ALBERT

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〉

Description: Ca(2+)-release-activated Ca(2+) (CRAC) channels generate sustained Ca(2+) signals that are essential for a range of cell functions, including antigen-stimulated T lymphocyte activation and proliferation. Recent studies have revealed that the depletion of Ca(2+) from the endoplasmic reticulum (ER) triggers the oligomerization of stromal interaction molecule 1 (STIM1), the ER Ca(2+) sensor, and its redistribution to ER-plasma membrane (ER-PM) junctions where the CRAC channel subunit ORAI1 accumulates in the plasma membrane and CRAC channels open. However, how the loss of ER Ca(2+) sets into motion these coordinated molecular rearrangements remains unclear. Here we define the relationships among [Ca(2+)](ER), STIM1 redistribution and CRAC channel activation and identify STIM1 oligomerization as the critical [Ca(2+)](ER)-dependent event that drives store-operated Ca(2+) entry. In human Jurkat leukaemic T cells expressing an ER-targeted Ca(2+) indicator, CRAC channel activation and STIM1 redistribution follow the same function of [Ca(2+)](ER), reaching half-maximum at approximately 200 microM with a Hill coefficient of approximately 4. Because STIM1 binds only a single Ca(2+) ion, the high apparent cooperativity suggests that STIM1 must first oligomerize to enable its accumulation at ER-PM junctions. To assess directly the causal role of STIM1 oligomerization in store-operated Ca(2+) entry, we replaced the luminal Ca(2+)-sensing domain of STIM1 with the 12-kDa FK506- and rapamycin-binding protein (FKBP12, also known as FKBP1A) or the FKBP-rapamycin binding (FRB) domain of the mammalian target of rapamycin (mTOR, also known as FRAP1). A rapamycin analogue oligomerizes the fusion proteins and causes them to accumulate at ER-PM junctions and activate CRAC channels without depleting Ca(2+) from the ER. Thus, STIM1 oligomerization is the critical transduction event through which Ca(2+) store depletion controls store-operated Ca(2+) entry, acting as a switch that triggers the self-organization and activation of STIM1-ORAI1 clusters at ER-PM junctions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712442/" 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/PMC2712442/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luik, Riina M -- Wang, Bin -- Prakriya, Murali -- Wu, Minnie M -- Lewis, Richard S -- R01 GM045374/GM/NIGMS NIH HHS/ -- R01 GM045374-18/GM/NIGMS NIH HHS/ -- T32 AI007290/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Jul 24;454(7203):538-42. doi: 10.1038/nature07065. Epub 2008 Jul 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18596693" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2685185/" 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/PMC2685185/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bankston, J R -- Kass, R S -- R01 HL056810/HL/NHLBI NIH HHS/ -- R01 HL056810-11/HL/NHLBI NIH HHS/ -- England -- Nature. 2008 Nov 13;456(7219):183-5. doi: 10.1038/456183a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19005542" target="_blank"〉PubMed〈/a〉

