5 results on '"Barry Cabuay"'
Search Results
2. List of Contributors
- Author
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Samer Abbas, Shuaib Abdullah, Hasan Ahmad, Gorav Ailawadi, Wail Alkashkari, Osama Alsanjari, Jason H. Anderson, Judah Askew, Luis Asmarats, Ganesh Athappan, Rizwan Attia, Vasilis Babaliaros, Richard Y. Bae, Charles M. Baker, Subhash Banerjee, Vinayak N. Bapat, Colin M. Barker, Itsik Ben-Dor, Stefan Bertog, Phillipe Blanke, Peter Block, Patrick Boehm, Stephen Brecker, Emmanouil S. Brilakis, Marcus Burns, Christian Butter, Allison K. Cabalka, Barry Cabuay, Alex Campbell, John D. Carroll, Anson W. Cheung, Adnan K. Chhatriwalla, Martin Cohen, Mauricio G. Cohen, Frank Corrigan, Cameron Dowling, Tanya Dutta, Mackram Eleid, Robert Saeid Farivar, Ted Feldman, Thomas Flavin, Jessica Forcillo, Jennifer Franke, Sameer Gafoor, Evaldas Girdauskas, Steven L. Goldberg, Mario Gössl, Mayra Guerrero, Alexander Haak, Cameron Hague, Eva Harmel, Ziyad Hijazi, David Hildick-Smith, Ilona Hofmann, Samuel E. Horr, Nay M. Htun, Shaw Hua (Anthony) Kueh, Vladimir Jelnin, Brandon M. Jones, Ravi Joshi, Rami Kahwash, Ankur Kalra, Norihiko Kamioka, Samir R. Kapadia, Ryan K. Kaple, Judit Karacsonyi, Marc R. Katz, John J. Kelly, Samuel Kessel, Ung Kim, Neal S. Kleiman, Thomas Knickelbine, Amar Krishnaswamy, Vibhu Kshettry, Shaw-Hua Kueh, Ivandito Kuntijoro, Shingo Kuwata, Jonathon Leipsic, Stamatios Lerakis, John R. Lesser, Scott M. Lilly, D. Scott Lim, David Lin, Francesco Maisano, Gurdeep Mann, Christopher Meduri, Stephanie Mick, Michael Mooney, Aung Myat, Srihari S. Naidu, Michael Neuss, Fabian Nietlispach, Mickaël Ohana, Ioannis Parastatidis, Tilak K.R. Pasala, Ateet Patel, Paul Pearson, Wesley R. Pedersen, François Philippon, Augusto Pichard, Anil Poulose, Alberto Pozzoli, Matthew J. Price, Vivek Rajagopal, Claire Raphael, Michael J. Reardon, Evelyn Regar, Josep Rodés-Cabau, Jason H. Rogers, Carlos E. Ruiz, Michael Salinger, Muhamed Saric, Lowell Satler, Jacqueline Saw, Lynelle Schneider, Atman P. Shah, Rahul Sharma, Mark Victor Sherrid, Joy S. Shome, Horst Sievert, Gagan D. Singh, Thomas W. Smith, Benjamin Sun, Hussam Suradi, Gilbert H.L. Tang, Maurizio Taramasso, Jay Thakkar, Vinod H. Thourani, Stacey Tonne, Imre Ungi, Laura Vaskelyte, Joseph M. Venturini, Marko Vezmar, Ron Waksman, Zuyue Wang, John Graydon Webb, Dominik M. Wiktor, and Mathew R. Williams
- Published
- 2019
3. Accelerated Allograft Vasculopathy With Rituximab After Cardiac Transplantation
- Author
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Randall C. Starling, Brian Armstrong, Nancy D. Bridges, Howard Eisen, Michael M. Givertz, Abdallah G. Kfoury, Jon Kobashigawa, David Ikle, Yvonne Morrison, Sean Pinney, Josef Stehlik, Sudipta Tripathi, Mohamed H. Sayegh, Anil Chandraker, Barbara Gus, Karen Keslar, Bill Magyar, John Petrich, W. H. Wilson Tang, Kimberly Brooks, Michael Givertz, Charles Kelly, Katie Klein, Kerry Crisalli, Sandra DeBronkart, Joren Madsen, Marc Semigran, John Vetrano, Teresa DeMarco, Scott Fields, Carol Maguire, Robert Gordon, Allen Anderson, Jane Regalado, Anna Warzecha, Lee Goldberg, Caroline Olt, Kenneth Rockwell, Ashley Harris, Maryl Johnson, Susan Johnston, Chris Roginski, Rashid Ahmed, Ivy Cohen, Denise Peace, Tina Yao, Gloria Araujo, Arvind Bhimaraj, Eunice Karanga, Varsha Patel, Julie Chait, Mario Deng, Gregg Fonarow, Christina Shin, Charles Gibbs, Judson Hunt, Melissa Johnson, Tina Worley, Jeff Gibbs, John Kirk, Winter Redd, Julia Bryan, Anna French, A.G. Kfoury, Kristin Konery, Erika Feller, Myounghee Lee, Richard Pierson, Cindi Young, Theodora Hollifield, Kimberley Porter, Mariann Schulz, Adrian VanBakel, Kiran Khush, Helen Luikart, Son Nguyen, Michael Pham, David DeNofrio, Ryan O’Kelly, Lucilla Garcia, Sean Sana, Brandy Starks, Maria Thottam, Annie Yi, Barry Cabuay, Rachel Olson, Larry Tucker, Laura Uppgaard, Denise Lai, Colleen Poisker, Klaudija Dragicevic, Harrison Kelner, Darlette Luke, Jennifer Nelson, Ganesh Raveendran, Nick Kleissas, Srinivas Murali, Kenneth Rayl, Sarah Sherry, and Michele Cosgrove
