@article{ThierschmannArnoldMittermuelleretal.2015, author = {Thierschmann, H and Arnold, F and Mitterm{\"u}ller, M and Maier, L and Heyn, C and Hansen, W and Buhmann, H and Molenkamp, L W}, title = {Thermal gating of charge currents with Coulomb coupled quantum dots}, series = {New Journal of Physics}, volume = {17}, journal = {New Journal of Physics}, number = {113003}, doi = {10.1088/1367-2630/17/11/113003}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-145196}, year = {2015}, abstract = {We have observed thermal gating, i.e. electrostatic gating induced by hot electrons. The effect occurs in a device consisting of two capacitively coupled quantum dots. The double dot system is coupled to a hot electron reservoir on one side (QD1), while the conductance of the second dot (QD2) is monitored. When a bias across QD2 is applied we observe a current which is strongly dependent on the temperature of the heat reservoir. This current can be either enhanced or suppressed, depending on the relative energetic alignment of the QD levels. Thus, the system can be used to control a charge current by hot electrons.}, language = {en} } @article{ThierschmannHenkeKnorretal.2013, author = {Thierschmann, H. and Henke, M. and Knorr, J. and Maier, L. and Heyn, C. and Hansen, W. and Buhmann, H. and Molenkamp, L. W.}, title = {Diffusion thermopower of a serial double quantum dot}, series = {New Journal of Physics}, volume = {15}, journal = {New Journal of Physics}, number = {123010}, doi = {10.1088/1367-2630/15/12/123010}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-129714}, year = {2013}, abstract = {We have experimentally studied the diffusion thermopower of a serial double quantum dot, defined electrostatically in a GaAs/AlGaAs heterostructure. We present the thermopower stability diagram for a temperature difference 1T = (20±10)mK across the device and find a maximum thermovoltage signal of several μV in the vicinity of the triple points. Along a constant energy axis in this regime, the data show a characteristic pattern which is in agreement with Mott's relation and can be well understood within a model of sequential transport.}, language = {en} } @article{BlancoKuchenbaeckerCuadrasetal.2015, author = {Blanco, Ignacio and Kuchenbaecker, Karoline and Cuadras, Daniel and Wang, Xianshu and Barrowdale, Daniel and Ruiz de Garibay, Gorka and Librado, Pablo and Sanchez-Gracia, Alejandro and Rozas, Julio and Bonifaci, N{\´u}ria and McGuffog, Lesley and Pankratz, Vernon S. and Islam, Abul and Mateo, Francesca and Berenguer, Antoni and Petit, Anna and Catal{\`a}, Isabel and Brunet, Joan and Feliubadal{\´o}, Lidia and Tornero, Eva and Ben{\´i}tez, Javier and Osorio, Ana and Ram{\´o}n y Cajal, Teresa and Nevanlinna, Heli and Aittom{\"a}ki, Kristina and Arun, Banu K. and Toland, Amanda E. and Karlan, Beth Y. and Walsh, Christine and Lester, Jenny and Greene, Mark H. and Mai, Phuong L. and Nussbaum, Robert L. and Andrulis, Irene L. and Domchek, Susan M. and Nathanson, Katherine L. and Rebbeck, Timothy R. and Barkardottir, Rosa B. and Jakubowska, Anna and Lubinski, Jan and Durda, Katarzyna and Jaworska-Bieniek, Katarzyna and Claes, Kathleen and Van Maerken, Tom and D{\´i}ez, Orland and Hansen, Thomas V. and J{\o}nson, Lars and Gerdes, Anne-Marie and Ejlertsen, Bent and De la Hoya, Miguel and Cald{\´e}s, Trinidad and Dunning, Alison M. and Oliver, Clare and Fineberg, Elena and Cook, Margaret and Peock, Susan and McCann, Emma and Murray, Alex and Jacobs, Chris