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Start Over Author "Klein, Christoph" Publisher elsevier b.v.
128 results on '"Klein, Christoph"'

9. Transcatheter Aortic Valve Replacement for Isolated Aortic Regurgitation Using a New Self-Expanding TAVR System.

Author

Adam, Matti, Tamm, Alexander, Wienemann, Hendrik, Unbehaun, Axel, Klein, Christoph, Arnold, Martin, Marwan, Mohamed, Theiss, Hans, Braun, Daniel, Bleiziffer, Sabine, Geyer, Martin, Goncharov, Arseniy, Kuhn, Elmar, Falk, Volkmar, von Bardeleben, R.S., Achenbach, Stephan, Massberg, Steffen, Baldus, Stephan, Treede, Hendrik, and Rudolph, Tanja Katharina

Abstract

Patients with severe aortic regurgitation (AR) are often not considered for surgery because of increased surgical risk. Because of unique anatomical characteristics among patients with AR, interventional treatment options are limited, and implantation results are inconsistent compared with those among patients with aortic stenosis. The authors describe the initial commercial experience of the first Conformité Européenne–marked transfemoral transcatheter aortic valve replacement system (JenaValve Trilogy [JV]) for the treatment of patients with AR. This multicenter registry included 58 consecutive patients from 6 centers across Germany. Transcatheter aortic valve replacement was performed with the JV system for isolated severe and symptomatic AR. Patient characteristics, primary implantation outcomes, and valve performance up to 30 days were analyzed using Valve Academic Research Consortium 3 definitions. The mean patient age was 76.5 ± 9 years, with a mean Society of Thoracic Surgeons score of 4.2% ± 4.3%. Device success was achieved in 98% of patients. The mean gradient was 4.3 ± 1.6 mm Hg, and no moderate or severe paravalvular regurgitation occurred. No conversion to open heart surgery or valve embolization was reported. There were no major vascular complications or bleeding events. The rate of new permanent pacemaker implantation was 19.6%. At 30 days, 92% of the patients were in NYHA functional class I or II, and the 30-day mortality rate was 1.7%. Treatment of patients with severe symptomatic AR using the transfemoral JV system is safe and effective. Given its favorable hemodynamic performance and low complication rates, this system may offer a new treatment option for patients with AR not suitable for surgery. [Display omitted] [ABSTRACT FROM AUTHOR]

Published
2023
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16. First-in-Human Dedicated Leaflet Splitting Device for Prevention of Coronary Obstruction in Transcatheter Aortic Valve Replacement.

Author

Dvir, Danny, Leon, Martin B., Abdel-Wahab, Mohamed, Unbehaun, Axel, Kodali, Susheel, Tchetche, Didier, Pibarot, Philippe, Leipsic, Jonathon, Blanke, Philipp, Gerckens, Ulrich, Manoharan, Ganesh, Harari, Emanuel, Hellou, Elias, Wolak, Arik, Ben-Assa, Eyal, Jubeh, Rami, Shuvy, Mony, Koifman, Edward, Klein, Christoph, and Kempfert, Joerg

Abstract

Coronary artery obstruction is a life-threatening complication of transcatheter aortic valve replacement (TAVR) procedures. Current preventive strategies are suboptimal. The aim of this study was to describe bench testing and clinical experience with a novel device that splits valve leaflets that are at risk for causing coronary obstruction after TAVR, allowing normal coronary flow. The ShortCut device was initially tested in vitro and preclinically in a porcine model for functionality and safety. The device was subsequently offered to patients at elevated risk for coronary obstruction. Risk for coronary obstruction was based on computed tomography–based anatomical characteristics. Procedure success was determined as patient survival at 30 days with a functioning new valve, without stroke or coronary obstruction. Following a successful completion of bench testing and preclinical trial, the device was used in 8 patients with failed bioprosthetic valves (median age 81 years; IQR: 72-85 years; 37.5% man) at 2 medical centers. A total of 11 leaflets were split: 5 patients (63.5%) were considered at risk for left main obstruction alone, and 3 patients (37.5%) were at risk for double coronary obstruction. All patients underwent successful TAVR without evidence of coronary obstruction. All patients were discharged from the hospital in good clinical condition, and no adverse neurologic events were noted. Procedure success was 100%. Evaluation of the first dedicated transcatheter leaflet-splitting device shows that the device can successfully split degenerated bioprosthetic valve leaflets. The procedure was safe and successfully prevented coronary obstruction in patients at risk for this complication following TAVR. [Display omitted] [ABSTRACT FROM AUTHOR]

Published
2023
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18. Measurement of the associated production of a Higgs boson decaying into b-quarks with a vector boson at high transverse momentum in pp collisions at sqrt(s)=13 TeV with the ATLAS detector

