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2. Inhibition of IL-11 signalling extends mammalian healthspan and lifespan

Author

Widjaja, Anissa A., Lim, Wei-Wen, Viswanathan, Sivakumar, Chothani, Sonia, Corden, Ben, Dasan, Cibi Mary, Goh, Joyce Wei Ting, Lim, Radiance, Singh, Brijesh K., Tan, Jessie, Pua, Chee Jian, Lim, Sze Yun, Adami, Eleonora, Schafer, Sebastian, George, Benjamin L., Sweeney, Mark, Xie, Chen, Tripathi, Madhulika, Sims, Natalie A., Hübner, Norbert, Petretto, Enrico, Withers, Dominic J., Ho, Lena, Gil, Jesus, Carling, David, and Cook, Stuart A.

Published
2024
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3. Dominance is common in mammals and is associated with trans-acting gene expression and alternative splicing.

Author

Cui, Leilei, Yang, Bin, Xiao, Shijun, Gao, Jun, Baud, Amelie, Graham, Delyth, McBride, Martin, Dominiczak, Anna, Schafer, Sebastian, Aumatell, Regina, Mont, Carme, Teruel, Albert, Hübner, Norbert, Flint, Jonathan, Mott, Richard, and Huang, Lusheng

Subjects
Mice, Rats, Animals, Swine, Alternative Splicing, Genome-Wide Association Study, Quantitative Trait Loci, Mammals, Gene Expression
Abstract

BACKGROUND: Dominance and other non-additive genetic effects arise from the interaction between alleles, and historically these phenomena play a major role in quantitative genetics. However, most genome-wide association studies (GWAS) assume alleles act additively. RESULTS: We systematically investigate both dominance-here representing any non-additive within-locus interaction-and additivity across 574 physiological and gene expression traits in three mammalian stocks: F2 intercross pigs, rat heterogeneous stock, and mice heterogeneous stock. Dominance accounts for about one quarter of heritable variance across all physiological traits in all species. Hematological and immunological traits exhibit the highest dominance variance, possibly reflecting balancing selection in response to pathogens. Although most quantitative trait loci (QTLs) are detectable as additive QTLs, we identify 154, 64, and 62 novel dominance QTLs in pigs, rats, and mice respectively that are undetectable as additive QTLs. Similarly, even though most cis-acting expression QTLs are additive, gene expression exhibits a large fraction of dominance variance, and trans-acting eQTLs are enriched for dominance. Genes causal for dominance physiological QTLs are less likely to be physically linked to their QTLs but instead act via trans-acting dominance eQTLs. In addition, thousands of eQTLs are associated with alternatively spliced isoforms with complex additive and dominant architectures in heterogeneous stock rats, suggesting a possible mechanism for dominance. CONCLUSIONS: Although heritability is predominantly additive, many mammalian genetic effects are dominant and likely arise through distinct mechanisms. It is therefore advantageous to consider both additive and dominance effects in GWAS to improve power and uncover causality.

Published
2023

4. Magnetic Tunnel Junction Performance Under Mechanical Strain

Author

Roschewsky, Niklas, Schafer, Sebastian, Hellman, Frances, and Nikitin, Vladimir

Subjects
Condensed Matter - Mesoscale and Nanoscale Physics
Abstract

In this work we investigate the effect of the mechanical stress on the performance of magnetic tunnel junctions (MTJ) with perpendicular magnetic anisotropy. We developed a 4-point bending setup, that allows us to apply a constant stress over a large substrate area with access to electrical measurements and external magnetic field. This setup enables us to measure key device performance parameters, such as tunnel magnetoresistance (TMR), switching current ($I_c^{50\%}$) and thermal stability ($\Delta$), as a function of applied stress. We find that variations in these parameters are negligible: less than $\SI{2}{\percent}$ over the entire measured range between the zero stress condition and the maximum stress at the point of wafer breakage., Comment: 4 pages, 4 figures

Published
2018
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6. A high-resolution map of human RNA translation

