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Your search keyword '"Schmitt, Joachim P."' showing total 170 results
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170 results on '"Schmitt, Joachim P."'

1. SPINEPS -- Automatic Whole Spine Segmentation of T2-weighted MR images using a Two-Phase Approach to Multi-class Semantic and Instance Segmentation

Author

Möller, Hendrik, Graf, Robert, Schmitt, Joachim, Keinert, Benjamin, Atad, Matan, Sekuboyina, Anjany, Streckenbach, Felix, Schön, Hanna, Kofler, Florian, Kroencke, Thomas, Bette, Stefanie, Willich, Stefan, Keil, Thomas, Niendorf, Thoralf, Pischon, Tobias, Endemann, Beate, Menze, Bjoern, Rueckert, Daniel, and Kirschke, Jan S.

Subjects
Electrical Engineering and Systems Science - Image and Video Processing, Computer Science - Computer Vision and Pattern Recognition
Abstract

Purpose. To present SPINEPS, an open-source deep learning approach for semantic and instance segmentation of 14 spinal structures (ten vertebra substructures, intervertebral discs, spinal cord, spinal canal, and sacrum) in whole body T2w MRI. Methods. During this HIPPA-compliant, retrospective study, we utilized the public SPIDER dataset (218 subjects, 63% female) and a subset of the German National Cohort (1423 subjects, mean age 53, 49% female) for training and evaluation. We combined CT and T2w segmentations to train models that segment 14 spinal structures in T2w sagittal scans both semantically and instance-wise. Performance evaluation metrics included Dice similarity coefficient, average symmetrical surface distance, panoptic quality, segmentation quality, and recognition quality. Statistical significance was assessed using the Wilcoxon signed-rank test. An in-house dataset was used to qualitatively evaluate out-of-distribution samples. Results. On the public dataset, our approach outperformed the baseline (instance-wise vertebra dice score 0.929 vs. 0.907, p-value<0.001). Training on auto-generated annotations and evaluating on manually corrected test data from the GNC yielded global dice scores of 0.900 for vertebrae, 0.960 for intervertebral discs, and 0.947 for the spinal canal. Incorporating the SPIDER dataset during training increased these scores to 0.920, 0.967, 0.958, respectively. Conclusions. The proposed segmentation approach offers robust segmentation of 14 spinal structures in T2w sagittal images, including the spinal cord, spinal canal, intervertebral discs, endplate, sacrum, and vertebrae. The approach yields both a semantic and instance mask as output, thus being easy to utilize. This marks the first publicly available algorithm for whole spine segmentation in sagittal T2w MR imaging., Comment: https://github.com/Hendrik-code/spineps

Published
2024

2. Deficiency of the sphingosine-1-phosphate (S1P) transporter Mfsd2b protects the heart against hypertension-induced cardiac remodeling by suppressing the L-type-Ca2+ channel

Author

Duse, Dragos Andrei, Schröder, Nathalie Hannelore, Srivastava, Tanu, Benkhoff, Marcel, Vogt, Jens, Nowak, Melissa Kim, Funk, Florian, Semleit, Nina, Wollnitzke, Philipp, Erkens, Ralf, Kötter, Sebastian, Meuth, Sven Günther, Keul, Petra, Santos, Webster, Polzin, Amin, Kelm, Malte, Krüger, Martina, Schmitt, Joachim, and Levkau, Bodo

Published
2024
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3. Denoising diffusion-based MRI to CT image translation enables automated spinal segmentation

Author

Graf, Robert, Schmitt, Joachim, Schlaeger, Sarah, Möller, Hendrik Kristian, Sideri-Lampretsa, Vasiliki, Sekuboyina, Anjany, Krieg, Sandro Manuel, Wiestler, Benedikt, Menze, Bjoern, Rueckert, Daniel, and Kirschke, Jan Stefan

Subjects
Electrical Engineering and Systems Science - Image and Video Processing, Computer Science - Computer Vision and Pattern Recognition, Computer Science - Machine Learning, 68T99 68U10, I.2.1
Abstract

Background: Automated segmentation of spinal MR images plays a vital role both scientifically and clinically. However, accurately delineating posterior spine structures presents challenges. Methods: This retrospective study, approved by the ethical committee, involved translating T1w and T2w MR image series into CT images in a total of n=263 pairs of CT/MR series. Landmark-based registration was performed to align image pairs. We compared 2D paired (Pix2Pix, denoising diffusion implicit models (DDIM) image mode, DDIM noise mode) and unpaired (contrastive unpaired translation, SynDiff) image-to-image translation using "peak signal to noise ratio" (PSNR) as quality measure. A publicly available segmentation network segmented the synthesized CT datasets, and Dice scores were evaluated on in-house test sets and the "MRSpineSeg Challenge" volumes. The 2D findings were extended to 3D Pix2Pix and DDIM. Results: 2D paired methods and SynDiff exhibited similar translation performance and Dice scores on paired data. DDIM image mode achieved the highest image quality. SynDiff, Pix2Pix, and DDIM image mode demonstrated similar Dice scores (0.77). For craniocaudal axis rotations, at least two landmarks per vertebra were required for registration. The 3D translation outperformed the 2D approach, resulting in improved Dice scores (0.80) and anatomically accurate segmentations in a higher resolution than the original MR image. Conclusion: Two landmarks per vertebra registration enabled paired image-to-image translation from MR to CT and outperformed all unpaired approaches. The 3D techniques provided anatomically correct segmentations, avoiding underprediction of small structures like the spinous process., Comment: 35 pages, 7 figures, Code and a model weights available https://doi.org/10.5281/zenodo.8221159 and https://doi.org/10.5281/zenodo.8198697

Published
2023
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6. Molecular and cellular evidence for the impact of a hypertrophic cardiomyopathy-associated RAF1 variant on the structure and function of contractile machinery in bioartificial cardiac tissues

Author

Nakhaei-Rad, Saeideh, Haghighi, Fereshteh, Bazgir, Farhad, Dahlmann, Julia, Busley, Alexandra Viktoria, Buchholzer, Marcel, Kleemann, Karolin, Schänzer, Anne, Borchardt, Andrea, Hahn, Andreas, Kötter, Sebastian, Schanze, Denny, Anand, Ruchika, Funk, Florian, Kronenbitter, Annette Vera, Scheller, Jürgen, Piekorz, Roland P., Reichert, Andreas S., Volleth, Marianne, Wolf, Matthew J., Cirstea, Ion Cristian, Gelb, Bruce D., Tartaglia, Marco, Schmitt, Joachim P., Krüger, Martina, Kutschka, Ingo, Cyganek, Lukas, Zenker, Martin, Kensah, George, and Ahmadian, Mohammad R.

