@article{TaalStPourcainThieringetal.2012,
  author    = {Taal, H. Rob and St Pourcain, Beate and Thiering, Elisabeth and Das, Shikta and Mook-Kanamori, Dennis O. and Warrington, Nicole M. and Kaakinen, Marika and Kreiner-Moller, Eskil and Bradfield, Jonathan P. and Freathy, Rachel M. and Geller, Frank and Guxens, Monica and Cousminer, Diana L. and Kerkhof, Marjan and Timpson, Nicholas J. and Ikram, M. Arfan and Beilin, Lawrence J. and Bonnelykke, Klaus and Buxton, Jessica L. and Charoen, Pimphen and Chawes, Bo Lund Krogsgaard and Eriksson, Johan and Evans, David M. and Hofman, Albert and Kemp, John P. and Kim, Cecilia E. and Klopp, Norman and Lahti, Jari and Lye, Stephen J. and McMahon, George and Mentch, Frank D. and Mueller-Nurasyid, Martina and O'Reilly, Paul F. and Prokopenko, Inga and Rivadeneira, Fernando and Steegers, Eric A. P. and Sunyer, Jordi and Tiesler, Carla and Yaghootkar, Hanieh and Breteler, Monique M. B. and Debette, Stephanie and Fornage, Myriam and Gudnason, Vilmundur and Launer, Lenore J. and van der Lugt, Aad and Mosley, Thomas H. and Seshadri, Sudha and Smith, Albert V. and Vernooij, Meike W. and Blakemore, Alexandra I. F. and Chiavacci, Rosetta M. and Feenstra, Bjarke and Fernandez-Banet, Julio and Grant, Struan F. A. and Hartikainen, Anna-Liisa and van der Heijden, Albert J. and Iniguez, Carmen and Lathrop, Mark and McArdle, Wendy L. and Molgaard, Anne and Newnham, John P. and Palmer, Lyle J. and Palotie, Aarno and Pouta, Annneli and Ring, Susan M. and Sovio, Ulla and Standl, Marie and Uitterlinden, Andre G. and Wichmann, H-Erich and Vissing, Nadja Hawwa and DeCarli, Charles and van Duijn, Cornelia M. and McCarthy, Mark I. and Koppelman, Gerard H. and Estivill, Xavier and Hattersley, Andrew T. and Melbye, Mads and Bisgaard, Hans and Pennell, Craig E. and Widen, Elisabeth and Hakonarson, Hakon and Smith, George Davey and Heinrich, Joachim and Jarvelin, Marjo-Riitta and Jaddoe, Vincent W. V. and Adair, Linda S. and Ang, Wei and Atalay, Mustafa and van Beijsterveldt, Toos and Bergen, Nienke and Benke, Kelly and Berry, Diane J. and Bradfield, Jonathan P. and Charoen, Pimphen and Coin, Lachlan and Cousminer, Diana L. and Das, Shikta and Davis, Oliver S. P. and Elliott, Paul and Evans, David M. and Feenstra, Bjarke and Flexeder, Claudia and Frayling, Tim and Freathy, Rachel M. and Gaillard, Romy and Geller, Frank and Groen-Blokhuis, Maria and Goh, Liang-Kee and Guxens, Monica and Haworth, Claire M. A. and Hadley, Dexter and Hebebrand, Johannes and Hinney, Anke and Hirschhorn, Joel N. and Holloway, John W. and Holst, Claus and Hottenga, Jouke Jan and Horikoshi, Momoko and Huikari, Ville and Hypponen, Elina and Iniguez, Carmen and Kaakinen, Marika and Kilpelainen, Tuomas O. and Kirin, Mirna and Kowgier, Matthew and Lakka, Hanna-Maaria and Lange, Leslie A. and Lawlor, Debbie A. and Lehtimaki, Terho and Lewin, Alex and Lindgren, Cecilia and Lindi, Virpi and Maggi, Reedik and Marsh, Julie and Middeldorp, Christel and Millwood, Iona and Mook-Kanamori, Dennis O. and Murray, Jeffrey C. and Nivard, Michel and Nohr, Ellen Aagaard and Ntalla, Ioanna and Oken, Emily and O'Reilly, Paul F. and Palmer, Lyle J. and Panoutsopoulou, Kalliope and Pararajasingham, Jennifer and Prokopenko, Inga and Rodriguez, Alina and Salem, Rany M. and Sebert, Sylvain and Siitonen, Niina and Sovio, Ulla and St Pourcain, Beate and Strachan, David P. and Sunyer, Jordi and Taal, H. Rob and Teo, Yik-Ying and Thiering, Elisabeth and Tiesler, Carla and Uitterlinden, Andre G. and Valcarcel, Beatriz and Warrington, Nicole M. and White, Scott and Willemsen, Gonneke and Yaghootkar, Hanieh and Zeggini, Eleftheria and Boomsma, Dorret I. and Cooper, Cyrus and Estivill, Xavier and Gillman, Matthew and Grant, Struan F. A. and Hakonarson, Hakon and Hattersley, Andrew T. and Heinrich, Joachim and Hocher, Berthold and Jaddoe, Vincent W. V. and Jarvelin, Marjo-Riitta and Lakka, Timo A. and McCarthy, Mark I. and Melbye, Mads and Mohlke, Karen L. and Dedoussis, George V. and Ong, Ken K. and Pearson, Ewan R. and Pennell, Craig E. and Price, Thomas S. and Power, Chris and Raitakari, Olli T. and Saw, Seang-Mei and Scherag, Andre and Simell, Olli and Sorensen, Thorkild I. A. and Timpson, Nicholas J. and