Author

Chothani, Sonia P., Adami, Eleonora, Widjaja, Anissa A., Langley, Sarah R., Viswanathan, Sivakumar, Pua, Chee Jian, Zhihao, Nevin Tham, Harmston, Nathan, D’Agostino, Giuseppe, Whiffin, Nicola, Mao, Wang, Ouyang, John F., Lim, Wei Wen, Lim, Shiqi, Lee, Cheryl Q.E., Grubman, Alexandra, Chen, Joseph, Kovalik, J.P., Tryggvason, Karl, Polo, Jose M., Ho, Lena, Cook, Stuart A., Rackham, Owen J.L., and Schafer, Sebastian

Published
2022
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7. Perpendicular magnetic tunnel junction performance under mechanical strain

Author

Roschewsky, Niklas, Schafer, Sebastian, Hellman, Frances, and Nikitin, Vladimir

Subjects
Bioengineering, Physical Sciences, Engineering, Technology, Applied Physics
Abstract

In this work, we investigate effect of the mechanical stress on the performance of magnetic tunnel junctions with perpendicular magnetic anisotropy. We developed a 4-point bending setup that allows us to apply a constant stress over a large substrate area with access to electrical measurements and an external magnetic field. This setup enables us to measure key device performance parameters, such as tunnel magnetoresistance, switching current (I c 50%), and thermal stability (Δ), as a function of applied stress. We find that variations in these parameters are negligible: less than 2% over the entire measured range between the zero stress condition and the maximum stress at the point of wafer breakage.

Published
2018

11. An indirect transmission measurement-based spectrum estimation method for computed tomography

Author

Zhao, Wei, Niu, Kai, Schafer, Sebastian, and Royalty, Kevin

Subjects
Physics - Medical Physics
Abstract

The characteristics of an x-ray spectrum can greatly influence imaging and related tasks. In practice, due to the pile-up effect of the detector, it's difficult to directly measure the spectrum of a CT scanner using an energy resolved detector. An alternative solution is to estimate the spectrum using transmission measurements with a step phantom or other CT phantom. In this work, we present a new spectrum estimation method based on indirect transmission measurement and model spectra mixture approach. The estimated x-ray spectrum was expressed as weighted summation of a set of model spectra, which can significantly reduce the degrees of freedom (DOF) of the spectrum estimation problem. Next, an estimated projection can be calculated with the assumed spectrum. By iteratively updating the unknown weights, we minimized the difference between the estimated projection data and the raw projection data. The final spectrum was calculated with these calibrated weights and the model spectra. Both simulation and experimental data were used to evaluate the proposed method. In the simulation study, the estimated spectra were compared to the raw spectra which were used to generate the raw projection data. For the experimental study, the ground truth measurement of the raw x-ray spectrum was not available. Therefore, the estimated spectrum was compared against spectra generated using the SpekCalc software with tube configurations provided by the scanner manufacturer. The results show the proposed method has potential to accurately estimate x-ray spectra using the raw projection data. The difference between the mean energy of the raw spectra and the mean energy of the estimated spectra were smaller than 0.5 keV for both simulation and experimental data. Further tests show the method was robust with respect to the model spectra generator., Comment: 22 pages, 9 figures

Published
2015
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12. A patient-specific scatter artifacts correction method

Author

Zhao, Wei, Brunner, Stephen, Niu, Kai, Schafer, Sebastian, Royalty, Kevin, and Chen, Guang-Hong

Subjects
Physics - Medical Physics
Abstract

This paper provides a fast and patient-specific scatter artifact correction method for cone-beam computed tomography (CBCT) used in image-guided interventional procedures. Due to increased irradiated volume of interest in CBCT imaging, scatter radiation has increased dramatically compared to 2D imaging, leading to a degradation of image quality. In this study, we propose a scatter artifact correction strategy using an analytical convolution-based model whose free parameters are estimated using a rough estimation of scatter profiles from the acquired cone-beam projections. It was evaluated using Monte Carlo simulations with both monochromatic and polychromatic X-ray sources. The results demonstrated that the proposed method significantly reduced the scatter-induced shading artifacts and recovered CT numbers.