Published
2023
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8. Diabetes disturbs functional adaptation of the remote myocardium after ischemia/reperfusion

Author

Funk, Florian, Kronenbitter, Annette, Isić, Malgorzata, Flocke, Vera, Gorreßen, Simone, Semmler, Dominik, Brinkmann, Maximilian, Beck, Katharina, Steinhoff, Oliver, Srivastava, Tanu, Barbosa, David Monteiro, Voigt, Katharina, Wang, Luzhou, Bottermann, Katharina, Kötter, Sebastian, Grandoch, Maria, Flögel, Ulrich, Krüger, Martina, and Schmitt, Joachim P.

Published
2022
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9. Regulation of titin-based cardiac stiffness by unfolded domain oxidation (UnDOx)

Author

Loescher, Christine M., Breitkreuz, Martin, Li, Yong, Nickel, Alexander, Unger, Andreas, Dietl, Alexander, Schmidt, Andreas, Mohamed, Belal A., Kötter, Sebastian, Schmitt, Joachim P., Krüger, Marcus, Krüger, Martina, Toischer, Karl, Maack, Christoph, Leichert, Lars I., Hamdani, Nazha, and Linke, Wolfgang A.

Published
2020

12. Extracorporeal Life Support Organization Registry International Report 2022: 100,000 Survivors

Author

Tonna, Joseph E., Boonstra, Philip S., MacLaren, Graeme, Paden, Matthew, Brodie, Daniel, Anders, Marc, Hoskote, Aparna, Ramanathan, Kollengode, Hyslop, Rob, Fanning, Jeffrey J., Rycus, Peter, Stead, Christine, Barrett, Nicholas A., Mueller, Thomas, Gómez, Rene D., Malhotra Kapoor, Poonam, Fraser, John F., Bartlett, Robert H., Alexander, Peta M.A., Barbaro, Ryan P., Abbasi, Adeel, Said Abdalmohsen, Ahmad, Abdelbary, Akram M., Abecasis, Francisco, Abel, Peter, Abu-Omar, Yasir, Adams, Douglas R, Manuel Africano, Juan, Aganga, Devon, Agati, Salvatore, Agerstrand, Cara, Aguillon, Mario V., Akers, Crystal S., Akhtarekhavari, Julia, Alazzam, Mohammad Izzat Salah, Albert, Martin, Alberti, Angela, Al-Fares, Abdulrahman A., Alfoudri, Huda, Allaert, Silvie, Allbert, Keesha N., Allen, Christopher T., Lescano Alva, Miguel Ángel, Alwardt, Cory M., Amigoni, Angela, Anandamurthy, Balaram, Anastasiadis, Kyriakos, Anders, Nicholas R., Anderson, Scott A., Anderson, Patricia L., Andrijević, Ana, Annoni, Alice, Anselmi, Michael, Anstey, James R., Antonini, Marta V., Antonitsis, Polychronis, Stein Araujo, Tays, Arcalas, Rhodney, Areinamo, Igor, Martin Arias, Anibal, Armijo-Garcia, Veronica, Aronsky, Vladimir, Arora, Lovkesh, Arora, Madhur, Leigh Aspenleiter, Marit, Atik, Fernando A., AugustGeorg Auzinger, Erin Colleen, Azzam, Ismail, Bacchetta, Matthew, Bak, Erica I., Balcells, Joan, Sánchez Ballesteros, Jesús, Banjac, Igor S., Barbaria, Jacqueline M., Barrigoto, Cleide L., Bass, Stephanie D., Batranović, Uroš, Bauer, Matthew H., Fernando Bautista, Diego, Beck, Robert M., Giraldo Bejarano, Estefania, Belohlavek, Jan, Bembea, Melania M., Benes, Jan, Benharash, Peyman, Benish, Lynne A., Bennett, Suzanne, Bento, Luís F.N., Bermudez, Christian A., Bertini, Pietro, Best, Derek, Bharat, Ankit, Bhutta, Omar J., Bizzell, Samantha J., Blakeman, Stephanie A., Blanco-Schweizer, Pablo, Blanton, Jessica K., Blood, Peggy S., Bohlmann, Allison S., Kyle Bohman, John, Bombino, Michela, Kathleen Bonadonna, Desiree, Bond, Ashley, Borgmann, Kristina M., Bourgoin, Pierre, Boville, Brian M., Boza, Raquel, Brady, Heather L., Brady, Alison, Braunlich, Jessica M., Bridges, Brian C., Brinkley, Karen K., Brookshire, Robert S., Brozzi Nicole Brueggemann, Nicolas A., Buckley, Dwight P., Buckley, Klayton, Budhani, Irfan B., Bukamal, Nazar, Burgos, Lucrecia M, Burša, Filip, Busby, Landon K., Buscher, Hergen, Butler, Menoly, Butt, Warwick W., Byrnes, Jonathan W., Calaritis, Christos, Caldwell, Lisa R., Calligaro, Gregory L., Campbell, Patrick T., Camporota, Luigi, Fernando Caneo, Luiz, Jovo Carapic, Vladimir, Carrasco-Carrasco, Cristina, Ivan Carrizo, Nestor, Carrow, Heidi, Carton, Edmund G., Casabella, Christian, Gomez Casal, Vanesa, Casey, Francis L., Castillo, Andres, Castleberry, Anthony W., Alexandros Cavayas, Yiorgos, Cerqua, Karey, Ming Chan, Kai Man ChanWai, Brian Chapman, Jason, Brahma Chari, Hari, Cheifetz, Omair ChaudharyIra M., Chen, Robin H.S, Chen, Weiting, Cheung, Eva W., Cheung, Anson, Chico, Juan I., Chiletti, Roberto, Jin Cho, Hwa, Cholette, Jill M., Christensen, Steffen, Chui, Betty S., Circelli, Alessandro, Clement, Katherine C., Cleuziou, Julie, Clouse, Brian, Cole, Gwendolen, Coles, Garrett M., Collins, Monika F., Collins, Monika F., Connelly, James, Conrad, Steven A., Cook, Marlene, Copeland, Hannah, Copus, Scott C., Cox, Charles S., Craig, Lynne K., Crain, Natasha, Cremonese, Ricardo V., Criswell, Emily A., Cross, Lisa M., Crowley, Moira A., Crowley, Jerome C., Cruz, Leonora, Cypel, Marcelo, Czarnik, Tomasz, Czuczwa, Miroslaw E., Sica da Rocha, Taís, Daddow, Samuel, Dali, Dante C., Dalton, Heidi J., Daly, Kathleen J.R., Damuth, Emily, Daniel, Dennis A., Daniel IV, John M., Daniel, Josiane M., Danis, Max D., Danko, Melissa E., Rodrigues Dantas, Joao Alberto, Daoust, Isabelle, Dauwe, Dieter F., Davidson, Mark, Davis, Joel C., Davis, Mitchell, D’Cunha, Jonathan, de Arruda Bravim, Bruno, de BoodeKim T. De La Cruz, Willem P., Gray DeAngelis, Kathryn, Debeuckelaere, Gerdy, Deitemyer, Matthew A., DellaVolpe, Jeffrey, Deneau, Jamie L., DeNino, Walter F., Denmark, Christopher G., Denney, Derek, DeValeria, Patrick A., Dewulf, Petra, Di Nardo, Matteo, DiBardino, Daniel J., DiMartino, Joseph, Dimopoulos, Stavros, Domico, Michele B., Dominy, Meaghan E., Donker, Dirk W., Dresbach, Till, Droogh, Joep M., Dunlap, Tiffany W., Dupon, Allsion, Durham, Lucian A., Durward, Andrew, Dvorak, Anna, Dyett, John F., Dziedzina, Carol L., Eaken, Carmen