Widen, Elisabeth and Wilson, James F. and Ang, Wei and van Beijsterveldt, Toos and Bergen, Nienke and Benke, Kelly and Berry, Diane J. and Bradfield, Jonathan P. and Charoen, Pimphen and Coin, Lachlan and Cousminer, Diana L. and Das, Shikta and Elliott, Paul and Evans, David M. and Frayling, Tim and Freathy, Rachel M. and Gaillard, Romy and Groen-Blokhuis, Maria and Guxens, Monica and Hadley, Dexter and Hottenga, Jouke Jan and Huikari, Ville and Hypponen, Elina and Kaakinen, Marika and Kowgier, Matthew and Lawlor, Debbie A. and Lewin, Alex and Lindgren, Cecilia and Marsh, Julie and Middeldorp, Christel and Millwood, Iona and Mook-Kanamori, Dennis O. and Nivard, Michel and O'Reilly, Paul F. and Palmer, Lyle J. and Prokopenko, Inga and Rodriguez, Alina and Sebert, Sylvain and Sovio, Ulla and St Pourcain, Beate and Standl, Marie and Strachan, David P. and Sunyer, Jordi and Taal, H. Rob and Thiering, Elisabeth and Tiesler, Carla and Uitterlinden, Andre G. and Valcarcel, Beatriz and Warrington, Nicole M. and White, Scott and Willemsen, Gonneke and Yaghootkar, Hanieh and Boomsma, Dorret I. and Estivill, Xavier and Grant, Struan F. A. and Hakonarson, Hakon and Hattersley, Andrew T. and Heinrich, Joachim and Jaddoe, Vincent W. V. and Jarvelin, Marjo-Riitta and McCarthy, Mark I. and Pennell, Craig E. and Power, Chris and Timpson, Nicholas J. and Widen, Elisabeth and Ikram, M. Arfan and Fornage, Myriam and Smith, Albert V. and Seshadri, Sudha and Schmidt, Reinhold and Debette, Stephanie and Vrooman, Henri A. and Sigurdsson, Sigurdur and Ropele, Stefan and Coker, Laura H. and Longstreth, W. T. and Niessen, Wiro J. and DeStefano, Anita L. and Beiser, Alexa and Zijdenbos, Alex P. and Struchalin, Maksim and Jack, Clifford R. and Nalls, Mike A. and Au, Rhoda and Hofman, Albert and Gudnason, Haukur and van der Lugt, Aad and Harris, Tamara B. and Meeks, William M. and Vernooij, Meike W. and van Buchem, Mark A. and Catellier, Diane and Gudnason, Vilmundur and Windham, B. Gwen and Wolf, Philip A. and van Duijn, Cornelia M. and Mosley, Thomas H. and Schmidt, Helena and Launer, Lenore J. and Breteler, Monique M. B. and DeCarli, Charles},
  title     = {Common variants at 12q15 and 12q24 are associated with infant head circumference},
  series = {Nature genetics},
  volume    = {44},
  journal   = {Nature genetics},
  number    = {5},
  publisher = {Nature Publ. Group},
  address   = {New York},
  organization    = {Cohorts Heart Aging Res Genetic Ep, Early Genetics Lifecourse Epidemio, Early Growth Genetics EGG Consorti},
  issn      = {1061-4036},
  doi       = {10.1038/ng.2238},
  pages     = {532 -- +},
  year      = {2012},
  abstract  = {To identify genetic variants associated with head circumference in infancy, we performed a meta-analysis of seven genome-wide association studies (GWAS) (N = 10,768 individuals of European ancestry enrolled in pregnancy and/or birth cohorts) and followed up three lead signals in six replication studies (combined N = 19,089). rs7980687 on chromosome 12q24 (P = 8.1 x 10(-9)) and rs1042725 on chromosome 12q15 (P = 2.8 x 10(-10)) were robustly associated with head circumference in infancy. Although these loci have previously been associated with adult height(1), their effects on infant head circumference were largely independent of height (P = 3.8 x 10(-7) for rs7980687 and P = 1.3 x 10(-7) for rs1042725 after adjustment for infant height). A third signal, rs11655470 on chromosome 17q21, showed suggestive evidence of association with head circumference (P = 3.9 x 10(-6)). SNPs correlated to the 17q21 signal have shown genome-wide association with adult intracranial volume(2), Parkinson's disease and other neurodegenerative diseases(3-5), indicating that a common genetic variant in this region might link early brain growth with neurological disease in later life.},
  language  = {en}
}
@article{IkramFornageSmithetal.2012,