Author

Aad, Georges, Abbott, Brad, Abbott, Dale Charles, Abed Abud, Adam, Abeling, Kira, Abhayasinghe, Deshan Kavishka, Abidi, Syed Haider, Abouzeid, Ossama, Abraham, Nicola, Abramowicz, Halina, Abreu, Henso, Abulaiti, Yiming, Acharya, Bobby Samir, Achkar, Baida, Adam, Lennart, Adam Bourdarios, Claire, Adamczyk, Leszek, Adamek, Lukas, Adelman, Jahred, Adersberger, Michael, Adiguzel, Aytul, Adorni, Sofia, Adye, Tim, Affolder, Tony, Afik, Yoav, Agapopoulou, Christina, Agaras, Merve Nazlim, Aggarwal, Anamika, Agheorghiesei, Catalin, Aguilar Saavedra, Juan Antonio, Ahmad, Ammara, Ahmadov, Faig, Ahmed, Waleed Syed, Ai, Xiaocong, Aielli, Giulio, Akatsuka, Shunichi, Akbiyik, Melike, Akesson, Torsten Paul Ake, Akilli, Ece, Akimov, Andrei, Al Khoury, Konie, Alberghi, Gian Luigi, Albert, Justin, Alconada Verzini, Maria Josefina, Alderweireldt, Sara Caroline, Aleksa, Martin, Aleksandrov, Igor, Alexa, Calin, Alexopoulos, Theodoros, Alfonsi, Alice, Alfonsi, Fabrizio, Alhroob, Muhammad, Ali, Babar, Ali, Shahzad, Aliev, Malik, Alimonti, Gianluca, Allaire, Corentin, Allbrooke, Benedict, Allen, Benjamin William, Allport, Phillip, Aloisio, Alberto, Alonso, Francisco, Alpigiani, Cristiano, Alunno Camelia, Elio, Alvarez Estevez, Manuel, Alviggi, Mariagrazia, Amaral Coutinho, Yara, Ambler, Alessandro, Ambroz, Luca, Amelung, Christoph, Amidei, Dante Eric, Amor dos Santos, Susana Patricia, Amoroso, Simone, Amrouche, Cherifa Sabrina, An, Fenfen, Anastopoulos, Christos, Andari, Nansi, Andeen, Timothy, Anders, John Kenneth, Andrean, Stefio Yosse, Andreazza, Attilio, Andrei, George Victor, Anelli, Christopher Ryan, Angelidakis, Stylianos, Angerami, Aaron, Anisenkov, Alexey, Annovi, Alberto, Antel, Claire, Anthony, Matthew Thomas, Antipov, Egor, Antonelli, Mario, Antrim, Daniel Joseph, Anulli, Fabio, Aoki, Masato, Aparisi Pozo, Javier Alberto, Aparo, Marco, Aperio Bella, Ludovica, Aranzabal, Nordin, Araujo Ferraz, Victor, Araujo Pereira, Rodrigo, Arcangeletti, Chiara, Arce, Ayana, Arduh, Francisco Anuar, Arguin, Jean-Francois, Argyropoulos, Spyridon, Arling, Jan-Hendrik, Armbruster, Aaron James, Armstrong, Alexander, Arnaez, Olivier, Arnold, Hannah, Arrubarrena Tame, Zulit Paola, Artoni, Giacomo, Asai, Kanae, Asai, Shoji, Asawatavonvanich, Thanawat, Asbah, Nedaa, Asimakopoulou, Eleni Myrto, Asquith, Lily, Assahsah, Jihad, Assamagan, Ketevi, Astalos, Robert, Atkin, Ryan Justin, Atkinson, Markus, Atlay, Naim Bora, Atmani, Hicham, Augsten, Kamil, Austrup, Volker Andreas, Avolio, Giuseppe, Ayoub, Mohamad Kassem, Azuelos, Georges, Bachacou, Henri, Bachas, Konstantinos, Backes, Moritz, Backman, Filip, Bagnaia, Paolo, Bahmani, Marzieh, Baluch Bahrasemani, Sina, Bailey, Adam, Bailey, Virginia Ruth, Baines, John, Bakalis, Christos, Baker, Keith, Bakker, Pepijn Johannes, Bakos, Evelin, Bakshi Gupta, Debottam, Balaji, Shyam, Baldin, Evgenii, Balek, Petr, Balli, Fabrice, Balunas, William Keaton, Balz, Johannes, Banas, Elzbieta, Bandieramonte, Marilena, Bandyopadhyay, Anjishnu, Banerjee, Swagato, Barak, Liron, Barbe, William Mickael, Barberio, Elisabetta Luigia, Barberis, Dario, Barbero, Marlon, Barbour, Gregory, Barillari, Teresa, Barisits, Martin-Stefan, Barkeloo, Jason Tylor Colt, Barklow, Timothy, Barnea, Rotem, Barnett, Bruce, Barnett, Michael, Blenessy, Zuzana, Baroncelli, Antonio, Barone, Gaetano, Barr, Alan, Barranco Navarro, Laura, Barreiro, Fernando, Barreiro Guimaraes da Costa, Joao, Barron, Uriel, Barsov, Sergey, Bartels, Falk, Bartoldus, Rainer, Bartolini, Giovanni, Barton, Adam Edward, Bartos, Pavol, Basalaev, Artem, Basan, Alexander, Bassalat, Ahmed, Basso, Matthew Joseph, Bates, Richard, Batlamous, Souad, Batley, Richard, Batool, Binish, Battaglia, Marco, Bauce, Matteo, Bauer, Florian, Bauer, Kevin Thomas, Bauer, Patrick, Bawa, Harinder Singh, Bayirli, Arif, Beacham, James Baker, Beau, Tristan, Beauchemin, Pierre-Hugues, Becherer, Fabian Horst, Bechtle, Philip, Beck, Helge Christoph, Beck, Hans Peter, Becker, Anne Kathrin, Becot, Cyril, Beddall, Ayda, Beddall, Andrew, Bednyakov, Vadim, Bedognetti, Matteo, Bee, Christopher, Beermann, Thomas Alfons, Begalli, Marcia, Begel, Michael, Behera, Arabinda, Behr, Katharina, Beisiegel, Florian, Belfkir, Mohamed, Bell, Andrew Stuart, Bella, Gideon, Bellagamba, Lorenzo, Bellerive, Alain, Bellos, Panagiotis, Beloborodov, Konstantin, Belotskiy, Konstantin, Belyaev, Nikita, Benchekroun, Driss, Benekos, Nektarios, Benhammou, Yan, Benjamin, Douglas, Benoit, Mathieu, Bensinger, James, Bentvelsen, Stan, Beresford, Lydia, Beretta, Matteo, Berge, David, Bergeaas Kuutmann, Elin, Berger, Nicolas, Bergmann, Benedikt, Bergsten, Laura Jean, Beringer, Juerg, Berlendis, Simon Paul, Bernardi, Gregorio, Bernius, Catrin, Bernlochner, Florian Urs, Berry, Tracey, Berta, Peter, Bertella, Claudia, Berthold, Anne-Sophie, Bertram, Iain Alexander, Bessidskaia Bylund, Olga, Besson, Nathalie, Bethani, Agni, Bethke, Siegfried, Betti, Alessandra, Bevan, Adrian John, Beyer, Julien-Christopher, Bhattacharya, Deb Sankar, Bhattarai, Prajita, Bhopatkar, Vallary Shashikant, Bi, Runyu, Bianchi, Riccardo Maria, Biebel, Otmar, Biedermann, Dustin, Bielski, Rafal, Bierwagen, Katharina, Biesuz, Nicolo Vladi, Biglietti, Michela, Billoud, Thomas, Bindi, Marcello, Bingul, Ahmet, Bini, Cesare, Biondi, Silvia, Birch-Sykes, Callum Jacob, Birman, Mattias, Bisanz, Tobias, Biswal, Jyoti Prakash, Biswas, Diptaparna, Bitadze, Alexandre, Bittrich, Carsten, Bjoerke, Kristian, Blazek, Tomas, Bloch, Ingo, Blocker, Craig, Blue, Andrew, Blumenschein, Ulrike, Bobbink, Gerjan, Bobrovnikov, Victor, Bocchetta, Simona Serena, Boerner, Daniela, Bogavac, Danijela, Bogdanchikov, Alexander, Bohm, Christian, Boisvert, Veronique, Bokan, Petar, Bold, Tomasz, Bolz, Arthur Eugen, Bomben, Marco, Bona, Marcella, Bonilla, Johan Sebastian, Boonekamp, Maarten, Booth, Callum Dale, Borbely, Albert, Borecka-Bielska, Hanna Maria, Borgna, Lucas Santiago, Borisov, Anatoly, Borissov, Guennadi, Bortoletto, Daniela, Boscherini, Davide, Bosman, Martine, Bossio Sola, Jonathan David, Bouaouda, Khalil, Boudreau, Joseph, Bouhova-Thacker, Evelina Vassileva, Boumediene, Djamel Eddine, Boutle, Sarah Kate, Boveia, Antonio, Boyd, James, Boye, Diallo, Boyko, Igor, Bozson, Adam James, Bracinik, Juraj, Brahimi, Nihal, Brandt, Gerhard, Brandt, Oleg, Braren, Frued, Brau, Benjamin, Brau, James, Breaden Madden, William Dmitri, Brendlinger, Kurt, Brener, Roy, Brenner, Lydia, Brenner, Richard, Bressler, Shikma, Brickwedde, Bernard, Briglin, Daniel Lawrence, Britton, Dave, Britzger, Daniel Andreas, Brock, Ian, Brock, Raymond, Brooijmans, Gustaaf, Brooks, William, Brost, Elizabeth, Bruckman de Renstrom, Pawel, Brueers, Ben, Bruncko, Dusan, Bruni, Alessia, Bruni, Graziano, Bruni, Lucrezia Stella, Bruno, Salvatore, Bruschi, Marco, Bruscino, Nello, Bryngemark, Lene, Buanes, Trygve, Buat, Quentin, Buchholz, Peter, Buckley, Andrew, Budagov, Ioulian, Bugge, Magnar Kopangen, Buehrer, Felix, Bulekov, Oleg, Bullard, Brendon Aurele, Burch, Tyler James, Burdin, Sergey, Burgard, Carsten Daniel, Burger, Angela Maria, Burghgrave, Blake, Burr, Jonathan Thomas, Burton, Charles Davis, Burzynski, Jackson Carl, Buescher, Volker, Buschmann, Eric, Bussey, Peter, Butler, John, Buttar, Craig, Butterworth, Jonathan, Butti, Pierfrancesco, Buttinger, William, Buxo Vazquez, Carlos Josue, Buzatu, Adrian, Buzykaev, Aleksey, Cabras, Grazia, Cabrera Urban, Susana, Caforio, Davide, Cai, Huacheng, Cairo, Valentina Maria, Cakir, Orhan, Calace, Noemi, Calafiura, Paolo, Calderini, Giovanni, Calfayan, Philippe, Callea, Giuseppe, Caloba, Luiz, Caltabiano, Alessandro, Calvente Lopez, Sergio, Calvet, David, Calvet, Samuel, Calvet, Thomas Philippe, Calvetti, Milene, Camacho Toro, Reina, Camarda, Stefano, Camarero Munoz, Daniel, Camarri, Paolo, Camerlingo, Maria Teresa, Cameron, David, Camincher, Clement, Campana, Simone, Campanelli, Mario, Camplani, Alessandra, Canale, Vincenzo, Canesse, Auriane, Cano Bret, Marc, Cantero, Josu, Cao, Tingting, Cao, Yumeng, Capeans Garrido, Maria del Mar, Capua, Marcella, Cardarelli, Roberto, Cardillo, Fabio, Carducci, Giovandomenico, Carli, Ina, Carli, Tancredi, Carlino, Gianpaolo, Carlson, Benjamin Taylor, Carlson, Evan Michael, Carminati, Leonardo, Carney, Rebecca, Caron, Sascha, Carquin, Edson, Carra, Sonia, Carratta, Giuseppe, Carter, Joseph William, Carter, Thomas Michael, Casado, Maria Pilar, Casha, Albert Francis, Castillo, Florencia Luciana, Castillo Garcia, Lucia, Castillo Gimenez, Victoria, Castro, Nuno Filipe, Catinaccio, Andrea, Catmore, James, Cattai, Ariella, Cavaliere, Viviana, Cavasinni, Vincenzo, Celebi, Emre, Celli, Federico, Cerny, Karel, Santiago Cerqueira, Augusto, Cerri, Alessandro, Cerrito, Lucio, Cerutti, Fabio, Cervelli, Alberto, Cetin, Serkant Ali, Chadi, Zakaria, Chakraborty, Dhiman, Chan, Jay, Chan, Wing Sheung, Chan, Wai Yuen, Chapman, John Derek, Chargeishvili, Bakar, Charlton, Dave, Charman, Thomas Paul, Chau, Chav Chhiv, Che, Siinn, Chekanov, Sergei, Chekulaev, Sergey, Chelkov, Gueorgui, Chen, Boping, Chen, Cheng, Chen, Chunhui, Chen, Hucheng, Chen, Jing, Chen, Jue, Chen, Jiayi, Chen, Shion, Chen, Shenjian, Chen, Xin, Chen, Ye, Chen, Yu-Heng, Cheng, Hok Chuen, Cheng, Huajie, Cheplakov, Alexander, Cheremushkina, Evgenia, Cherkaoui El Moursli, Rajaa, Cheu, Elliott, Cheung, Kingman, Chevalerias, Thibault Jean Aime, Chevalier, Laurent, Chiarella, Vitaliano, Chiarelli, Giorgio, Chiodini, Gabriele, Chisholm, Andrew, Chitan, Adrian, Chiu, I-Huan, Chiu, Yu Him Justin, Chizhov, Mihail, Choi, Kyungeon, Chomont, Arthur Rene, Chow, Yun Sang, Christopher, Lawrence Davou, Chu, Ming Chung, Chu, Xiaotong, Chudoba, Jiri, Chwastowski, Janusz, Chytka, Ladislav, Cieri, Davide, Ciesla, Krzysztof Marcin, Cinca, Diane, Cindro, Vladimir, Cioara, Irina Antonela, Ciocio, Alessandra, Cirotto, Francesco, Citron, Zvi Hirsh, Citterio, Mauro, Ciubotaru, Dan Andrei, Ciungu, Bianca Monica, Clark, Allan G., Clark, Michael Ryan, Clark, Philip James, Clawson, Savannah Ellen, Clement, Christophe, Coadou, Yann, Cobal, Marina, Coccaro, Andrea, Cochran, James H., Coelho Barrue, Ricardo Filipe, Coelho Lopes de Sa, Rafael, Cohen, Hadar Yosef, Coimbra, Artur Cardoso, Cole, Brian, Colijn, Auke-Pieter, Collot, Johann, Conde Muino, Patricia, Connell, Simon Henry, Connelly, Ian, Constantinescu, Serban, Conventi, Francesco, Cooper-Sarkar, Amanda, Cormier, Felix, Cormier, Kyle James Read, Corpe, Louie Dartmoor, Corradi, Massimo, Corrigan, Eric Edward, Corriveau, Francois, Costa, Maria Jose, Costanza, Francesco, Costanzo, Davide, Cowan, Glen, Cowley, James William, Crane, Jonathan, Cranmer, Kyle, Creager, Rachael Ann, Crépé-Renaudin, Sabine, Crescioli, Francesco, Cristinziani, Markus, Croft, Vincent, Crosetti, Giovanni, Cueto Gomez, Ana Rosario, Cuhadar Donszelmann, Tulay, Cui, Han, Cukierman, Aviv Ruben, Cunningham, William Reilly, Czekierda, Sabina, Czodrowski, Patrick, Czurylo, Marta Maja, da Cunha Sargedas de Sousa, Mario Jose, da Fonseca Pinto, Joao Victor, da Via, Cinzia, Dabrowski, Wladyslaw, Dachs, Florian, Dado, Tomas, Dahbi, Salah-Eddine, Dai, Tiesheng, Dallapiccola, Carlo, Dam, Mogens, d'Amen, Gabriele, d'Amico, Valerio, Damp, Johannes Frederic, Dandoy, Jeffrey Rogers, Daneri, Maria Florencia, Danninger, Matthias, Dao, Valerio, Darbo, Giovanni, Dartsi, Olympia, Dattagupta, Aparajita, Daubney, Thomas, d'Auria, Saverio, David, Claire, Davidek, Tomas, Davis, Douglas, Dawson, Ian, De, Kaushik, de Asmundis, Riccardo, de Beurs, Marcus, de Castro, Stefano, de Groot, Nicolo, de Jong, Paul, de la Torre, Hector, de Maria, Antonio, de Pedis, Daniele, de Salvo, Alessandro, de Sanctis, Umberto, de Santis, Maurizio, de Santo, Antonella, de Vivie de Regie, Jean-Baptiste, Debenedetti, Chiara, Dedovich, Dmitri, Deiana, Allison Mccarn, del Peso, Jose, Delabat Diaz, Yasiel, Delgove, David, Deliot, Frederic, Delitzsch, Chris Malena, Della Pietra, Massimo, Della Volpe, Domenico, Dell'Acqua, Andrea, Dell'Asta, Lidia, Delmastro, Marco, Delporte, Charles, Delsart, Pierre-Antoine, Demarco, David, Demers, Sarah, Demichev, Mikhail, Demontigny, Gabriel, Denisov, Sergey, d'Eramo, Louis, Derendarz, Dominik, Derkaoui, Jamal Eddine, Derue, Frederic, Dervan, Paul, Desch, Klaus Kurt, Dette, Karola, Deutsch, Christopher, Devesa, Maria Roberta, Deviveiros, Pier-Olivier, Di Bello, Francesco Armando, Di Ciaccio, Anna, Di Ciaccio, Lucia, Di Clemente, William Kennedy, Di Donato, Camilla, Di Girolamo, Alessandro, Di Gregorio, Giulia, Di Micco, Biagio, Di Nardo, Roberto, Di Petrillo, Karri Folan, Di Sipio, Riccardo, Diaconu, Cristinel, de Almeida Dias, Flavia, Dias Do Vale, Tiago, Diaz, Marco Aurelio, Diaz Capriles, Federico Guillermo, Dickinson, Jennet, Didenko, Mariya, Diehl, Edward, Dietrich, Janet, Díez Cornell, Sergio, Diez Pardos, Carmen, Dimitrievska, Aleksandra, Ding, Wei, Dingfelder, Jochen, Dittmeier, Sebastian Johannes, Dittus, Fido, Djama, Fares, Djobava, Tamar, Djuvsland, Julia Isabell, Barros Do Vale, Maria Aline, Dobre, Monica, Dodsworth, David, Doglioni, Caterina, Dolejsi, Jiri, Dolezal, Zdenek, Donadelli, Marisilvia, Dong, Binbin, Donini, Julien, d'Onofrio, Adelina, d'Onofrio, Monica, Dopke, Jens, Doria, Alessandra, Dova, Maria-Teresa, Doyle, Tony, Drechsler, Eric, Dreyer, Etienne, Dreyer, Timo, Drobac, Alec Swenson, Du, Dongshuo, Du Pree, Tristan Arnoldus, Duan, Yanyun, Dubinin, Filipp, Dubovsky, Michal, Dubreuil, Arnaud, Duchovni, Ehud, Duckeck, Guenter, Ducu, Otilia Anamaria, Duda, Dominik, Dudarev, Alexey, Dudder, Andreas Christian, Duffield, Emily Marie, d'Uffizi, Matteo, Duflot, Laurent, Duehrssen, Michael, Dulsen, Carsten, Dumancic, Mirta, Dumitriu, Ana Elena, Dunford, Monica, Duperrin, Arnaud, Duran Yildiz, Hatice, Dueren, Michael, Durglishvili, Archil, Duschinger, Dirk, Dutta, Baishali, Duvnjak, Damir, Dyckes, George, Dyndal, Mateusz, Dysch, Samuel, Dziedzic, Bartosz Sebastian, Eggleston, Michael Glenn, Eifert, Till, Eigen, Gerald, Einsweiler, Kevin, Ekelof, Tord, El Jarrari, Hassnae, Ellajosyula, Venugopal, Ellert, Mattias, Ellinghaus, Frank, Elliot, Alison, Ellis, Nicolas, Elmsheuser, Johannes, Elsing, Markus, Emeliyanov, Dmitry, Emerman, Alexander, Enari, Yuji, Epland, Matthew Berg, Erdmann, Johannes, Ereditato, Antonio, Erland, Paula Agnieszka, Errenst, Martin, Escalier, Marc, Escobar, Carlos, Estrada Pastor, Oscar, Etzion, Erez, Evans, Hal, Evans, Meirin Oan, Ezhilov, Alexey, Fabbri, Federica, Fabbri, Laura, Fabiani, Veronica, Facini, Gabriel John, Fakhrutdinov, Rinat, Falciano, Speranza, Falke, Peter Johannes, Falke, Saskia, Faltova, Jana, Fang, Yi, Fang, Yaquan, Fanourakis, Georgios, Fanti, Marcello, Faraj, Mohammed, Farbin, Amir, Farilla, Addolorata, Farina, Edoardo Maria, Farooque, Trisha, Farrington, Sinead, Farthouat, Philippe, Fassi, Farida, Fassnacht, Patrick, Fassouliotis, Dimitrios, Faucci Giannelli, Michele, Fawcett, William James, Fayard, Louis, Fedin, Oleg, Fedorko, Woiciech, Fehr, Armin, Feickert, Matthew, Feligioni, Lorenzo, Fell, Alexandra, Feng, Cunfeng, Feng, Minyu, Fenton, Michael James, Fenyuk, Alexander, Ferguson, Sarah Whitney, Ferrando, James, Ferrante, Andrew, Ferrari, Arnaud, Ferrari, Pamela, Ferrari, Roberto, Ferreira de Lima, Danilo Enoque, Ferrer, Antonio, Ferrere, Didier, Ferretti, Claudio, Fiedler, Frank, Filipcic, Andrej, Filthaut, Frank, Finelli, Kevin Daniel, Fiolhais, Miguel, Fiorini, Luca, Fischer, Florian Christoph, Fischer, Julian, Fisher, Wade Cameron, Fitschen, Tobias, Fleck, Ivor, Fleischmann, Philipp, Flick, Tobias, Flierl, Bernhard Matthias, Flores, Lucas Macrorie, Flores Castillo, Luis, Follega, Francesco Maria, Fomin, Nikolai, Foo, Joel Hengwei, Forcolin, Giulio Tiziano, Forland, Blake Christopher, Formica, Andrea, Foerster, Fabian Alexander, Forti, Alessandra, Fortin, Etienne, Foti, Maria Giovanna, Fournier, Daniel, Fox, Harald, Francavilla, Paolo, Francescato, Simone, Franchini, Matteo, Franchino, Silvia, Francis, David, Franco, Luca, Franconi, Laura, Franklin, Melissa, Frattari, Guglielmo, Fray, Antony, Freeman, Patrick Moriishi, Freund, Benjamin, Spolidoro Freund, Werner, Freundlich, Elena Murielle, Frizzell, Dylan Cooper, Froidevaux, Daniel, Frost, James, Fujimoto, Minori, Fukunaga, Chikara, Fullana Torregrosa, Esteban, Fusayasu, Takahiro, Fuster, Juan, Gabrielli, Alessandro, Gabrielli, Andrea, Gadatsch, Stefan, Gadow, Paul Philipp, Gagliardi, Guido, Gagnon, Louis Guillaume, Gallardo, Gabriel Emmanuel, Gallas, Elizabeth, Gallop, Bruce, Gamboa Goni, Rodrigo, Gan, K.K., Ganguly, Sanmay, Gao, Jun, Gao, Yanyan, Gao, Yongsheng, Garay Walls, Francisca, Garcia, Carmen, García Navarro, José Enrique, Garcia Pascual, Juan Antonio, Garcia Argos, Carlos, Garcia-Sciveres, Maurice, Gardner, Robert, Garelli, Nicoletta, Gargiulo, Simona, Garner, Christopher Andrew, Garonne, Vincent, Gasiorowski, Sean Joseph, Do Nascimento Gaspar, Philipp, Gaudiello, Andrea, Gaudio, Gabriella, Gavrilenko, Igor, Gavrilyuk, Alexander, Gay, Colin, Gaycken, Goetz, Gazis, Evangelos, Geanta, Andrei Alexandru, Gee, Carolyn Mei, Gee, Norman, Geisen, Jannik, Geisen, Marc, Gemme, Claudia, Genest, Marie-Helene, Geng, Cong, Gentile, Simonetta, George, Simon, Geralis, Theodoros, Gerlach, Lino Oscar, Gessinger-Befurt, Paul, Gessner, Gregor, Ghasemi, Sara, Ghasemi Bostanabad, Meisam, Ghneimat, Mazuza, Ghosh, Aishik, Ghosh, Anindya, Giacobbe, Benedetto, Giagu, Stefano, Giangiacomi, Nico, Giannetti, Paola, Giannini, Antonio, Giannini, Giulia, Gibson, Stephen, Gignac, Matthew, Gil, Damian Tomasz, Gilbert, Benjamin Jacob, Gillberg, Dag Ingemar, Gilles, Geoffrey, Gingrich, Douglas, Giordani, Mariopaolo, Giraud, Pierre-Francois, Giugliarelli, Gilberto, Giugni, Danilo, Giuli, Francesco, Gkaitatzis, Stamatios, Gkialas, Ioannis, Gkougkousis, Evangelos, Gkountoumis, Panagiotis, Gladilin, Leonid, Glasman, Claudia, Glatzer, Julian Maximilian Volker, Glaysher, Paul, Glazov, Alexandre, Gledhill, Galen Rhodes, Gnesi, Ivan, Goblirsch-Kolb, Maximilian, Godin, Dominique, Goldfarb, Steven, Golling, Tobias, Golubkov, Dmitry, Gomes, Agostinho, Goncalves Gama, Rafael, Goncalo, Ricardo, Gonella, Giulia, Gonella, Laura, Gongadze, Alexi, Gonnella, Francesco, Gonski, Julia Lynne, Gonzalez de la Hoz, Santiago, Gonzalez Fernandez, Sergio, Gonzalez Lopez, Ricardo, Gonzalez Renteria, Cesar, Gonzalez Suarez, Rebeca, Gonzalez-Sevilla, Sergio, Gonzalvo Rodriguez, Galo Rafael, Goossens, Luc, Gorasia, Nandish Arjan, Gorbounov, Petr Andreevich, Gordon, Howard, Gorini, Benedetto, Gorini, Edoardo, Gorisek, Andrej, Goshaw, Alfred, Gostkin, Mikhail Ivanovitch, Gottardo, Carlo Alberto, Gouighri, Mohamed, Goussiou, Anna, Govender, Nicolin, Goy, Corinne, Grabowska-Bold, Iwona, Graham, Emily Charlotte, Gramling, Johanna, Gramstad, Eirik, Grancagnolo, Sergio, Grandi, Mario, Gratchev, Vadim, Gravila, Paul Mircea, Gravili, Francesco Giuseppe, Gray, Chloe, Gray, Heather, Grefe, Christian, Gregersen, Kristian, Gregor, Ingrid-Maria, Grenier, Philippe, Grevtsov, Kirill, Grieco, Chiara, Grieser, Nathan Allen, Grillo, Alexander, Grimm, Kathryn, Grinstein, Sebastian, 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Owen, Rhys Edward, Ozcan, Veysi Erkcan, Ozturk, Nurcan, Pacalt, Josef, Pacey, Holly Ann, Pachal, Katherine, Pacheco Pages, Andres, Padilla Aranda, Cristobal, Pagan Griso, Simone, Palacino, Gabriel, Palazzo, Serena, Palestini, Sandro, Palka, Marek, Palni, Prabhakar, Pandini, Carlo Enrico, Panduro Vazquez, Jose