L., Eaton, Jonathan S., Eberle, Christopher J., Edwards, Linda, Efseviou, Christakis, Eigner, Juliann M., Ahmed Elhamrawi, Hazem, Elhazmi, Alyaa M., Elizondo, Tammy, Ellersick, Beverly L., Emling, Jonathan A., Ernst, Andreas, Pablo Escalante, Juan, Espinoza, Otoniel, Evey, Lee W., Fan, Eddy, Fang, Gary, Faulkner, Gail M., Fauman, Karen R, Ferguson, Niall, Ferreira, Benigno, Fiane, Arnt E., Andrade Fierro, Dario, Martha Filippi, María, Findeisen, Michael C., Finlay, Katie, Finlayson, Gordon, Fischer, Gwenyth A., Fischer, Courtney D., Fischer, William J., Fisher, Caleb M., Fitriasari, Reni, Fitzgerald, Jillian, Fix, Melissa K., Fleming, Sarah B., Flynn, Brigid C., Forst, Beth A., Fortuna, Philip P., Foti, Giuseppe, Fox, Matthew P., Franco, Thais O., David Freeland, C., Fried, Justin A., Friedman, Matthew L., Furlanetto, Beatriz, Fux, Thomas, Gaião, Sérgio, Gale, Michael J., Garcia, Joann Kathleen G., Garcia-Montilla, Romel, Gardner, Eric R., Garg, Meena, Garrison, Lawrence L., Gavrilovic, Srdjan M., Gawda, Ryszard, Geer, Laura W., Gelandt, Elton A., Gelvin, Michael G., Genovese, Bradley M., George, Jeffrey A., George, Timothy J, George, Sangley, Ghimire, Anup, Giani, Marco, Gill, Baljit S., Glikes, Erin, Golecki, Michael, Gongora, Enrique, Govener, Sara, Graf, Amanda, Grasselli, Giacomo, Gray, Brian W., Greenlee, Joseph A., Gregoric, Igor D., Gregory, Melinda, Grins, Edgars, Volker Groesdonk, Heinrich, Group, Kimberly F., Guarracino, Fabio, Joy Guidi-Solloway, Alexandra, Gunn, Tyler M., Guru, Pramod K, Haddle, John C., Haft, Jonathan W., Haisz, Emma, Hall, Julie L., Hall, Cameron, Hamaguchi, Jun, Hammond, Terese C., Han, Peggy K., Hardison, Daphne C., Harischandra, Dickwelle T., Hart, Shaun M., Harting, Matthew T., Hartley, Louise, Harvey, Chris J., Hasan, Zubair, Fawzy Hassan, Ibrahim, Hastings, Jennifer R., Hatcher, Renee’, Hatton, Kevin W., Haught, Christopher K., Awori Hayanga, Jeremiah, Peter Haydon, Timothy, Healy, Aaron H., Heard, Micheal L., Heather, Beth M., Hendrix, Rik H.J., Hennig, Felix, Hermens, Greet HermansJeannine A.J., Hernandez, Deborah A., Hernandez-Montfort, Jaime, Herrera, Guillermo, Hickman, Keri, Hittel, Ashley, Hobbs, Crystal, Hoffman, Jordan R.H., Hollinger, Laura E., Homishak, Michael, Horigoshi, Nelson K., Hoshino, Kota, Huang, Shu-Chien, Huenges, Katharina, Hussey, Alexander D., Hyslop, Robert W., Ihle, Rayan E., Ingemansson, Ola, Ivulich, Daniel, Jackson, Amanda L., Garcia Jacques, Rogelio, Jain, Harsh, Jakobs, Sharon M., Jan, Robert, Janowiak, Lisa M., Jara, Claire B., Jarden, Angela M., Jarzembowski, Jamie L., Jaudon, Andrew, Kishore Jayanthi, Venkata Krishna, Jennings, Joseph A., Jeong, Inseok, Meza Jiménez, Rafael, Jimenez-Rodriguez, Gian M., Joachim, Sabrina, Joelsons, Daniel, Johnson, Caroline A., Johnson, Andrea L., Jones, Jeffry H., Joseph, Mark, Joseph, Sunimol, Joshi, Raja, Joyce, Christopher J., Seung Jung, Jae, Carone Junior, José, Kallas, Harry J., KamerkarPilje Kang, Asavari, Kar, Biswajit, Karapanagiotidis, Georgios T., Kattan, Javier, Kaufman, David A., Kawauchi, Akira, Keene, Sarah D., Keller, Norma M., Keller, Roberta, Kelley, Emily W., Kelley, Kellie, Kelly-Geyer, Janet F., Kenderessy, Peter, Kenny, Laura E., Keshavjee, Shaf, Kessel, D., Kessler, Heather, Keuler, Suzanne, Khicha, Sanjay, Wan Kim, Do, Kim, Richard Y., Maxwell Kime, Aaron, Kincade, Robert C., Kipfmueller, Florian, Kirk, Douglas A., Klein, Liviu, Knapp, Randall S., Knapp, Randall S., Kneyber, Martin C.J., Knowles, Andrea L., Koch, Jillian M., Koepke, Stephanie, Kogelmann, Klaus M., Elzo Kraemer, Carlos, Krauklis, Amanda, Krumroy, Samantha L., Kumar, Madhan, Kumar, Arun, Kumpf, Matthias E, Kyle, Kimberly, Laffin, Anna, Kees Lagrand, Wim, Lahiji, Parshawn A., Keung Lai, Peter Chi, Ka Lai, Cally Ho, Danielle Laird, Amanda, Landsberg, Michelle LaMarreDavid M., Lanmueller, Pia, Oude Lansink-Hartgring, Annemieke, Beth Larson, Sharon, Laufenberg, De’Ann M., Lavana, Jayshree, Layne, Tracie L., John Lazar, Michael, Ledoux, Matthew R., Lee, Raymond C., Leek, Thomas M., Lequier, Laurance, Lesbekov, Timur, Leslie, Robert, Anne Leung, Kit Hung, Lillie, Jon, Phang Lim, Yeong, Lim, Sang-Hyun, Lin, Ling, Lindsey, Thomas, Ho Ling, Steven Kin, Lingle, Kaitlyn J., Lipes, Jed, Liu, Songqiao, Llevadias, Judit, Lomas, Erin A., Longenecker, Robert D., Lorusso, Roberto, Ann Low, Tracy, Steven Lubinsky, Anthony, Lucas, Matthias LubnowMark T., Lucchini, Alberto, Luze, Lisa E., Lynch, William R., Manoj, M.C., Maas, Jacinta J., MacNamara, Vanessa, Madden, Jesse L., Maimone, Justin, Malhotra, Rajiv, Malone, Matthew P., Mangukia, Chirantan, Manzur-Sandoval, Daniel, Maráczi, Veronika, Marinaro, Jonathan L., Marinucci, Christina R., Marshall, Tammy, Martin, Mark, Marwali, Eva M., Maslach-Hubbard, Anna, Matijašević, Jovan, Mattke, Adrian, Mattucci, Joseph, Maul, Timothy M., Maybauer, Marc O., Mayette, Michael, Mayville, Joni R., McAllister, Catherine, McBride, Martha W., Scott McCaul, David, McClelland, Samantha L.S., Gregory McCloskey, Colin, McGregor, Randy, McKamie, Wesley A., McKee, Andrew D., McMahon, Chelsea M., McMullin, Kaye, McNicol, Jane, McNulty, John P., McRae, Thomas, Meade, Maureen E., Meersseman, Philippe, Mekeirele, Michael, Ito Mendes, Elisa, Menon, Anuradha P., Meyer, Jason P., Meyers, Jourdan E., Meyns, Bart, Mignone, John L., Miller, Brittany D., Miller, Malcolm G.A., Miller, Deborah, Mintak, Renee, Minter, Sarah M., Reis Miranda, Dinis, Mirza, Farrukh, Mishkin, Joseph D., Modelewski, Paul, Mohan, Rajeev C., Hui Mok, Yee, Money, Dustin, Monteagudo, Julie, Moores, Russell