  author    = {Ikram, M. Arfan and Fornage, Myriam and Smith, Albert V. and Seshadri, Sudha and Schmidt, Reinhold and Debette, Stephanie and Vrooman, Henri A. and Sigurdsson, Sigurdur and Ropele, Stefan and Taal, H. Rob and Mook-Kanamori, Dennis O. and Coker, Laura H. and Longstreth, W. T. and Niessen, Wiro J. and DeStefano, Anita L. and Beiser, Alexa and Zijdenbos, Alex P. and Struchalin, Maksim and Jack, Clifford R. and Rivadeneira, Fernando and Uitterlinden, Andre G. and Knopman, David S. and Hartikainen, Anna-Liisa and Pennell, Craig E. and Thiering, Elisabeth and Steegers, Eric A. P. and Hakonarson, Hakon and Heinrich, Joachim and Palmer, Lyle J. and Jarvelin, Marjo-Riitta and McCarthy, Mark I. and Grant, Struan F. A. and St Pourcain, Beate and Timpson, Nicholas J. and Smith, George Davey and Sovio, Ulla and Nalls, Mike A. and Au, Rhoda and Hofman, Albert and Gudnason, Haukur and van der Lugt, Aad and Harris, Tamara B. and Meeks, William M. and Vernooij, Meike W. and van Buchem, Mark A. and Catellier, Diane and Jaddoe, Vincent W. V. and Gudnason, Vilmundur and Windham, B. Gwen and Wolf, Philip A. and van Duijn, Cornelia M. and Mosley, Thomas H. and Schmidt, Helena and Launer, Lenore J. and Breteler, Monique M. B. and DeCarli, Charles and Adair, Linda S. and Ang, Wei and Atalay, Mustafa and vanBeijsterveldt, Toos and Bergen, Nienke and Benke, Kelly and Berry, Diane J. and Coin, Lachlan and Davis, Oliver S. P. and Elliott, Paul and Flexeder, Claudia and Frayling, Tim and Gaillard, Romy and Groen-Blokhuis, Maria and Goh, Liang-Kee and Haworth, Claire M. A. and Hadley, Dexter and Hebebrand, Johannes and Hinney, Anke and Hirschhorn, Joel N. and Holloway, John W. and Holst, Claus and Hottenga, Jouke Jan and Horikoshi, Momoko and Huikari, Ville and Hypponen, Elina and Kilpelainen, Tuomas O. and Kirin, Mirna and Kowgier, Matthew and Lakka, Hanna-Maaria and Lange, Leslie A. and Lawlor, Debbie A. and Lehtimaki, Terho and Lewin, Alex and Lindgren, Cecilia and Lindi, Virpi and Maggi, Reedik and Marsh, Julie and Middeldorp, Christel and Millwood, Iona and Murray, Jeffrey C. and Nivard, Michel and Nohr, Ellen Aagaard and Ntalla, Ioanna and Oken, Emily and Panoutsopoulou, Kalliope and Pararajasingham, Jennifer and Rodriguez, Alina and Salem, Rany M. and Sebert, Sylvain and Siitonen, Niina and Strachan, David P. and Teo, Yik-Ying and Valcarcel, Beatriz and Willemsen, Gonneke and Zeggini, Eleftheria and Boomsma, Dorret I. and Cooper, Cyrus and Gillman, Matthew and Hocher, Berthold and Lakka, Timo A. and Mohlke, Karen L. and Dedoussis, George V. and Ong, Ken K. and Pearson, Ewan R. and Price, Thomas S. and Power, Chris and Raitakari, Olli T. and Saw, Seang-Mei and Scherag, Andre and Simell, Olli and Sorensen, Thorkild I. A. and Wilson, James F.},
  title     = {Common variants at 6q22 and 17q21 are associated with intracranial volume},
  series = {Nature genetics},
  volume    = {44},
  journal   = {Nature genetics},
  number    = {5},
  publisher = {Nature Publ. Group},
  address   = {New York},
  organization    = {Early Growth Genetics EGG Consorti, Cohorts Heart Aging Res Genomic Ep},
  issn      = {1061-4036},
  doi       = {10.1038/ng.2245},
  pages     = {539 -- +},
  year      = {2012},
  abstract  = {During aging, intracranial volume remains unchanged and represents maximally attained brain size, while various interacting biological phenomena lead to brain volume loss. Consequently, intracranial volume and brain volume in late life reflect different genetic influences. Our genome-wide association study (GWAS) in 8,175 community-dwelling elderly persons did not reveal any associations at genome-wide significance (P < 5 x 10(-8)) for brain volume. In contrast, intracranial volume was significantly associated with two loci: rs4273712 (P = 3.4 x 10(-11)), a known height-associated locus on chromosome 6q22, and rs9915547 (P = 1.5 x 10(-12)), localized to the inversion on chromosome 17q21. We replicated the associations of these loci with intracranial volume in a separate sample of 1,752 elderly persons (P = 1.1 x 10(-3) for 6q22 and 1.2 x 10(-3) for 17q21). Furthermore, we also found suggestive associations of the 17q21 locus with head circumference in 10,768 children (mean age of 14.5 months). Our data identify two loci associated with head size, with the inversion at 17q21 also likely to be involved in attaining maximal brain size.},
  language  = {en}
}
@article{PesicekEngdahlThurberetal.2012,
  author    = {Pesicek, J. D. and Engdahl, E. R. and Thurber, C. H. and DeShon, H. R. and Lange, Dietrich},