and Pichert, Gabriella and Lalloo, Fiona and Chu, Carol and Dorkins, Huw and Paterson, Joan and Ong, Kai-Ren and Teixeira, Manuel R. and Hogervorst, Frans B. L. and Van der Hout, Annemarie H. and Seynaeve, Caroline and Van der Luijt, Rob B. and Ligtenberg, Marjolijn J. L. and Devilee, Peter and Wijnen, Juul T. and Rookus, Matti A. and Meijers-Heijboer, Hanne E. J. and Blok, Marinus J. and Van den Ouweland, Ans M. W. and Aalfs, Cora M. and Rodriguez, Gustavo C. and Phillips, Kelly-Anne A. and Piedmonte, Marion and Nerenstone, Stacy R. and Bae-Jump, Victoria L. and O'Malley, David M. and Schmutzler, Rita K. and Wappenschmidt, Barbara and Rhiem, Kerstin and Engel, Christoph and Meindl, Alfons and Ditsch, Nina and Arnold, Norbert and Plendl, Hansjoerg J. and Niederacher, Dieter and Sutter, Christian and Wang-Gohrke, Shan and Steinemann, Doris and Preisler-Adams, Sabine and Kast, Karin and Varon-Mateeva, Raymonda and Gehrig, Andrea and Bojesen, Anders and Pedersen, Inge Sokilde and Sunde, Lone and Birk Jensen, Uffe and Thomassen, Mads and Kruse, Torben A. and Foretova, Lenka and Peterlongo, Paolo and Bernard, Loris and Peissel, Bernard and Scuvera, Giulietta and Manoukian, Siranoush and Radice, Paolo and Ottini, Laura and Montagna, Marco and Agata, Simona and Maugard, Christine and Simard, Jacques and Soucy, Penny and Berger, Andreas and Fink-Retter, Anneliese and Singer, Christian F. and Rappaport, Christine and Geschwantler-Kaulich, Daphne and Tea, Muy-Kheng and Pfeiler, Georg and John, Esther M. and Miron, Alex and Neuhausen, Susan L. and Terry, Mary Beth and Chung, Wendy K. and Daly, Mary B. and Goldgar, David E. and Janavicius, Ramunas and Dorfling, Cecilia M. and Van Rensburg, Elisabeth J. and Fostira, Florentia and Konstantopoulou, Irene and Garber, Judy and Godwin, Andrew K. and Olah, Edith and Narod, Steven A. and Rennert, Gad and Paluch, Shani Shimon and Laitman, Yael and Friedman, Eitan and Liljegren, Annelie and Rantala, Johanna and Stenmark-Askmalm, Marie and Loman, Niklas and Imyanitov, Evgeny N. and Hamann, Ute and Spurdle, Amanda B. and Healey, Sue and Weitzel, Jeffrey N. and Herzog, Josef and Margileth, David and Gorrini, Chiara and Esteller, Manel and G{\´o}mez, Antonio and Sayols, Sergi and Vidal, Enrique and Heyn, Holger and Stoppa-Lyonnet, Dominique and L{\´e}on{\´e}, Melanie and Barjhoux, Laure and Fassy-Colcombet, Marion and Pauw, Antoine de and Lasset, Christine and Fert Ferrer, Sandra and Castera, Laurent and Berthet, Pascaline and Cornelis, Fran{\c{c}}ois and Bignon, Yves-Jean and Damiola, Francesca and Mazoyer, Sylvie and Sinilnikova, Olga M. and Maxwell, Christopher A. and Vijai, Joseph and Robson, Mark and Kauff, Noah and Corines, Marina J. and Villano, Danylko and Cunningham, Julie and Lee, Adam and Lindor, Noralane and L{\´a}zaro, Conxi and Easton, Douglas F. and Offit, Kenneth and Chenevix-Trench, Georgia and Couch, Fergus J. and Antoniou, Antonis C. and Pujana, Miguel Angel}, title = {Assessing associations between the AURKA-HMMR-TPX2-TUBG1 functional module and breast cancer risk in BRCA1/2 mutation carriers}, series = {PLoS ONE}, volume = {10}, journal = {PLoS ONE}, number = {4}, doi = {10.1371/journal.pone.0120020}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-143469}, pages = {e0120020}, year = {2015}, abstract = {While interplay between BRCA1 and AURKA-RHAMM-TPX2-TUBG1 regulates mammary epithelial polarization, common genetic variation in HMMR (gene product RHAMM) may be associated with risk of breast