Guillermo, Pani, Priscilla, Panizzo, Giancarlo, Paolozzi, Lorenzo, Papadatos, Constantine, Papageorgiou, Konstantinos, Parajuli, Santosh, Paramonov, Alexander, Paraskevopoulos, Christos, Paredes Hernandez, Daniela, Paredes Saenz, Santiago Rafael, Parida, Bibhuti, Park, Tae Hyoun, Parker, Adam Jackson, Parker, Andy, Parodi, Fabrizio, Parrish, Elliot Wesley, Parsons, John, Parzefall, Ulrich, Pascual Dominguez, Luis, Pascuzzi, Vincent, Pasner, Jacob Martin, Pasquali, Federica, Pasqualucci, Enrico, Passaggio, Stefano, Pastore, Francesca, Pasuwan, Patrawan, Pataraia, Sophio, Pater, Joleen, Pathak, Atanu, Patton, Joseph, Pauly, Thilo, Pearkes, Jannicke, Pearson, Benjamin, Pedersen, Maiken, Pedraza Diaz, Lucia, Costa Batalha Pedro, Rute, Peiffer, Thomas, Peleganchuk, Sergey, Penc, Ondrej, Peng, Haiping, Sotto-Maior Peralva, Bernardo, Perego, Marta Maria, Pereira Peixoto, Ana Paula, Pereira Sanchez, Laura, Perepelitsa, Dennis, Perez Codina, Estel, Peri, Francesco, Perini, Laura, Pernegger, Heinz, Perrella, Sabrina, Perrevoort, Ann-Kathrin, Peters, Krisztian, Peters, Reinhild, Petersen, Brian, Petersen, Troels, Petit, Elisabeth, Petousis, Vlasios, Petridis, Andreas, Petridou, Chariclia, Petroff, Pierre, Petrucci, Fabrizio, Pettee, Mariel Nelson, Pettersson, Nora Emilia, Petukhova, Krystsina, Peyaud, Alan, Pezoa, Raquel, Pezzotti, Lorenzo, Pham, Thu, Phillips, Forrest Hays, Phillips, Peter William, Phipps, Michael William, Piacquadio, Giacinto, Pianori, Elisabetta, Picazio, Attilio, Pickles, Rebecca Hayley, Piegaia, Ricardo, Pietreanu, Dorel, Pilcher, James, Pilkington, Andrew, Pinamonti, Michele, Pinfold, James, Pitman Donaldson, Charlie, Pitt, Michael, Pizzimento, Luca, Pizzini, Alessio, Pleier, Marc-Andre, Plesanovs, Vladislavs, Pleskot, Vojtech, Plotnikova, Elena, Podberezko, Pavel, Poettgen, Ruth, Poggi, Riccardo, Poggioli, Luc, Pogrebnyak, Ivan, Pohl, David-Leon, Pokharel, Ishan, Polesello, Giacomo, Poley, Anne-Luise, Policicchio, Antonio, Polifka, Richard, Polini, Alessandro, Pollard, Christopher Samuel, Polychronakos, Venetios, Ponomarenko, Daniil, Pontecorvo, Ludovico, Popa, Stefan, Popeneciu, Gabriel Alexandru, Portales, Louis Adrien Paul, Portillo Quintero, Dilia Maria, Pospisil, Stanislav, Potamianos, Karolos Jozef, Potrap, Igor, Potter, Christina, Potti, Harish, Poulsen, Trine, Poveda, Joaquin, Powell, Thomas Dennis, Pownall, Gavin, Pozo Astigarraga, Mikel Eukeni, Pralavorio, Pascal, Prell, Soeren, Price, Darren, Primavera, Margherita, Proffitt, Mason Louis, Proklova, Nadezda, Prokofiev, Kirill, Prokoshin, Fedor, Protopopescu, Serban, Proudfoot, James, Przybycien, Mariusz, Pudzha, Denis, Puri, Akshat, Puzo, Patrick, Pyatiizbyantseva, Diana, Qian, Jianming, Qin, Yang, Quadt, Arnulf, Queitsch-Maitland, Michaela, Racko, Michal, Ragusa, Francesco, Rahal, Ghita, Raine, John Andrew, Rajagopalan, Srinivasan, Ramirez Morales, Andres, Ran, Kunlin, Rauch, Daniel Mauricio, Rauscher, Felix, Rave, Stefan, Ravina, Baptiste, Ravinovich, Ilia, Rawling, Jacob Henry, Raymond, Michel, Read, Alexander Lincoln, Readioff, Nathan Peter, Reale, Marilea, Rebuzzi, Daniela, Redlinger, George, Reeves, Kendall, Reichert, Joseph, Reikher, David, Reiss, Andreas, Rej, Amartya, Rembser, Christoph, Renardi, Alessia, Renda, Michele, Rendel, Marian Benedikt, Rennie, Adam Graham, Resconi, Silvia, Resseguie, Elodie Deborah, Rettie, Sebastien, Reynolds, Bryan John Gardner, Reynolds, Elliot, Rezanova, Olga, Reznicek, Pavel, Ricci, Ester, Richter, Robert, Richter, Stefan, Richter-Was, Elzbieta, Ridel, Melissa, Rieck, Patrick, Rifki, Othmane, Rijssenbeek, Michael, Rimoldi, Adele, Rimoldi, Marco, Rinaldi, Lorenzo, Rinn, Timothy Thomas, Ripellino, Giulia, Riu, Imma, Rivadeneira, Pablo, Rivera Vergara, Juan Cristobal, Rizatdinova, Flera, Rizvi, Eram, Rizzi, Chiara, Robertson, Steven, Robin, Matthieu, Robinson, Dave, Robles Gajardo, Carolina Michel, Robles Manzano, Maria, Robson, Aidan, Rocchi, Alessandro, Rocco, Elena, Roda, Chiara, Rodriguez Bosca, Sergi, Rodriguez Vera, Ana Maria, Roe, Shaun, Roggel, Jens, Rohne, Ole, Roehrig, Rainer, Rojas, Rimsky Alejandro, Roland, Benoit, Roland, Christophe Pol A., Roloff, Jennifer Kathryn, Romaniouk, Anatoli, Romano, Marino, Rompotis, Nikolaos, Ronzani, Manfredi, Roos, Lydia, Rosati, Stefano, Rosin, Guy, Rosser, Benjamin John, Rossi, Edoardo, Rossi, Eleonora, Rossi, Elvira, Rossi, Leonardo Paolo, Rossini, Lorenzo, Rosten, Rachel, Rotaru, Marina, Rottler, Benjamin Tobias, Rousseau, David, Rovelli, Giulia, Roy, Avik, Roy, Debarati, Rozanov, Alexander, Rozen, Yoram, Ruan, Xifeng, Ruggeri, Tristan Andrew, Ruehr, Frederik, Ruiz-Martinez, Aranzazu, Rummler, Andre, Rurikova, Zuzana, Rusakovich, Nikolai, Russell, Heather Lynn, Rustige, Lennart, Rutherfoord, John, Ruettinger, Elias Michael, Rybar, Martin, Rybkin, Grigori, Rye, Eli Baverfjord, Ryzhov, Andrey, Sabater Iglesias, Jorge Andres, Sabatini, Paolo, Sabetta, Luigi, Sacerdoti, Sabrina, Sadrozinski, Hartmut, Sadykov, Renat, Safai Tehrani, Francesco, Safarzadeh Samani, Batool, Safdari, Murtaza, Saha, Puja, Saha, Shreya, Sahinsoy, Merve, Sahu, Arunika, Saimpert, Matthias, Saito, Masahiko, Saito, Tomoyuki, Sakamoto, Hiroshi, Salamani, Dalila, Salamanna, Giuseppe, Salnikov, Andrei, Salt, José, Salvador Salas, Adrian, Salvatore, Daniela, Salvatore, Pasquale Fabrizio, Salvucci, Antonio, Salzburger, Andreas, Samarati, Jerome, Sammel, Dirk, Sampsonidis, Dimitrios, Sampsonidou, Despoina, Sánchez, Javier, Sanchez Pineda, Arturo Rodolfo, Sandaker, Heidi, Sander, Christian Oliver, Sanderswood, Izaac Gregory, Sandhoff, Marisa, Sandoval Usme, Carlos, Sankey, Dave, Sannino, Mario, Sano, Yuta, Sansoni, Andrea, Santoni, Claudio, Santos, Helena, Santpur, Sai Neha, Santra, Arka, Saoucha, Kamal Abdelouadoud, Sapronov, Andrey, Saraiva, Joao, Sasaki, Osamu, Sato, Koji, Sauerburger, Frank, Sauvan, Emmanuel, Savard, Pierre, Sawada, Ryu, Sawyer, Craig, Sawyer, Lee, Sayago Galvan, Ivan, Sbarra, Carla, Sbrizzi, Antonio, Scanlon, Timothy Paul, Schaarschmidt, Jana, Schacht, Peter, Schaefer, Douglas, Schaefer, Leigh, Schaepe, Steffen, Schaefer, Uli, Schaffer, Arthur, Schaile, Dorothee, Schamberger, R. Dean, Schanet, Eric, Scharf, Christian, Scharmberg, Nicolas, Schegelsky, Valery, Scheirich, Daniel, Schenck, Ferdinand, Schernau, Michael, Schiavi, Carlo, Schildgen, Lara Katharina, Schillaci, Zachary Michael, Schioppa, Enrico, Schioppa, Marco, Schleicher, Katharina, Schlenker, Stefan, Schmidt-Sommerfeld, Korbinian Ralf, Schmieden, Kristof, Schmitt, Christian, Schmitt, Stefan, Schmoeckel, Julian Constantin, Schoeffel, Laurent, Schoening, Andre, Scholer, Patrick Gerhard, Schopf, Elisabeth, Schott, Matthias, Schouwenberg, Jeroen, Schovancova, Jaroslava, Schramm, Steven, Schroeder, Frederic, Schulte, Alexandra, Schultz-Coulon, Hans-Christian, Schumacher, Markus, Schumm, Bruce, Schune, Philippe, Schwartzman, Ariel, Schwarz, Thomas Andrew, Schwemling, Philippe, Schwienhorst, Reinhard, Sciandra, Andrea, Sciolla, Gabriella, Scornajenghi, Matteo, Scuri, Fabrizio, Scutti, Federico, Scyboz, Ludovic Michel, Sebastiani, Cristiano David, Seema, Pienpen, Seidel, Sally, Seiden, Abraham, Seidlitz, Blair Daniel, Seiss, Todd, Seitz, Claudia, Seixas, Jose, Sekhniaidze, Givi, Sekula, Stephen Jacob, Semprini-Cesari, Nicola, Sen, Sourav, Serfon, Cedric, Serin, Laurent, Serkin, Leonid, Sessa, Marco, Severini, Horst, Sevova, Stanislava, Sforza, Federico, Sfyrla, Anna, Shabalina, Elizaveta, Shahinian, Jeffrey David, Shaikh, Nabila Wahab, Shaked, Dan, Shan, Lianyou, Shapiro, Marjorie, Sharma, Abhishek, Shatalov, Pavel, Shaw, Kate, Shaw, Savanna Marie, Shehade, Mahran, Shen, Yu-Ting, Sherman, Alexander David, Sherwood, Peter, Shi, Liaoshan, Shimizu, Shima, Shimmin, Chase Owen, Shimogama, Yoshihiro, Shimojima, Makoto, Shipsey, Ian Peter Joseph, Shirabe, Shohei, Shiyakova, Mariya, Shlomi, Jonathan, Shmeleva, Alevtina, Shochet, Mel, Shojaii, Jafar, Shope, David Richard, Shrestha, Suyog, Shrif, Esra Mohammed, Shulga, Evgeny, Sicho, Petr, Sickles, Anne Marie, Sideras Haddad, Elias, Sidiropoulou, Ourania, Sidoti, Antonio, Siegert, Frank, Sijacki, Djordje, Silva, Manuel, Silva Oliveira, Marcos Vinicius, Silverstein, Samuel, Simion, Stefan, Simoniello, Rosa, Simpson-Allsop, Cameron James, Simsek, Sinem, Sinervo, Pekka, Sinetckii, Viktor, Singh, Sundeep, Sioli, Maximiliano, Siral, Ismet, Sivoklokov, Serguei, Sjoelin, Joergen, Skaf, Ali, Skorda, Eleni, Skubic, Patrick, Slawinska, Magdalena, Sliwa, Krzysztof, Slovak, Radim, Smakhtin, Vladimir, Smart, Ben, Smiesko, Juraj, Smirnov, Nikita, Smirnov, Sergei, Smirnov, Yury, Smirnova, Lidia, Smirnova, Oxana, Smith, Emily Ann, Smith, Hayden Alexander, Smizanska, Maria, Smolek, Karel, Smykiewicz, Andrzej, Snesarev, Andrei, Snoek, Hella Leonie, Snyder, Ian Michael, Snyder, Scott, Sobie, Randall, Soffer, Abner, Sogaard, Andreas, Sohns, Fabian, Solans, Carlos, Soldatov, Evgeny, Soldevila- Serrano, Urmila, Solodkov, Alexander, Soloshenko, Alexei, Solovyanov, Oleg, Solovyev, Victor, Sommer, Philip, Son, Hyungsuk, Song, Weimin, Song, Wen Yi, Sopczak, Andre, Sopio, Alexander Linus, Sopkova, Filomena, Sottocornola, Simone, Soualah, Rachik, Soukharev, Andrey, South, David, Spagnolo, Stefania, Spalla, Margherita, Spangenberg, Martin, Spano, Francesco, Sperlich, Dennis, Spieker, Thomas Malte, Spigo, Giancarlo, Spina, Mario, Spiteri, Dwayne Patrick, Spousta, Martin, Stabile, Alberto, Stamas, Brianna Lynn, Stamen, Rainer, Stamenkovic, Marko, Stanecka, Ewa, Stanislaus, Beojan, Stanitzki, Marcel Michael, Stankaityte, Migle, Stapf, Birgit Sylvia, Starchenko, Evgeny, Stark, Giordon Holtsberg, Stark, Jan, Staroba, Pavel, Starovoitov, Pavel, Staerz, Steffen, Staszewski, Rafal, Stavropoulos, Georgios, Stegler, Martin, Steinberg, Peter, Steinhebel, Amanda Lynn, Stelzer, Bernd, Stelzer, Harald Joerg, Stelzer-Chilton, Oliver, Stenzel, Hasko, Stevenson, Thomas James, Stewart, Graeme, Stockton, Mark, Stoicea, Gabriel, Stolarski, Marcin, Stonjek, Stefan, Straessner, Arno, Strandberg, Jonas, Strandberg, Sara Kristina, Strauss, Michael, Strebler, Thomas, Strizenec, Pavol, Stroehmer, Raimund, Strom, David, Stroynowski, Ryszard, Struebig, Antonia, Stucci, Stefania Antonia, Stugu, Bjarne, Stupak, John, Styles, Nicholas Adam, Su, Dong, Su, Wanyun, Su, Xiaowen, Sulin, Vladimir, Sullivan, Matthew James, Sultan, Dms, Sultanov, Saleh, Sumida, Toshi, Sun, Siyuan, Sun, Xiaohu, Suruliz, Kerim, Suster, Carl, Sutton, Mark, Suzuki, Shota, Svatos, Michal, Swiatlowski, Maximilian J., Swift, Stewart Patrick, Swirski, Thorben, Sydorenko, Alexander, Sykora, Ivan, Sykora, Martin, Sykora, Tomas, Ta, Duc Bao, Tackmann, Kerstin, Kinghorn-Taenzer, Joseph Peter, Taffard, Anyes, Tafirout, Reda, Tagiev, Emin, Takashima, Ryuichi, Takeda, Kosuke, Takeshita, Tohru, Takeva, Emily Petrova, Takubo, Yosuke, Talby, Mossadek, Talyshev, Alexey, Tam, Kai Chung, Tamir, Nadav Michael, Tanaka, Junichi, Tanaka, Reisaburo, Tapia Araya, Sebastian, Tapprogge, Stefan, Tarek Abouelfadl Mohamed, Ahmed, Tarem, Shlomit, Tariq, Khuram, Tarna, Grigore, Tartarelli, Giuseppe Francesco, Tas, Petr, Tasevsky, Marek, Tashiro, Takuya, Tassi, Enrico, Tavares Delgado, Ademar, Tayalati, Yahya, Taylor, Alan James, Taylor, Geoffrey, Taylor, Wendy, Teagle, Hamish, Teixeira de Lima, Rafael, Teixeira-Dias, Pedro, ten Kate, Herman, Teoh, Jia Jian, Terada, Susumu, Terashi, Koji, Terron, Juan, Terzo, Stefano, Testa, Marianna, Teuscher, Richard, Thais, Savannah Jennifer, Themistokleous, Neofytos, Theveneaux-Pelzer, Timothee, Thiele, Fabian, Thomas, David William, Thomas, James Oscar, Thomas, Juergen, Thompson, Emily Anne, Thompson, Paul, Thomson, Evelyn, Thorpe, Edward James, Ticse Torres, Royer Edson, Tikhomirov, Vladimir, Tikhonov, Yury, Timoshenko, Sergey, Tipton, Paul, Tisserant, Sylvain, Todome, Kazuki, Todorova-Nova, Sharka, Todt, Stefanie, Tojo, Junji, Tokar, Stanislav, Tokushuku, Katsuo, Tolley, Emma, Tombs, Rupert, Tomiwa, Kehinde Gbenga, Tomoto, Makoto, Tompkins, Lauren, Tornambe, Peter, Torrence, Eric, Torres, Heberth, Torro Pastor, Emma, Tosciri, Cecilia, Toth, Jozsef, Tovey, Daniel, Traeet, Are Sivertsen, Treado, Colleen Jennifer, Trefzger, Thomas, Tresoldi, Fabio, Tricoli, Alessandro, Trigger, Isabel Marian, Trincaz-Duvoid, Sophie, Trischuk, Dominique Anderson, Trischuk, William, Trocme, Benjamin, Trofymov, Artur, Troncon, Clara, Trovato, Fabrizio, Truong, Loan, Trzebinski, Maciej, Trzupek, Adam, Tsai, Fang-Ying, Tseng, Jeffrey, Tsiareshka, Pavel, Tsirigotis, Apostolos, Tsiskaridze, Vakhtang, Tskhadadze, Edisher, Tsopoulou, Maria-Evanthia, Tsukerman, Ilya, Tsulaia, Vakhtang, Tsuno, Soshi, Tsybychev, Dmitri, Tu, Yanjun, Tudorache, Alexandra, Tudorache, Valentina, Tulbure, Traian Tiberiu, Tuna, Alexander Naip, Turchikhin, Semen, Turgeman, Daniel, Turk Cakir, Ilkay, Turner, Russell James, Turra, Ruggero, Tuts, Michael, Tzamarias, Spyros, Tzovara, Eftychia, Uchida, Kenta, Ukegawa, Fumihiko, Unal, Guillaume, Unal, Mesut, Undrus, Alexander, Unel, Gokhan, Ungaro, Francesca, Unno, Yoshinobu, Uno, Kenta, Urban, Jozef, Urquijo, Phillip, Usai, Giulio, Uysal, Zekeriya, Vacek, Vaclav, Vachon, Brigitte, Vadla, Knut Oddvar Hoie, Vafeiadis, Theodoros, Vaidya, Amal, Valderanis, Chrysostomos, Valdes Santurio, Eduardo, Valente, Marco, Valentinetti, Sara, Valero, Alberto, Valery, Loic, Vallance, Robert Adam, Vallier, Alexis Roger Louis, Valls Ferrer, Juan Antonio, van Daalen, Tal Roelof, van Gemmeren, Peter, van Stroud, Samuel, van Vulpen, Ivo, Vanadia, Marco, Vandelli, Wainer, Vandenbroucke, Maxence, Vandewall, Evan Richard, Vaniachine, Alexandre, Vannicola, Damiano, Vari, Riccardo, Varnes, Erich, Varni, Carlo, Varol Mete, Tulin, Varouchas, Dimitris, Varvell, Kevin, Vasile, Matei Eugen, Vasquez Arenas, Gerardo Alexis, Vazeille, Francois, Vazquez Furelos, David, Vazquez Schroeder, Tamara, Veatch, Jason, Vecchio, Valentina, Veen, Michiel Jan, Veloce, Laurelle Maria, Veloso, Filipe, Veneziano, Stefano, Ventura, Andrea, Verbytskyi, Andrii, Vercesi, Valerio, Verducci, Monica, Vergel Infante, Carlos Miguel, Vergis, Christos, Verkerke, Wouter, Vermeulen, Ambrosius Thomas, Vermeulen, Jos, Vernieri, Caterina, Vetterli, Michel, Viaux Maira, Nicolas, Vickey, Trevor, Vickey Boeriu, Oana Elena, Viehhauser, Georg, Vigani, Luigi, Villa, Mauro, Villaplana Perez, Miguel, Villhauer, Elena Michelle, Vilucchi, Elisabetta, Vincter, Manuella, Virdee, Govindraj Singh, Vishwakarma, Akanksha, Vittori, Camilla, Vivarelli, Iacopo, Vogel, Marcelo, Vokac, Petr, von Buddenbrock, Stefan Erich, von Toerne, Eckhard, Vorobel, Vit, Vorobev, Konstantin, Vos, Marcel, Vossebeld, Joost, Vozak, Matous, Vranjes, Nenad, Vranjes Milosavljevic, Marija, Vrba, Vaclav, Vreeswijk, Marcel, Vuillermet, Raphael, Vukotic, Ilija, Wada, Sayaka, Wagner, Peter, Wagner, Wolfgang, Wagner-Kuhr, Jeannine, Wahdan, Shayma, Wahlberg, Hernan, Wakasa, Rena, Walbrecht, Verena Maria, Walder, James, Walker, Rodney, Walker, Stuart Derek, Walkowiak, Wolfgang, Wallangen, Veronica, Wang, Ann Miao, Wang, Alex Zeng, Wang, Chen, Wang, Chenliang, Wang, Fuquan, Wang, Haichen, Wang, Hulin, Wang, Jiawei, Wang, Peilong, Wang, Qing, Wang, Renjie, Wang, Rongkun, Wang, Rui, Wang, Song-Ming, Wang, Weitao, Wang, Wei, Wang, Wenxiao, Wang, Yufeng, Wang, Zirui, Wanotayaroj, Chaowaroj, Warburton, Andreas, Ward, Patricia, Wardrope, David Robert, Warrack, Neil, Watson, Alan, Watson, Miriam, Watts, Gordon, Waugh, Ben, Webb, Aaron Foley, Weber, Christian, Weber, Michele, Weber, Stephen Albert, Weber, Sebastian Mario, Weidberg, Anthony, Weingarten, Jens, Weirich, Marcel, Weiser, Christian, Wells, Pippa, Wenaus, Torre, Wendland, Bjorn, Wengler, Thorsten, Wenig, Siegfried, Wermes, Norbert, Wessels, Martin, Weston, Thomas Daniel, Whalen, Kathleen, Wharton, Andrew Mark, White, Aaron, White, Andrew, White, Martin, Whiteson, Daniel, Whitmore, Ben William, Wiedenmann, Werner, Wiel, Christian, Wielers, Monika, Wieseotte, Natalie, Wiglesworth, Craig, Wiik, Liv Antje Mari, Wilkens, Henric George, Wilkins, Lewis Joseph, Williams, Hugh, Williams, Sarah, Willocq, Stephane, Windischhofer, Philipp Jonas, Wingerter-Seez, Isabelle, Winkels, Emma, Winklmeier, Frank, Winter, Benedict Tobias, Wittgen, Matthias, Wobisch, Markus, Wolf, Anton, Woelker, Ricardo, Wollrath, Julian, Wolter, Marcin Wladyslaw, Wolters, Helmut, Wong, Vincent Wai Sum, Woods, Natasha Lee, Worm, Steven, Wosiek, Barbara, Wozniak, Krzysztof, Wraight, Kenneth, Wu, Sau Lan, Wu, Xin, Wu, Yusheng, Wuerzinger, Jonas, Wyatt, Terry Richard, Wynne, Benjamin, Xella, Stefania, Xia, Ligang, Xiang, Jianhuan, Xiao, Xiong, Xie, Xiangyu, Xiotidis, Ioannis, Xu, Da, Xu, Hanlin, Xu, Hao, Xu, Lailin, Xu, Tairan, Xu, Wenhao, Xu, Zhongyukun, Xu, Zijun, Yabsley, Bruce, Yacoob, Sahal, Yajima, Kazuki, Yallup, David Paul, Yamaguchi, Naoki, Yamaguchi, Yohei, Yamamoto, Akira, Yamatani, Masahiro, Yamazaki, Tomohiro, Yamazaki, Yuji, Yan, Jun, Yan, Zhen, Yang, Haijun, Yang, Hongtao, Yang, Siqi, Yang, Tianyi, Yang, Xuan, Yang, Yi-Lin, Yang, Zhe, Yao, Weiming, Yap, Yee Chinn, Yasu, Yoshiji, Yatsenko, Elena, Ye, Hanfei, Ye, Jingbo, Ye, Shuwei, Yeletskikh, Ivan, Yexley, Melissa Rebecca, Yigitbasi, Efe, Yin, Pengqi, Yorita, Kohei, Yoshihara, Keisuke, Young, Christopher, Young, Charles, Yu, Jie, Yuan, Rui, Yue, Xiaoguang, Zaazoua, Mohamed, Zabinski, Bartlomiej, Zacharis, George, Zaffaroni, Ettore, Zahreddine, Jad, Zaitsev, Alexander, Zakareishvili, Tamar, Zakharchuk, Nataliia, Zambito, Stefano, Zanzi, Daniele, Zaripovas, Donatas Ramilas, Zeissner, Sonja Verena, Zeitnitz, Christian, Zemaityte, Gabija, Zeng, Jian Cong, Zenin, Oleg, Zenis, Tibor, Zerwas, Dirk, Zgubic, Miha, Zhang, Bowen, Zhang, Dengfeng, Zhang, Gang, Zhang, Jinlong, Zhang, Kaili, Zhang, Lei, Zhang, Liqing, Zhang, Matt, Zhang, Rui, Zhang, Shuzhou, Zhang, Xiangke, Zhang, Xueyao, Zhang, Yu, Zhang, Zhidong, Zhang, Zhiqing, Zhao, Pingchuan, Zhao, Zhengguo, Zhemchugov, Alexey, Zheng, Zhi, Zhong, Dewen, Zhou, Bing, Zhou, Chen, Zhou, Hao, Zhou, Maosen, Zhou, Mingliang, Zhou, Ning, Zhou, You, Zhu, Cheng Guang, Zhu, Chenzheng, Zhu, Heling, Zhu, Hongbo, Zhu, Junjie, Zhu, Yingchun, Zhuang, Xuai, Zhukov, Konstantin, Zhulanov, Vladimir, Zieminska, Daria, Zimine, Nikolai, Zimmermann, Stephanie, Zinonos, Zinonas, Ziolkowski, Michael, Zivkovic, Lidija, Zobernig, Georg, Zoccoli, Antonio, Zoch, Knut, Zorbas, Theodoros Georgio, Zou, Rui, Zwalinski, Lukasz, Centre de Physique des Particules de Marseille (CPPM), Aix Marseille Université (AMU)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'Annecy de Physique des Particules (LAPP), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry])-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique des 2 Infinis Irène Joliot-Curie (IJCLab), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique de Clermont (LPC), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université Clermont Auvergne (UCA), Institut de Recherches sur les lois Fondamentales de l'Univers (IRFU), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, Laboratoire de Physique Nucléaire et de Hautes Énergies (LPNHE (UMR_7585)), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique Subatomique et de Cosmologie (LPSC), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes (UGA)-Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP ), Université Grenoble Alpes (UGA), Centre de Calcul de l'IN2P3 (CC-IN2P3), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), ATLAS, and Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)