R., Moran, Patrick, Morelock, Shawn, Moreno, Marsha R., Blanco Morillo, Juan, Morrison, Tracy, Morton, John M., Morton, Brenda, Moscatelli, Andrea, Mosier, Jarrod M., Muellenbach, Ralf M., Mueller, Andreas, Mueller, Dale, Musca, Steven C., Nagpal, Dave, Najaf, Tasnim, Narasimhan, Mangala, Nater, Melissa, Natividad, Zynthia, Nedeljkov, Djordje, Nelson, Bryan D., Newman, Sally F., Newton, Debra E., Neyman, Jonathan L., George Ng, Wing Yiu, Nicholson, Meghan C., Nicolaas, Christine, Nix, Charlie, Nkwantabisa, Raymond, Nolan, Shirley, Norese, Mariano, Norton, Bridget M., Norton, Bridget M., O’Brien, Serena G., O’Callaghan, Maura, Oishi, Peter, O’Leary, Tony D., Olia, Salim E., O’Meara, Carlisle, Oppel, Emily E., Arias Ortiz, Julian, Oza, Pranay L., Ozment, Caroline P., Pacific, Marjorie, Pálizas, Fernando, Palmer, David, Paoletti, Luca, Pardo, Diego H., Paredes, Pablo, Patel, Thomas PasgaardMrunal G., Patel, Sandeep M., Patel, Vijay S., Patel, Brijesh V., PatelDrisya Paul, Sameer, Pawale, Amit A., Pearson, Nicole M., Renee Pearson, Crystal, Peek, Giles J., Pellecchia, Crescens M., Pellegrino, Vincent, Peperstraete, Harlinde, Perkins, Rebecca L., Perkins, Brandon, Peterec, Steven, Peterman, Claire, Phillips, Cooper W., Piekutowski, Richard R., Pilan, María L., Luisa Pilan, Maria, Mark Pincus, Jason, Pino, Melissa, Plambeck, Robert W., Plisco, Michael S., Plumley, Donald A., Plunkett, Mark D., Poffo, Robinson, Poh, Pei-Fen, Polito, Angelo, Pollema, Travis L, Pozzi, Matteo, Pozzi, Matteo, Pranikoff, Thomas, Prekker, Matthew E., Prossen, Erik F., Puligandla, Pramod S., Puslecki, Mateusz, Raheel Qureshi, Muhammad, Emilia Rabanal, Lily, Abdulhamid Rabie, Ahmed, Rackley, Craig R., Radovancevic, Rajko, Raes, Matthias, Allen Raff, Lauren Desiree, Rahban, Youssef, Raimer, Patricia L., Rajbanshi, Bijoy G., Ramanan, Raj, Rambaud, Jerome, Ramírez-Arce, Jorge A., Simões Ramos, Ana Carolina, Rao, Suresh G., Rector, Raymond, Redfors, Bengt, Regmi, Ashim, Alejandro Rey, Jose, Miguel Ribeiro, Joao, Richards, Chelsea E, Joan Richardson, C., Riddle, Christy C., Riera, Jordi, Ripardo, Marina, Rivas, Fernando M., Roan, Ronald M., Robertson, Elizabeth, Robinson, Megan, Röder, Daniel, Rodrigus, Inez E.R., Paul Roeleveld, Peter, Romano, Jennifer C., Rona, Roberto, Ann Rosenberg, Carol, Rosenow, Felix, Rowe, Robert J., Rower, Katy E., Rudolph, Kristina L., Fernando Rueda, Luis, Ruf, Bettina, Russell, Hyde M., Russell, Nichole, Ryan, Kathleen, Saberi, Asif A., Said, Ahmed S., Sailor, Caitlin, Sakal, Angela, Lujan Salas, Gisela, Salazar, Leonardo, Saleem, Kashif, Samoukovic, Gordan, Sanchez, Pablo G., Marie Santiago, Lian, Sargin, Murat, Miguel Sassine, Assad, Satou, Nancy L., Saunders, Paul C., Schachinger, Scott, Schaible, Thomas, Schellongowski, Peter, Schlager, Gerald W., Schmid, Christof, Schmitt, Joachim, Schnell, LeeAndra, Schnur, Janos, Schroeder, Lukas, Schubach, Scott, Schuetz, Michael T., Schwartz, Gary S., Schwarz, Patricia, Scriven, Nicole M., Seabrook, Ruth B., Seefeldt, Cassandra, Seelhammer, Troy G., Segura-Matute, Susana, Sen, Ayan, Adrian Seoane, Leonardo, Shaffer, Jamie, Shafi, Bilal M., Shambley, Shannon, Shankar, Shyam, Shapland, Amanda, Sharng, Yih, Shavelle, David, Sheldrake, Jayne, Mohan Shetty, Rajesh, Shiber, Joseph R., Shimzu, Naoki, Lou Short, Billie, Sichting, Kay A., Sidehamer, Keith E., Siebenaler, Teka, Silvestry, Scott C., Sinclair, Jennifer T, Sinclair, Andrew, Singh, Aalok R., Singh, Gurmeet, Skinner, Sean C., Smart, Alexandra, Smith, Reanna M., Smith, Adam, Smith, Karen, Sommer-Candelario, Sherri, Song, Seunghwan, Sorensen, Gro, Sousa, Eduardo, Sower, Christopher T., Spadea, Nicholas V, Spangle, April, Speicher, David G., Spieth, Peter M., Srivastava, Ankur, Srivastava, Neeraj, Stahl, Mark, Stallkamp, Eric D., Stanley, Vanessa J., Starr, Joanne P., Staudinger, Thomas, Stevens, Berkeley E., Stevens, Kimberly, Stocker, Christian, Strickland, Richard, Suarez, Erik E., Kumar Subramanian, Rakesh, Sudakevych, Serhii, Summerall, Charlene, Sundararajan, Santosh, Susupaus, Attapoom, Suzuki, Hiroyuki, Sweberg, Todd, Sydzyik, Troy, Anh Ta, Tuan, Tagliari, Luciana, Tanaka, Hiroyuki, Tanski, Christopher T., Tasset, Mark, Taylor, Donna M., Teman, Nicholas R., Ramesh Thangaraj, Paul, Thiagarajan, Ravi R., Thiruchelvam, Timothy, Thomas, James A., Thomas, Owain D., Thompson, Shaun L., Thomson, David A., Thukaram, Roopa, Todd, Mark L., Toeg, Hadi, Torres, Silvio F., Trautner, Simon, Trombino, Terry, Tuazon, Divina M., Tuel, Julie, Tukacs, Monika, Turner, April N., Tyree, Melissa M., Uchiyama, Makoto, Vaijyanath, Prashant, van den Brule, Judith M.D., van Dyck, Marlice A., van Gijlswijk, Mascha, Van Meurs, Krisa P., VanDyck, Tyler J., Vardi, Amir, Vega, Alejandra, Ventetuolo, Corey E., Vera, Magdalena, Vercaemst, Leen, Vets, Philippe, Viamonte, Heather, Vidlund, Mårten, Vitali, Sally H., Vlaa, Alexander P.J., Vuylsteke, Alain, Loon Wan, Kah, Watkins, Reuben, Watson, Pia, Weast, Travis A., Weaver, Karen E., Welkovics, Norbert, Wellner, Heidi L., Wells, Jason C., Welter, Karen, Westpheling, Amber G., Whalen, Lesta D.S., Whebell, Stephen, Wiersema, Ubbo, Wiisanen, Matthew E., Eugene Wilcox, Bradley, Wille, Keith, Jan Will, Ellyne, Wilson, Brock J., Win, April M., Winearls, James R., Wise, Linda J., Witter, Tobias, Ruby Wong, Hoi Mei, Worku, Berhane, Wright, Tina M, Wu, James K., Yalon, Larissa A., Yantosh, Garrett, Yaranov, Dmitry M., Yee, Pat, Yi, Cassia, Yost, Christian C., Young, John, Younger, Katrina, Zaborowski, Steven, Zachmann, Brenda, Zainab, Asma, Zanai, Rosanna, Zhao, Ju, Zhou, Chengbin, and Zinger, Marcia

