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2. Health status after invasive or conservative care in coronary and advanced kidney disease

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Spertus J. A., Jones P. G., Maron D. J., Mark D. B., O'Brien S. M., Fleg J. L., Reynolds H. R., Stone G. W., Sidhu M. S., Chaitman B. R., Chertow G. M., Hochman J. S., Bangalore S, ISCHEMIA-CKD Research Group: Abdallah M Abdallah, Abel E Moreyra, Abhay A Laddu, Abhishek Dubey, Abhishek Goyal, Abigail Knighton, Adedayo Adeboye, Agne Juceviciene, Agne Urboniene, Agnieszka Szramowska, Ahmed Abdel-Latif, Ahmed Ayoub, Ahmed Elghamaz, Ahmed Kamal, Ahmed Talaat, Ajay Sharma, Ajit Singh Narula, Akshay Bagai, Akvile Smigelskaite, Alain Raymond, Alain Rheault, Alaine Melanie Loehr, Albert Varga, Aldo P Maggioni, Alec Moorman, Alejandro Chevaile Ramos, Alejandro Gisbert, Aleksandra Fratczak, Aleksandras Laucevicius, Alexander M Chernyavskiy, Alexander Sergeevich Borisov, Alexandra Craft, Alexandra Hunter, Alexandre Ciappina Hueb, Alexandre Schaan de Quadros, Alice Manica Muller, Aline Peixoto Deiro, Allegra Stone, Almudena Castro, Amar Uxa, Amaryllis Van Craenenbroeck, Ambuj Roy, Amit Kakkar, Amy Flowers, Amy Iskandrian, Ana D Djordjevic-Dikic, Ana Gomes Almeida, Ana Rita Francisco, Ana S Mladenovic, Ana Santana, Anandaroop Lahiri, Anastasia M Kuzmina-Krutetskaya, Anastasia Vamvakidou, Andras Vertes, Andre Gabriel, Andrea Bartykowszki, Andrea Lorimer, Andrea Pascual, Andreia Coelho, Andreia Rocha, Andrés García-Rincón, Andrew Starovoytov, Andrzej Łabyk, Anelise Kawakami, Angela Hoye, Angelo Nobre, Anjali Acharya, Anjali Anand, Anjana Rishmawi, Ann Banfield, Ann Luyten, Anna Cichocka-Radwan, Anna Fojt, Anna Plachcinska, Anna Teresinska, Anne Marie Webb, Anne Heath, Anoop Mathew, Antonia Vega, Antonio Carvalho, Antonio Colombo, Antonio Fiarresga, Anu Tharini, Anupama Rao, Aquiles Valdespino-Estrada, Ariel Diaz, Arif Asif, Arnold H Seto, Arturo S Campos-Santaolalla, Asim N Cheema, Asker Ahmed, Atul Mathur, Audrey W Leong, Axel Åkerblom, Axelle Fuentes, Aynun Naher, Badhma Valaiyapathi, Balaji Srinivasan, Baljeet Kaur, Balram Bhargava, Bandula Guruge, Barbara Wicklund, Bartosz Czarniak, Bebek Singh, Begoña Igual, Bela Merkely, Benoy N Shah, Bernard de Bruyne, Beth Abramson, Beth Stefanchik, Bethany Harvey, Bharati Shivalkar, Bilal Malik, Binoy Mannekkattukudy Kurian, Bougrida Hammouche, Branko D Beleslin, Bruce Ferguson, Bruce McManus, Bruna Maria Ascoli, Bryn Smith, Byron J Allen, C Michael Gibson, C Noel Bairey Merz, Calin Pop, Carl-Éric Gagné, Carly Ohmart, Carol M Kartje, Caroline Alsweiler, Caroline Rodgers, Caroline Spindler, Carolyn J Gruber, Catherine Albert, Catherine Bone, Catherine Lemay, Cezary Kepka, Chandini Suvarna, Chantale Mercure, Charlene Wiyarand, Chetan Patel, Chiara Attanasio, Chi-Ming Chow, Ching Min Er, Ching-Ching Ong, Cholenahally Nanjappa Manjunath, Chris Buller, Christel Vassaliere, Christiaan Vrints, Christian Witzke, Christie Ballantyne, Christina Björklund, Christine Roraff, Christophe Laure, Christophe Thuaire, Christopher Chan, Christopher Fordyce, Christopher Kinsey, Chunli Xia, Cidney Schultz, Claes Held, Claudia Cortés, Claudia Escobar, Cláudia Freixo, Clemens T Kadalie, Corine Thobois, Courtney Page, Cristina Bare, Dalisa Espinosa, Dan Gao, Dana Rizk, Daniela Puzhevsky, Data Analyst, David M Charytan, David O Williams, David Booth, David Charytan, David Cohen, David DeMets, David Foo, David Goldfarb, David Schlichting, David Sisson, David Taggart, David Waters, David Wheeler, David Williams, Davis Vo, Dawid Teodorczyk, Dawn D Shelstad, Dean Kereiakes, Deborah Yip, Deepa Ramaswamy, Deirdre Mattina, Deirdre Murphy, Dengke Jiang, Derek Cyr, Diana Cukali, Diane Camara, Dimitrios Stournaras, Dipti Patel, Dongze Li, Donna Exley, Doreen Reimann, Doron Schwartz, Duarte Cacela, Dwayne S G Conway, Eapen Punnoose, Edgar L Tay, Edgar Karanjah, Eduardo Gomes Lima, Eduardo Hernandez-Rangel, Edward D Nicol, Edyta Kaczmarska, Elena Refoyo Salicio, Eli Feen, Elihú Durán-Cortés, Elisabeth M Janzen, Elise van Dongen, Elissa Restelli Piloto, Elizabeta Srbinovska Kostovska, Elizabeth Capasso-Gulve, Elizaveta V Zbyshevskaya, Ellie Fridell, Ellis W Lader, Elvira Gosmanova, Emilie Tachot, Emma Howard, Emmanuel Sorbets, Encarnación Alonso-Álvarez, Eric Daugas, Erick Alexánderson Rosas, Estelle Montpetit, Eugene Passamani, Evgeny Shutov, Ewa Szczerba, Ewelina Wojtala, Expedito Eustáquio Ribeiro Silva, Fabio Fimiani, Fadi Hage, Fahim Haider Jafary, Fang Feng, Fatima Ranjbaran, Fausto J Pinto, Fernando Caeiro, Fernando Nolasco, Filipa Silva, Filippo Ottani, Firas Al Solaiman, Flávia Egydio, Florina Chereches, Francesca De Micco, Francesca Bianchini, Francesca Pietrucci, Francesco Orso, Francesco Pisano, Francisca Patuleia Figueiras, François Madore, Frank Harrell, Frank Rockhold, Frans Van de Werf, Franziska Guenther, Fred Mohr, G Karthikeyan, Gabriel Galeote, Gabriel Grossmann, Gabriel Steg, Gabriela Guzman, Gabriele Gabrielli, Gang Chen, Gautam Sharma, Gaylin Petty, Gelmina Mikolaitiene, Gennie Yee, Gerard Patrick Devlin, Gerard Esposito, Gergely Ágoston, Gervasio Lamas, Gia Cobb, Gian Piero Perna, Gianpiero Leone, Girish Mishra, Gonzalo Barge-Caballero, Grace M Young, Graciela Scaro, Graham Wong, Gregg Pressman, Gregor Simonis, Gudrun Steinmaurer, Guilherme Portugal, Guilhermina Cantinho Lopes, Guillermo Garcia-Garcia, Guoqin Wang, Gurpreet S Wander, Gurpreet Gulati, Haibo Zhang, Halina Marciniak, Hao Dai, Haojian Dong, Harold Franch, Harvey White, Hatem Elabd, Hayley Pomeroy, Heather Golden, Heidi Wilson, Helene Abergel, Hemalata Siddaram, Hemant Shakhar Mahapatra, Henry C Stokes, Hermine Osseni, Herwig Schuchlenz, Hicham Skali, Holly Mattix-Kramer, Hong Cheng, Hossam Mahrous, Hristo Pejkov, Hugo Marques, Hui Zhong, Hussien El Fishawy, Ian Webb, Iftikhar Kullo, Igor O Grazhdankin, Ikraam Hassan, Ileana L Pina, Ilona Tamasauskiene, Inês Zimbarra Cabrita, Ines Rodrigues, Inga Soveri, Irena Peovska Mitevska, Irene Marthe Lang, Irina Subbotina, Irma Kalibataite-Rutkauskiene, Isabelle Roy, Ishita Tejani, Ivan A Naryshkin, Ivana Jankovic, Iwona Niedzwiecka, Jacek Kusmierek, Jackie Chow, Jaekyeong Heo, Jakub Maksym, James E Davies, James J Jang, James Hirsch, James Tatoulis, Jan Henzel, Janaina Oliveira, Janani Rangaswami, Jane Eckstein, Janitha Raj, Jaqueline Pozzibon, Jaroslaw Drozdz, Jason Loh Kwok Kong, Jason T Call, Jason Linefsky, Javier J Garcia, Jay Meisner, Jayne Scales, Jean Michel Juliard, Jean Diodati, Jean-Michel Juliard, Jeanne Russo, Jeannette J M Schoep, Jeff Leimberger, Jeffrey C Milliken, Jeffrey Anderson, Jeffrey Kanters, Jeffrey Lorin, Jeffrey Moses, Jelena J Stepanovic, Jelena Celutkiene, Jelena Stojkovic, Jenne M Jose, Jennifer L Stanford, Jennifer Hogan, Jennifer Horst, Jennifer Isaacs, Jennifer Thomson, Jennifer Tomfohr, Jennifer White, Jerry Yee, Jessica Berg, Jesus Peteiro, Jesús Peteiro, Jia Li, Jiamin Liu, Jianxin Zhang, Jill Marcus, Jim Blankenship, Jing Dong, Jiyan Chen, Jo Evans, Joaquín V Peñafiel, Joe Sabik, Johann Christopher, John B Kostis, John Joseph Graham, John Doan, John Jose, John Kotter, John Lehman, John Middleton, John Pownall, Jonathan M Gleadle, Jonathan S Chavez-Iñiguez, Jonathan Byrne, Jonathan Himmelfarb, Jonathan Lebowitz, Jonean Thorsen, Jorge Carrillo Calvillo, Jorge Escobedo, José A Ortega-Ramírez, José J Cuenca-Castillo, Jose L Diez, José Luis Narro Villanueva, José Luiz da Costa Vieira, José M Flores-Palacios, Jose Fragata, Jose Lopes, Jose Lopez-Sendon, José Lopez-Sendon, Jose Rueda, Joseph B Selvanayagam, Joseph Sacco, Joshua P Loh, Joy Burkhardt, Juan Manuel López Quijano, Juan Gaztanaga, Judit Sebo, Judith Wright, Juergen Stumpf, Julia de Aveiro Morata, Julio César Figal, Julio Hernandez Jaras, Junqing Yang, Jyotsna Garg, K Manjula Rani, K Preethi, Kaatje Goetschalckx, Karen Calfas, Karen Petrosyan, Karen Servilla, Karen Swan, Karin Ploetze, Karolina Kryczka, Karolina Wojtczak-Soska, Karolina Wojtera, Karthik Ramasamy, Katarzyna Łuczak, Katarzyna Malinowska, Katharina