Subjects
associated production [Higgs particle], lepton, transverse momentum: high, 13000 GeV-cms, measured [channel cross section], S126SBB, cross section: ratio, bottom: particle identification, vector boson: transverse momentum, W: leptonic decay, high [transverse momentum], High Energy Physics - Experiment, High Energy Physics - Experiment (hep-ex), effective field theory, scattering [p p], [PHYS.HEXP]Physics [physics]/High Energy Physics - Experiment [hep-ex], associated production [Z0], Nuclear Experiment, vector boson: associated production, gauge boson, associated production [W], decay [Higgs particle], ATLAS, bottom [jet], upper limit [coupling constant], pair production [bottom], CERN LHC Coll, particle identification [bottom], colliding beams [p p], W: associated production, anomaly [coupling], jet: bottom, channel cross section: measured, Particle Physics - Experiment, p p: scattering, transverse momentum [vector boson], FOS: Physical sciences, bottom: pair production, coupling constant: upper limit, ddc:530, coupling: anomaly, hep-ex, High Energy Physics::Phenomenology, Higgs particle: associated production, leptonic decay [Z0], Z0: associated production, leptonic decay [W], hadronic decay [Higgs particle], Higgs particle: hadronic decay, Z0: leptonic decay, associated production [vector boson], High Energy Physics::Experiment, ratio [cross section], p p: colliding beams, pair [quark], experimental results
Abstract