  title     = {Mantle subducting slab structure in the region of the 2010 M8.8 Maule earthquake (30-40 degrees S), Chile},
  series = {Geophysical journal international},
  volume    = {191},
  journal   = {Geophysical journal international},
  number    = {1},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {0956-540X},
  doi       = {10.1111/j.1365-246X.2012.05624.x},
  pages     = {317 -- 324},
  year      = {2012},
  abstract  = {We present a new tomographic model of the mantle in the area of the 2010 M8.8 Maule earthquake and surrounding regions. Increased ray coverage provided by the aftershock data allows us to image the detailed subducting slab structure in the mantle, from the region of flat slab subduction north of the Maule rupture to the area of overlapping rupture between the 1960 M9.5 and the 2010 M8.8 events to the south. We have combined teleseismic primary and depth phase arrivals with available local arrivals to better constrain the teleseismic earthquake locations in the region, which we use to conduct nested regionalglobal tomography. The new model reveals the detailed structure of the flat slab and its transition to a more moderately dipping slab in the Maule region. South of the Maule region, a steeply dipping relic slab is imaged from similar to 200 to 1000 km depth that is distinct from the moderately dipping slab above it and from the more northerly slab at similar depths. We interpret the images as revealing both horizontal and vertical tearing of the slab at similar to 38 degrees S to explain the imaged pattern of slab anomalies in the southern portion of the model. In contrast, the transition from a horizontal to moderately subducting slab in the northern portion of the model is imaged as a continuous slab bend. We speculate that the tearing was most likely facilitated by a fracture zone in the downgoing plate or alternatively by a continental scale terrane boundary in the overriding plate.},
  language  = {en}
}
@article{MuellerCooperLangeetal.2017,
  author    = {M{\"u}ller, B. R. and Cooper, R. C. and Lange, A. and Kupsch, Andreas and Wheeler, M. and Hentschel, M. P. and Staude, A. and Pandey, A. and Shyam, A. and Bruno, Giovanni},
  title     = {Stress-induced microcrack density evolution in beta-eucryptite ceramics},
  series = {Acta materialia},
  volume    = {144},
  journal   = {Acta materialia},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {1359-6454},
  doi       = {10.1016/j.actamat.2017.10.030},
  pages     = {627 -- 641},
  year      = {2017},
  abstract  = {In order to investigate their microcracking behaviour, the microstructures of several beta-eucryptite ceramics, obtained from glass precursor and cerammed to yield different grain sizes and microcrack densities, were characterized by laboratory and synchrotron x-ray refraction and tomography. Results were compared with those obtained from scanning electron microscopy (SEM). In SEM images, the characterized materials appeared fully dense but computed tomography showed the presence of pore clusters. Uniaxial tensile testing was performed on specimens while strain maps were recorded and analyzed by Digital Image Correlation (DIC). X-ray refraction techniques were applied on specimens before and after tensile testing to measure the amount of the internal specific surface (i.e., area per unit volume). X-ray refraction revealed that (a) the small grain size (SGS) material contained a large specific surface, originating from the grain boundaries and the interfaces of TiO2 precipitates; (b) the medium (MGS) and large grain size (LGS) materials possessed higher amounts of specific surface compared to SGS material due to microcracks, which decreased after tensile loading; (c) the precursor glass had negligible internal surface. The unexpected decrease in the internal surface of MGS and LGS after tensile testing is explained by the presence of compressive regions in the DIC strain maps and further by theoretical arguments. It is suggested that while some microcracks merge via propagation, more close mechanically, thereby explaining the observed X-ray refraction results. The mechanisms proposed would allow the development of a strain hardening route in ceramics.},
  language  = {en}
}