Knaut, Katherine Martin, Kathleen Claes, Kathryn Mason, Ken Mahaffey, Kenneth Gin, Kerry Lee, Kerstin Bonin, Kerstin Mikes, Kevin R Bainey, Kevin T Harley, Kevin Marzo, Kevin McMahon, Khaled Abdul-Nour, Khaled Alfakih, Khaled Dajani, Khrystyna Kushniriuk, Kian-Keong Poh, Kim Holland, Kimberly E Halverson, Kinnari Murphy, Kiran Reddy, Kirsten J Quiles, Kirsty Abercrombie, Klaus Matschke, Konrad Szymczyk, Koo Hui Chan, Kreton Mavromatis, Krishnakumar Hongalgi, Kristian Thygesen, Kristin M Salmi, Kristin Newby, Kristine Arges, Kristine Teoh, Krzysztof Drzymalski, Lalathaksha Kumbar, Laszlone Matics, LaTonya J Hickson, Laura Keinaite, Laura Sarti, Laura True, Lawrence M Phillips, Lawrence Friedman, Leandro C Maranan, Leda Lotaif, Lekshmi Dharmarajan, Leo A Bockeria, Leonardo Pizzol Caetano, Leonardo Bridi, Leonid L Bershtein, Li Hai Yan, Li Li, Lidia Sousa, Lihong Xu, Lihua Zhang, Lili Zhang, Lilian Mazza Barbosa, Liljana Tozija, Linda Arcand, Lino Patricio, Liping Zhang, Lisa Hatch, Lixin Jiang, Liz Low, Loay Salman, Lorena Lopez, Lori Pritchard, Luis Bernanrdes, Luis Guzman, Lynette L Teo, M Sowjanya Reddy, Maarten Simoons, Maayan Konigstein, Mafalda Selas, Magdalena Madero, Magdalena Miller, Magdalena Misztal-Teodorczyk, Magdy Abdelhamid, Magid Fahim, Mahevamma Mylarappa, Majo X Joseph, Malgorzata Frach, Manjula Rani, Marcello Galvani, Marcin Demkow, Marcin Szkopiak, Marco De Fabritis, Marco Magnoni, Marco Marini, Marco Sicuro, Marek Roik, Maria A Alfonso, Maria Antonieta Pereira de Moraes, María Dolores Martínez-Ruíz, Maria Eugenia Canziani, Maria Eugenia Martin, Maria Inês Caetano, Maria P Corral, Maria Pérez García, Maria Andreasson, Maria Posada, Marianna D A Dracoulakis, Mariano Rubio, Marija T Petrovic, Marina Vieira, Mario J Garcia, Mario D'arezzo, Maris Orgera, Marius Miglinas, Mark Garand, Mark Peterson, Mark Xavier, Marlowe Mosley, Marta Capinha, Marta Swiderek, Martha Meyer, Martina Ceseri, Martinia Tricoli, Mary Wiilliams, Mary Ann Champagne, Mary Streif, Massoud Leesar, Matei Claudia, Mateusz Solecki, Matías Nicolás Mungo, Matthew Shinseki, Matthew Weir, Maura Carina Nédio, Max-Paul Winter, Mayil S Krishnam, Meenakshi Mishra, Mei Hwang, Melemadathil Srilatha, Melissa LeFevre, Mengistu Simegn, Michael A Gibson, Michael B Rubens, Michael D Shapiro, Michael Chobanian, Michael Davidson, Michael Farkouh, Michael Mack, Michal Wlodarczyk, Michel G Khouri, Michelle Crowder, Michelle Ratliff, Miguel Borges Santos, Miguel Nobre Menezes, Miguel Perez Fontan, Miguel Barrero, Mihaly Tapolyai, Mikhail T Torosoff, Milan R Dobric, Milind Avdhoot Gadkari, Min Tun Kyaw, Miri Revivo, Mitchel B Lustre, Mohamed Adel, Mohamed Hassan, Mohammad El-Hajjar, Mohammed Hussain, Mohammed Saleem, Moisés Blanco-Calvo, Moisés Jiménez-Santos, Monika Laukyte, Muhamed Saric, Myrthes Emy Takiuti, Nadia Asif, Nagaraja Moorthy, Naima L Ogletree, Nana O Katamadze, Nandita Nataraj, Naomi Uchida, Nasrul Ismail, Natalia S Oliveira, Natalia de Carvalho Maffei, Nathalie Brosens, Naved Aslam, Naveed Akhtar, Neamat Mowafy, Neeraj Pandit, Neeraj Parakh, Neesh Pannu, Neill Duncan, Nevena Garcevic, Ngaire Meadows, Nicholas Danchin, Nicole Deming, Nikola N Boskovic, Nikolaos Karogiannis, Ning Zhang, Nirmal Kumar, Niruta Sharma, Nitika Chadha, Nitish Naik, Noelle M Durfee, Nora M Cosgrove, Norbert Urbanski, Norma Hogg, Olga Walesiak, Olga Zdończyk, Olga Zhdanova, Olivia Anaya, Olugbenga Bello, Omar Almousalli, Omar Thompson, Orit Kliuk, Oscar Méndiz, Óscar Prada-Delgado, Oz Shapira, Pablo Raffaele, Page Salanger, Pal Maurovich-Horvat, Pallav Garg, Paloma Moraga, Pam Singh, Pamela Ouyang, Pamela Woodard, Paola Emanuela Poggio Smanio, Paola Smanio, Paolo Calabro, Patricia K Nguyen, Patricia Alarie, Patricia Carrilho, Patricia Endsley, Patricia Pellikka, Patrycja Lebioda, Paul Der Mesropian, Paul Hauptman, Paula García-González, Paula Wilson, Paulo Cury Rezende, Paulo Novis Rocha, Pedro Canas Silva, Pedro Farto E Abreu, Pedro Píccaro de Oliveira, Pedro Carvalho, Pedro Modas, Pedro Rio, Peiyu He, Peter A McCullough, Peter H Stone, Peter Douglass, Peter Sizeland, Peter Voros, Philippe Gabriel Steg, Philippe Genereux, Philippe Généreux, Philippe Menasche, Philippe Rheault, Piero Tassinario, Pierre Gervais, Pilar Calvillo, Ping Chai, Piotr Jakubowski, Piotr Pruszczyk, Poay-Huan Loh, Pouneh Samadi, Prakash Deedwania, Pranav M Patel, Praneeth Polamuri, Pratiksha Sharma, Preeti Kamath, Prince Thomas, Priyadarshani Arambam, Puneet Sodhi, Pushpa Naik, Qi Zhong, Qian Zhao, Qianqian Yuan, Qiulan Xie, Rachel Murphy, Radmila Lyubarova, Radmilar Lyubarova, Raewyn Fisher, Rafael Diaz, Rafael Maldonado, Rafael Selgas, Raffaele Bugiardini, Rafia Chaudhry, Raisa Kavalakkat, Rajalekshmi Vs, Rajesh Gopalan Nair, Rajiv Narang, Rakesh Yadav, Ramiro Carvalho, Ramon de Jesús-Pérez, Ran Leng, Ranjan Kachru, Raquel Sanchez, Raven R Dwyer, Raven Lee, Ray Wyman, Raymond C Wong, Reinette Hampson, Renato Abdala Karam Kalil, Renato D Lopes, Renato George Eick, Renato Lopes, Reshma Ravindran, Reto Andreas Gamma, Ricardo Costa, Richa Bhatt, Richard H J Trimlett, Risha Patel, Rita Coram, Robert K Riezebos, Robert M Donnino, Robert Guyton, Robert Harrington, Robert Malecki, Roberto René Favaloro, Robyn Elliott, Rodolfo G S D Lima, Rohit Tandon, Rolf Doerr, Roma Tewari, Ron Wald, Rongrong Hu, Rory Collins, Roxana Mehran, Roxy Senior, Rubén Baleón-Espinosa, Ruben Ramos, Rui Ferreira, Ruth Kirby, Ruth Pérez-Fernández, S Ramakrishnan, S K Dwivedi, Sadath Lubna, Sadiq Ahmed, Sajeev Chakanalil Govindan, Salamah Alfalahi, Salvador Cruz-Flores, Salvatore P Costa, Sampoornima Setty, Samuel Nwosu, Sandeep Mahajan, Sandeep Seth, Sandeep Singh, Sander R Niehe, Sandy Carr, Sanja Simic Ogrizovic, Sanja Ogrizovic, Sanjeev Gulati, Sanjeev Sharma, Sara Fernandez, Sarah Williams, Sarju Ralhan, Sasko Kedev, Satinder Singh, Satish Sankaranarayanan, Satvic Cholenahally Manjunath, Sau Lee, Schawana Thaxton, Sean M O'Brien, Sebastian Sobczak, Seema Nour, Sergey A Sayganov, Sérgio Bravo Baptista, Sergio Draibe, Seth Sokol, Sharad Chandra, Shari Mackedanz, Shaun Goodman, Shayan Shirazian, Sheetal Rupesh Karwa, Sheri Ussery, Sheromani Bajaj, Shirin Heydari, Shiv Kumar Choudhary, Shivali Patel, Shruti Pandey, Shuyang Zhang, Siddharth Gadage, Sik-Yin V Tan, Sílvia Zottis Poletti, Silvia Valbuena, Simone Savaris, Solomon Yakubov, Songlin Zhu, Sonika Gupta, Sorin Brener, Sothinathan Gurunathan, Soundarya Nayak, Sowjanya Reddy, Stanley E Cobos, Stefan Weikl, Stephanie M Lane, Stephanie Ferket, Stephanie Mavromichalis, Stephen Fremes, Steven A Fein, Steven P Sedlis, Steven Giovannone, Steven Weitz, Subhash Banerjee, Sudhanva S Hegde, Suellen Hosino, Sulagna Mookherjee, Suman Singh, Sumith Abeygunasekara, Sundeep Mishra, Sunil Kumar Verma, Suresh Kumar, Suryaprakash Narayanappa, Susan K Milbrandt, Susana Silva, Susanna Stevens, Suvarna Kolhe, Suzana Tavares, Suzanne Welsh, T A Kishore, Tamara Colaiácovo Soares, Tapan Umesh Pillay, Tarek Rashid, Tarun K Mittal, Tauane Bello Duarte, Téodora Dutoiu, Teresa Delgadillo, Terrance Chua, Terrance Welch, Theodoros Kofidis, Thierry Lefevre, Tiago Silva, Timea Boros, Titus Lau, Tiziana Formisano, Tomasz Ciurus, Tomasz Tarchalski, Tracy Tan, Umesh Lingaraj, V K Bahl, V S Narain, Valentina Pellu, Valentine Lobo, Valerie Robesyn, Vandana Yadav, Veerabhadra Gupta, Verghese Mathew, Vicente Miro, Victoria Gumerova, Victoria Hernandez, Vijay Kher, Vijay Kumar, Vikas Makkar, Vikranth Reddy, Viktoria Bulkley, Vinoi George David, Virendra Misra, Virginia Fernández-Figares, Vladimir Ryasniansky, Vojislav L Giga, Wael A Almahmeed, Wan Xian Chan, Wanda C Marfori, Wanda Parker, Wayne Pennachi, Wei Ling Lau, Weibing Xing, Weijing Bian, Wendy L Stewart, Wendy Drewes, Whady Hueb, William Weintraub, Winnie C Sia, Xacobe Flores-Ríos, Xiang Ma, Xiangqiong Gu, Xiaomei Li, Xiaoyi Xu, Xin Fu, Xuemei Li, Xutong Wang, Yanek Pépin-Dubois, Yaron Arbel, Yechen Han, Yiming Lit, Ying Tung Sia, Ying Wang, Yining Yang, Yitong Ma, Yolayfi Peralta, Yves Smets, Yvonne Taul, Zalina Kudzoeva, Zeljko