Published
2015
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14. 52 Genetic Loci Influencing Myocardial Mass

Author

van der Harst, Pim, van Setten, Jessica, Verweij, Niek, Vogler, Georg, Franke, Lude, Maurano, Matthew T, Wang, Xinchen, Leach, Irene Mateo, Eijgelsheim, Mark, Sotoodehnia, Nona, Hayward, Caroline, Sorice, Rossella, Meirelles, Osorio, Lyytikäinen, Leo-Pekka, Polašek, Ozren, Tanaka, Toshiko, Arking, Dan E, Ulivi, Sheila, Trompet, Stella, Müller-Nurasyid, Martina, Smith, Albert V, Dörr, Marcus, Kerr, Kathleen F, Magnani, Jared W, Del Greco M., Fabiola, Zhang, Weihua, Nolte, Ilja M, Silva, Claudia T, Padmanabhan, Sandosh, Tragante, Vinicius, Esko, Tõnu, Abecasis, Gonçalo R, Adriaens, Michiel E, Andersen, Karl, Barnett, Phil, Bis, Joshua C, Bodmer, Rolf, Buckley, Brendan M, Campbell, Harry, Cannon, Megan V, Chakravarti, Aravinda, Chen, Lin Y, Delitala, Alessandro, Devereux, Richard B, Doevendans, Pieter A, Dominiczak, Anna F, Ferrucci, Luigi, Ford, Ian, Gieger, Christian, Harris, Tamara B, Haugen, Eric, Heinig, Matthias, Hernandez, Dena G, Hillege, Hans L, Hirschhorn, Joel N, Hofman, Albert, Hubner, Norbert, Hwang, Shih-Jen, Iorio, Annamaria, Kähönen, Mika, Kellis, Manolis, Kolcic, Ivana, Kooner, Ishminder K, Kooner, Jaspal S, Kors, Jan A, Lakatta, Edward G, Lage, Kasper, Launer, Lenore J, Levy, Daniel, Lundby, Alicia, Macfarlane, Peter W, May, Dalit, Meitinger, Thomas, Metspalu, Andres, Nappo, Stefania, Naitza, Silvia, Neph, Shane, Nord, Alex S, Nutile, Teresa, Okin, Peter M, Olsen, Jesper V, Oostra, Ben A, Penninger, Josef M, Pennacchio, Len A, Pers, Tune H, Perz, Siegfried, Peters, Annette, Pinto, Yigal M, Pfeufer, Arne, Pilia, Maria Grazia, Pramstaller, Peter P, Prins, Bram P, Raitakari, Olli T, Raychaudhuri, Soumya, Rice, Ken M, Rossin, Elizabeth J, Rotter, Jerome I, Schafer, Sebastian, Schlessinger, David, and Schmidt, Carsten O

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Heart Disease - Coronary Heart Disease, Human Genome, Heart Disease, Biotechnology, Cardiovascular, Genetics, 2.1 Biological and endogenous factors, Animals, Cardiomegaly, Genetic Loci, Genome-Wide Association Study, Humans, electrocardiogram, genetic association study, heart failure, left ventricular hypertrophy, QRS, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundMyocardial mass is a key determinant of cardiac muscle function and hypertrophy. Myocardial depolarization leading to cardiac muscle contraction is reflected by the amplitude and duration of the QRS complex on the electrocardiogram (ECG). Abnormal QRS amplitude or duration reflect changes in myocardial mass and conduction, and are associated with increased risk of heart failure and death.ObjectivesThis meta-analysis sought to gain insights into the genetic determinants of myocardial mass.MethodsWe carried out a genome-wide association meta-analysis of 4 QRS traits in up to 73,518 individuals of European ancestry, followed by extensive biological and functional assessment.ResultsWe identified 52 genomic loci, of which 32 are novel, that are reliably associated with 1 or more QRS phenotypes at p < 1 × 10(-8). These loci are enriched in regions of open chromatin, histone modifications, and transcription factor binding, suggesting that they represent regions of the genome that are actively transcribed in the human heart. Pathway analyses provided evidence that these loci play a role in cardiac hypertrophy. We further highlighted 67 candidate genes at the identified loci that are preferentially expressed in cardiac tissue and associated with cardiac abnormalities in Drosophila melanogaster and Mus musculus. We validated the regulatory function of a novel variant in the SCN5A/SCN10A locus in vitro and in vivo.ConclusionsTaken together, our findings provide new insights into genes and biological pathways controlling myocardial mass and may help identify novel therapeutic targets.