Abstract

The Extracorporeal Life Support Organization (ELSO) maintains the world’s largest extracorporeal membrane oxygenation (ECMO) registry by volume, center participation, and international scope. This 2022 ELSO Registry Report describes the program characteristics of ECMO centers, processes of ECMO care, and reported outcomes. Neonates (0–28 days), children (29 days–17 years), and adults (≥18 years) supported with ECMO from 2009 through 2022 and reported to the ELSO Registry were included. This report describes adjunctive therapies, support modes, treatments, complications, and survival outcomes. Data are presented descriptively as counts and percent or median and interquartile range (IQR) by year, group, or level. Missing values were excluded before calculating descriptive statistics. Complications are reported per 1,000 ECMO hours. From 2009 to 2022, 154,568 ECMO runs were entered into the ELSO Registry. Seven hundred and eighty centers submitted data during this time (557 in 2022). Since 2009, the median annual number of adult ECMO runs per center per year increased from 4 to 15, whereas for pediatric and neonatal runs, the rate decreased from 12 to 7. Over 50% of patients were transferred to the reporting ECMO center; 20% of these patients were transported with ECMO. The use of prone positioning before respiratory ECMO increased from 15% (2019) to 44% (2021) for adults during the coronavirus disease-2019 (COVID-19) pandemic. Survival to hospital discharge was greatest at 68.5% for neonatal respiratory support and lowest at 29.5% for ECPR delivered to adults. By 2022, the Registry had enrolled its 200,000th ECMO patient and 100,000th patient discharged alive. Since its inception, the ELSO Registry has helped centers measure and compare outcomes across its member centers and strategies of care. Continued growth and development of the Registry will aim to bolster its utility to patients and centers.