Z Markovic, Zhangsuo Liu, Zhenyu Liu, Zhiming Ye, Zixiang Yu, Zoltan Davidovits, Zvezdana Petronijevic, Spertus J.A., Jones P.G., Maron D.J., Mark D.B., O'Brien S.M., Fleg J.L., Reynolds H.R., Stone G.W., Sidhu M.S., Chaitman B.R., Chertow G.M., Hochman J.S., Bangalore S, and ISCHEMIA-CKD Research Group: Abdallah M Abdallah, Abel E Moreyra, Abhay A Laddu, Abhishek Dubey, Abhishek Goyal, Abigail Knighton, Adedayo Adeboye, Agne Juceviciene, Agne Urboniene, Agnieszka Szramowska, Ahmed Abdel-Latif, Ahmed Ayoub, Ahmed Elghamaz, Ahmed Kamal, Ahmed Talaat, Ajay Sharma, Ajit Singh Narula, Akshay Bagai, Akvile Smigelskaite, Alain Raymond, Alain Rheault, Alaine Melanie Loehr, Albert Varga, Aldo P Maggioni, Alec Moorman, Alejandro Chevaile Ramos, Alejandro Gisbert, Aleksandra Fratczak, Aleksandras Laucevicius, Alexander M Chernyavskiy, Alexander Sergeevich Borisov, Alexandra Craft, Alexandra Hunter, Alexandre Ciappina Hueb, Alexandre Schaan de Quadros, Alice Manica Muller, Aline Peixoto Deiro, Allegra Stone, Almudena Castro, Amar Uxa, Amaryllis Van Craenenbroeck, Ambuj Roy, Amit Kakkar, Amy Flowers, Amy Iskandrian, Ana D Djordjevic-Dikic, Ana Gomes Almeida, Ana Rita Francisco, Ana S Mladenovic, Ana Santana, Anandaroop Lahiri, Anastasia M Kuzmina-Krutetskaya, Anastasia Vamvakidou, Andras Vertes, Andre Gabriel, Andrea Bartykowszki, Andrea Lorimer, Andrea Pascual, Andreia Coelho, Andreia Rocha, Andrés García-Rincón, Andrew Starovoytov, Andrzej Łabyk, Anelise Kawakami, Angela Hoye, Angelo Nobre, Anjali Acharya, Anjali Anand, Anjana Rishmawi, Ann Banfield, Ann Luyten, Anna Cichocka-Radwan, Anna Fojt, Anna Plachcinska, Anna Teresinska, Anne Marie Webb, Anne Heath, Anoop Mathew, Antonia Vega, Antonio Carvalho, Antonio Colombo, Antonio Fiarresga, Anu Tharini, Anupama Rao, Aquiles Valdespino-Estrada, Ariel Diaz, Arif Asif, Arnold H Seto, Arturo S Campos-Santaolalla, Asim N Cheema, Asker Ahmed, Atul Mathur, Audrey W Leong, Axel Åkerblom, Axelle Fuentes, Aynun Naher, Badhma Valaiyapathi, Balaji Srinivasan, Baljeet Kaur, Balram Bhargava, Bandula Guruge, Barbara Wicklund, Bartosz Czarniak, Bebek Singh, Begoña Igual, Bela Merkely, Benoy N Shah, Bernard de Bruyne, Beth Abramson, Beth Stefanchik, Bethany Harvey, Bharati Shivalkar, Bilal Malik, Binoy Mannekkattukudy Kurian, Bougrida Hammouche, Branko D Beleslin, Bruce Ferguson, Bruce McManus, Bruna Maria Ascoli, Bryn Smith, Byron J Allen, C Michael Gibson, C Noel Bairey Merz, Calin Pop, Carl-Éric Gagné, Carly Ohmart, Carol M Kartje, Caroline Alsweiler, Caroline Rodgers, Caroline Spindler, Carolyn J Gruber, Catherine Albert, Catherine Bone, Catherine Lemay, Cezary Kepka, Chandini Suvarna, Chantale Mercure, Charlene Wiyarand, Chetan Patel, Chiara Attanasio, Chi-Ming Chow, Ching Min Er, Ching-Ching Ong, Cholenahally Nanjappa Manjunath, Chris Buller, Christel Vassaliere, Christiaan Vrints, Christian Witzke, Christie Ballantyne, Christina Björklund, Christine Roraff, Christophe Laure, Christophe Thuaire, Christopher Chan, Christopher Fordyce, Christopher Kinsey, Chunli Xia, Cidney Schultz, Claes Held, Claudia Cortés, Claudia Escobar, Cláudia Freixo, Clemens T Kadalie, Corine Thobois, Courtney Page, Cristina Bare, Dalisa Espinosa, Dan Gao, Dana Rizk, Daniela Puzhevsky, Data Analyst, David M Charytan, David O Williams, David Booth, David Charytan, David Cohen, David DeMets, David Foo, David Goldfarb, David Schlichting, David Sisson, David Taggart, David Waters, David Wheeler, David Williams, Davis Vo, Dawid Teodorczyk, Dawn D Shelstad, Dean Kereiakes, Deborah Yip, Deepa Ramaswamy, Deirdre Mattina, Deirdre Murphy, Dengke Jiang, Derek Cyr, Diana Cukali, Diane Camara, Dimitrios Stournaras, Dipti Patel, Dongze Li, Donna Exley, Doreen Reimann, Doron Schwartz, Duarte Cacela, Dwayne S G Conway, Eapen Punnoose, Edgar L Tay, Edgar Karanjah, Eduardo Gomes Lima, Eduardo Hernandez-Rangel, Edward D Nicol, Edyta Kaczmarska, Elena Refoyo Salicio, Eli Feen, Elihú Durán-Cortés, Elisabeth M Janzen, Elise van Dongen, Elissa Restelli Piloto, Elizabeta Srbinovska Kostovska, Elizabeth Capasso-Gulve, Elizaveta V Zbyshevskaya, Ellie Fridell, Ellis W Lader, Elvira Gosmanova, Emilie Tachot, Emma Howard, Emmanuel Sorbets, Encarnación Alonso-Álvarez, Eric Daugas, Erick Alexánderson Rosas, Estelle Montpetit, Eugene Passamani, Evgeny Shutov, Ewa Szczerba, Ewelina Wojtala, Expedito Eustáquio Ribeiro Silva, Fabio Fimiani, Fadi Hage, Fahim Haider Jafary, Fang Feng, Fatima Ranjbaran, Fausto J Pinto, Fernando Caeiro, Fernando Nolasco, Filipa Silva, Filippo Ottani, Firas Al Solaiman, Flávia Egydio, Florina Chereches, Francesca De Micco, Francesca Bianchini, Francesca Pietrucci, Francesco Orso, Francesco Pisano, Francisca Patuleia Figueiras, François Madore, Frank Harrell, Frank Rockhold, Frans Van de Werf, Franziska Guenther, Fred Mohr, G Karthikeyan, Gabriel Galeote, Gabriel Grossmann, Gabriel Steg, Gabriela Guzman, Gabriele Gabrielli, Gang Chen, Gautam Sharma, Gaylin Petty, Gelmina Mikolaitiene, Gennie Yee, Gerard Patrick Devlin, Gerard Esposito, Gergely Ágoston, Gervasio Lamas, Gia Cobb, Gian Piero Perna, Gianpiero Leone, Girish Mishra, Gonzalo Barge-Caballero, Grace M Young, Graciela Scaro, Graham Wong, Gregg Pressman, Gregor Simonis, Gudrun Steinmaurer, Guilherme Portugal, Guilhermina Cantinho Lopes, Guillermo Garcia-Garcia, Guoqin Wang, Gurpreet S Wander, Gurpreet Gulati, Haibo Zhang, Halina Marciniak, Hao Dai, Haojian Dong, Harold Franch, Harvey White, Hatem Elabd, Hayley Pomeroy, Heather Golden, Heidi Wilson, Helene Abergel, Hemalata Siddaram, Hemant Shakhar Mahapatra, Henry C Stokes, Hermine Osseni, Herwig Schuchlenz, Hicham Skali, Holly Mattix-Kramer, Hong Cheng, Hossam Mahrous, Hristo Pejkov, Hugo Marques, Hui Zhong, Hussien El Fishawy, Ian Webb, Iftikhar Kullo, Igor O Grazhdankin, Ikraam Hassan, Ileana L Pina, Ilona Tamasauskiene, Inês Zimbarra Cabrita, Ines Rodrigues, Inga Soveri, Irena Peovska Mitevska, Irene Marthe Lang, Irina Subbotina, Irma Kalibataite-Rutkauskiene, Isabelle Roy, Ishita Tejani, Ivan A Naryshkin, Ivana Jankovic, Iwona Niedzwiecka, Jacek Kusmierek, Jackie Chow, Jaekyeong Heo, Jakub Maksym, James E Davies, James J Jang, James Hirsch, James Tatoulis, Jan Henzel, Janaina Oliveira, Janani Rangaswami, Jane Eckstein, Janitha Raj, Jaqueline Pozzibon, Jaroslaw Drozdz, Jason Loh Kwok Kong, Jason T Call, Jason Linefsky, Javier J Garcia, Jay Meisner, Jayne Scales, Jean Michel Juliard, Jean Diodati, Jean-Michel Juliard, Jeanne Russo, Jeannette J M Schoep, Jeff Leimberger, Jeffrey C Milliken, Jeffrey Anderson, Jeffrey Kanters, Jeffrey Lorin, Jeffrey Moses, Jelena J Stepanovic, Jelena Celutkiene, Jelena Stojkovic, Jenne M Jose, Jennifer L Stanford, Jennifer Hogan, Jennifer Horst, Jennifer Isaacs, Jennifer Thomson, Jennifer Tomfohr, Jennifer White, Jerry Yee, Jessica Berg, Jesus Peteiro, Jesús Peteiro, Jia Li, Jiamin Liu, Jianxin Zhang, Jill Marcus, Jim Blankenship, Jing Dong, Jiyan Chen, Jo Evans, Joaquín V Peñafiel, Joe Sabik, Johann Christopher, John B Kostis, John Joseph Graham, John Doan, John Jose, John Kotter, John Lehman, John Middleton, John Pownall, Jonathan M Gleadle, Jonathan S Chavez-Iñiguez, Jonathan Byrne, Jonathan Himmelfarb, Jonathan Lebowitz, Jonean Thorsen, Jorge Carrillo Calvillo, Jorge Escobedo, José A Ortega-Ramírez, José J Cuenca-Castillo, Jose L Diez, José Luis Narro Villanueva, José Luiz da Costa Vieira, José M Flores-Palacios, Jose Fragata, Jose Lopes, Jose Lopez-Sendon, José Lopez-Sendon, Jose Rueda, Joseph B Selvanayagam, Joseph Sacco, Joshua P Loh, Joy Burkhardt, Juan Manuel López Quijano, Juan Gaztanaga, Judit Sebo, Judith Wright, Juergen Stumpf, Julia de Aveiro Morata, Julio César Figal, Julio Hernandez Jaras, Junqing Yang, Jyotsna Garg, K Manjula Rani, K Preethi, Kaatje Goetschalckx, Karen Calfas, Karen Petrosyan, Karen Servilla, Karen Swan, Karin Ploetze, Karolina Kryczka, Karolina Wojtczak-Soska, Karolina Wojtera, Karthik Ramasamy, Katarzyna Łuczak, Katarzyna Malinowska, Katharina Knaut, Katherine Martin, Kathleen Claes, Kathryn Mason, Ken Mahaffey, Kenneth Gin, Kerry