cancer in BRCA1 mutation carriers. Following on these observations, we further assessed the link between the AURKA-HMMR-TPX2-TUBG1 functional module and risk of breast cancer in BRCA1 or BRCA2 mutation carriers. Forty-one single nucleotide polymorphisms (SNPs) were genotyped in 15,252 BRCA1 and 8,211 BRCA2 mutation carriers and subsequently analyzed using a retrospective likelihood approach. The association of HMMR rs299290 with breast cancer risk in BRCA1 mutation carriers was confirmed: per-allele hazard ratio (HR) = 1.10, 95\% confidence interval (CI) 1.04 - 1.15, p = 1.9 x 10\(^{-4}\) (false discovery rate (FDR)-adjusted p = 0.043). Variation in CSTF1, located next to AURKA, was also found to be associated with breast cancer risk in BRCA2 mutation carriers: rs2426618 per-allele HR = 1.10, 95\% CI 1.03 - 1.16, p = 0.005 (FDR-adjusted p = 0.045). Assessment of pairwise interactions provided suggestions (FDR-adjusted p\(_{interaction}\) values > 0.05) for deviations from the multiplicative model for rs299290 and CSTF1 rs6064391, and rs299290 and TUBG1 rs11649877 in both BRCA1 and BRCA2 mutation carriers. Following these suggestions, the expression of HMMR and AURKA or TUBG1 in sporadic breast tumors was found to potentially interact, influencing patients' survival. Together, the results of this study support the hypothesis of a causative link between altered function of AURKA-HMMR-TPX2-TUBG1 and breast carcinogenesis in BRCA1/2 mutation carriers.}, language = {en} } @article{EdgecockCarettaDavenneetal.2013, author = {Edgecock, T. R. and Caretta, O. and Davenne, T. and Densam, C. and Fitton, M. and Kelliher, D. and Loveridge, P. and Machida, S. and Prior, C. and Rogers, C. and Rooney, M. and Thomason, J. and Wilcox, D. and Wildner, E. and Efthymiopoulos, I. and Garoby, R. and Gilardoni, S. and Hansen, C. and Benedetto, E. and Jensen, E. and Kosmicki, A. and Martini, M. and Osborne, J. and Prior, G. and Stora, T. and Melo Mendonca, T. and Vlachoudis, V. and Waaijer, C. and Cupial, P. and Chanc{\´e}, A. and Longhin, A. and Payet, J. and Zito, M. and Baussan, E. and Bobeth, C. and Bouquerel, E. and Dracos, M. and Gaudiot, G. and Lepers, B. and Osswald, F. and Poussot, P. and Vassilopoulos, N. and Wurtz, J. and Zeter, V. and Bielski, J. and Kozien, M. and Lacny, L. and Skoczen, B. and Szybinski, B. and Ustrycka, A. and Wroblewski, A. and Marie-Jeanne, M. and Balint, P. and Fourel, C. and Giraud, J. and Jacob, J. and Lamy, T. and Latrasse, L. and Sortais, P. and Thuillier, T. and Mitrofanov, S. and Loiselet, M. and Keutgen, Th. and Delbar, Th. and Debray, F. and Trophine, C. and Veys, S. and Daversin, C. and Zorin, V. and Izotov, I. and Skalyga, V. and Burt, G. and Dexter, A. C. and Kravchuk, V. L. and Marchi, T. and Cinausero, M. and Gramegna, F. and De Angelis, G. and Prete, G. and Collazuol, G. and Laveder, M. and Mazzocco, M. and Mezzetto, M. and Signorini, C. and Vardaci, E. and Di Nitto, A. and Brondi, A. and La Rana, G. and Migliozzi, P. and Moro, R. and Palladino, V. and Gelli, N. and Berkovits, D. and Hass, M. and Hirsh, T. Y. and Schuhmann, M. and Stahl, A. and Wehner, J. and Bross, A. and Kopp, J. and Neuffer, D. and Wands, R. and Bayes, R. and Laing, A. and Soler, P. and Agarwalla, S. K. and Cervera Villanueva, A. and Donini, A. and Ghosh, T. and G{\´o}mez Cadenas, J. J. and Hern{\´a}ndez, P. and Mart{\´i}n-Albo, J. and Mena, O. and Burguet-Castell, J. and Agostino, L. and Buizza-Avanzini, M. and Marafini, M. and Patzak, T. and