Published
2016

19. Inhibiting Interleukin 11 Signaling Reduces Hepatocyte Death and Liver Fibrosis, Inflammation, and Steatosis in Mouse Models of Nonalcoholic Steatohepatitis

Author

Widjaja, Anissa A., Singh, Brijesh K., Adami, Eleonora, Viswanathan, Sivakumar, Dong, Jinrui, D’Agostino, Giuseppe A., Ng, Benjamin, Lim, Wei Wen, Tan, Jessie, Paleja, Bhairav S., Tripathi, Madhulika, Lim, Sze Yun, Shekeran, Shamini Guna, Chothani, Sonia P., Rabes, Anne, Sombetzki, Martina, Bruinstroop, Eveline, Min, Lio Pei, Sinha, Rohit A., Albani, Salvatore, Yen, Paul M., Schafer, Sebastian, and Cook, Stuart A.

Published
2019
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20. The Translational Landscape of the Human Heart

Author

van Heesch, Sebastiaan, Witte, Franziska, Schneider-Lunitz, Valentin, Schulz, Jana F., Adami, Eleonora, Faber, Allison B., Kirchner, Marieluise, Maatz, Henrike, Blachut, Susanne, Sandmann, Clara-Louisa, Kanda, Masatoshi, Worth, Catherine L., Schafer, Sebastian, Calviello, Lorenzo, Merriott, Rhys, Patone, Giannino, Hummel, Oliver, Wyler, Emanuel, Obermayer, Benedikt, Mücke, Michael B., Lindberg, Eric L., Trnka, Franziska, Memczak, Sebastian, Schilling, Marcel, Felkin, Leanne E., Barton, Paul J.R., Quaife, Nicholas M., Vanezis, Konstantinos, Diecke, Sebastian, Mukai, Masaya, Mah, Nancy, Oh, Su-Jun, Kurtz, Andreas, Schramm, Christoph, Schwinge, Dorothee, Sebode, Marcial, Harakalova, Magdalena, Asselbergs, Folkert W., Vink, Aryan, de Weger, Roel A., Viswanathan, Sivakumar, Widjaja, Anissa A., Gärtner-Rommel, Anna, Milting, Hendrik, dos Remedios, Cris, Knosalla, Christoph, Mertins, Philipp, Landthaler, Markus, Vingron, Martin, Linke, Wolfgang A., Seidman, Jonathan G., Seidman, Christine E., Rajewsky, Nikolaus, Ohler, Uwe, Cook, Stuart A., and Hubner, Norbert

Published
2019
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23. Interleukin-11 is important for vascular smooth muscle phenotypic switching and aortic inflammation, fibrosis and remodeling in mouse models

Author

Lim, Wei-Wen, Corden, Ben, Ng, Benjamin, Vanezis, Konstantinos, D’Agostino, Giuseppe, Widjaja, Anissa A., Song, Wei-Hua, Xie, Chen, Su, Liping, Kwek, Xiu-Yi, Tee, Nicole G. Z., Dong, Jinrui, Ko, Nicole S. J., Wang, Mao, Pua, Chee Jian, Jamal, Muhammad H., Soh, Beeyong, Viswanathan, Sivakumar, Schafer, Sebastian, and Cook, Stuart A.