Lee, Kerstin Bonin, Kerstin Mikes, Kevin R Bainey, Kevin T Harley, Kevin Marzo, Kevin McMahon, Khaled Abdul-Nour, Khaled Alfakih, Khaled Dajani, Khrystyna Kushniriuk, Kian-Keong Poh, Kim Holland, Kimberly E Halverson, Kinnari Murphy, Kiran Reddy, Kirsten J Quiles, Kirsty Abercrombie, Klaus Matschke, Konrad Szymczyk, Koo Hui Chan, Kreton Mavromatis, Krishnakumar Hongalgi, Kristian Thygesen, Kristin M Salmi, Kristin Newby, Kristine Arges, Kristine Teoh, Krzysztof Drzymalski, Lalathaksha Kumbar, Laszlone Matics, LaTonya J Hickson, Laura Keinaite, Laura Sarti, Laura True, Lawrence M Phillips, Lawrence Friedman, Leandro C Maranan, Leda Lotaif, Lekshmi Dharmarajan, Leo A Bockeria, Leonardo Pizzol Caetano, Leonardo Bridi, Leonid L Bershtein, Li Hai Yan, Li Li, Lidia Sousa, Lihong Xu, Lihua Zhang, Lili Zhang, Lilian Mazza Barbosa, Liljana Tozija, Linda Arcand, Lino Patricio, Liping Zhang, Lisa Hatch, Lixin Jiang, Liz Low, Loay Salman, Lorena Lopez, Lori Pritchard, Luis Bernanrdes, Luis Guzman, Lynette L Teo, M Sowjanya Reddy, Maarten Simoons, Maayan Konigstein, Mafalda Selas, Magdalena Madero, Magdalena Miller, Magdalena Misztal-Teodorczyk, Magdy Abdelhamid, Magid Fahim, Mahevamma Mylarappa, Majo X Joseph, Malgorzata Frach, Manjula Rani, Marcello Galvani, Marcin Demkow, Marcin Szkopiak, Marco De Fabritis, Marco Magnoni, Marco Marini, Marco Sicuro, Marek Roik, Maria A Alfonso, Maria Antonieta Pereira de Moraes, María Dolores Martínez-Ruíz, Maria Eugenia Canziani, Maria Eugenia Martin, Maria Inês Caetano, Maria P Corral, Maria Pérez García, Maria Andreasson, Maria Posada, Marianna D A Dracoulakis, Mariano Rubio, Marija T Petrovic, Marina Vieira, Mario J Garcia, Mario D'arezzo, Maris Orgera, Marius Miglinas, Mark Garand, Mark Peterson, Mark Xavier, Marlowe Mosley, Marta Capinha, Marta Swiderek, Martha Meyer, Martina Ceseri, Martinia Tricoli, Mary Wiilliams, Mary Ann Champagne, Mary Streif, Massoud Leesar, Matei Claudia, Mateusz Solecki, Matías Nicolás Mungo, Matthew Shinseki, Matthew Weir, Maura Carina Nédio, Max-Paul Winter, Mayil S Krishnam, Meenakshi Mishra, Mei Hwang, Melemadathil Srilatha, Melissa LeFevre, Mengistu Simegn, Michael A Gibson, Michael B Rubens, Michael D Shapiro, Michael Chobanian, Michael Davidson, Michael Farkouh, Michael Mack, Michal Wlodarczyk, Michel G Khouri, Michelle Crowder, Michelle Ratliff, Miguel Borges Santos, Miguel Nobre Menezes, Miguel Perez Fontan, Miguel Barrero, Mihaly Tapolyai, Mikhail T Torosoff, Milan R Dobric, Milind Avdhoot Gadkari, Min Tun Kyaw, Miri Revivo, Mitchel B Lustre, Mohamed Adel, Mohamed Hassan, Mohammad El-Hajjar, Mohammed Hussain, Mohammed Saleem, Moisés Blanco-Calvo, Moisés Jiménez-Santos, Monika Laukyte, Muhamed Saric, Myrthes Emy Takiuti, Nadia Asif, Nagaraja Moorthy, Naima L Ogletree, Nana O Katamadze, Nandita Nataraj, Naomi Uchida, Nasrul Ismail, Natalia S Oliveira, Natalia de Carvalho Maffei, Nathalie Brosens, Naved Aslam, Naveed Akhtar, Neamat Mowafy, Neeraj Pandit, Neeraj Parakh, Neesh Pannu, Neill Duncan, Nevena Garcevic, Ngaire Meadows, Nicholas Danchin, Nicole Deming, Nikola N Boskovic, Nikolaos Karogiannis, Ning Zhang, Nirmal Kumar, Niruta Sharma, Nitika Chadha, Nitish Naik, Noelle M Durfee, Nora M Cosgrove, Norbert Urbanski, Norma Hogg, Olga Walesiak, Olga Zdończyk, Olga Zhdanova, Olivia Anaya, Olugbenga Bello, Omar Almousalli, Omar Thompson, Orit Kliuk, Oscar Méndiz, Óscar Prada-Delgado, Oz Shapira, Pablo Raffaele, Page Salanger, Pal Maurovich-Horvat, Pallav Garg, Paloma Moraga, Pam Singh, Pamela Ouyang, Pamela Woodard, Paola Emanuela Poggio Smanio, Paola Smanio, Paolo Calabro, Patricia K Nguyen, Patricia Alarie, Patricia Carrilho, Patricia Endsley, Patricia Pellikka, Patrycja Lebioda, Paul Der Mesropian, Paul Hauptman, Paula García-González, Paula Wilson, Paulo Cury Rezende, Paulo Novis Rocha, Pedro Canas Silva, Pedro Farto E Abreu, Pedro Píccaro de Oliveira, Pedro Carvalho, Pedro Modas, Pedro Rio, Peiyu He, Peter A McCullough, Peter H Stone, Peter Douglass, Peter Sizeland, Peter Voros, Philippe Gabriel Steg, Philippe Genereux, Philippe Généreux, Philippe Menasche, Philippe Rheault, Piero Tassinario, Pierre Gervais, Pilar Calvillo, Ping Chai, Piotr Jakubowski, Piotr Pruszczyk, Poay-Huan Loh, Pouneh Samadi, Prakash Deedwania, Pranav M Patel, Praneeth Polamuri, Pratiksha Sharma, Preeti Kamath, Prince Thomas, Priyadarshani Arambam, Puneet Sodhi, Pushpa Naik, Qi Zhong, Qian Zhao, Qianqian Yuan, Qiulan Xie, Rachel Murphy, Radmila Lyubarova, Radmilar Lyubarova, Raewyn Fisher, Rafael Diaz, Rafael Maldonado, Rafael Selgas, Raffaele Bugiardini, Rafia Chaudhry, Raisa Kavalakkat, Rajalekshmi Vs, Rajesh Gopalan Nair, Rajiv Narang, Rakesh Yadav, Ramiro Carvalho, Ramon de Jesús-Pérez, Ran Leng, Ranjan Kachru, Raquel Sanchez, Raven R Dwyer, Raven Lee, Ray Wyman, Raymond C Wong, Reinette Hampson, Renato Abdala Karam Kalil, Renato D Lopes, Renato George Eick, Renato Lopes, Reshma Ravindran, Reto Andreas Gamma, Ricardo Costa, Richa Bhatt, Richard H J Trimlett, Risha Patel, Rita Coram, Robert K Riezebos, Robert M Donnino, Robert Guyton, Robert Harrington, Robert Malecki, Roberto René Favaloro, Robyn Elliott, Rodolfo G S D Lima, Rohit Tandon, Rolf Doerr, Roma Tewari, Ron Wald, Rongrong Hu, Rory Collins, Roxana Mehran, Roxy Senior, Rubén Baleón-Espinosa, Ruben Ramos, Rui Ferreira, Ruth Kirby, Ruth Pérez-Fernández, S Ramakrishnan, S K Dwivedi, Sadath Lubna, Sadiq Ahmed, Sajeev Chakanalil Govindan, Salamah Alfalahi, Salvador Cruz-Flores, Salvatore P Costa, Sampoornima Setty, Samuel Nwosu, Sandeep Mahajan, Sandeep Seth, Sandeep Singh, Sander R Niehe, Sandy Carr, Sanja Simic Ogrizovic, Sanja Ogrizovic, Sanjeev Gulati, Sanjeev Sharma, Sara Fernandez, Sarah Williams, Sarju Ralhan, Sasko Kedev, Satinder Singh, Satish Sankaranarayanan, Satvic Cholenahally Manjunath, Sau Lee, Schawana Thaxton, Sean M O'Brien, Sebastian Sobczak, Seema Nour, Sergey A Sayganov, Sérgio Bravo Baptista, Sergio Draibe, Seth Sokol, Sharad Chandra, Shari Mackedanz, Shaun Goodman, Shayan Shirazian, Sheetal Rupesh Karwa, Sheri Ussery, Sheromani Bajaj, Shirin Heydari, Shiv Kumar Choudhary, Shivali Patel, Shruti Pandey, Shuyang Zhang, Siddharth Gadage, Sik-Yin V Tan, Sílvia Zottis Poletti, Silvia Valbuena, Simone Savaris, Solomon Yakubov, Songlin Zhu, Sonika Gupta, Sorin Brener, Sothinathan Gurunathan, Soundarya Nayak, Sowjanya Reddy, Stanley E Cobos, Stefan Weikl, Stephanie M Lane, Stephanie Ferket, Stephanie Mavromichalis, Stephen Fremes, Steven A Fein, Steven P Sedlis, Steven Giovannone, Steven Weitz, Subhash Banerjee, Sudhanva S Hegde, Suellen Hosino, Sulagna Mookherjee, Suman Singh, Sumith Abeygunasekara, Sundeep Mishra, Sunil Kumar Verma, Suresh Kumar, Suryaprakash Narayanappa, Susan K Milbrandt, Susana Silva, Susanna Stevens, Suvarna Kolhe, Suzana Tavares, Suzanne Welsh, T A Kishore, Tamara Colaiácovo Soares, Tapan Umesh Pillay, Tarek Rashid, Tarun K Mittal, Tauane Bello Duarte, Téodora Dutoiu, Teresa Delgadillo, Terrance Chua, Terrance Welch, Theodoros Kofidis, Thierry Lefevre, Tiago Silva, Timea Boros, Titus Lau, Tiziana Formisano, Tomasz Ciurus, Tomasz Tarchalski, Tracy Tan, Umesh Lingaraj, V K Bahl, V S Narain, Valentina Pellu, Valentine Lobo, Valerie Robesyn, Vandana Yadav, Veerabhadra Gupta, Verghese Mathew, Vicente Miro, Victoria Gumerova, Victoria Hernandez, Vijay Kher, Vijay Kumar, Vikas Makkar, Vikranth Reddy, Viktoria Bulkley, Vinoi George David, Virendra Misra, Virginia Fernández-Figares, Vladimir Ryasniansky, Vojislav L Giga, Wael A Almahmeed, Wan Xian Chan, Wanda C Marfori, Wanda Parker, Wayne Pennachi, Wei Ling Lau, Weibing Xing, Weijing Bian, Wendy L Stewart, Wendy Drewes, Whady Hueb, William Weintraub, Winnie C Sia, Xacobe Flores-Ríos, Xiang Ma, Xiangqiong Gu, Xiaomei Li, Xiaoyi Xu, Xin Fu, Xuemei Li, Xutong Wang, Yanek Pépin-Dubois, Yaron Arbel, Yechen Han, Yiming Lit, Ying Tung Sia, Ying Wang, Yining Yang, Yitong Ma, Yolayfi Peralta, Yves Smets, Yvonne Taul, Zalina Kudzoeva, Zeljko Z Markovic, Zhangsuo Liu, Zhenyu Liu, Zhiming Ye, Zixiang Yu, Zoltan Davidovits, Zvezdana Petronijevic