Description: We present a draft genome sequence of the platypus, Ornithorhynchus anatinus. This monotreme exhibits a fascinating combination of reptilian and mammalian characters. For example, platypuses have a coat of fur adapted to an aquatic lifestyle; platypus females lactate, yet lay eggs; and males are equipped with venom similar to that of reptiles. Analysis of the first monotreme genome aligned these features with genetic innovations. We find that reptile and platypus venom proteins have been co-opted independently from the same gene families; milk protein genes are conserved despite platypuses laying eggs; and immune gene family expansions are directly related to platypus biology. Expansions of protein, non-protein-coding RNA and microRNA families, as well as repeat elements, are identified. Sequencing of this genome now provides a valuable resource for deep mammalian comparative analyses, as well as for monotreme biology and conservation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803040/" 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/PMC2803040/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warren, Wesley C -- Hillier, LaDeana W -- Marshall Graves, Jennifer A -- Birney, Ewan -- Ponting, Chris P -- Grutzner, Frank -- Belov, Katherine -- Miller, Webb -- Clarke, Laura -- Chinwalla, Asif T -- Yang, Shiaw-Pyng -- Heger, Andreas -- Locke, Devin P -- Miethke, Pat -- Waters, Paul D -- Veyrunes, Frederic -- Fulton, Lucinda -- Fulton, Bob -- Graves, Tina -- Wallis, John -- Puente, Xose S -- Lopez-Otin, Carlos -- Ordonez, Gonzalo R -- Eichler, Evan E -- Chen, Lin -- Cheng, Ze -- Deakin, Janine E -- Alsop, Amber -- Thompson, Katherine -- Kirby, Patrick -- Papenfuss, Anthony T -- Wakefield, Matthew J -- Olender, Tsviya -- Lancet, Doron -- Huttley, Gavin A -- Smit, Arian F A -- Pask, Andrew -- Temple-Smith, Peter -- Batzer, Mark A -- Walker, Jerilyn A -- Konkel, Miriam K -- Harris, Robert S -- Whittington, Camilla M -- Wong, Emily S W -- Gemmell, Neil J -- Buschiazzo, Emmanuel -- Vargas Jentzsch, Iris M -- Merkel, Angelika -- Schmitz, Juergen -- Zemann, Anja -- Churakov, Gennady -- Kriegs, Jan Ole -- Brosius, Juergen -- Murchison, Elizabeth P -- Sachidanandam, Ravi -- Smith, Carly -- Hannon, Gregory J -- Tsend-Ayush, Enkhjargal -- McMillan, Daniel -- Attenborough, Rosalind -- Rens, Willem -- Ferguson-Smith, Malcolm -- Lefevre, Christophe M -- Sharp, Julie A -- Nicholas, Kevin R -- Ray, David A -- Kube, Michael -- Reinhardt, Richard -- Pringle, Thomas H -- Taylor, James -- Jones, Russell C -- Nixon, Brett -- Dacheux, Jean-Louis -- Niwa, Hitoshi -- Sekita, Yoko -- Huang, Xiaoqiu -- Stark, Alexander -- Kheradpour, Pouya -- Kellis, Manolis -- Flicek, Paul -- Chen, Yuan -- Webber, Caleb -- Hardison, Ross -- Nelson, Joanne -- Hallsworth-Pepin, Kym -- Delehaunty, Kim -- Markovic, Chris -- Minx, Pat -- Feng, Yucheng -- Kremitzki, Colin -- Mitreva, Makedonka -- Glasscock, Jarret -- Wylie, Todd -- Wohldmann, Patricia -- Thiru, Prathapan -- Nhan, Michael N -- Pohl, Craig S -- Smith, Scott M -- Hou, Shunfeng -- Nefedov, Mikhail -- de Jong, Pieter J -- Renfree, Marilyn B -- Mardis, Elaine R -- Wilson, Richard K -- 062023/Wellcome Trust/United Kingdom -- HG002238/HG/NHGRI NIH HHS/ -- MC_U137761446/Medical Research Council/United Kingdom -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-37/CA/NCI NIH HHS/ -- R01 GM59290/GM/NIGMS NIH HHS/ -- R01 HG002939/HG/NHGRI NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG004037-02/HG/NHGRI NIH HHS/ -- R01HG02385/HG/NHGRI NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2008 May 8;453(7192):175-83. doi: 10.1038/nature06936.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genome Sequencing Center, Washington University School of Medicine, Campus Box 8501, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA. wwarren@wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18464734" target="_blank"〉PubMed〈/a〉

Description: The onset of major glaciations in the Northern Hemisphere about 2.7 million years ago was most probably induced by climate cooling during the late Pliocene epoch. These glaciations, during which the Northern Hemisphere ice sheets successively expanded and retreated, are superimposed on this long-term climate trend, and have been linked to variations in the Earth's orbital parameters. One intriguing problem associated with orbitally driven glacial cycles is the transition from 41,000-year to 100,000-year climatic cycles that occurred without an apparent change in insolation forcing. Several hypotheses have been proposed to explain the transition, both including and excluding ice-sheet dynamics. Difficulties in finding a conclusive answer to this palaeoclimatic problem are related to the lack of sufficiently long records of ice-sheet volume or sea level. Here we use a comprehensive ice-sheet model and a simple ocean-temperature model to extract three-million-year mutually consistent records of surface air temperature, ice volume and sea level from marine benthic oxygen isotopes. Although these records and their relative phasings are subject to considerable uncertainty owing to limited availability of palaeoclimate constraints, the results suggest that the gradual emergence of the 100,000-year cycles can be attributed to the increased ability of the merged North American ice sheets to survive insolation maxima and reach continental-scale size. The oversized, wet-based ice sheet probably responded to the subsequent insolation maximum by rapid thinning through increased basal-sliding, thereby initiating a glacial termination. Based on our assessment of the temporal changes in air temperature and ice volume during individual glacials, we demonstrate the importance of ice dynamics and ice-climate interactions in establishing the 100,000-year glacial cycles, with enhanced North American ice-sheet growth and the subsequent merging of the ice sheets being key elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bintanja, R -- van de Wal, R S W -- England -- Nature. 2008 Aug 14;454(7206):869-72. doi: 10.1038/nature07158.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Royal Netherlands Meteorological Institute (KNMI), Wilhelminalaan 10, 3732 GK De Bilt, The Netherlands. bintanja@knmi.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18704083" target="_blank"〉PubMed〈/a〉