The associated production of a Higgs boson with a $W$ or $Z$ boson decaying into leptons and where the Higgs boson decays to a $b\bar{b}$ pair is measured in the high vector-boson transverse momentum regime, above 250 GeV, with the ATLAS detector. The analysed data, corresponding to an integrated luminosity of 139 fb$^{-1}$, were collected in proton-proton collisions at the Large Hadron Collider between 2015 and 2018 at a centre-of-mass energy of $\sqrt{s} = 13$ TeV. The measured signal strength, defined as the ratio of the measured signal yield to that predicted by the Standard Model, is $0.72 ^{+0.39}_{-0.36}$ corresponding to an observed (expected) significance of 2.1 (2.7) standard deviations. Cross-sections of associated production of a Higgs boson decaying into $b$ quark pairs with a $W$ or $Z$ gauge boson, decaying into leptons, are measured in two exclusive vector boson transverse momentum regions, 250-400 GeV and above 400 GeV, and interpreted as constraints on anomalous couplings in the framework of a Standard Model effective field theory., Comment: 49 pages in total, author list starting page 33, 7 figures, 9 tables, published in Phys. Lett. B. All figures including auxiliary figures are available at https://atlas.web.cern.ch/Atlas/GROUPS/PHYSICS/PAPERS/HIGG-2018-52. The results presented in this paper including the correlation matrix have been inserted in HEPdata with the following record: https://www.hepdata.net/record/94801

Published
2021
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19. BIOACTIVE INTERLEUKIN-1 DETECTED IN IBD PATIENT INTESTINAL BIOPSIES IS A HALLMARK OF ULCERS AND CORRELATES WITH TRANSCRIPTOMIC ASSESSMENTS, INCLUDING AN ULCER-ASSOCIATED GENE MODULE.

Author

Losa, Marco, Field, Michael, Collen, Lauren, Barends, Jared, Ringel, Amit, Bresnahan, Mairead, Yang, Jessica, Tumminkatti, Rhea, Sveen, Mia, Bearup, Richelle, Kotlarz, Daniel, Klein, Christoph, Argmann, Carmen, Schadt, Eric, Muise, Aleixo, Thiagarajah, Jay, Eran, Alal, Horwitz, Bruce, Snapper, Scott, and Mitsialis, Vanessa

Published
2024
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20. TAVR - From inoperable to younger, lower-risk patients: A slippery slope?

Author

Unbehaun, Axel, Abdullah, Mohamed, Hooda, Amit, Gedela, Maheedhar, Kempfert, Joerg, Klein, Christoph, and Tang, Gilbert H.L.

Abstract

Despite current valve guidelines recommending both transcatheter and surgical aortic valve replacement (TAVR and SAVR, respectively) in patients with symptomatic severe aortic stenosis (AS), TAVR has recently become the preferred treatment over SAVR, driven by its minimal invasiveness, faster recovery and earlier improvement in quality of life. However, several limitations and unresolved issues remain with TAVR, including stroke, conduction system disorder, durability, bicuspid anatomy, coronary reaccess and lifetime management with aortic valve reintervention. Our review aims to highlight the above issues and discuss them in depth, to demonstrate the complementary role of TAVR and SAVR in the treatment of AS. [ABSTRACT FROM AUTHOR]

Published
2022
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21. 335 BIOACTIVE INTERLEUKIN-1 DETECTED IN IBD PATIENT INTESTINAL BIOPSIES IS A HALLMARK OF ULCERS AND CORRELATES WITH TRANSCRIPTOMIC ASSESSMENTS, INCLUDING AN ULCER-SPECIFIC GENE MODULE ASSOCIATED WITH STROMAL CELL DIFFERENTIATION.

Author

Losa, Marco, Field, Michael, Nandy, Anubhab, Collen, Lauren, Barends, Jared, Ringel, Amit, Bresnahan, Mairead, Yang, Jessica, Tumminkatti, Rhea, Sveen, Mia, Bearup, Richelle, Kotlarz, Daniel, Klein, Christoph, Argmann, Carmen A., Schadt, Eric E., Muise, Aleixo, Thiagarajah, Jay R., Eran, Alal, Horwitz, Bruce, and Snapper, Scott B.

Published
2024
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22. A Systematic Review of Monogenic Inflammatory Bowel Disease.