@article{GorskiJungLietal.2020,
  author    = {Gorski, Mathias and Jung, Bettina and Li, Yong and Matias-Garcia, Pamela R. and Wuttke, Matthias and Coassin, Stefan and Thio, Chris H. L. and Kleber, Marcus E. and Winkler, Thomas W. and Wanner, Veronika and Chai, Jin-Fang and Chu, Audrey Y. and Cocca, Massimiliano and Feitosa, Mary F. and Ghasemi, Sahar and Hoppmann, Anselm and Horn, Katrin and Li, Man and Nutile, Teresa and Scholz, Markus and Sieber, Karsten B. and Teumer, Alexander and Tin, Adrienne and Wang, Judy and Tayo, Bamidele O. and Ahluwalia, Tarunveer S. and Almgren, Peter and Bakker, Stephan J. L. and Banas, Bernhard and Bansal, Nisha and Biggs, Mary L. and Boerwinkle, Eric and B{\"o}ttinger, Erwin and Brenner, Hermann and Carroll, Robert J. and Chalmers, John and Chee, Miao-Li and Chee, Miao-Ling and Cheng, Ching-Yu and Coresh, Josef and de Borst, Martin H. and Degenhardt, Frauke and Eckardt, Kai-Uwe and Endlich, Karlhans and Franke, Andre and Freitag-Wolf, Sandra and Gampawar, Piyush and Gansevoort, Ron T. and Ghanbari, Mohsen and Gieger, Christian and Hamet, Pavel and Ho, Kevin and Hofer, Edith and Holleczek, Bernd and Foo, Valencia Hui Xian and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Josyula, Navya Shilpa and Kahonen, Mika and Khor, Chiea-Chuen and Koenig, Wolfgang and Kramer, Holly and Kraemer, Bernhard K. and Kuehnel, Brigitte and Lange, Leslie A. and Lehtimaki, Terho and Lieb, Wolfgang and Loos, Ruth J. F. and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Milaneschi, Yuri and Mishra, Pashupati P. and Mononen, Nina and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and O'Donoghue, Michelle L. and Orho-Melander, Marju and Pendergrass, Sarah A. and Penninx, Brenda W. J. H. and Preuss, Michael H. and Psaty, Bruce M. and Raffield, Laura M. and Raitakari, Olli T. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Rosenkranz, Alexander R. and Rossing, Peter and Rotter, Jerome and Sabanayagam, Charumathi and Schmidt, Helena and Schmidt, Reinhold and Schoettker, Ben and Schulz, Christina-Alexandra and Sedaghat, Sanaz and Shaffer, Christian M. and Strauch, Konstantin and Szymczak, Silke and Taylor, Kent D. and Tremblay, Johanne and Chaker, Layal and van der Harst, Pim and van der Most, Peter J. and Verweij, Niek and Voelker, Uwe and Waldenberger, Melanie and Wallentin, Lars and Waterworth, Dawn M. and White, Harvey D. and Wilson, James G. and Wong, Tien-Yin and Woodward, Mark and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Yan and Snieder, Harold and Wanner, Christoph and Boger, Carsten A. and Kottgen, Anna and Kronenberg, Florian and Pattaro, Cristian and Heid, Iris M.},
  title     = {Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline},
  series = {Kidney international : official journal of the International Society of Nephrology},
  volume    = {99},
  journal   = {Kidney international : official journal of the International Society of Nephrology},
  number    = {4},
  publisher = {Elsevier},
  address   = {New York},
  organization    = {Lifelines Cohort Study<br /> Regeneron Genetics Ctr},
  issn      = {0085-2538},
  doi       = {10.1016/j.kint.2020.09.030},
  pages     = {926 -- 939},
  year      = {2020},
  abstract  = {Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25\% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95\% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.},
  language  = {en}
}
@article{FoersterTischendorfRhedeetal.2005,
  author    = {F{\"o}rster, Hans-J{\"u}rgen and Tischendorf, Gerhard and Rhede, Dieter and Naumann, R. and Gottesmann, B{\"a}rbel and Lange, W},
  title     = {Cs-rich lithium micas and Mn-rich lithian siderophyllite in miarolitic NYF pegmatites of the Konigshain granite, Lausitz, Germany},
  year      = {2005},