Published
2024
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16. Red blood cell eNOS is cardioprotective in acute myocardial infarction

Author

Cortese-Krott, Miriam M., primary, Suvorava, Tatsiana, additional, Leo, Francesca, additional, Heuser, Sophia K., additional, LoBue, Anthea, additional, Li, Junjie, additional, Becher, Stefanie, additional, Schneckmann, Rebekka, additional, Srivrastava, Tanu, additional, Erkens, Ralf, additional, Wolff, Georg, additional, Schmitt, Joachim P., additional, Grandoch, Maria, additional, Lundberg, Jon O., additional, Pernow, John, additional, Isakson, Brant E., additional, Weitzberg, Eddie, additional, and Kelm, Malte, additional

Published
2022
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17. Downregulation of eNOS and preserved endothelial function in endothelial-specific arginase 1-deficient mice

Author

Heuser, Sophia K., primary, LoBue, Anthea, additional, Li, Junjie, additional, Zhuge, Zhengbing, additional, Leo, Francesca, additional, Suvorava, Tatsiana, additional, Olsson, Annika, additional, Schneckmann, Rebekka, additional, Guimaraes Braga, Drielle D., additional, Srivrastava, Tanu, additional, Montero, Lidia, additional, Schmitz, Oliver J., additional, Schmitt, Joachim P., additional, Grandoch, Maria, additional, Weitzberg, Eddie, additional, Lundberg, Jon O., additional, Pernow, John, additional, Kelm, Malte, additional, Carlström, Mattias, additional, and Cortese-Krott, Miriam M., additional

Published
2022
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18. Cardiac RKIP induces a beneficial [beta]-adrenoceptor-dependent positive inotropy

Author

Schmid, Evelyn, Neef, Stefan, Berlin, Christopher, Tomasovic, Angela, Kahlert, Katrin, Nordbeck, Peter, Deiss, Katharina, Denzinger, Sabrina, Herrmann, Sebastian, Wettwer, Erich, Weidendorfer, Markus, Becker, Daniel, Schäfer, Florian, Wagner, Nicole, Ergün, Süleyman, Schmitt, Joachim P, Katus, Hugo A, Weidemann, Frank, Ravens, Ursula, Maack, Christoph, Hein, Lutz, Ertl, Georg, Müller, Oliver J, Maier, Lars S, Lohse, Martin J, and Lorenz, Kristina

Subjects
Heart failure -- Care and treatment, Nervous system -- Management, Phosphorylation -- Research, Echocardiography -- Usage, Genetically modified mice -- Research, Company business management, Biological sciences, Health
Abstract

In heart failure therapy, it is generally assumed that attempts to produce a long-term increase in cardiac contractile force are almost always accompanied by structural and functional damage. Here we show that modest overexpression of the Raf kinase inhibitor protein (RKIP), encoded by Pebp1 in mice, produces a well-tolerated, persistent increase in cardiac contractility that is mediated by the [beta][sub.1]-adrenoceptor ([beta][sub.1]AR). This result is unexpected, as [beta][sub.1]AR activation, a major driver of cardiac contractility, usually has long-term adverse effects. RKIP overexpression achieves this tolerance via simultaneous activation of the [beta][sub.2]AR subtype. Analogously, RKIP deficiency exaggerates pressure overload-induced cardiac failure. We find that RKIP expression is upregulated in mouse and human heart failure, indicative of an adaptive role for RKIP. Pebp1 gene transfer in a mouse model of heart failure has beneficial effects, suggesting a new therapeutic strategy for heart failure therapy., Author(s): Evelyn Schmid [1]; Stefan Neef [2]; Christopher Berlin [1]; Angela Tomasovic [1]; Katrin Kahlert [1]; Peter Nordbeck [3, 4]; Katharina Deiss [1]; Sabrina Denzinger [1]; Sebastian Herrmann [3, 4]; [...]

Published
2015
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21. Inducible over‐expression of cardiac Nos1ap causes short QT syndrome in transgenic mice.

Author

Jänsch, Monique, Lubomirov, Lubomir T., Trum, Maximilian, Williams, Tatjana, Schmitt, Joachim, Schuh, Kai, Qadri, Fatimunnisa, Maier, Lars S., Bader, Michael, and Ritter, Oliver

Subjects
ARRHYTHMIA, TRANSGENIC mice, CALCIUM channels, NITRIC-oxide synthases, ION channels, CARDIAC arrest, VENTRICULAR arrhythmia
Abstract

Recent evidence demonstrated that alterations in the QT interval duration on the ECG are not only determined by mutations in genes for ion channels, but also by modulators of ion channels. Changes in the QT interval duration beyond certain thresholds are pathological and can lead to sudden cardiac death. We here focus on the ion channel modulator nitric oxide synthase 1 adaptor protein (Nos1ap). Whole‐cell patch‐clamp measurements of a conditional transgenic mouse model exhibiting cardiac‐specific Nos1ap over‐expression revealed a Nos1ap‐dependent increase of L‐type calcium channel nitrosylation, which led to increased susceptibility to ventricular tachycardias associated with a decrease in QT duration and shortening of APD90 duration. Survival was significantly reduced (60% after 12 weeks vs. 100% in controls). Examination of the structural features of the hearts of transgenic mice revealed constant heart dimensions and wall thickness without abnormal fibrosis content or BNP production after 3 months of Nos1ap over‐expression compared to controls. Nos1ap over‐expression did not alter cGMP production or ROS concentration. Our study showed that myocardial over‐expression of Nos1ap leads to the shortening of the QT interval and reduces the survival rate of transgenic animals, perhaps via the development of ventricular arrhythmias. We conclude that Nos1ap overexpression causes targeted subcellular localization of Nos1 to the CaV1.2 with a subsequent decrease of ADP90 and the QT interval. This causes detrimental cardiac arrhythmias in transgenic mice. [ABSTRACT FROM AUTHOR]

Published
2023
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24. Cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non-myocyte proliferation and requires Tgf-β

Author

Teekakirikul, Polakit, Eminaga, Seda, Toka, Okan, Alcalai, Ronny, Wang, Libin, Wakimoto, Hiroko, Nayor, Matthew, Konno, Tetsuo, Gorham, Joshua M., Wolf, Cordula M., Kim, Jae B., Schmitt, Joachim P., Molkentin, Jefferey D., Norris, Russell A., Tager, Andrew M., Hoffman, Stanley R., Markwald, Roger R., Seidman, Christine E., and Seidman, Jonathan G.