- Subjects
Adult ,Male ,medicine.medical_specialty ,medicine.medical_treatment ,Population ,030204 cardiovascular system & hematology ,Placebo ,Gastroenterology ,03 medical and health sciences ,Young Adult ,0302 clinical medicine ,Postoperative Complications ,Double-Blind Method ,hemic and lymphatic diseases ,Internal medicine ,Intravascular ultrasound ,medicine ,Humans ,Immunologic Factors ,030212 general & internal medicine ,Prospective Studies ,Vascular Diseases ,education ,CD20 ,education.field_of_study ,medicine.diagnostic_test ,biology ,business.industry ,Immunosuppression ,Middle Aged ,Allografts ,Transplantation ,Clinical trial ,biology.protein ,Heart Transplantation ,Rituximab ,Female ,Cardiology and Cardiovascular Medicine ,business ,medicine.drug - Abstract
Background The CTOT-11 (Prevention of Cardiac Allograft Vasculopathy Using Rituximab Therapy in Cardiac Transplantation [Clinical Trials in Organ Transplantation-11]) study was a randomized, placebo-controlled, multicenter, double-blinded clinical trial in nonsensitized primary heart transplant (HTX) recipients. Objectives The study sought to determine whether B cell depletion therapy would attenuate the development of cardiac allograft vasculopathy. Methods A total of 163 HTX recipients were randomized to rituximab 1,000 mg intravenous or placebo on days 0 and 12 post-transplant. Primary outcome was change in percent atheroma volume (PAV) from baseline to 1 year measured by intravascular ultrasound. Secondary outcomes included treated episodes of acute rejection, de novo anti-HLA antibodies (including donor-specific antibodies), and phenotypic differentiation of B cells. Results There were no significant differences at study entry between the rituximab and placebo groups. Paired intravascular ultrasound measures were available at baseline and 1 year in 86 subjects (49 rituximab, 37 placebo). The mean ± SD change in PAV at 12 months was +6.8 ± 8.2% rituximab versus +1.9 ± 4.4% placebo (p = 0.0019). Mortality at 12 months was 3.4% rituximab versus 6.8% placebo (p = 0.47); there were no retransplants or post-transplant lymphoproliferative disorder. The rate of treated rejection was 24.7% rituximab versus 32.4% placebo (p = 0.28). Rituximab therapy effectively eliminated CD20+/CD19+ B cells followed by a gradual expansion of a CD19– cell population in the rituximab-treated group. Conclusions A marked, unexpected increase in coronary artery PAV with rituximab was observed during the first year in HTX recipients. One-year mortality was not impacted; however, longer-term follow-up and mechanistic explanations are required. (Prevention of Cardiac Allograft Vasculopathy Using Rituximab [Rituxan] Therapy in Cardiac Transplantation; NCT01278745)
- Published
- 2018
4. Door-to-VAD time: an expedient management strategy for cardiogenic shock
- Author
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Barry, Cabuay, Katarzyna, Hryniewicz, Benjamin, Sun, and David, Feldman
- Subjects
Time Factors ,Shock, Cardiogenic ,Humans ,Heart-Assist Devices ,Severity of Illness Index - Abstract