  abstract  = {Annite and Fe-rich siderophyllite constitute the rock-forming micas in the late-Variscan composite granite pluton of Konigshain, Lausitz, Germany. This multiphase pluton is composed of three fractionated, but not chemically specialized monzogranite types, which contain lithophile elements such as Li, Rb, Cs, Sn, and F in average quantities. Abundant miarolitic pegmatites of the NYF family with a broad diversity of rare minerals occur in the apical part of the pluton. These pegmatitic cavities locally contain di- and trioctabedral micas as well as cation-deficient micas. Trioctahedral micas comprise F-rich manganoan lithian siderophyllite to manganoan zinnwaldite, zinnwaldite, and minor lepidolite. The formula [calculated on the basis of 22 anion valencies and 2 (F + OH + Cl)] of the most Mn-rich siderophyllite is (K0.85Rb0.08Na0.04)(0.97)(Al0.99Li0.91Fe0.51Mn0.42Ti0.01Zn0.01)(2.85) (Si3.21Al0.79)(4)O- 10(F1.80OH0.19Cl0.01)(2). This mica constitutes one of the most Mn-rich siderophyllite compositions reported to date. The lithium micas poorer in Mn are distinguished by elevated concentrations of Rb (up to 2.5 wt \% Rb2O), CS (UP to 1.2 wt \% Cs2O), and F (up to 9.6 wt \%). This fluorine content is probably consistent with the maximum possible F occupation of 2 of the (F,OH,Cl)-site. The structural formula of the most Li-rich lepidolite is (K0.83Rb0.07Cs0.03)(0.93) (Li1.62Al1.00Fe0.38)(3.00)(Si3.62Al0.38)(4) O-10(F1.91OH0.09)(2). During hydrothermal alteration, lepidolite and zinnwaldite became partially depleted in K, Li, Rb, Cs, and F and gradually transformed into cation-deficient micas (lithian phengite to illite of phengitic affinity)},
  language  = {en}
}
@article{BauernschmittMalbergWesseletal.2004,
  author    = {Bauernschmitt, Robert and Malberg, Hagen and Wessel, Niels and Kopp, B. and Schirmbeck, E. U. and Lange, R.},
  title     = {Impairment of cardiovascular autonomic control in patients early after cardiac surgery},
  issn      = {1010-7940},
  year      = {2004},
  abstract  = {Objective: Impairment of the baroreceptor reflex activity reflects an alteration of the autonomous regulation of the cardiovascular system and has proven to predict fatal outcome in patients after acute myocardial infarction. The following study was performed to analyse the baroreceptor sensitivity, heart rate variability and blood pressure variability in patients early after coronary surgery. Methods: Twenty-five male patients undergoing coronary artery bypass were examined in a prospective study; normal values were obtained from healthy volunteers. Arterial pressure signals were recorded from a radial artery catheter for 30 min preoperatively and in short intervals after surgery. Mechanical manipulations and pharmacological interventions were avoided during the sampling periods. Baroreflex function was calculated according to the dual sequence method, heart rate variability and blood pressure variability were calculated including nonlinear methods. Results: Initial values of the patients did not differ from healthy volunteers. The strength of baroreflex sensitivity (increase in blood pressure causing a synchronous decrease of heart rate) is low 2 It postoperatively. The number of delayed tachycardic changes of heart rate, which are caused by sympathetic activation, is only moderately reduced as compared to values obtained from healthy volunteers. Heart rate variability is widely unchanged as compared to preoperative values; blood pressure variability showed an increase of low-frequency components, again indicating sympathetic predominance. Nonlinear analyses revealed reduced system complexity at the beginning of the postoperative course. Conclusion: Obviously, there is a vagal suppression 20 h after surgery, while the sympathetic tonus works in a normal range. This unbalanced interaction of the autonomous systems is similar to findings in patients after myocardial infarction. The predictive value of these markers has to be elucidated in further clinical studies. (C) 2003 Elsevier B.V. All rights reserved},
  language  = {en}
}
@misc{HetenyiMolinariClintonetal.2018,