Author

Nambu, Ryusuke, Warner, Neil, Mulder, Daniel J., Kotlarz, Daniel, McGovern, Dermot P.B., Cho, Judy, Klein, Christoph, Snapper, Scott B., Griffiths, Anne M., Iwama, Itaru, and Muise, Aleixo M.

Abstract

Advances in genomic technologies have led to increasing reports of monogenic inflammatory bowel disease (IBD). Here, we systematically review the literature to determine the clinical features, genetic profile, and previously used treatment strategies in monogenic IBD. A systematic review of MEDLINE articles published between January 2000 and December 2020 was conducted. A total of 750 individual monogenic IBD cases were identified from 303 eligible articles. The most frequently reported monogenic IBD genes were IL10RA / B , XIAP , CYBB , LRBA , and TTC7A. In total, 63.4% of patients developed IBD before 6 years of age, 17.4% developed IBD between ages 10 and 17.9 years, and 10.9% developed IBD after age 18. There was a substantial difference between these age groups and the underlying monogenic disorders. Only 31.7% had any history of extraintestinal comorbidity (EIC) before IBD onset, but 76.0% developed at least 1 EIC during their clinical course. The most common EICs were atypical infection (44.7%), dermatologic abnormality (38.4%), and autoimmunity (21.9%). Bowel surgery, biologic therapy, and hematopoietic stem cell transplantation were performed in 27.1%, 32.9%, and 23.1% of patients, respectively. Monogenic IBD cases, although rare, have varied extraintestinal comorbidities and limited treatment options including surgery and transplant. Early identification and improved understanding of the characteristics of the genes and underlying disease processes in monogenic IBD is important for effective management. [Display omitted] [ABSTRACT FROM AUTHOR]

Published
2022
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26. Drug Screen Identifies Leflunomide for Treatment of Inflammatory Bowel Disease Caused by TTC7A Deficiency.

Author

Jardine, Sasha, Anderson, Sierra, Babcock, Stephen, Leung, Gabriella, Pan, Jie, Dhingani, Neel, Warner, Neil, Guo, Conghui, Siddiqui, Iram, Kotlarz, Daniel, Dowling, James J., Melnyk, Roman A., Snapper, Scott B., Klein, Christoph, Thiagarajah, Jay R., and Muise, Aleixo M.

Abstract

Mutations in the tetratricopeptide repeat domain 7A gene (TTC7A) cause intestinal epithelial and immune defects. Patients can become immune deficient and develop apoptotic enterocolitis, multiple intestinal atresia, and recurrent intestinal stenosis. The intestinal disease in patients with TTC7A deficiency is severe and untreatable, and it recurs despite resection or allogeneic hematopoietic stem cell transplant. We screened drugs for those that prevent apoptosis of in cells with TTC7A deficiency and tested their effects in an animal model of the disease. We developed a high-throughput screen to identify compounds approved by the US Food and Drug Administration that reduce activity of caspases 3 and 7 in TTC7A - knockout (TTC7A-KO) HAP1 (human haploid) cells and reduce the susceptibility to apoptosis. We validated the effects of identified agents in HeLa cells that stably express TTC7A with point mutations found in patients. Signaling pathways in cells were analyzed by immunoblots. We tested the effects of identified agents in zebrafish with disruption of ttc7a , which develop intestinal defects, and colonoids derived from biopsy samples of patients with and without mutations in TTC7A. We performed real-time imaging of intestinal peristalsis in zebrafish and histologic analyses of intestinal tissues from patients and zebrafish. Colonoids were analyzed by immunofluorescence and for ion transport. TTC7A-KO HAP1 cells have abnormal morphology and undergo apoptosis, due to increased levels of active caspases 3 and 7. We identified drugs that increased cell viability; leflunomide (used to treat patients with inflammatory conditions) reduced caspase 3 and 7 activity in cells by 96%. TTC7A-KO cells contained cleaved caspase 3 and had reduced levels of phosphorylated AKT and X-linked inhibitor of apoptosis (XIAP); incubation of these cells with leflunomide increased levels of phosphorylated AKT and XIAP and reduced levels of cleaved caspase 3. Administration of leflunomide to ttc7a –/– zebrafish increased gut motility, reduced intestinal tract narrowing, increased intestinal cell survival, increased sizes of intestinal luminal spaces, and restored villi and goblet cell morphology. Exposure of patient-derived colonoids to leflunomide increased cell survival, polarity, and transport function. In a drug screen, we identified leflunomide as an agent that reduces apoptosis and activates AKT signaling in TTC7A-KO cells. In zebrafish with disruption of ttc7a , leflunomide restores gut motility, reduces intestinal tract narrowing, and increases intestinal cell survival. This drug might be repurposed for treatment of TTC7A deficiency. [ABSTRACT FROM AUTHOR]

Published
2020
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28. Su1760 BULK RNA-SEQUENCING OF BLOOD INFORMS MOLECULAR DIAGNOSES IN VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE.

Author

Collen, Lauren, Field, Michael, Eran, Alal, Mitsialis, Vanessa, Barends, Jared, Saccocia, Gwen, Bresnahan, Mairead, Yang, Jessica, Buijsen, Fleur, Combs, Abigail, Tuthill, Margaret, Bearup, Richelle, Okoroafor, Ibeawuchi, Ouahed, Jodie, Grushkin-Lerner, Leslie, Beckman, Noam D., Muise, Aleixo, Klein, Christoph, Schadt, Eric E., and Argmann, Carmen A.

Published
2023
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29. Sa1858 DEFECTIVE STAT3 SIGNALING IN TREATMENT-REFRACTORY VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE IS ASSOCIATED WITH A TRANSCRIPTIONAL SIGNATURE WHICH PREDICTS RESPONSE TO USTEKINUMAB.

Author

Collen, Lauren, Beckman, Noam D., Mitsialis, Vanessa, Eran, Alal, Field, Michael, Kim, David Y., Bao, Bin, Barends, Jared, Saccocia, Gwen, Bresnahan, Mairead, Yang, Jessica, Combs, Abigail, Tuthill, Margaret, Bearup, Richelle, Okoroafor, Ibeawuchi, Patik, Izabel, Grushkin-Lerner, Leslie, Ouahed, Jodie, Muise, Aleixo, and Klein, Christoph

Published
2023
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30. Myb-like, SWIRM, and MPN domains 1 (MYSM1) deficiency: Genotoxic stress-associated bone marrow failure and developmental aberrations.

Author

Bahrami, Ehsan, Witzel, Maximilian, Racek, Tomas, Puchałka, Jacek, Hollizeck, Sebastian, Greif-Kohistani, Naschla, Kotlarz, Daniel, Horny, Hans-Peter, Feederle, Regina, Schmidt, Heinrich, Sherkat, Roya, Steinemann, Doris, Göhring, Gudrun, Schlegelbeger, Brigitte, Albert, Michael H., Al-Herz, Waleed, and Klein, Christoph

Abstract

Background Myb-like, SWIRM, and MPN domains 1 (MYSM1) is a transcriptional regulator mediating histone deubiquitination. Its role in human immunity and hematopoiesis is poorly understood. Objectives We sought to investigate the clinical, cellular, and molecular features in 2 siblings presenting with progressive bone marrow failure (BMF), immunodeficiency, and developmental aberrations. Methods We performed genome-wide homozygosity mapping, whole-exome and Sanger sequencing, immunophenotyping studies, and analysis of genotoxic stress responses. p38 activation, reactive oxygen species levels, rate of apoptosis and clonogenic survival, and growth in immune and nonimmune cells were assessed. The outcome of allogeneic hematopoietic stem cell transplantation (HSCT) was monitored. Results We report 2 patients with progressive BMF associated with myelodysplastic features, immunodeficiency affecting B cells and neutrophil granulocytes, and complex developmental aberrations, including mild skeletal anomalies, neurocognitive developmental delay, and cataracts. Whole-exome sequencing revealed a homozygous premature stop codon mutation in the gene encoding MYSM1. MYSM1-deficient cells are characterized by increased sensitivity to genotoxic stress associated with sustained induction of phosphorylated p38 protein, increased reactive oxygen species production, and decreased survival following UV light–induced DNA damage. Both patients were successfully treated with allogeneic HSCT with sustained reconstitution of hematopoietic defects. Conclusions Here we show that MYSM1 deficiency is associated with developmental aberrations, progressive BMF with myelodysplastic features, and increased susceptibility to genotoxic stress. HSCT represents a curative therapy for patients with MYSM1 deficiency. [ABSTRACT FROM AUTHOR]

Published
2017
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31. Biallelic TLR4 deficiency in humans.

Author

Capitani, Melania, Al-Shaibi, Ahmad A., Pandey, Sumeet, Gartner, Lisa, Taylor, Henry, Hubrack, Satanay Z., Agrebi, Nourhen, Al-Mohannadi, Muneera Jassim, Al Kaabi, Saad, Vogl, Thomas, Roth, Johannes, Kotlarz, Daniel, Klein, Christoph, Charles, Adrian K., Vijayakumar, Vinayan, Karim, Mohammed Yousuf, George, Bruce, Travis, Simon P., Elawad, Mamoun, and Lo, Bernice

Abstract

Toll-like receptors (TLRs) mediate functions for host defense and inflammatory responses. TLR4 recognizes LPS, a component of gram-negative bacteria as well as host-derived endogenous ligands such as S100A8 and S100A9 proteins. We sought to report phenotype and cellular function of individuals with complete TLR4 deficiency. We performed genome sequencing and investigated exome and genome sequencing databases. Cellular responses were studied on primary monocytes, macrophages, and neutrophils, as well as cell lines using flow cytometry, reporter, and cytokine assays. We identified 2 individuals in a family of Qatari origin carrying a homozygous stop codon variant p.Q188X in TLR4 presenting with a variable phenotype (asymptomatic and inflammatory bowel disease consistent with severe perianal Crohn disease). A third individual with homozygous p.Y794X was identified in a population database. In contrast to hypomorphic polymorphisms p.D299G and p.T399I, the variants p.Q188X and p.Y794X completely abrogated LPS-induced cytokine responses whereas TLR2 response was normal. TLR4 deficiency causes a neutrophil CD62L shedding defect, whereas antimicrobial activity toward intracellular Salmonella was intact. Biallelic TLR4 deficiency in humans causes an inborn error of immunity in responding to LPS. This complements the spectrum of known primary immunodeficiencies, in particular myeloid differentiation primary response 88 (MYD88) or the IL-1 receptor-associated kinase 4 (IRAK4) deficiency that are downstream of TLR4 and TLR2 signaling. [ABSTRACT FROM AUTHOR]

Published
2023
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32. Human MD2 deficiency—an inborn error of immunity with pleiotropic features.

Author

Li, Yue, Yu, Ziqi, Schenk, Madlin, Lagovsky, Irena, Illig, David, Walz, Christoph, Rohlfs, Meino, Conca, Raffaele, Muise, Aleixo M., Snapper, Scott B., Uhlig, Holm H., Garty, Ben Zion, Klein, Christoph, and Kotlarz, Daniel

Abstract

[Display omitted] Toll-like receptors (TLRs) are important pattern recognition receptors that sense microbes and control host defense. Myeloid differentiation protein 2 (MD2) is the indispensable coreceptor for TLR4, facilitating the binding to the gram-negative bacterial cell wall component LPS and activation of downstream signaling. We sought to provide phenotypic and mechanistic insights into human MD2 deficiency. To elucidate the genetic cause in a patient with very early onset inflammatory bowel disease, we performed whole-exome sequencing and studied the functional consequences of the identified mutation in LY96 (encoding for MD2) in genetically engineered induced pluripotent stem cell–derived macrophages with knockout of MD2 or knockin of the patient-specific mutation, including TLR4-mediated signaling, cytokine production, and bacterial handling. Whole-exome sequencing identified a homozygous in-frame deletion in the LY96 gene (c.347_349delCAA; p.Thr116del) in a patient with very early onset inflammatory bowel disease and a sibling presenting with pneumonia and otitis media. Induced pluripotent stem cell–derived macrophages with knockout of MD2 or expression of the Thr116del mutation showed impaired activation of nuclear factor kappa B and mitogen-activated protein kinase signaling as well as TLR4 endocytosis on challenge with LPS or bacteria. In addition, MD2-deficient macrophages showed decreased cytokine expression (eg, IL-6, TNF, and IL-10) in response to LPS or gram-negative but not gram-positive bacteria. Human MD2 deficiency causes defective TLR4 signaling in response to LPS or gram-negative bacteria. The clinical manifestations and expressivity might be variable due to unknown secondary risk factors. Because TLR4 represents a therapeutic target for multiple inflammatory conditions, our study may provide insights into potential side effects of pharmacological TLR4 targeting. [ABSTRACT FROM AUTHOR]

Published
2023
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33. A program of successive gene expression in mouse one-cell embryos.

Author

Asami, Maki, Lam, Brian Y.H., Hoffmann, Martin, Suzuki, Toru, Lu, Xin, Yoshida, Naoko, Ma, Marcella K., Rainbow, Kara, Gužvić, Miodrag, VerMilyea, Matthew D., Yeo, Giles S.H., Klein, Christoph A., and Perry, Anthony C.F.