Subjects
Male, Intention to Treat Analysi, medicine.medical_treatment, Health Status, Myocardial Ischemia, 030204 cardiovascular system & hematology, Coronary Angiography, law.invention, Health Statu, 0302 clinical medicine, Randomized controlled trial, law, Surveys and Questionnaires, Odds Ratio, Surveys and Questionnaire, 030212 general & internal medicine, Myocardial infarction, Coronary Artery Bypass, medicine.diagnostic_test, General Medicine, Middle Aged, Intention to Treat Analysis, Cardiology, Female, Human, medicine.medical_specialty, Revascularization, Follow-Up Studie, 03 medical and health sciences, Percutaneous Coronary Intervention, Internal medicine, medicine, Humans, cardiovascular diseases, Healthy Lifestyle, Renal Insufficiency, Chronic, Proportional Hazards Models, Aged, Intention-to-treat analysis, business.industry, Coronary Artery Bypa, Percutaneous coronary intervention, Odds ratio, medicine.disease, Angiography, Exercise Test, Proportional Hazards Model, business, Kidney disease, Follow-Up Studies
Abstract

BACKGROUND In the ISCHEMIA-CKD trial, the primary analysis showed no significant difference in the risk of death or myocardial infarction with initial angiography and revascularization plus guideline-based medical therapy (invasive strategy) as compared with guideline-based medical therapy alone (conservative strategy) in participants with stable ischemic heart disease, moderate or severe ischemia, and advanced chronic kidney disease (an estimated glomerular filtration rate of