  author    = {Hetenyi, Gyorgy and Molinari, Irene and Clinton, John and Bokelmann, Gotz and Bondar, Istvan and Crawford, Wayne C. and Dessa, Jean-Xavier and Doubre, Cecile and Friederich, Wolfgang and Fuchs, Florian and Giardini, Domenico and Graczer, Zoltan and Handy, Mark R. and Herak, Marijan and Jia, Yan and Kissling, Edi and Kopp, Heidrun and Korn, Michael and Margheriti, Lucia and Meier, Thomas and Mucciarelli, Marco and Paul, Anne and Pesaresi, Damiano and Piromallo, Claudia and Plenefisch, Thomas and Plomerova, Jaroslava and Ritter, Joachim and Rumpker, Georg and Sipka, Vesna and Spallarossa, Daniele and Thomas, Christine and Tilmann, Frederik and Wassermann, Joachim and Weber, Michael and Weber, Zoltan and Wesztergom, Viktor and Zivcic, Mladen and Abreu, Rafael and Allegretti, Ivo and Apoloner, Maria-Theresia and Aubert, Coralie and Besancon, Simon and de Berc, Maxime Bes and Brunel, Didier and Capello, Marco and Carman, Martina and Cavaliere, Adriano and Cheze, Jerome and Chiarabba, Claudio and Cougoulat, Glenn and Cristiano, Luigia and Czifra, Tibor and Danesi, Stefania and Daniel, Romuald and Dannowski, Anke and Dasovic, Iva and Deschamps, Anne and Egdorf, Sven and Fiket, Tomislav and Fischer, Kasper and Funke, Sigward and Govoni, Aladino and Groschl, Gidera and Heimers, Stefan and Heit, Ben and Herak, Davorka and Huber, Johann and Jaric, Dejan and Jedlicka, Petr and Jund, Helene and Klingen, Stefan and Klotz, Bernhard and Kolinsky, Petr and Kotek, Josef and Kuhne, Lothar and Kuk, Kreso and Lange, Dietrich and Loos, Jurgen and Lovati, Sara and Malengros, Deny and Maron, Christophe and Martin, Xavier and Massa, Marco and Mazzarini, Francesco and Metral, Laurent and Moretti, Milena and Munzarova, Helena and Nardi, Anna and Pahor, Jurij and Pequegnat, Catherine and Petersen, Florian and Piccinini, Davide and Pondrelli, Silvia and Prevolnik, Snjezan and Racine, Roman and Regnier, Marc and Reiss, Miriam and Salimbeni, Simone and Santulin, Marco and Scherer, Werner and Schippkus, Sven and Schulte-Kortnack, Detlef and Solarino, Stefano and Spieker, Kathrin and Stipcevic, Josip and Strollo, Angelo and Sule, Balint and Szanyi, Gyongyver and Szucs, Eszter and Thorwart, Martin and Ueding, Stefan and Vallocchia, Massimiliano and Vecsey, Ludek and Voigt, Rene and Weidle, Christian and Weyland, Gauthier and Wiemer, Stefan and Wolf, Felix and Wolyniec, David and Zieke, Thomas},
  title     = {The AlpArray seismic network},
  series = {Surveys in Geophysics},
  volume    = {39},
  journal   = {Surveys in Geophysics},
  number    = {5},
  publisher = {Springer},
  address   = {Dordrecht},
  organization    = {ETHZ SED Elect Lab AlpArray Seismic Network Team AlpArray OBS Cruise Crew AlpArray Working Grp},
  issn      = {0169-3298},
  doi       = {10.1007/s10712-018-9472-4},
  pages     = {1009 -- 1033},
  year      = {2018},
  abstract  = {The AlpArray programme is a multinational, European consortium to advance our understanding of orogenesis and its relationship to mantle dynamics, plate reorganizations, surface processes and seismic hazard in the Alps-Apennines-Carpathians-Dinarides orogenic system. The AlpArray Seismic Network has been deployed with contributions from 36 institutions from 11 countries to map physical properties of the lithosphere and asthenosphere in 3D and thus to obtain new, high-resolution geophysical images of structures from the surface down to the base of the mantle transition zone. With over 600 broadband stations operated for 2 years, this seismic experiment is one of the largest simultaneously operated seismological networks in the academic domain, employing hexagonal coverage with station spacing at less than 52 km. This dense and regularly spaced experiment is made possible by the coordinated coeval deployment of temporary stations from numerous national pools, including ocean-bottom seismometers, which were funded by different national agencies. They combine with permanent networks, which also required the cooperation of many different operators. Together these stations ultimately fill coverage gaps. Following a short overview of previous large-scale seismological experiments in the Alpine region, we here present the goals, construction, deployment, characteristics and data management of the AlpArray Seismic Network, which will provide data that is expected to be unprecedented in quality to image the complex Alpine mountains at depth.},
  language  = {en}
}
@article{CollingsRietbrockLangeetal.2013,
  author    = {Collings, R. and Rietbrock, Andreas and Lange, Dietrich and Tilmann, F. and Nippress, Stuart and Natawidjaja, D.},
  title     = {Seismic anisotropy in the sumatra subduction zone},
  series = {Journal of geophysical research : Solid earth},
  volume    = {118},