Published
2020
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24. Contributors

Author

Abolmaesumi, Purang, primary, Ahmad, Sahar, additional, Anderson, William S., additional, Asman, Andrew J., additional, Ben-Cohen, Avi, additional, Biswas, Pradipta, additional, Boctor, Emad, additional, Bodenstedt, Sebastian, additional, Breton, Elodie, additional, Cao, Xiaohuan, additional, Carass, Aaron, additional, Cardoso, M. Jorge, additional, Castillo Tovar, Jose M., additional, Chen, Elvis C.S., additional, Chen, Hao, additional, Chen, Zhi, additional, Cheng, Jie-Zhi, additional, Cootes, T.F., additional, Davatzikos, Christos, additional, de Ribaupierre, Sandrine, additional, Dewey, Blake E., additional, DiPietro, Robert, additional, Dong, Pei, additional, Dou, Qi, additional, Eagleson, Roy, additional, Elson, Daniel S., additional, Erus, Guray, additional, Esposito, M., additional, Essert, Caroline, additional, Fan, Jingfan, additional, Fenster, Aaron, additional, Fichtinger, Gabor, additional, Gangi, Afshin, additional, Garnon, Julien, additional, Gilbert, Kathleen, additional, Glocker, Ben, additional, Greenspan, Hayit, additional, Habes, Mohamad, additional, Hacihaliloglu, Ilker, additional, Hager, Gregory D., additional, Hammernik, Kerstin, additional, Heinrich, Mattias P., additional, Heng, Pheng-Ann, additional, Hennersperger, C., additional, Hensen, Bennet, additional, Holden, Matthew, additional, Huo, Yuankai, additional, Ilse, Maximilian, additional, Išgum, Ivana, additional, Joskowicz, Leo, additional, Judy, Brendan F., additional, Kägebein, Urte, additional, Kamnitsas, Konstantinos, additional, Kashyap, Satyananda, additional, Kazanzides, Peter, additional, Klein, Stefan, additional, Knoll, Florian, additional, Konukoglu, Ender, additional, Kulkarni, Pankaj Pramod, additional, Landman, Bennett A., additional, Lasso, Andras, additional, Ledig, Christian, additional, Lee, Kyungmoo, additional, Linte, Cristian A., additional, Lu, Le, additional, Lyu, Ilwoo, additional, Maier-Hein, Lena, additional, Metaxas, Dimitris N., additional, Miller, Karol, additional, Modat, Marc, additional, Mori, Kensaku, additional, Moriakov, Nikita, additional, Mousavi, Parvin, additional, Navab, N., additional, Niessen, Wiro J., additional, Ortiz, Marilu, additional, Ourselin, Sebastien, additional, Papież, Bartłomiej W., additional, Peng, Yifan, additional, Pham, Dzung L., additional, Pontre, Beau, additional, Prince, Jerry L., additional, Qi, Xiaojuan, additional, Rothgang, Eva, additional, Roy, Snehashis, additional, Schafer, Sebastian, additional, Shen, Dinggang, additional, Sikander, Sakura, additional, Siewerdsen, Jeffrey H., additional, Song, Sang-Eun, additional, Sonka, Milan, additional, Speidel, Stefanie, additional, Starmans, Martijn P.A., additional, Stefan, P., additional, Stoyanov, Danail, additional, Sudre, Carole H., additional, Suinesiaputra, Avan, additional, Taylor, Russell H., additional, Teuwen, Jonas, additional, Tomczak, Jakub M., additional, Traub, J., additional, Ungi, Tamas, additional, van der Voort, Sebastian R., additional, Vasconcelos, Francisco, additional, Vedula, S. Swaroop, additional, Veenland, Jifke F., additional, Wacker, Frank K., additional, Wang, Xiaosong, additional, Welling, Max, additional, Wittek, Adam, additional, Wolterink, Jelmer M., additional, Xiong, Tao, additional, Xu, Daguang, additional, Xu, Zhoubing, additional, Yan, Zhennan, additional, Yang, Dong, additional, Yang, Lin, additional, Yap, Pew-Thian, additional, Young, Alistair A., additional, Zevin, Boris, additional, Zhang, Honghai, additional, Zhang, Zizhao, additional, Zhao, Can, additional, Zheng, Yefeng, additional, and Zhou, S. Kevin, additional