Description: When continents break apart, the rifting is sometimes accompanied by the production of large volumes of molten rock. The total melt volume, however, is uncertain, because only part of it has erupted at the surface. Furthermore, the cause of the magmatism is still disputed-specifically, whether or not it is due to increased mantle temperatures. We recorded deep-penetration normal-incidence and wide-angle seismic profiles across the Faroe and Hatton Bank volcanic margins in the northeast Atlantic. Here we show that near the Faroe Islands, for every 1 km along strike, 360-400 km(3) of basalt is extruded, while 540-600 km(3) is intruded into the continent-ocean transition. We find that lower-crustal intrusions are focused mainly into a narrow zone approximately 50 km wide on the transition, although extruded basalts flow more than 100 km from the rift. Seismic profiles show that the melt is intruded into the lower crust as sills, which cross-cut the continental fabric, rather than as an 'underplate' of 100 per cent melt, as has often been assumed. Evidence from the measured seismic velocities and from igneous thicknesses are consistent with the dominant control on melt production being increased mantle temperatures, with no requirement for either significant active small-scale mantle convection under the rift or the presence of fertile mantle at the time of continental break-up, as has previously been suggested for the North Atlantic Ocean.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, R S -- Smith, L K -- Roberts, A W -- Christie, P A F -- Kusznir, N J -- iSIMM Team -- Roberts, A M -- Healy, D -- Spitzer, R -- Chappell, A -- Eccles, J D -- Fletcher, R -- Hurst, N -- Lunnon, Z -- Parkin, C J -- Tymms, V J -- England -- Nature. 2008 Mar 27;452(7186):460-4. doi: 10.1038/nature06687.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bullard Laboratories, University of Cambridge, Madingley Road, Cambridge CB3 0EZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18368115" target="_blank"〉PubMed〈/a〉

Description: Recent studies of galaxies approximately 2-3 Gyr after the Big Bang have revealed large, rotating disks, similar to those of galaxies today. The existence of well-ordered rotation in galaxies during this peak epoch of cosmic star formation indicates that gas accretion is likely to be the dominant mode by which galaxies grow, because major mergers of galaxies would completely disrupt the observed velocity fields. But poor spatial resolution and sensitivity have hampered this interpretation; such studies have been limited to the largest and most luminous galaxies, which may have fundamentally different modes of assembly from those of more typical galaxies (which are thought to grow into the spheroidal components at the centres of galaxies similar to the Milky Way). Here we report observations of a typical star-forming galaxy at z = 3.07, with a linear resolution of approximately 100 parsecs. We find a well-ordered compact source in which molecular gas is being converted efficiently into stars, likely to be assembling a spheroidal bulge similar to those seen in spiral galaxies at the present day. The presence of undisrupted rotation may indicate that galaxies such as the Milky Way gain much of their mass by accretion rather than major mergers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stark, Daniel P -- Swinbank, A Mark -- Ellis, Richard S -- Dye, Simon -- Smail, Ian R -- Richard, Johan -- England -- Nature. 2008 Oct 9;455(7214):775-7. doi: 10.1038/nature07294.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Astronomy, California Institute of Technology, Pasadena, California 91125, USA. dps@astro.caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18843363" target="_blank"〉PubMed〈/a〉

Description: Angiogenesis and the development of a vascular network are required for tumour progression, and they involve the release of angiogenic factors, including vascular endothelial growth factor (VEGF-A), from both malignant and stromal cell types. Infiltration by cells of the myeloid lineage is a hallmark of many tumours, and in many cases the macrophages in these infiltrates express VEGF-A. Here we show that the deletion of inflammatory-cell-derived VEGF-A attenuates the formation of a typical high-density vessel network, thus blocking the angiogenic switch in solid tumours in mice. Vasculature in tumours lacking myeloid-cell-derived VEGF-A was less tortuous, with increased pericyte coverage and decreased vessel length, indicating vascular normalization. In addition, loss of myeloid-derived VEGF-A decreases the phosphorylation of VEGF receptor 2 (VEGFR2) in tumours, even though overall VEGF-A levels in the tumours are unaffected. However, deletion of myeloid-cell VEGF-A resulted in an accelerated tumour progression in multiple subcutaneous isograft models and an autochthonous transgenic model of mammary tumorigenesis, with less overall tumour cell death and decreased tumour hypoxia. Furthermore, loss of myeloid-cell VEGF-A increased the susceptibility of tumours to chemotherapeutic cytotoxicity. This shows that myeloid-derived VEGF-A is essential for the tumorigenic alteration of vasculature and signalling to VEGFR2, and that these changes act to retard, not promote, tumour progression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3103772/" 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/PMC3103772/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stockmann, Christian -- Doedens, Andrew -- Weidemann, Alexander -- Zhang, Na -- Takeda, Norihiko -- Greenberg, Joshua I -- Cheresh, David A -- Johnson, Randall S -- AI060840/AI/NIAID NIH HHS/ -- CA118165/CA/NCI NIH HHS/ -- CA82515/CA/NCI NIH HHS/ -- R01 CA082515/CA/NCI NIH HHS/ -- R01 CA082515-12/CA/NCI NIH HHS/ -- R01 CA118165/CA/NCI NIH HHS/ -- England -- Nature. 2008 Dec 11;456(7223):814-8. doi: 10.1038/nature07445. Epub 2008 Nov 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Section, Division of Biological Sciences, Moores Cancer Center, University of California, San Diego, San Diego, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18997773" target="_blank"〉PubMed〈/a〉