Subjects
Gene expression -- Research -- Usage -- Genetic aspects -- Physiological aspects, Cardiomyopathy, Hypertrophic -- Risk factors -- Genetic aspects -- Research -- Care and treatment, Fibrosis -- Genetic aspects -- Risk factors -- Care and treatment -- Research, Immunohistochemistry -- Usage -- Research -- Physiological aspects, Transforming growth factors -- Physiological aspects -- Genetic aspects -- Research -- Usage, Health care industry
Abstract

Mutations in sarcomere protein genes can cause hypertrophic cardiomyopathy (HCM), a disorder characterized by myocyte enlargement, fibrosis, and impaired ventricular relaxation. Here, we demonstrate that sarcomere protein gene mutations activate proliferative and profibrotic signals in non-myocyte cells to produce pathologic remodeling in HCM. Gene expression analyses of non-myocyte cells isolated from HCM mouse hearts showed increased levels of RNAs encoding cell-cycle proteins, Tgf- β, periostin, and other profibrotic proteins. Markedly increased BrdU labeling, Ki67 antigen expression, and periostin immunohistochemistry in the fibrotic regions of HCM hearts confirmed the transcriptional profiling data. Genetic ablation of periostin in HCM mice reduced but did not extinguish non-myocyte proliferation and fibrosis. In contrast, administration of Tgf-β-neutralizing antibodies abrogated non-myocyte proliferation and fibrosis. Chronic administration of the angiotensin II type 1 receptor antagonist losartan to mutation-positive, hypertrophy-negative (prehypertrophic) mice prevented the emergence of hypertrophy, non-myocyte proliferation, and fibrosis. Losartan treatment did not reverse pathologic remodeling of established HCM but did reduce non-myocyte proliferation. These data define non-myocyte activation of Tgf-β signaling as a pivotal mechanism for increased fibrosis in HCM and a potentially important factor contributing to diastolic dysfunction and heart failure. Preemptive pharmacologic inhibition of Tgf-β signals warrants study in human patients with sarcomere gene mutations., Introduction Dominant mutations in sarcomere protein genes cause hypertrophic cardiomyopathy (HCM), a primary myocardial disorder characterized by myocyte enlargement, increased myocardial fibrosis, and impaired ventricular relaxation that predisposes patients to [...]

Published
2010
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25. A new type of ERK1/2 autophosphorylation causes cardiac hypertrophy

Author

Lorenz, Kristina, Schmitt, Joachim P., Schmitteckert, Eva M., and Lohse, Martin J.

Subjects
Gene expression -- Research, Heart enlargement -- Risk factors, Heart enlargement -- Genetic aspects, Heart enlargement -- Research, Phosphorylation -- Research, Protein kinases -- Physiological aspects, Protein kinases -- Research
Abstract

The extracellular-regulated kinases ERK1 and ERK2 (commonly referred to as ERK1/2) have a crucial role in cardiac hypertrophy. ERK1/2 is activated by mitogen-activated protein kinase kinase-1 (MEK1) and MEK2 (commonly referred to as MEK1/2)-dependent phosphorylation in the TEY motif of the activation loop, but how ERK1/2 is targeted toward specific substrates is not well understood. Here we show that autophosphorylation of ERK1/2 on Thr188 directs ERK1/2 to phosphorylate nuclear targets known to cause cardiac hypertrophy. Thr188 autophosphorylation requires the activation and assembly of the entire Raf-MEK-ERK kinase cascade, phosphorylation of the TEY motif, dimerization of ERK1/2 and binding to G protein [beta][gamma] subunits released from activated [G.sub.q]. Thr188 phosphorylation of ERK1/2 was observed in isolated cardiomyocytes induced to undergo hypertrophic growth, in mice upon stimulation of [G.sub.q]-coupled receptors or after aortic banding and in failing human hearts. Experiments using transgenic mouse models carrying mutations at the Thr188 phosphorylation site of ERK2 suggested a causal relationship to cardiac hypertrophy. We propose that specific phosphorylation events on ERK1/2 integrate differing upstream signals (Raf1-MEK1/2 or G protein-coupled receptor-[G.sub.q]) to induce cardiac hypertrophy., Cardiac hypertrophy occurs in response to increased mechanical load on the heart and through the action of several hormones and mediators (1-3). It involves increased protein synthesis, cardiomyocyte growth and [...]

Published
2009

30. Differential cross-bridge kinetics of FHC myosin mutations R403Q and R453C in heterozygous mouse myocardium

Author

Palmer, Bradley M., Fishbaugher, David E., Schmitt, Joachim P., Wang, Yuan, Alpert, Norman R., Seidman, Christine E., Seidman, J.G., VanBuren, Peter, and Maughan, David W.

Subjects
Myosin -- Research, Biological sciences
Abstract

The kinetic effects of the cardiac myosin point mutations R403Q and R453C, which underlie lethal forms of familial hypertrophic cardiomyopathy (FHC), were assessed using isolated myosin and skinned strips taken from beterozygous (R403Q/+ and R453C/+) male mouse hearts. Compared with wild-type (WT) mice, actin-activated ATPase was increased by 38% in R403Q/+ and reduced by 45% in R453C/+, maximal velocity of regulated thin filament ([V.sub.RTF]) in the in vitro motility assay was increased by 8% in R403Q/+ and was not different in R453C/+, myosin concentration at half-maximal [V.sub.RTF] was reduced by 30% in R403Q/+ and not different in R453C/+, and the characteristic frequency for oscillatory work production (b frequency), determined by sinusoidal analysis in the skinned strip at maximal calcium activation, was 27% lower in R403Q/+ and 18% higher in R453C/+. The calcium sensitivity for isometric tension in the skinned strip was not different in R403Q/+ (p[Ca.sub.50] 5.64 [+ or -] 0.02) and significantly enhanced in R453C/+ (5.82 [+ or -] 0.03) compared with WT (5.58 [+ or -] 0.02). We conclude that isolated myosin and skinned strips of R403Q/+ and R453C/+ myocardium show marked differences in cross-bridge kinetic parameters and in calcium sensitivity of force production that indicate different functional roles associated with the location of each point mutation at the molecular level. myosin heavy chain; ATPase; myosin motility; isometric tension; sinusoidal analysis

Published
2004

32. A murine model of Holt-Oram syndrome defines roles of the T-box transcription factor Tbx5 in cardiogenesis and disease

Author

Bruneau, Benoit G., Nemer, Georges, Schmitt, Joachim P., Charron, Frederic, Robitaille, Lynda, Caron, Sophie, Conner, David A., Gessler, Manfred, Nemer, Mona, Seidman, Christine E., and Seidman, J. G.