Published
2020
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27. Author Correction: WWP2 regulates pathological cardiac fibrosis by modulating SMAD2 signaling

Author

Chen, Huimei, Moreno-Moral, Aida, Pesce, Francesco, Devapragash, Nithya, Mancini, Massimiliano, Heng, Ee Ling, Rotival, Maxime, Srivastava, Prashant K., Harmston, Nathan, Shkura, Kirill, Rackham, Owen J. L., Yu, Wei-Ping, Sun, Xi-Ming, Tee, Nicole Gui Zhen, Tan, Elisabeth Li Sa, Barton, Paul J. R., Felkin, Leanne E., Lara-Pezzi, Enrique, Angelini, Gianni, Beltrami, Cristina, Pravenec, Michal, Schafer, Sebastian, Bottolo, Leonardo, Hubner, Norbert, Emanueli, Costanza, Cook, Stuart A., and Petretto, Enrico

Published
2019
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28. WWP2 regulates pathological cardiac fibrosis by modulating SMAD2 signaling

Author

Chen, Huimei, Moreno-Moral, Aida, Pesce, Francesco, Devapragash, Nithya, Mancini, Massimiliano, Heng, Ee Ling, Rotival, Maxime, Srivastava, Prashant K., Harmston, Nathan, Shkura, Kirill, Rackham, Owen J. L., Yu, Wei-Ping, Sun, Xi-Ming, Tee, Nicole Gui Zhen, Tan, Elisabeth Li Sa, Barton, Paul J. R., Felkin, Leanne E., Lara-Pezzi, Enrique, Angelini, Gianni, Beltrami, Cristina, Pravenec, Michal, Schafer, Sebastian, Bottolo, Leonardo, Hubner, Norbert, Emanueli, Costanza, Cook, Stuart A., and Petretto, Enrico

Published
2019
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29. Differences in 5'untranslated regions highlight the importance of translational regulation of dosage sensitive genes

Author

Wieder, Nechama, primary, D'Souza, Elston N., additional, Martin-Geary, Alexandra C., additional, Lassen, Frederik H., additional, Talbot-Martin, Jonathan, additional, Fernandes, Maria, additional, Chothani, Sonia P., additional, Rackham, Owen J.L., additional, Schafer, Sebastian, additional, Aspden, Julie L., additional, MacArthur, Daniel G., additional, Davies, Robert W., additional, and Whiffin, Nicola, additional

Published
2023
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30. Dominance is common in mammals and is associated with trans-acting gene expression and alternative splicing

Author

Cui, Leilei, primary, Yang, Bin, additional, Xiao, Shijun, additional, Gao, Jun, additional, Baud, Amelie, additional, Graham, Delyth, additional, McBride, Martin, additional, Dominiczak, Anna, additional, Schafer, Sebastian, additional, Lopez Aumatell, Regina, additional, Mont, Carme, additional, Fernandez Teruel, Albert, additional, Hubner, Norbert, additional, Flint, Jonathan, additional, Mott, Richard, additional, and Huang, Lusheng, additional

Published
2023
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31. IL-11 is a crucial determinant of cardiovascular fibrosis

Author

Schafer, Sebastian, Viswanathan, Sivakumar, Widjaja, Anissa A., Lim, Wei-Wen, Moreno-Moral, Aida, DeLaughter, Daniel M., Ng, Benjamin, Patone, Giannino, Chow, Kingsley, Khin, Ester, Tan, Jessie, Chothani, Sonia P., Ye, Lei, Rackham, Owen J. L., Ko, Nicole S. J., Sahib, Norliza E., Pua, Chee Jian, Zhen, Nicole T. G., Xie, Chen, Wang, Mao, Maatz, Henrike, Lim, Shiqi, Saar, Kathrin, Blachut, Susanne, Petretto, Enrico, Schmidt, Sabine, Putoczki, Tracy, Guimares-Camboa, Nuno, Wakimoto, Hiroko, van Heesch, Sebastiaan, Sigmundsson, Kristmundur, Lim, See L., Soon, Jia L., Chao, Victor T. T., Chua, Yeow L., Tan, Teing E., Evans, Sylvia M., Loh, Yee J., Jamal, Muhammad H., Ong, Kim K., Chua, Kim C., Ong, Boon-Hean, Chakaramakkil, Mathew J., Seidman, Jonathan G., Seidman, Christine E., Hubner, Norbert, Sin, Kenny Y. K., and Cook, Stuart A.