Published
2020

6. In old BALB/c mice, bone marrow pre-B cell and surrogate light chain reduction is associated with increased B cell reactivity to phosphorylcholine, but reduced T15 idiotype dominance

Author

Bonnie B. Blomberg, Michelle Ratliff, Richard L. Riley, Kelly Khomtchouk, and Sarah Alter

Subjects
0301 basic medicine, Idiotype, Aging, Phosphorylcholine, Cell, Receptors, Antigen, B-Cell, Bone Marrow Cells, Biology, Article, BALB/c, Mice, 03 medical and health sciences, 0302 clinical medicine, medicine, Animals, Receptor, B cell, Autoantibodies, Mice, Inbred BALB C, Precursor Cells, B-Lymphoid, biology.organism_classification, Molecular biology, 030104 developmental biology, medicine.anatomical_structure, biology.protein, Immunoglobulin Light Chains, Bone marrow, Antibody, Signal Transduction, 030215 immunology, Developmental Biology
Abstract

In young adult BALB/c mice, antibodies to phosphorylcholine (PC) bearing the T15 (TEPC 15) idiotype confer protection against pneumococcal infections. In old age, even though PC reactive B cells are often increased, the proportion of T15+ antibodies declines. We hypothesize that limited surrogate light chain (SLC) and compromise of the pre-B cell receptor checkpoint in old mice contribute to both reduced new B cell generation and changes in the anti-PC antibodies seen in old age. In old mice: 1) early pre-B cell loss is most pronounced at the preBCR checkpoint; however, the reduced pool of early pre-B cells continues to proliferate consistent with preBCR signaling; 2) increased PC reactivity is seen in bone marrow immature B cells; 3) deficient SLC promotes increased B cell PC reactivity and diminished T15 idiotype within a subset of young adult mice; and 4) in old mice, as pre-B cell losses and reduced SLC become progressively more severe, increased T15 negative PC reactive B cells occur. These results associate a reduction in pre-B cells, imposed at the preBCR checkpoint, with increased reactivity to PC, but more limited expression of the protective T15 idiotype among PC reactive antibodies in old age.