Emerging devices are now providing full hemodynamic support and may improve survival in patients who present with cardiogenic shock. This manuscript will present the framework strategy for utilizing current advancements in temporary device therapy for acutely decompensated patients with cardiogenic shock, as a stabilizing bridge-to-decision (BTD) modality. We identify criteria for the clinical presentation of cardiogenic shock and a list of factors that suggest inferior outcomes.Cardiogenic shock continues to be associated with significant morbidity and mortality. The observed poor outcomes are usually impacted by delayed recognition and limited pharmacologic options. Initial therapeutic responses are often temporarily successful, but fail to adequately resuscitate many patients who ultimately die of multiorgan system or septic deaths.We will describe essential clinical components to assist in identifying such patients for short-term circulatory support as a BTD for advanced durable ventricular assist devices. Improved outcomes of patients with cardiogenic shock may be achieved by both early clinical recognition and early strategic implementation of sustainable temporary circulatory support.
- Published
- 2012
5. Targeted inhibition of calcineurin in pressure-overload cardiac hypertrophy. Preservation of systolic function
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Joseph A, Hill, Beverly, Rothermel, Ki-Dong, Yoo, Barry, Cabuay, Elaine, Demetroulis, Robert M, Weiss, William, Kutschke, Rhonda, Bassel-Duby, and R Sanders, Williams
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Male ,DNA, Complementary ,Time Factors ,Dose-Response Relationship, Drug ,Heart Diseases ,Calcineurin ,Myocardium ,Calcineurin Inhibitors ,Blood Pressure ,Electroencephalography ,Mice, Transgenic ,Hypertrophy ,Blotting, Northern ,Up-Regulation ,Mice ,Echocardiography ,Pressure ,Animals ,Humans ,Protein Isoforms ,RNA ,RNA, Messenger ,Aorta ,Protein Binding - Abstract
Calcineurin is a Ca(2+)/calmodulin-activated protein phosphatase that transduces hypertrophic stimuli to regulate transcriptional control of myocyte transformation. It is not known whether overexpression of MCIP1, a recently described endogenous inhibitor of calcineurin, impacts the hypertrophic response to pathophysiologically relevant pressure overload. Further, the functional consequences of calcineurin inhibition by MCIP1 under conditions of hemodynamic stress are unknown. Transgenic mice expressing a human cDNA encoding hMCIP1 in the myocardium were subjected to thoracic aortic banding. Transgenic mice and wild type littermates tolerated pressure overload equally well. Wild type mice developed left ventricular hypertrophy, but the hypertrophic response in transgenics was significantly blunted. An isoform of MCIP1 transcript was up-regulated by pressure stress, whereas MCIP2 transcript was not. Expression patterns of fetal genes were differentially regulated in banded MCIP1 hearts compared with wild type. Echocardiography performed at 3 weeks and 3 months revealed preservation of both left ventricular size and systolic function in banded MCIP1 mice despite the attenuated hypertrophic response. These data demonstrate attenuation of hypertrophic transformation when calcineurin is inhibited by MCIP1. Further, these data suggest that activation of hypertrophic marker genes may not be directly dependent on calcineurin activity. Finally, they demonstrate that ventricular performance is preserved despite attenuation of compensatory hypertrophy.
- Published
- 2002
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