Subjects
Physiological aspects, Health aspects, Interleukins -- Health aspects, Cardiovascular diseases -- Physiological aspects, Fibrosis -- Physiological aspects
Abstract

Author(s): Sebastian Schafer [1, 2]; Sivakumar Viswanathan [2]; Anissa A. Widjaja [2]; Wei-Wen Lim [1]; Aida Moreno-Moral [2]; Daniel M. DeLaughter [3]; Benjamin Ng [1]; Giannino Patone [4]; Kingsley Chow [...]

Published
2017
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33. AAPM Task Group Report 238: 3D C‐arms with volumetric imaging capability*

Author

Supanich, Mark, primary, Siewerdsen, Jeff, additional, Fahrig, Rebecca, additional, Farahani, Keyvan, additional, Gang, Grace Jianan, additional, Helm, Pat, additional, Jans, Jan, additional, Jones, Kyle, additional, Koenig, Thomas, additional, Kuhls‐Gilcrist, Andrew, additional, Lin, MingDe, additional, Riddell, Cyril, additional, Ritschl, Ludwig, additional, Schafer, Sebastian, additional, Schueler, Beth, additional, Silver, Mike, additional, Timmer, Jan, additional, Trousset, Yves, additional, and Zhang, Jie, additional

Published
2023
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34. Talk to your crowd: principles for effective communication in crowdsourcing: a few key principles for communicating with solvers can help contest sponsors maintain and grow their base of participants

Author

Schafer, Sebastian, Antons, David, Luttgens, Dirk, Piller, Frank, and Salge, Torsten Oliver

Subjects
Organizational communication -- Methods, Problem solving -- Methods, Crowdsourcing -- Methods, Business, general, Business, Engineering and manufacturing industries
Abstract

OVERVIEW: When crowdsourcing intermediaries lose crowd members, they lose potential high-quality solutions in the future. As the number of contests and intermediaries grows, it is increasingly critical for crowdsourcers to meet the needs of solvers and avoid seeing them migrate to the competition. Besides winning contests, intensive communication and customized feedback are solvers' most central needs. For this study, we surveyed 202 solvers about the importance of communication in crowdsourcing contests. Based on our quantitative and qualitative insights, we derive key principles that can help crowdsourcers maintain and grow their solver base. KEYWORDS: Crowdsourcing contests, Solvers, Problem solving, Crowdsourcing contests are becoming mainstream (Boudreau and Lakhani 2013) as an increasing number of firms and other organizations recognize the vast potential of sourcing ideas and solutions from crowds of [...]

Published
2017
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37. Fine Mapping of the 1p36 Deletion Syndrome Identifies Mutation of PRDM16 as a Cause of Cardiomyopathy

Author

Arndt, Anne-Karin, Schafer, Sebastian, Drenckhahn, Jorg-Detlef, Sabeh, M. Khaled, Plovie, Eva R., Caliebe, Almuth, Klopocki, Eva, Musso, Gabriel, Werdich, Andreas A., Kalwa, Hermann, Heinig, Matthias, Padera, Robert F., Wassilew, Katharina, Bluhm, Julia, Harnack, Christine, Martitz, Janine, Barton, Paul J., Greutmann, Matthias, Berger, Felix, Hubner, Norbert, Siebert, Reiner, Kramer, Hans-Heiner, Cook, Stuart A., MacRae, Calum A., and Klaassen, Sabine

Published
2013
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40. Engineered cell homing

Author

Sarkar, Debanjan, Spencer, Joel A., Phillips, Joseph A., Zhao, Weian, Schafer, Sebastian, Spelke, Dawn P., Mortensen, Luke J., Ruiz, Juan P., Vemula, Praveen Kumar, Sridharan, Rukmani, Kumar, Sriram, Karnik, Rohit, Lin, Charles P., and Karp, Jeffrey M.