  journal   = {Journal of geophysical research : Solid earth},
  number    = {10},
  publisher = {American Geophysical Union},
  address   = {Washington},
  issn      = {2169-9313},
  doi       = {10.1002/jgrb.50157},
  pages     = {5372 -- 5390},
  year      = {2013},
  abstract  = {An important tool for understanding deformation occurring within a subduction zone is the measurement of seismic anisotropy through observations of shear wave splitting (SWS). In Sumatra, two temporary seismic networks were deployed between December 2007 and February 2009, covering the fore arc between the fore-arc islands to the back arc. We use SKS and local SWS measurements to determine the type, amount, and location of anisotropy. Local SWS measurements from the fore-arc islands exhibit trench-parallel fast directions which can be attributed to shape preferred orientation of cracks/fractures in the overriding sediments. In the Sumatran Fault region, the predominant fast direction is fault/trench parallel, while in the back-arc region it is trench perpendicular. The trench-perpendicular measurements exhibit a positive correlation between delay time and raypath length in the mantle wedge, while the fault-parallel measurements are similar to the fault-parallel fast directions observed for two crustal events at the Sumatran Fault. This suggests that there are two layers of anisotropy: one due to entrained flow within the mantle wedge and a second layer within the overriding crust due to the shear strain caused by the Sumatran Fault. SKS splitting results show a NNW-SSE fast direction with delay times of 0.8-3.0s. The fast directions are approximately parallel to the absolute plate motion of the subducting Indo-Australian Plate. The small delay times exhibited by the local SWS (0.05-0.45s), in combination with the large SKS delay times, suggest that the anisotropy generating the teleseismic SWS is dominated by entrained flow in the asthenosphere below the slab.},
  language  = {en}
}
@article{CollingsLangeRietbrocketal.2012,
  author    = {Collings, R. and Lange, Dietrich and Rietbrock, Andreas and Tilmann, F. and Natawidjaja, D. and Suwargadi, B. and Miller, M. and Saul, Joschim},
  title     = {Structure and seismogenic properties of the Mentawai segment of the Sumatra subduction zone revealed by local earthquake traveltime tomography},
  series = {Journal of geophysical research : Solid earth},
  volume    = {117},
  journal   = {Journal of geophysical research : Solid earth},
  number    = {3},
  publisher = {American Geophysical Union},
  address   = {Washington},
  issn      = {2169-9313},
  doi       = {10.1029/2011JB008469},
  pages     = {23},
  year      = {2012},
  abstract  = {On 12 September 2007, an M-w 8.4 earthquake occurred within the southern section of the Mentawai segment of the Sumatra subduction zone, where the subduction thrust had previously ruptured in 1833 and 1797. Traveltime data obtained from a temporary local seismic network, deployed between December 2007 and October 2008 to record the aftershocks of the 2007 event, was used to determine two-dimensional (2-D) and three-dimensional (3-D) velocity models of the Mentawai segment. The seismicity distribution reveals significant activity along the subduction interface and within two clusters in the overriding plate either side of the forearc basin. The downgoing slab is clearly distinguished by a dipping region of high Vp (8.0 km/s), which can be a traced to similar to 50 km depth, with an increased Vp/Vs ratio (1.75 to 1.90) beneath the islands and the western side of the forearc basin, suggesting hydrated oceanic crust. Above the slab, a shallow continental Moho of less than 30 km depth can be inferred, suggesting that the intersection of the continental mantle with the subducting slab is much shallower than the downdip limit of the seismogenic zone despite localized serpentinization being present at the toe of the mantle wedge. The outer arc islands are characterized by low Vp (4.5-5.8 km/s) and high Vp/Vs (greater than 2.0), suggesting that they consist of fluid saturated sediments. The very low rigidity of the outer forearc contributed to the slow rupture of the M-w 7.7 Mentawai tsunami earthquake on 25 October 2010.},
  language  = {en}
}