Subjects
Cell research -- Analysis, Genetic transcription -- Genetic aspects, Proteins -- Genetic aspects, Gene mutations -- Physiological aspects, Cardia -- Genetic aspects, Biological sciences
Abstract

Research has been conducted on the T-box proteins. The role of these proteins in cardiac development and the consequences of the TBX5 mutations have been investigated via the engineered mice containing a deletion in Tbx5 alleles and the results are discussed.

Published
2001

36. Raf kinase inhibitor protein: lessons of a better way for β-adrenergic receptor activation in the heart

Author

Lorenz, Kristina, Rosner, Marsha Rich, Brand, Theresa, and Schmitt, Joachim P

Subjects
Medizin
Abstract

Stimulation of β-adrenergic receptors (βARs) provides the most efficient physiological mechanism to enhance contraction and relaxation of the heart. Activation of βARs allows rapid enhancement of myocardial function in order to fuel the muscles for running and fighting in a fight-or-flight response. Likewise, βARs become activated during cardiovascular disease in an attempt to counteract the restrictions of cardiac output. However, long-term stimulation of βARs increases the likelihood of cardiac arrhythmias, adverse ventricular remodelling, decline of cardiac performance and premature death, thereby limiting the use of βAR agonists in the treatment of heart failure. Recently the endogenous Raf kinase inhibitor protein (RKIP) was found to activate βAR signalling of the heart without adverse effects. This review will summarize the current knowledge on RKIP-driven compared to receptor-mediated signalling in cardiomyocytes. Emphasis is given to the differential effects of RKIP on β₁- and β₂-ARs and their downstream targets, the regulation of myocyte calcium cycling and myofilament activity. OA hybrid - CA Lorenz

Published
2017

37. Corrigendum to ‘Impaired Ca2+ cycling of nonischemic myocytes contributes to sarcomere dysfunction early after myocardial infarction’ [J. Mol. Cell. Cardiol. 119 (2018) 28–39]

Author

Kronenbitter, Annette, primary, Funk, Florian, additional, Hackert, Katarzyna, additional, Gorreßen, Simone, additional, Glaser, Dennis, additional, Boknik, Peter, additional, Poschmann, Gereon, additional, Stühler, Kai, additional, Isić, Malgorzata, additional, Krüger, Martina, additional, and Schmitt, Joachim P., additional

Published
2018
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39. Adaptive Ventricular Remodelling after Myocardial Infarction Involves Titin-Based Cardiomyocyte Stiffening and Elevated Titin Turnover

Author

Kötter, Sebastian, primary, Kazmierowska, Malgorzata, additional, Andresen, Christian, additional, Bottermann, Katharina, additional, Grandoch, Maria, additional, Gorressen, Simone, additional, Heinen, Andre, additional, Moll, Jens M., additional, Scheller, Jürgen, additional, Gödecke, Axel, additional, Fischer, Jens W., additional, Schmitt, Joachim P., additional, and Krüger, Martina, additional

Published
2017
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40. Titin-Based Cardiac Myocyte Stiffening Contributes to Early Adaptive Ventricular Remodeling After Myocardial Infarction

Author

Kötter, Sebastian, primary, Kazmierowska, Malgorzata, additional, Andresen, Christian, additional, Bottermann, Katharina, additional, Grandoch, Maria, additional, Gorressen, Simone, additional, Heinen, Andre, additional, Moll, Jens M., additional, Scheller, Jürgen, additional, Gödecke, Axel, additional, Fischer, Jens W., additional, Schmitt, Joachim P., additional, and Krüger, Martina, additional

Published
2016
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41. Erratum: Cardiac RKIP induces a beneficial β-adrenoceptor–dependent positive inotropy

Author

Schmid, Evelyn, primary, Neef, Stefan, additional, Berlin, Christopher, additional, Tomasovic, Angela, additional, Kahlert, Katrin, additional, Nordbeck, Peter, additional, Deiss, Katharina, additional, Denzinger, Sabrina, additional, Herrmann, Sebastian, additional, Wettwer, Erich, additional, Weidendorfer, Markus, additional, Becker, Daniel, additional, Schäfer, Florian, additional, Wagner, Nicole, additional, Ergün, Süleyman, additional, Schmitt, Joachim P, additional, Katus, Hugo A, additional, Weidemann, Frank, additional, Ravens, Ursula, additional, Maack, Christoph, additional, Hein, Lutz, additional, Ertl, Georg, additional, Müller, Oliver J, additional, Maier, Lars S, additional, Lohse, Martin J, additional, and Lorenz, Kristina, additional

Published
2016
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42. Cardiac RKIP induces a beneficial β-adrenoceptor–dependent positive inotropy

Author

Schmid, Evelyn, primary, Neef, Stefan, additional, Berlin, Christopher, additional, Tomasovic, Angela, additional, Kahlert, Katrin, additional, Nordbeck, Peter, additional, Deiss, Katharina, additional, Denzinger, Sabrina, additional, Herrmann, Sebastian, additional, Wettwer, Erich, additional, Weidendorfer, Markus, additional, Becker, Daniel, additional, Schäfer, Florian, additional, Wagner, Nicole, additional, Ergün, Süleyman, additional, Schmitt, Joachim P, additional, Katus, Hugo A, additional, Weidemann, Frank, additional, Ravens, Ursula, additional, Maack, Christoph, additional, Hein, Lutz, additional, Ertl, Georg, additional, Müller, Oliver J, additional, Maier, Lars S, additional, Lohse, Martin J, additional, and Lorenz, Kristina, additional

Published
2015
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46. INHIBITION OF CARDIAC FIBROSIS MEDIATED BY NON-MYOCYTE PROLIFERATION IN HYPERTROPHIC CARDIOMYOPATHY

Author

Teekakirikul, Polakit, primary, Eminaga, Seda, additional, Toka, Okan, additional, Wang, Libin, additional, Wakimoto, Hiroko, additional, Nayor, Matthew, additional, Konno, Tetsuo, additional, Wolf, Cordula M., additional, Alcalai, Ronny, additional, Gorham, Joshua, additional, Schmitt, Joachim P., additional, Caine, Brendan, additional, Markwald, Roger R., additional, Hoffman, Standley R., additional, Molkentin, Jeffery D., additional, Seidman, Christine E., additional, and Seidman, Jonathan G., additional

Published
2010
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