Abstract

At the moment of union in fertilization, sperm and oocyte are transcriptionally silent. The ensuing onset of embryonic transcription (embryonic genome activation [EGA]) is critical for development, yet its timing and profile remain elusive in any vertebrate species. We here dissect transcription during EGA by high-resolution single-cell RNA sequencing of precisely synchronized mouse one-cell embryos. This reveals a program of embryonic gene expression (immediate EGA [iEGA]) initiating within 4 h of fertilization. Expression during iEGA produces canonically spliced transcripts, occurs substantially from the maternal genome, and is mostly downregulated at the two-cell stage. Transcribed genes predict regulation by transcription factors (TFs) associated with cancer, including c-Myc. Blocking c-Myc or other predicted regulatory TF activities disrupts iEGA and induces acute developmental arrest. These findings illuminate intracellular mechanisms that regulate the onset of mammalian development and hold promise for the study of cancer. [Display omitted] • A gene expression program, iEGA, initiates within 4 h of mouse fertilization • Upregulated genes are normatively spliced, protein coded, and soon downregulated • iEGA genes predict cancer-associated pathways and transcription regulators • Inhibiting predicted transcription regulators acutely disrupts iEGA and development How and when embryonic transcription begins following fertilization remains elusive. Asami et al. generate a high-resolution time course to reveal a transcription program initiating within 4 h of fertilization in mouse one-cell embryos. The program predicts embryonic and cancer-associated pathway expression, and inhibiting inferred regulators acutely blocks transcription and development. [ABSTRACT FROM AUTHOR]

Published
2023
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34. Interleukin 1β Mediates Intestinal Inflammation in Mice and Patients With Interleukin 10 Receptor Deficiency.

Author

Shouval, Dror S., Biswas, Amlan, Kang, Yu Hui, Griffith, Alexandra E., Konnikova, Liza, Mascanfroni, Ivan D., Redhu, Naresh S., Frei, Sandra M., Field, Michael, Doty, Andria L., Goldsmith, Jeffrey D., Bhan, Atul K., Loizides, Anthony, Weiss, Batia, Yerushalmi, Baruch, Yanagi, Tadahiro, Lui, Xiuli, Quintana, Francisco J., Muise, Aleixo M., and Klein, Christoph

Abstract

Interleukin 10 receptor (IL10R)−deficient mice develop spontaneous colitis and, similarly, patients with loss-of-function mutations in IL10R develop severe infant-onset inflammatory bowel disease. Loss of IL10R signaling in mouse and human macrophages is associated with increased production of interleukin 1β. We demonstrated that innate immune production of IL1β mediates colitis in IL10R-deficient mice. Transfer of Il1r1 −/− CD4 + T cells into Rag1 − / − /Il10rb − / − mice reduced the severity of their colitis (compared to mice that received CD4 + T cells that express IL1R), accompanied by decreased production of interferon gamma, tumor necrosis factor−α, and IL17A. In macrophages from mice without disruption of IL10R signaling or from healthy humans (controls), incubation with IL10 reduced canonical activation of the inflammasome and production of IL1β through transcriptional and post-translational regulation of NLRP3 . Lipopolysaccharide and adenosine triphosphate stimulation of macrophages from Il10rb − / − mice or IL10R-deficient patients resulted in increased production of IL1β. Moreover, in human IL10R-deficient macrophages, lipopolysaccharide stimulation alone triggered IL1β secretion via non-canonical, caspase 8−dependent activation of the inflammasome. We treated 2 IL10R-deficient patients with severe and treatment-refractory infant-onset inflammatory bowel disease with the IL1−receptor antagonist anakinra. Both patients had marked clinical, endoscopic, and histologic responses after 4–7 weeks. This treatment served as successful bridge to allogeneic hematopoietic stem cell transplantation in 1 patient. Our findings indicate that loss of IL10 signaling leads to intestinal inflammation, at least in part, through increased production of IL1 by innate immune cells, leading to activation of CD4 + T cells. Agents that block IL1 signaling might be used to treat patients with inflammatory bowel disease resulting from IL10R deficiency. [ABSTRACT FROM AUTHOR]

Published
2016
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35. A Novel Technique for Transcatheter Aortic Valve Replacement in Pure Aortic Regurgitation.

Author

Unbehaun, Axel, Klein, Christoph, Buz, Semih, Meyer, Alexander, Wamala, Isaac, Potapov, Evgenij, Schoenrath, Felix, Falk, Volkmar, and Kempfert, Joerg

Abstract

Transcatheter aortic valve replacement (TAVR) in pure aortic regurgitation (AR) is challenging, because of the subsequent difficulty in anchoring the transcatheter valve in a noncalcified device landing zone (DLZ). Prestenting can help to prepare a stable DLZ for TAVR in pure AR and prevent valve migration. Here we report the first-in-human implantation of an uncovered stent into a noncalcified aortic valve as a prestenting strategy to prepare an easy DLZ for TAVR in pure AR. We consider this technique a useful novel tool to improve device success, at least as long as specific TAVR devices for pure AR are lacking. [ABSTRACT FROM AUTHOR]

Published
2019
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38. Estimation of Geothermal Reservoir Properties Using the Ensemble Kalman Filter.

Author

Marquart, Gabriele, Vogt, Christian, Klein, Christoph, and Widera, André

Abstract

Abstract: Information on the permeability at depth is important for the exploitation of geothermal reservoirs. The Ensemble Kalman Filter (EnKF) is tool for property estimation if temporal observations are available. Observations can be temperature, hydraulic head during pumping tests, and chemical concentrations from tracer experiments at a few boreholes. The EnKF is a recursive Bayesian method incorporating observations in a Monte-Carlo-ensemble of reservoir simulations considering probability distributions. We present in synthetic test cases the application of the EnKF for estimating permeability and demonstrate its use for exploration planning. We apply the method to the 2005-tracer experiment of the Soultz-sous-Forêts geothermal reservoir. [Copyright &y& Elsevier]

Published
2013
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39. Framework models of tumor dormancy from patient-derived observations

Author

Klein, Christoph A

Subjects
*CARCINOGENESIS, *CANCER cell proliferation, *HOMEOSTASIS, *GROWTH rate, *CELLULAR mechanics, *MEDICAL research, *PREVENTION
Abstract

Unusually long latency periods between the treatment of primary tumors and metastatic recurrences are commonly thought to prove the existence and relevance of clinical tumor dormancy. However, careful consideration of disease courses and cancer growth rates leads to the conclusion that clinical dormancy may be everything from non-existent to much more frequent than originally thought. On the other hand, cellular dormancy defined as a non-productive state of disseminated tumor cells is very frequent, while homeostatic mechanisms such as angiogenic and immunological control contribute to the chronicity of cancer. This review attempts to provide a conceptual framework for the study of dormancy, which may guide clinical and experimental research. [ABSTRACT FROM AUTHOR]

Published
2011
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40. Long-Term Prognostic Value of Dobutamine Stress CMR.

Author

Kelle, Sebastian, Chiribiri, Amedeo, Vierecke, Juliane, Egnell, Christina, Hamdan, Ashraf, Jahnke, Cosima, Paetsch, Ingo, Wellnhofer, Ernst, Fleck, Eckart, Klein, Christoph, and Gebker, Rolf

Subjects
DOBUTAMINE, CARDIAC magnetic resonance imaging, HEART disease prognosis, CORONARY disease, CORONARY artery bypass, CONFIDENCE intervals, ECHOCARDIOGRAPHY, MYOCARDIAL infarction
Abstract

Objectives: The aim of this study was to assess the long-term value of high-dose dobutamine cardiac magnetic resonance (DCMR) for the prediction of cardiac events in a large cohort of patients with known or suspected coronary artery disease. Background: High-dose DCMR has been shown to be a useful technique for diagnosis and intermediate-term prognostic stratification. Methods: Clinical data and DCMR results were analyzed in 1,463 consecutive patients undergoing DCMR between 2000 and 2004. Ninety-four patients were lost to follow-up. The remaining 1,369 patients were followed up for a mean of 44 ± 24 months. Cardiac events, defined as cardiac death and nonfatal myocardial infarction, were related to clinical and DCMR results. Results: Three-hundred fifty-two patients underwent early revascularization (≤3 months of DCMR) and were excluded from analysis. Of the remaining 1,017 patients, 301 patients (29.6%) experienced inducible wall motion abnormalities (WMA). Forty-six cardiac events were reported. In those with and without inducible WMA, the proportion of patients with cardiac events was 8.0% versus 3.1%, respectively, p = 0.001 (hazard ratio: 3.3; 95% confidence interval: 1.8 to 5.9 for the presence of inducible WMA; p < 0.001). A DCMR without inducible WMA carried an excellent prognosis, with a 6-year cardiac event-free survival of 96.8%. In all 1,369 patients in the patient group with stress-inducible WMA, those patients with medical therapy demonstrated a trend to a higher cardiac event rate (8.0%) than those with early revascularization (5.4%) (p = 0.234). Patients with normal DCMR and medical therapy or early revascularization demonstrated similar cumulative cardiac event rates (3.1% vs. 3.2%, p = 0.964). Conclusions: In a large cohort of patients, DCMR has an added value for predicting cardiac events during long-term follow-up, improving the differentiation between high-risk and low-risk patients. Patients with inducible WMA and following early revascularization, demonstrate lower cardiac event rates than patients with medical therapy alone. [Copyright &y& Elsevier]

Published
2011
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41. Individuals differ in the attentional blink: Mental speed and intra-subject stability matter

Author

Klein, Christoph, Arend, Isabel C., Beauducel, Andre, and Shapiro, Kimron L.

Subjects
*VISUAL perception, *SHORT-term memory, *PSYCHOMETRICS, *INTELLECT, *VARIABILITY (Psychometrics), *DIFFERENTIAL psychology, *STABILITY (Mechanics), *RELIABILITY (Personality trait)
Abstract

Abstract: The failure to correctly report two targets (“T1”, “T2”) that follow each other in close temporal proximity has been called the “attentional blink” (AB). The AB has, so far, mainly been studied using experimental approaches. The present studies investigated individual differences in AB performance, revealing (among further findings) a high positive correlation between the accuracies of detecting the two targets correctly (r=0.69); and between T2∣T1 accuracy and psychometric intelligence (0.41≤r≤0.43) and RT variability in short-term and working memory (−0.38≤r≤−0.45). Together, these results support important aspects of major theoretical accounts of the AB from an individual differences perspective and introduce intelligence and intra-subject stability as contributing factors in AB performance. [ABSTRACT FROM AUTHOR]

Published
2011
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42. A Prospective Study for Comparison of MR and CT Imaging for Detection of Coronary Artery Stenosis.

Author

Hamdan, Ashraf, Asbach, Patrick, Wellnhofer, Ernst, Klein, Christoph, Gebker, Rolf, Kelle, Sebastian, Kilian, Harald, Huppertz, Alexander, and Fleck, Eckart

Subjects
CORONARY artery stenosis, LONGITUDINAL method, CARDIAC magnetic resonance imaging, TOMOGRAPHY, SIGNAL-to-noise ratio, ELECTROCARDIOGRAPHY, ANGIOGRAPHY, MAGNETIC resonance imaging
Abstract

Objectives: The purpose of the present study was to directly compare the diagnostic accuracy of magnetic resonance imaging (MRI) and multislice computed tomography (CT) for the detection of coronary artery stenosis. Background: Both imaging modalities have emerged as potential noninvasive coronary imaging modalities; however, CT—unlike MRI—exposes patients to radiation and iodinated contrast agent. Methods: One hundred twenty consecutive patients with suspected or known coronary artery disease prospectively underwent 32-channel 3.0-T MRI and 64-slice CT before elective X-ray angiography. The diagnostic accuracy of the 2 modalities for detecting significant coronary stenosis (≥50% luminal diameter stenosis) in segments ≥1.5 mm diameter was compared with quantitative invasive coronary angiography as the reference standard. Results: In the patient-based analysis MRI and CT angiography showed similar diagnostic accuracy of 83% (95% confidence interval [CI]: 75 to 87) versus 87% (95% CI: 80 to 92), p = 0.38; sensitivity of 87% (95% CI: 76 to 93) versus 90% (95% CI: 80 to 95), p = 0.16; and specificity of 77% (95% CI: 63 to 87) versus 83% (95% CI: 70 to 91), p = 0.06, respectively. All cases of left main or 3-vessel disease were correctly diagnosed by MRI and CT angiography. In the patient-based analysis MRI and CT angiography were similar in their ability to identify patients who subsequently underwent revascularization: the area under the receiver-operator characteristic curve was 0.78 (95% CI: 0.69 to 0.87) for MRI and 0.82 (95% CI: 0.74 to 0.90) for CT angiography. Conclusions: Thirty-two channel 3.0-T MRI and 64-slice CT angiography similarly identify significant coronary stenosis in patients with suspected or known coronary artery disease scheduled for elective coronary angiography. However, CT angiography showed a favorable trend toward higher diagnostic performance. [ABSTRACT FROM AUTHOR]

Published
2011
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43. Transapical Aortic Valve Implantation in 194 Patients: Problems, Complications, and Solutions.