Tonazzo, A. and Duchesneau, D. and Mosca, L. and Bogomilov, M. and Karadzhov, Y. and Matev, R. and Tsenov, R. and Akhmedov, E. and Blennow, M. and Lindner, M. and Schwetz, T. and Fern{\´a}ndez Martinez, E. and Maltoni, M. and Men{\´e}ndez, J. and Giunti, C. and Gonz{\´a}lez Garc{\´i}a, M. C. and Salvado, J. and Coloma, P. and Huber, P. and Li, T. and L{\´o}pez Pav{\´o}n, J. and Orme, C. and Pascoli, S. and Meloni, D. and Tang, J. and Winter, W. and Ohlsson, T. and Zhang, H. and Scotto-Lavina, L. and Terranova, F. and Bonesini, M. and Tortora, L. and Alekou, A. and Aslaninejad, M. and Bontoiu, C. and Kurup, A. and Jenner, L. J. and Long, K. and Pasternak, J. and Pozimski, J. and Back, J. J. and Harrison, P. and Beard, K. and Bogacz, A. and Berg, J. S. and Stratakis, D. and Witte, H. and Snopok, P. and Bliss, N. and Cordwell, M. and Moss, A. and Pattalwar, S. and Apollonio, M.}, title = {High intensity neutrino oscillation facilities in Europe}, series = {Physical Review Special Topics-Accelerators and Beams}, volume = {16}, journal = {Physical Review Special Topics-Accelerators and Beams}, number = {2}, doi = {10.1103/PhysRevSTAB.16.021002}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-126611}, pages = {21002}, year = {2013}, abstract = {The EUROnu project has studied three possible options for future, high intensity neutrino oscillation facilities in Europe. The first is a Super Beam, in which the neutrinos come from the decay of pions created by bombarding targets with a 4 MW proton beam from the CERN High Power Superconducting Proton Linac. The far detector for this facility is the 500 kt MEMPHYS water Cherenkov, located in the Frejus tunnel. The second facility is the Neutrino Factory, in which the neutrinos come from the decay of mu(+) and mu(-) beams in a storage ring. The far detector in this case is a 100 kt magnetized iron neutrino detector at a baseline of 2000 km. The third option is a Beta Beam, in which the neutrinos come from the decay of beta emitting isotopes, in particular He-6 and Ne-18, also stored in a ring. The far detector is also the MEMPHYS detector in the Frejus tunnel. EUROnu has undertaken conceptual designs of these facilities and studied the performance of the detectors. Based on this, it has determined the physics reach of each facility, in particular for the measurement of CP violation in the lepton sector, and estimated the cost of construction. These have demonstrated that the best facility to build is the Neutrino Factory. However, if a powerful proton driver is constructed for another purpose or if the MEMPHYS detector is built for astroparticle physics, the Super Beam also becomes very attractive.}, language = {en} } @article{BittnerBobakFeuchtenbergeretal.2011, author = {Bittner, Stefan and Bobak, Nicole and Feuchtenberger, Martin and Herrmann, Alexander M and G{\"o}bel, Kerstin and Kinne, Raimund W and Hansen, Anker J and Budde, Thomas and Kleinschnitz, Christoph and Frey, Oliver and Tony, Hans-Peter and Wiendl, Heinz and Meuth, Sven G}, title = {Expression of K\(_2\)\(_P\)5.1 potassium channels on CD4\(^+\)T lymphocytes correlates with disease activity in rheumatoid arthritis patients}, series = {Arthritis Research \& Therapy}, volume = {13}, journal = {Arthritis Research \& Therapy}, number = {R21}, doi = {10.1186/ar3245}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-139334}, year = {2011}, abstract = {Introduction CD4+ T cells express K2P5.1 (TWIK-related acid-sensitive potassium channel 2 (TASK2); KCNK5), a member of the two-pore domain potassium channel family, which has been shown to influence T cell effector functions. Recently, it was shown that K2P5.1 is upregulated upon (autoimmune) T cell stimulation. The aim of this study was to correlate expression levels of K2P5.1 on T cells from patients with rheumatoid arthritis (RA) to disease activity in these patients. Methods Expression levels of K2P5.1 were measured by RT-PCR in the peripheral blood of 58 patients with RA and correlated with disease activity parameters (C-reactive protein levels, erythrocyte sedimentation rates, disease activity score (DAS28) scores). Twenty patients undergoing therapy change were followed-up for six months. Additionally, synovial fluid and synovial biopsies were investigated for T lymphocytes expressing K2P5.1. Results K2P5.1 expression levels in CD4+ T cells show a strong correlation to DAS28 scores in RA patients. Similar correlations were found for serological inflammatory parameters (erythrocyte sedimentation rate, C-reactive protein). In addition, K2P5.1 expression levels of synovial fluid-derived T cells are higher compared to peripheral blood T cells. Prospective data in individual patients show a parallel behaviour of K2P5.1 expression to disease activity parameters during a longitudinal follow-up for six months. Conclusions Disease activity in RA patients correlates strongly with K2P5.1 expression levels in CD4+ T lymphocytes in the peripheral blood in cross-sectional as well as in longitudinal observations. Further studies are needed to investigate the exact pathophysiological mechanisms and to evaluate the possible use of K2P5.1 as a potential biomarker for disease activity and differential diagnosis.}, language = {en} } @article{BleinBardelDanjeanetal.2015, author = {Blein, Sophie and Bardel, Claire and Danjean, Vincent and McGuffog, Lesley and Healay, Sue and Barrowdale, Daniel and Lee, Andrew and Dennis, Joe and Kuchenbaecker, Karoline B. and Soucy, Penny and Terry, Mary Beth and Chung, Wendy K. and Goldgar, David E. and Buys, Saundra S. and Janavicius, Ramunas and Tihomirova, Laima and Tung, Nadine and Dorfling, Cecilia M. and van Rensburg, Elizabeth J. and Neuhausen, Susan L. and Ding, Yuan Chun and Gerdes, Anne-Marie and Ejlertsen, Bent and Nielsen, Finn C. and Hansen, Thomas V. O. and Osorio, Ana and Benitez, Javier and Andreas Conejero, Raquel and Segota, Ena and Weitzel, Jeffrey N. and Thelander, Margo and Peterlongo, Paolo and Radice, Paolo and Pensotti, Valeria and Dolcetti, Riccardo and Bonanni, Bernardo and Peissel, Bernard and Zaffaroni, Daniela and Scuvera, Giulietta and Manoukian, Siranoush and Varesco, Liliana and Capone, Gabriele L. and Papi, Laura and Ottini, Laura and Yannoukakos, Drakoulis and Konstantopoulou, Irene and Garber, Judy and Hamann, Ute and Donaldson, Alan and Brady, Angela and Brewer, Carole and Foo, Claire and Evans, D. Gareth and Frost, Debra and Eccles, Diana and Douglas, Fiona and Cook, Jackie and Adlard, Julian and Barwell, Julian and Walker, Lisa and Izatt, Louise and Side, Lucy E. and Kennedy, M. John and Tischkowitz, Marc and Rogers, Mark T. and Porteous, Mary E. and Morrison, Patrick J. and Platte, Radka and Eeles, Ros and Davidson, Rosemarie and Hodgson, Shirley and Cole, Trevor and Godwin, Andrew K and Isaacs, Claudine and Claes, Kathleen and De Leeneer, Kim and Meindl, Alfons and Gehrig, Andrea and Wappenschmidt, Barbara and Sutter, Christian and Engel, Christoph and Niederacher, Dieter