- Frasconi, F -- Frede, M -- Frei, M -- Frei, Z -- Freise, A -- Frey, R -- Fricke, T -- Fritschel, P -- Frolov, V V -- Fyffe, M -- Galdi, V -- Gammaitoni, L -- Garofoli, J A -- Garufi, F -- Genin, E -- Gennai, A -- Gholami, I -- Giaime, J A -- Giampanis, S -- Giardina, K D -- Giazotto, A -- Goda, K -- Goetz, E -- Goggin, L M -- Gonzalez, G -- Gorodetsky, M L -- Gobler, S -- Gouaty, R -- Granata, M -- Granata, V -- Grant, A -- Gras, S -- Gray, C -- Gray, M -- Greenhalgh, R J S -- Gretarsson, A M -- Greverie, C -- Grimaldi, F -- Grosso, R -- Grote, H -- Grunewald, S -- Guenther, M -- Guidi, G -- Gustafson, E K -- Gustafson, R -- Hage, B -- Hallam, J M -- Hammer, D -- Hammond, G D -- Hanna, C -- Hanson, J -- Harms, J -- Harry, G M -- Harry, I W -- Harstad, E D -- Haughian, K -- Hayama, K -- Heefner, J -- Heitmann, H -- Hello, P -- Heng, I S -- Heptonstall, A -- Hewitson, M -- Hild, S -- Hirose, E -- Hoak, D -- Hodge, K A -- Holt, K -- Hosken, D J -- Hough, J -- Hoyland, D -- Huet, D -- Hughey, B -- Huttner, S H -- Ingram, D R -- Isogai, T -- Ito, M -- Ivanov, A -- Johnson, B -- Johnson, W W -- Jones, D I -- Jones, G -- Jones, R -- Sancho de la Jordana, L -- Ju, L -- Kalmus, P -- Kalogera, V -- Kandhasamy, S -- Kanner, J -- Kasprzyk, D -- Katsavounidis, E -- Kawabe, K -- Kawamura, S -- Kawazoe, F -- Kells, W -- Keppel, D G -- Khalaidovski, A -- Khalili, F Y -- Khan, R -- Khazanov, E -- King, P -- Kissel, J S -- Klimenko, S -- Kokeyama, K -- Kondrashov, V -- Kopparapu, R -- Koranda, S -- Kozak, D -- Krishnan, B -- Kumar, R -- Kwee, P -- La Penna, P -- Lam, P K -- Landry, M -- Lantz, B -- Laval, M -- Lazzarini, A -- Lei, H -- Lei, M -- Leindecker, N -- Leonor, I -- Leroy, N -- Letendre, N -- Li, C -- Lin, H -- Lindquist, P E -- Littenberg, T B -- Lockerbie, N A -- Lodhia, D -- Longo, M -- Lorenzini, M -- Loriette, V -- Lormand, M -- Losurdo, G -- Lu, P -- Lubinski, M -- Lucianetti, A -- Luck, H -- Machenschalk, B -- Macinnis, M -- Mackowski, J-M -- Mageswaran, M -- Mailand, K -- Majorana, E -- Man, N -- Mandel, I -- Mandic, V -- Mantovani, M -- Marchesoni, F -- Marion, F -- Marka, S -- Marka, Z -- Markosyan, A -- Markowitz, J -- Maros, E -- Marque, J -- Martelli, F -- Martin, I W -- Martin, R M -- Marx, J N -- Mason, K -- Masserot, A -- Matichard, F -- Matone, L -- Matzner, R A -- Mavalvala, N -- McCarthy, R -- McClelland, D E -- McGuire, S C -- McHugh, M -- McIntyre, G -- McKechan, D J A -- McKenzie, K -- Mehmet, M -- Melatos, A -- Melissinos, A C -- Mendell, G -- Menendez, D F -- Menzinger, F -- Mercer, R A -- Meshkov, S -- Messenger, C -- Meyer, M S -- Michel, C -- Milano, L -- Miller, J -- Minelli, J -- Minenkov, Y -- Mino, Y -- Mitrofanov, V P -- Mitselmakher, G -- Mittleman, R -- Miyakawa, O -- Moe, B -- Mohan, M -- Mohanty, S D -- Mohapatra, S R P -- Moreau, J -- Moreno, G -- Morgado, N -- Morgia, A -- Morioka, T -- Mors, K -- Mosca, S -- Mossavi, K -- Mours, B -- Mowlowry, C -- Mueller, G -- Muhammad, D -- Muhlen, H Zur -- Mukherjee, S -- Mukhopadhyay, H -- Mullavey, A -- Muller-Ebhardt, H -- Munch, J -- Murray, P G -- Myers, E -- Myers, J -- Nash, T -- Nelson, J -- Neri, I -- Newton, G -- Nishizawa, A -- Nocera, F -- Numata, K -- Ochsner, E -- O'Dell, J -- Ogin, G H -- O'Reilly, B -- O'Shaughnessy, R -- Ottaway, D J -- Ottens, R S -- Overmier, H -- Owen, B J -- Pagliaroli, G -- Palomba, C -- Pan, Y -- Pankow, C -- Paoletti, F -- Papa, M A -- Parameshwaraiah, V -- Pardi, S -- Pasqualetti, A -- Passaquieti, R -- Passuello, D -- Patel, P -- Pedraza, M -- Penn, S -- Perreca, A -- Persichetti, G -- Pichot, M -- Piergiovanni, F -- Pierro, V -- Pinard, L -- Pinto, I M -- Pitkin, M -- Pletsch, H J -- Plissi, M V -- Poggiani, R -- Postiglione, F -- Principe, M -- Prix, R -- Prodi, G A -- Prokhorov, L -- Punken, O -- Punturo, M -- Puppo, P -- Putten, S van der -- Quetschke, V -- Raab, F J -- Rabaste, O -- Rabeling, D S -- Radkins, H -- Raffai, P -- Raics, Z -- Rainer, N -- Rakhmanov, M -- Rapagnani, P -- Raymond, V -- Re, V -- Reed, C M -- Reed, T -- Regimbau, T -- Rehbein, H -- Reid, S -- Reitze, D H -- Ricci, F -- Riesen, R -- Riles, K -- Rivera, B -- Roberts, P -- Robertson, N A -- Robinet, F -- Robinson, C -- Robinson, E L -- Rocchi, A -- Roddy, S -- Rolland, L -- Rollins, J -- Romano, J D -- Romano, R -- Romie, J H -- Rover, C -- Rowan, S -- Rudiger, A -- Ruggi, P -- Russell, P -- Ryan, K -- Sakata, S -- Salemi, F -- Sandberg, V -- Sannibale, V -- Santamaria, L -- Saraf, S -- Sarin, P -- Sassolas, B -- Sathyaprakash, B S -- Sato, S -- Satterthwaite, M -- Saulson, P R -- Savage, R -- Savov, P -- Scanlan, M -- Schilling, R -- Schnabel, R -- Schofield, R -- Schulz, B -- Schutz, B F -- Schwinberg, P -- Scott, J -- Scott, S M -- Searle, A C -- Sears, B -- Seifert, F -- Sellers, D -- Sengupta, A S -- Sentenac, D -- Sergeev, A -- Shapiro, B -- Shawhan, P -- Shoemaker, D H -- Sibley, A -- Siemens, X -- Sigg, D -- Sinha, S -- Sintes, A M -- Slagmolen, B J J -- Slutsky, J -- van der Sluys, M V -- Smith, J R -- Smith, M R -- Smith, N D -- Somiya, K -- Sorazu, B -- Stein, A -- Stein, L C -- Steplewski, S -- Stochino, A -- Stone, R -- Strain, K A -- Strigin, S -- Stroeer, A -- Sturani, R -- Stuver, A L -- Summerscales, T Z -- Sun, K-X -- Sung, M -- Sutton, P J -- Swinkels, B L -- Szokoly, G P -- Talukder, D -- Tang, L -- Tanner, D B -- Tarabrin, S P -- Taylor, J R -- Taylor, R -- Terenzi, R -- Thacker, J -- Thorne, K A -- Thorne, K S -- Thuring, A -- Tokmakov, K V -- Toncelli, A -- Tonelli, M -- Torres, C -- Torrie, C -- Tournefier, E -- Travasso, F -- Traylor, G -- Trias, M -- Trummer, J -- Ugolini, D -- Ulmen, J -- Urbanek, K -- Vahlbruch, H -- Vajente, G -- Vallisneri, M -- Vass, S -- Vaulin, R -- Vavoulidis, M -- Vecchio, A -- Vedovato, G -- van Veggel, A A -- Veitch, J -- Veitch, P -- Veltkamp, C -- Verkindt, D -- Vetrano, F -- Vicere, A -- Villar, A -- Vinet, J-Y -- Vocca, H -- Vorvick, C -- Vyachanin, S P -- Waldman, S J -- Wallace, L -- Ward, H -- Ward, R L -- Was, M -- Weidner, A -- Weinert, M -- Weinstein, A J -- Weiss, R -- Wen, L -- Wen, S -- Wette, K -- Whelan, J T -- Whitcomb, S E -- Whiting, B F -- Wilkinson, C -- Willems, P A -- Williams, H R -- Williams, L -- Willke, B -- Wilmut, I -- Winkelmann, L -- Winkler, W -- Wipf, C C -- Wiseman, A G -- Woan, G -- Wooley, R -- Worden, J -- Wu, W -- Yakushin, I -- Yamamoto, H -- Yan, Z -- Yoshida, S -- Yvert, M -- Zanolin, M -- Zhang, J -- Zhang, L -- Zhao, C -- Zotov, N -- Zucker, M E -- Zweizig, J -- England -- Nature. 2009 Aug 20;460(7258):990-4. doi: 10.1038/nature08278.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lists of participants and their affiliations appear at the end of the paper.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19693079" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...