Published
2017
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10. Drug-eluting stents versus bare-metal stents in saphenous vein grafts: a double-blind, randomised trial

Author

Emmanouil S Brilakis, Robert Edson, Deepak L Bhatt, Steven Goldman, David R Holmes, Sunil V Rao, Kendrick Shunk, Bavana V Rangan, Kreton Mavromatis, Kodangudi Ramanathan, Anthony A Bavry, Santiago Garcia, Faisal Latif, Ehrin Armstrong, Hani Jneid, Todd A Conner, Todd Wagner, Judit Karacsonyi, Lauren Uyeda, Beverly Ventura, Aaron Alsleben, Ying Lu, Mei-Chiung Shih, Subhash Banerjee, Bina Ahmed, D Michelle Ratliff, Mark Ricciardi, Mark Sheldon, Milton Icenogle, Richard Snider, Amer Ardati, Brahmajee Nallamothu, Claire Duvernoy, Daniel S Menees, Hitinder Gurm, Michael P Thomas, Paul Grossman, Kristine Owen, On Topaz, Gautam Kumar, Peter Block, David A Zidar, Hiram Bezerra, Jonathan Goldberg, Jose Ortiz, Joseph Jozic, Mohammed Osman, Noah Rosenthal, Sahil A Parikh, Tom A Lassar, Albert Chan, Arun Kumar, Kul Aggarwal, Tillmann Cyrus, Jerrold Grodin, Brack Hattler, Ivan Casserly, John Messenger, Michael Kim, R Kevin Rogers, Stephen Waldo, Thomas Tsai, Kenneth Morris, Mitchell Krucoff, Sunil Rao, Thomas J Povsic, William S Jones, Anthony Bavry, Calvin Choi, Ki Park, Jayson Liu, MD, Biswajit Kar, David Paniagua, Jeffrey Breall, Islam Bolad, Rita Mukerji, Roopa Subbarao, Ahmed Abdel-Latif, David C Booth, Khaled M Ziada, Lawrence Rajan, Abdul Hakeem, Barry F Uretsky, Mayank Agrawal, Rajesh Sachdeva, Zubair Ahmed, Jesse McGee, Rahman Shah, Alok Sharma, Edward McFalls, Rizwan Siddiqui, Selcuk Adabag, Stefan Bertog, Anand Irimpen, Drew Baldwin, Nidal Abi Rafeh, Owen Mogabgab, Patrice Delafontaine, Jeffrey Lorin, Steven Sedlis, Eliot Schechter, Mazen Abu-Fadel, Talla Rousan, Udho Thadani, Fady Malik, Jeffrey Zimmet, Tony Chou, Alexis Beatty, Kenneth Lehmann, Michael Stadius, Andrew Klein, Caroline Rowe, Megumi Taniuchi, Andrew J Klein, Michael Forsberg, Divya Kapoor, Elizabeth Juneman, Huu Tam Truong, Kapildeo Lotun, Ryan Tsuda, Sergio Thai, Hoang Thai, David Lu, Vasilios Papademetriou, David Faxon, Kevin Croce, Sammy Elmariah, and Scott Kinlay

Subjects
Graft Rejection, Male, medicine.medical_specialty, medicine.medical_treatment, Clinical Trials and Supportive Activities, Self Expandable Metallic Stents, Bioengineering, 030204 cardiovascular system & hematology, Cardiovascular, Medical and Health Sciences, law.invention, 03 medical and health sciences, 0302 clinical medicine, Percutaneous Coronary Intervention, Randomized controlled trial, Double-Blind Method, law, Clinical Research, General & Internal Medicine, Clinical endpoint, medicine, Humans, Saphenous Vein, 030212 general & internal medicine, Myocardial infarction, Veterans Affairs, Heart Disease - Coronary Heart Disease, Aged, Assistive Technology, business.industry, Hazard ratio, Percutaneous coronary intervention, Stent, Thrombosis, Drug-Eluting Stents, General Medicine, Middle Aged, medicine.disease, Atherosclerosis, Surgery, Stenosis, Treatment Outcome, Heart Disease, Female, Patient Safety, business, DIVA Trial Investigators
Abstract

Summary Background Few studies have examined the efficacy of drug-eluting stents (DES) for reducing aortocoronary saphenous vein bypass graft (SVG) failure compared with bare-metal stents (BMS) in patients undergoing stenting of de-novo SVG lesions. We assessed the risks and benefits of the use of DES versus BMS in de-novo SVG lesions. Methods Patients were recruited to our double-blind, randomised controlled trial from 25 US Department of Veterans Affairs centres. Eligible participants were aged at least 18 years and had at least one significant de-novo SVG lesion (50–99% stenosis of a 2·25–4·5 mm diameter SVG) requiring percutaneous coronary intervention with intent to use embolic protection devices. Enrolled patients were randomly assigned, in a 1:1 ratio, by phone randomisation system to receive a DES or BMS. Randomisation was stratified by presence or absence of diabetes and number of target SVG lesions requiring percutaneous coronary intervention (one or two or more) within each participating site by use of an adaptive scheme intended to balance the two stent type groups on marginal totals for the stratification factors. Patients, referring physicians, study coordinators, and outcome assessors were masked to group allocation. The primary endpoint was the 12-month incidence of target vessel failure, defined as the composite of cardiac death, target vessel myocardial infarction, or target vessel revascularisation. The DIVA trial is registered with ClinicalTrials.gov, number NCT01121224. Findings Between Jan 1, 2012, and Dec 31, 2015, 599 patients were randomly assigned to the stent groups, and the data for 597 patients were used. The patients' mean age was 68·6 (SD 7·6) years, and 595 (>99%) patients were men. The two stent groups were similar for most baseline characteristics. At 12 months, the incidence of target vessel failure was 17% (51 of 292) in the DES group versus 19% (58 of 305) in the BMS group (adjusted hazard ratio 0·92, 95% CI 0·63–1·34, p=0·70). Between-group differences in the components of the primary endpoint, serious adverse events, or stent thrombosis were not significant. Enrolment was stopped before the revised target sample size of 762 patients was reached. Interpretation In patients undergoing stenting of de-novo SVG lesions, no significant differences in outcomes between those receiving DES and BMS during 12 months of follow-up were found. The study results have important economic implications in countries with high DES prices such as the USA, because they suggest that the lower-cost BMS can be used in SVG lesions without compromising either safety or efficacy. Funding US Department of Veterans Affairs Cooperative Studies Program.