Author

Pasic, Miralem, Buz, Semih, Dreysse, Stephan, Drews, Thorsten, Unbehaun, Axel, Klein, Christoph, Kukucka, Marian, Mladenow, Alexander, Ivanitskaia–Kühn, Ekaterina, and Hetzer, Roland

Subjects
HEART valve transplantation, AORTIC valve, SURGICAL complications, MEDICAL statistics, ANGIOGRAPHY, POSTOPERATIVE care, HEART diseases, THERAPEUTICS
Abstract

Background: Transapical aortic valve implantation is a novel approach for high-risk patients with severe aortic stenosis. During our learning curve, we were faced with several problems, technical difficulties, and complications, and our strategy and procedural technique evolved accordingly. We report our experience during the learning curve for establishing this new method. Methods: Between April 2008 and January 2010, 194 patients (mean age, 80 ± 9 years; range, 36 to 99 years) were treated by transapical aortic valve implantation. The mean Society of Thoracic Surgeons score was 23.5% ± 19.4% (range, 2.7% to 89.5%; logistic EuroSCORE, 41% ± 20%; range, 6% to 97%). We have established institutional guidelines on how to act in particular situations, with regard to patient selection, procedural steps, and complications concerning the procedure that have evolved according to our own experience. Mandatory angiographic visualization of the aortic root during valve deployment was introduced, combined with slow and gradual inflation of the balloon with possible correction of the valve position and its definitive position higher than we had been taught. Results: Technical success was 99.5% with one conversion to conventional surgery (annulus rupture). One intraprocedural obstruction of the left coronary ostium was successfully treated by emergency stent implantation. The 30-day mortality was 5.7% for the whole group (11 of 194 patients), 3.8% for all patients without cardiogenic shock (7 of 182 patients), and 33% for the patients with cardiogenic shock (4 of 12 patients). There were 2 (1%) new clinical neurologic events postoperatively. Conclusions: A combination of patient-related evaluation and several small but precise technical modifications of the original transapical aortic valve implantation techniques reduced the rate of complications and increased success during the learning curve. [ABSTRACT FROM AUTHOR]

Published
2010
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44. Evaluation of contrast wash-in and peak enhancement in adenosine first pass perfusion CMR in patients post bypass surgery.

Author

Kelle, Sebastian, Graf, Kristof, Dreysse, Stefan, Schnackenburg, Bernhard, Fleck, Eckart, and Klein, Christoph

Subjects
HEART blood-vessels, ADENOSINES, CORONARY artery bypass, CARDIAC magnetic resonance imaging, ANGIOGRAPHY, RADIOSCOPIC diagnosis, CORONARY artery stenosis, BLOOD vessels, HEART beat
Abstract

Background: Adenosine first pass perfusion cardiovascular magnetic resonance (CMR) yields excellent results for the detection of significant coronary artery disease (CAD). In patients with coronary artery bypass grafts (CABG) the kinetics of a contrast bolus may by altered only due to different distances through the bypass grafts compared to native vessels, thereby possibly imitating a perfusion defect. The aim of the study was to evaluate semiquantitative perfusion parameters in order to assess possible differences in epicardial contrast kinetics in areas supplied by native coronaries and CABG, both without significant stenosis. Methods: Twenty patients with invasive exclusion of significant CAD (control group) and 38 patients with CABG without angiographically significant (≥50%) stenosis in unbypassed coronaries or grafts were retrospectively included in the study. They underwent adenosine first pass (0.05 mmol/kg Gd-DTPA) perfusion (3 short axis views/heart beat) and late gadolinium enhancement (LGE) imaging 1 day before invasive coronary angiography. Areas perfused by native coronaries and/or the different bypasses were identified in X-ray angiography using the 16 segment model. In each of these areas upslope and maximal signal intensity (SImax) relative to the left ventricular parameters, time to 50% maximal signal intensity (TSI50%max) and time to maximal signal intensity (TSImax) were calculated. Results: In areas perfused by coronary arteries with bypasses compared to native coronaries relative upslope and relative SImax did not show a significant difference. TSI50%max and TSImax in native coronaries and bypasses were 7.2s±1.9s vs. 7.5s±1.9s (p < 0.05) and 12.6s±3.0s vs. 13.1s±3.0s (p < 0.05), respectively. The delay in Tmax resulted in a significant (p < 0.05) delay of 0.5±1.1 heart beats (=images) when adjusted to the heart rate. Differences in time were most pronounced in areas perfused by left internal mammary artery grafts rather than by venous CABG, but were also present between native vessel territories in patients without CAD, albeit with smaller variability. Conclusion: Adenosine perfusion CMR in patients post CABG may be associated with a short delay in contrast arrival. However, once the contrast is in the myocardium there is similar wash-in kinetics and peak enhancement. Therefore, since the delay is only short, the possibly differing contrast kinetics through grafts and native vessels does not seem to be a limiting factor for the accuracy of first pass adenosine perfusion in patients post CABG. [ABSTRACT FROM AUTHOR]

Published
2010
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45. Novel genetic etiologies of severe congenital neutropenia

Author

Boztug, Kaan and Klein, Christoph

Subjects
*ETIOLOGY of diseases, *NEUTROPENIA, *GENETIC disorders, *IMMUNODEFICIENCY, *DEFICIENCY diseases, *NEUTROPHIL immunology, *ELASTASES, *LEUCOCYTE elastase, *GENETICS
Abstract

Severe congenital neutropenia (SCN) comprises a heterogenous group of primary immunodeficiency disorders collectively characterized by paucity of mature neutrophils. In recent years, progress has been made with respect to the elucidation of genetic causes underlying syndromic and non-syndromic variants of SCN. Most cases of autosomal dominant SCN are associated with mutations in the neutrophil elastase (ELA-2/ELANE) gene, autosomal recessive forms of this disorder can be caused by mutations in the gene encoding the mitochondrial protein HAX-1. Rarely, SCN can be caused by mutations in the gene encoding the transcription factor GFI1 or activating mutations in the Wiskott–Aldrich syndrome (WAS) gene, respectively. More recently, a complex disorder associating SCN and developmental aberrations was identified, caused by mutations in the glucose-6-phosphatase catalytic subunit 3 (G6PC3) gene. Despite our increasing knowledge of the genetic etiologies of SCN, the molecular pathophysiology underlying these disorders remains only partially understood. [Copyright &y& Elsevier]

Published
2009
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46. Magnetic Resonance Adenosine Perfusion Imaging in Patients After Coronary Artery Bypass Graft Surgery.

Author

Klein, Christoph, Nagel, Eike, Gebker, Rolf, Kelle, Sebastian, Schnackenburg, Bernhard, Graf, Kristof, Dreysse, Stefan, and Fleck, Eckart

Subjects
ADENOSINES, PERFUSION, CARDIAC magnetic resonance imaging, CORONARY artery bypass, NERVE grafting, PHYSIOLOGICAL stress, PATIENTS, THERAPEUTICS
Abstract

Objectives: The aim of the study was to evaluate the feasibility and diagnostic performance of the combination of adenosine stress perfusion and late gadolinium enhancement (LGE) in patients after coronary artery bypass graft surgery (CABG). Background: Cardiac magnetic resonance (CMR) imaging allows the detection of significant coronary artery disease by adenosine stress perfusion and infarct imaging. Myocardial contrast kinetics may be altered in patients after CABG owing to more complex myocardial perfusion and different distances of the contrast bolus through different bypasses and native coronary vessels. Additionally, all studies have excluded patients after CABG. Methods: In all, 78 patients (age 66 ± 8 years; 71 men) underwent CMR imaging including left ventricular function, first-pass adenosine stress perfusion (adenosine 140 μg/min/kg) using 0.05 mmol/kg body weight gadolinium-diethylenetriaminepenta-acetic acid and an additional 0.15 mmol/kg for LGE 1 day before invasive coronary angiography. Images were analyzed visually using the speed of contrast wash-in and maximal signal intensity. Transmural LGE defects of the size of a vessel or graft territory defined by angiography were considered true negatives, even when supplied by a stenosed/occluded vessel/graft. Stenoses >50% in grafts and grafted or ungrafted native vessels (diameter ≥2 mm) in invasive angiography were considered significant. Results: The prevalence of patients with significant stenosis was 63% (69% functionally 1-vessel, 28% 2-vessel, and 3% 3-vessel disease). Sensitivity and specificity were 77% and 90%, respectively, on a patient basis, and 71% and 89% on a vessel territory basis. Sensitivity, if only areas supplied by grafts (n = 196) were evaluated, was 78% and specificity was 94%, compared with territories supplied by ungrafted native vessels (n = 51) with sensitivity and specificity of 63% and 91%, respectively. Sensitivity and specificity for the 53 areas with prior infarction were 88% and 79%, respectively. Conclusions: For patients after surgical revascularization, the combination of stress perfusion and LGE yields good diagnostic accuracy for the detection and localization of significant stenoses. However, sensitivity is reduced compared with published data in patients without CABG. Prior myocardial infarction can be examined without loss of accuracy. [Copyright &y& Elsevier]

Published
2009
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47. Breakdown of T cell tolerance and autoimmunity in primary immunodeficiency—lessons learned from monogenic disorders in mice and men

Author

Westerberg, Lisa S, Klein, Christoph, and Snapper, Scott B

Subjects
*T cells, *AUTOIMMUNITY, *IMMUNODEFICIENCY, *MONOGENIC functions
Abstract

A key feature of the immune system is the capacity to monitor and control infections from non-self pathogens while maintaining tolerance to self-antigens. Primary immunodeficiencies (PID) are characterized by an increased susceptibility to infections, often associated with aberrant inflammatory responses and a concomitant high prevalence of autoimmunity. Autoimmunity in PID raises a conundrum: How can an immune system fail to respond to non-self pathogens while reacting vigorously to self-antigens? Recent advances from studies of PID patients and related animal models have revealed the crucial role of Aire-induced expression of self-antigens for deletion of autoreactive T cells in the thymus (central tolerance). Moreover, lessons from PID have provided unequivocal evidence for the essential role of regulatory T cells in suppressing autoreactive T cells in the periphery. Finally, findings from PID have broadened our understanding of how homeostatic proliferation and increased load or decreased clearance of apoptotic cells and non-self pathogens can lead to breakdown of peripheral tolerance. [Copyright &y& Elsevier]

Published
2008
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48. The direct molecular analysis of metastatic precursor cells in breast cancer: A chance for a better understanding of metastasis and for personalised medicine

Author

Klein, Christoph A.

Subjects
*GENETICS of breast cancer, *ADJUVANT treatment of cancer, *CANCER cells, *MEDICAL centers, *BONE marrow, *MOLECULAR oncology
Abstract

Abstract: The search for disseminated cancer cells has become a routine procedure in many clinical centres since the pioneering work of Riethmüller and Schlimok was published in the mid 1980s. Until today, clinical studies have mostly focused on the prognostic role of disseminated cancer cells that can be detected in bone marrow samples before manifestation of metastasis. As a more recent development, the field is increasingly concentrating on the prognostic information provided by tumour cells circulating in the peripheral blood instead of analysing the nature of disseminated tumour cells that have successfully homed to a new microenvironment and may eventually grow into metastases. This review critically questions that direction and proposes exploiting the unique opportunities provided by the direct molecular analysis of metastatic precursor cells for a better understanding of metastasis, tumour dormancy, therapy target identification, and personalised medicine in an adjuvant therapy setting. [Copyright &y& Elsevier]

Published
2008
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50. Lymphocyte-Dependent and Th2 Cytokine-Associated Colitis in Mice Deficient in Wiskott-Aldrich Syndrome Protein.

Author

Nguyen, Deanna D., Maillard, Michel H., Cotta–de–Almeida, Vinicius, Mizoguchi, Emiko, Klein, Christoph, Fuss, Ivan, Nagler, Cathryn, Mizoguchi, Atsushi, Bhan, Atul K., and Snapper, Scott B.

Subjects
DISEASES, ETIOLOGY of diseases, SICK leave, SICK people
Abstract

Background & Aims: Controversy exists as to whether patients with inflammatory bowel disease have an underlying immunodeficiency. We have focused on a murine model of the Wiskott-Aldrich syndrome, an immunodeficiency in which autoimmunity can manifest in the form of an inflammatory bowel disease-like illness. Wiskott-Aldrich syndrome protein (WASP) deficiency in mice results in similar clinical features. Herein, we characterized the colitis in WASP-deficient mice. Methods: WASP-deficient mice were followed clinically and histologically. Immunologic studies were performed to determine the pathogenic cell population(s), the predominant cytokine expression pattern, and the role of cytokine(s) in colitis pathogenesis. Results: All WASP-deficient mice develop colitis by 6 months of age. Lymphocytes are required for disease induction, and CD4+ T cells from WASP-deficient mice are sufficient to induce disease in lymphocyte-deficient hosts. Lamina propria preparations from WASP-deficient mice demonstrated elevations in interferon-γ, interleukin (IL)-4, and IL-13 levels but decreased IL-6 and no difference in IL-17 expression in comparison with wild-type controls. Treatment with neutralizing antibody to IL-4, but not to interferon-γ, abrogated colitis development. However, mice deficient in both WASP and IL-4 showed no difference in histologic colitis scores at 24 weeks of age compared with WASP-deficient mice. Conclusions: These results demonstrate a critical role for lymphocytes and a relative T helper 2 cytokine predominance in the colitis associated with WASP-deficient mice. This is the only model of colitis with elevated T helper 2 cytokines and aberrant natural regulatory T cell function and is unique in having a human disease counterpart with similar defects. [Copyright &y& Elsevier]

Published
2007
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