Published
2011
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42. Interleukin-11 drives human and mouse alcohol-related liver disease

Author

Effenberger, Maria, primary, Widjaja, Anissa A, additional, Grabherr, Felix, additional, Schaefer, Benedikt, additional, Grander, Christoph, additional, Mayr, Lisa, additional, Schwaerzler, Julian, additional, Enrich, Barbara, additional, Moser, Patrizia, additional, Fink, Julia, additional, Pedrini, Alisa, additional, Jaschke, Nikolai, additional, Kirchmair, Alexander, additional, Pfister, Alexandra, additional, Hausmann, Bela, additional, Bale, Reto, additional, Putzer, Daniel, additional, Zoller, Heinz, additional, Schafer, Sebastian, additional, Pjevac, Petra, additional, Trajanoski, Zlatko, additional, Oberhuber, Georg, additional, Adolph, Timon, additional, Cook, Stuart, additional, and Tilg, Herbert, additional

Published
2022
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43. IL11 Activates Pancreatic Stellate Cells and Causes Pancreatic Inflammation, Fibrosis and Atrophy in a Mouse Model of Pancreatitis

Author

Ng, Benjamin, primary, Viswanathan, Sivakumar, additional, Widjaja, Anissa A., additional, Lim, Wei-Wen, additional, Shekeran, Shamini G., additional, Goh, Joyce Wei Ting, additional, Tan, Jessie, additional, Kuthubudeen, Fathima, additional, Lim, Sze Yun, additional, Xie, Chen, additional, Schafer, Sebastian, additional, Adami, Eleonora, additional, and Cook, Stuart A., additional

Published
2022
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46. RNA-binding protein RBM20 represses splicing to orchestrate cardiac pre-mRNA processing

Author

Maatz, Henrike, Jens, Marvin, Liss, Martin, Schafer, Sebastian, Heinig, Matthias, Kirchner, Marieluise, Adami, Eleonora, Rintisch, Carola, Dauksaite, Vita, Radke, Michael H., Selbach, Matthias, Barton, Paul J.R., Cook, Stuart A., Rajewsky, Nikolaus, Gotthardt, Michael, Landthaler, Markus, and Hubner, Norbert

Subjects
Physiological aspects, Genetic aspects, Research, Risk factors, Heart failure -- Chemical properties -- Risk factors -- Genetic aspects -- Research, Binding proteins -- Physiological aspects -- Research, Messenger RNA -- Chemical properties -- Physiological aspects -- Research
Abstract

Introduction Alternative RNA processing is determined by RNA-binding splicing factors to generate different mRNA isoforms in a tissue-specific and developmental-regulated manner (1). Alterations in splicing factors or mutations in their [...], Mutations in the gene encoding the RNA-binding protein RBM20 have been implicated in dilated cardiomyopathy (DCM), a major cause of chronic heart failure, presumably through altering cardiac RNA splicing. Here, we combined transcriptome-wide crosslinking immunoprecipitation (CLIP-seq), RNA-seq, and quantitative proteomics in cell culture and rat and human hearts to examine how RBM20 regulates alternative splicing in the heart. Our analyses revealed the presence of a distinct RBM20 RNA-recognition element that is predominantly found within intronic binding sites and linked to repression of exon splicing with RBM20 binding near 3' and 5' splice sites. Proteomic analysis determined that RBM20 interacts with both U1 and U2 small nuclear ribonucleic particles (snRNPs) and suggested that RBM20-dependent splicing repression occurs through spliceosome stalling at complex A. Direct RBM20 targets included several genes previously shown to be involved in DCM as well as genes not typically associated with this disease. In failing human hearts, reduced expression of RBM20 affected alternative splicing of several direct targets, indicating that differences in RBM20 expression may affect cardiac function. Together, these findings identify RBM20-regulated targets and provide insight into the pathogenesis of human heart failure.

Published
2014
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