and Steinemann, Doris and Plendl, Hansjoerg and Kast, Karin and Rhiem, Kerstin and Ditsch, Nina and Arnold, Norbert and Varon-Mateeva, Raymonda and Schmutzler, Rita K. and Preisler-Adams, Sabine and Markov, Nadja Bogdanova and Wang-Gohrke, Shan and de Pauw, Antoine and Lefol, Cedrick and Lasset, Christine and Leroux, Dominique and Rouleau, Etienne and Damiola, Francesca and Dreyfus, Helene and Barjhoux, Laure and Golmard, Lisa and Uhrhammer, Nancy and Bonadona, Valerie and Sornin, Valerie and Bignon, Yves-Jean and Carter, Jonathan and Van Le, Linda and Piedmonte, Marion and DiSilvestro, Paul A. and de la Hoya, Miguel and Caldes, Trinidad and Nevanlinna, Heli and Aittom{\"a}ki, Kristiina and Jager, Agnes and van den Ouweland, Ans M. W. and Kets, Carolien M. and Aalfs, Cora M. and van Leeuwen, Flora E. and Hogervorst, Frans B. L. and Meijers-Heijboer, Hanne E. J. and Oosterwijk, Jan C. and van Roozendaal, Kees E. P. and Rookus, Matti A. and Devilee, Peter and van der Luijt, Rob B. and Olah, Edith and Diez, Orland and Teule, Alex and Lazaro, Conxi and Blanco, Ignacio and Del Valle, Jesus and Jakubowska, Anna and Sukiennicki, Grzegorz and Gronwald, Jacek and Spurdle, Amanda B. and Foulkes, William and Olswold, Curtis and Lindor, Noralene M. and Pankratz, Vernon S. and Szabo, Csilla I. and Lincoln, Anne and Jacobs, Lauren and Corines, Marina and Robson, Mark and Vijai, Joseph and Berger, Andreas and Fink-Retter, Anneliese and Singer, Christian F. and Rappaport, Christine and Geschwantler Kaulich, Daphne and Pfeiler, Georg and Tea, Muy-Kheng and Greene, Mark H. and Mai, Phuong L. and Rennert, Gad and Imyanitov, Evgeny N. and Mulligan, Anna Marie and Glendon, Gord and Andrulis, Irene L. and Tchatchou, Andrine and Toland, Amanda Ewart and Pedersen, Inge Sokilde and Thomassen, Mads and Kruse, Torben A. and Jensen, Uffe Birk and Caligo, Maria A. and Friedman, Eitan and Zidan, Jamal and Laitman, Yael and Lindblom, Annika and Melin, Beatrice and Arver, Brita and Loman, Niklas and Rosenquist, Richard and Olopade, Olufunmilayo I. and Nussbaum, Robert L. and Ramus, Susan J. and Nathanson, Katherine L. and Domchek, Susan M. and Rebbeck, Timothy R. and Arun, Banu K. and Mitchell, Gillian and Karlan, Bethy Y. and Lester, Jenny and Orsulic, Sandra and Stoppa-Lyonnet, Dominique and Thomas, Gilles and Simard, Jacques and Couch, Fergus J. and Offit, Kenenth and Easton, Douglas F. and Chenevix-Trench, Georgia and Antoniou, Antonis C. and Mazoyer, Sylvie and Phelan, Catherine M. and Sinilnikova, Olga M. and Cox, David G.}, title = {An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers}, series = {Breast Cancer Research}, volume = {17}, journal = {Breast Cancer Research}, number = {61}, doi = {10.1186/s13058-015-0567-2}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-145458}, year = {2015}, abstract = {Introduction: Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods: We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results: We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95\% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95\% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions: This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects.}, language = {en} } @article{FarmerStrzelczykFinisguerraetal.2021, author = {Farmer, Adam D. and Strzelczyk, Adam and Finisguerra, Alessandra and Gourine, Alexander V. and Gharabaghi, Alireza and Hasan, Alkomiet and Burger, Andreas M. and Jaramillo, Andr{\´e}s M. and Mertens, Ann and Majid, Arshad and Verkuil, Bart and Badran, Bashar W. and Ventura-Bort, Carlos and Gaul, Charly and Beste, Christian and Warren, Christopher M. and Quintana, Daniel S. and H{\"a}mmerer, Dorothea and Freri, Elena and Frangos, Eleni and Tobaldini, Eleonora and Kaniusas, Eugenijus and Rosenow, Felix and Capone, Fioravante and Panetsos, Fivos and Ackland, Gareth L. and Kaithwas, Gaurav and O'Leary, Georgia H. and Genheimer, Hannah and Jacobs, Heidi I. L. and Van Diest, Ilse and Schoenen, Jean and Redgrave, Jessica and Fang, Jiliang and Deuchars, Jim and Sz{\´e}les, Jozsef C. and Thayer, Julian F. and More, Kaushik and Vonck, Kristl and Steenbergen, Laura and Vianna, Lauro C. and McTeague, Lisa M. and Ludwig, Mareike and Veldhuizen, Maria G. and De Couck, Marijke and Casazza, Marina and Keute, Marius and Bikson, Marom and Andreatta, Marta and D'Agostini, Martina and Weymar, Mathias and Betts, Matthew and Prigge, Matthias and Kaess, Michael and Roden, Michael and Thai, Michelle and Schuster, Nathaniel M. and Montano, Nicola and Hansen, Niels and Kroemer, Nils B. and Rong, Peijing and Fischer, Rico and Howland, Robert H. and Sclocco, Roberta and Sellaro, Roberta and Garcia, Ronald G. and Bauer, Sebastian and Gancheva, Sofiya and Stavrakis, Stavros and Kampusch, Stefan and Deuchars, Susan A. and Wehner, Sven and Laborde, Sylvain and Usichenko, Taras and Polak, Thomas and Zaehle, Tino and Borges, Uirassu and Teckentrup, Vanessa and Jandackova, Vera K. and Napadow, Vitaly and Koenig, Julian}, title = {International Consensus Based Review and Recommendations for Minimum Reporting Standards in Research on Transcutaneous Vagus Nerve Stimulation (Version 2020)}, series = {Frontiers in Human Neuroscience}, volume = {14}, journal = {Frontiers in Human Neuroscience}, issn = {1662-5161}, doi = {10.3389/fnhum.2020.568051}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-234346}, year = {2021}, abstract = {Given its non-invasive nature, there is increasing interest in the use of transcutaneous vagus nerve stimulation (tVNS) across basic, translational and clinical research. Contemporaneously, tVNS can be achieved by stimulating either the auricular branch or the cervical bundle of the vagus nerve, referred to as transcutaneous auricular vagus nerve stimulation(VNS) and transcutaneous cervical VNS, respectively. In order to advance the field in a systematic manner, studies using these technologies need to adequately report sufficient methodological detail to enable comparison of results between studies, replication of studies, as well as enhancing study participant safety. We systematically reviewed the existing tVNS literature to evaluate current reporting practices. Based on this review, and consensus among participating authors, we propose a set of minimal reporting items to guide future tVNS studies. The suggested items address specific technical aspects of the device and stimulation parameters. We also cover general recommendations including inclusion and exclusion criteria for participants, outcome parameters and the detailed reporting of side effects. Furthermore, we review strategies used to identify the optimal stimulation parameters for a given research setting and summarize ongoing developments in animal research with potential implications for the application of tVNS in humans. Finally, we discuss the potential of tVNS in future research as well as the associated challenges across several disciplines in research and clinical practice.}, language = {en} }