Published
2018

11. The Transcription Factor ARID3a Is Important for In Vitro Differentiation of Human Hematopoietic Progenitors

Author

Joel M. Guthridge, Meenu Mishra, Michelle Ratliff, Carol F. Webb, and Mark Barton Frank

Subjects
0301 basic medicine, Immunology, Hematopoietic stem cell, Stem cell factor, Biology, Endothelial stem cell, 03 medical and health sciences, 030104 developmental biology, medicine.anatomical_structure, Cord blood, Cancer research, medicine, Immunology and Allergy, Hemangioblast, Progenitor cell, Stem cell, Adult stem cell
Abstract

We recently reported that the transcription factor ARID3a is expressed in a subset of human hematopoietic progenitor stem cells in both healthy individuals and in patients with systemic lupus erythematosus. Numbers of ARID3a+ lupus hematopoietic stem progenitor cells were associated with increased production of autoreactive Abs when those cells were introduced into humanized mouse models. Although ARID3a/Bright knockout mice died in utero, they exhibited decreased numbers of hematopoietic stem cells and erythrocytes, indicating that ARID3a is functionally important for hematopoiesis in mice. To explore the requirement for ARID3a for normal human hematopoiesis, hematopoietic stem cell progenitors from human cord blood were subjected to both inhibition and overexpression of ARID3a in vitro. Inhibition of ARID3a resulted in decreased B lineage cell production accompanied by increases in cells with myeloid lineage markers. Overexpression of ARID3a inhibited both myeloid and erythroid differentiation. Additionally, inhibition of ARID3a in hematopoietic stem cells resulted in altered expression of transcription factors associated with hematopoietic lineage decisions. These results suggest that appropriate regulation of ARID3a is critical for normal development of both myeloid and B lineage pathways.

Published
2016
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12. A developmentally plastic adult mouse kidney cell line spontaneously generates multiple adult kidney structures

Author

Celeste R. Wirsig-Wiechmann, Carol F. Webb, Rebecca Powell, Olga Lakiza, Tomoko Obara, and Michelle Ratliff

Subjects
medicine.medical_specialty, Oryzias, Biophysics, Kidney development, Biology, Kidney, Biochemistry, Article, Cell Line, Mice, Internal medicine, medicine, Animals, Induced pluripotent stem cell, Molecular Biology, Renal stem cell, Progenitor, Mice, Knockout, urogenital system, Stem Cells, Mesonephros, Cell Biology, Cell biology, DNA-Binding Proteins, Endocrinology, medicine.anatomical_structure, Cell culture, Stem cell, Cell Division, Transcription Factors
Abstract

Despite exciting new possibilities for regenerative therapy posed by the ability to induce pluripotent stem cells, recapitulation of three-dimensional kidneys for repair or replacement has not been possible. ARID3a-deficient mouse tissues generated multipotent, developmentally plastic cells. Therefore, we assessed the adult mouse ARID3a−/− kidney cell line, KKPS5, which expresses renal progenitor surface markers as an alternative cell source for modeling kidney development. Remarkably, these cells spontaneously developed into multicellular nephron-like structures in vitro, and engrafted into immunocompromised medaka mesonephros, where they formed mouse nephron structures. These data implicate KKPS5 cells as a new model system for studying kidney development. - Highlights: • An ARID3a-deficient mouse kidney cell line expresses multiple progenitor markers. • This cell line spontaneously forms multiple nephron-like structures in vitro. • This cell line formed mouse kidney structures in immunocompromised medaka fish kidneys. • Our data identify a novel model system for studying kidney development.

Published
2015
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13. In aged mice, low surrogate light chain promotes pro‐ <scp>B</scp> ‐cell apoptotic resistance, compromises the <scp>P</scp> re <scp>BCR</scp> checkpoint, and favors generation of autoreactive, phosphorylcholine‐specific <scp>B</scp> cells

Author

Sandra S. Zinkel, Daniela Frasca, Jacqueline A. Wright, Sarah Alter, Michelle Ratliff, Wasif N. Khan, Kelly McAvoy, Richard L. Riley, and Bonnie B. Blomberg

Subjects
0303 health sciences, Aging, Phosphorylcholine, Cellular differentiation, CD23, Cell Biology, Biology, Molecular biology, B-1 cell, 03 medical and health sciences, 0302 clinical medicine, medicine.anatomical_structure, Immunology, medicine, biology.protein, Tumor necrosis factor alpha, Bone marrow, Antibody, B cell, 030304 developmental biology, 030215 immunology
Abstract

In aged mice, new B-cell development is diminished and the antibody repertoire becomes more autoreactive. Our studies suggest that (i) apoptosis contributes to reduced B lymphopoiesis in old age and preferentially eliminates those B-cell precursors with higher levels of the surrogate light chain (SLC) proteins (λ5/VpreB) and (ii) λ5(low) B-cell precursors generate new B cells which show increased reactivity to the self-antigen/bacterial antigen phosphorylcholine (PC). Pro-B cells in old bone marrow as well as pro-B cells from young adult λ5-deficient mice are resistant to cytokine-induced apoptosis (TNFα; TGFβ), indicating that low λ5 expression in pro-B cells is sufficient to cause increased survival. Transfer of TNFα-producing 'age-associated B cells' (ABC; CD21/35(-) CD23(-)) or follicular (FO) B cells from aged mice into RAG-2 KO recipients led to preferential loss of λ5(high) pro-B cells, but retention of λ5(low), apoptosis-resistant pro-B cells. In old mice, there is increased reactivity to PC in both immature bone marrow B cells and mature splenic FO B cells. In young mice, absence of λ5 expression led to a similar increase in PC reactivity among bone marrow and splenic B cells. We propose that in old age, increased apoptosis, mediated in part by TNFα-producing B cells, results in preferential loss of SLC(high) pro-B cells within the bone marrow. Further B-cell development then occurs via an 'SLC(low)' pathway that not only impairs B-cell generation, but promotes autoreactivity within the naive antibody repertoires in the bone marrow and periphery.

Published
2015
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14. Abstract 425: Is Adventitial Thickening a Pathogenic Factor in Aortic Atherosclerosis?: A Controlled Transesophageal Echocardiographic Study

Author

Richard H. Snider, Michelle Ratliff, Luis P Roldan, Clifford Qualls, Carlos A. Roldan, Brennan N Gibbs, and Paola Roldan

Subjects
Aortic atherosclerosis, medicine.medical_specialty, Aorta, business.industry, Internal medicine, medicine.artery, Pathogenic factor, Cardiology, Medicine, Thickening, Cardiology and Cardiovascular Medicine, business
Abstract

Background: Aortic (Ao) atherosclerosis is common in systemic lupus erythematosus (SLE), is best assessed by transesophageal echocardiography (TEE), and is characterized by increased intima-media thickness (IMT) and plaques. Although TEE may also allow characterization of Ao adventitial thickness (AT), there is limited data on the pathogenic role of adventitial thickening in Ao atherosclerosis. Methods: 68 SLE patients (62 women, age 36 ± 12 years) and 25 age-and-gender matched healthy controls (22 women, age 34 ± 11 years) underwent multiplane TEE. At a depth of 3-4 cm using narrow sector scan, 2-dimensional guided M-mode images were obtained to assess the presence of plaques, IMT outside of plaques, AT outside of plaques, and AT in plaques at three different levels of the thoracic Ao (proximal, mid, distal). At each aortic level, 3 IMT and 3 AT measurements were taken during end diastole using electronic calipers. These measurements were then averaged. Unaware of subjects’ clinical data, one observer assessed for IMT and plaques while a second observer assessed AT. For purpose of analysis, intima-media thickening was defined as >1 mm which is >2SD above the corresponding overall mean IMT in controls (0.66 ± 0.17 mm), and adventitial thickening as >1.07 mm which is >2SD above the corresponding overall mean AT in controls (0.81 ± 0.13 mm). Plaques were defined as focal-protruding IMT >50% of the surrounding vessel wall at any aortic level. Results: As shown in Table 1A, intima-media thickening and plaques were greater in patients than in controls. Similarly, adventitial thickening was more common in patients than in controls. In addition, AT was greater in patients with intima media thickening, plaques, and intima-media thickening or plaques ( Table 1B) . Furthermore, AT was greater in plaques than AT outside of plaques ( Table 1C ). Conclusion: Adventitial thickening is a pathogenic factor of Ao atherosclerosis in SLE.

Published
2017
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15. Reduced Expression of the DNA-Binding Protein ARID3a, a Mediator of Human Hematopoiesis, in Hematopoietic Progenitors Contributes to Age-Related Transcriptional Changes

Author

Michelle Ratliff, Joshua W Garton, Judith A James, and Carol Webb

Subjects
Immunology, Immunology and Allergy
Abstract

Population studies estimate that 40% of European and US populations will be over the age of 60 by 2050. Aged individuals exhibit impaired immune responses consisting of poor responses to vaccines and increases in myeloid lineage cells. The reasons for decreased immunity in the elderly haven’t been completely elucidated, making studies of the mechanisms leading to these poor responses important. One possibility is that defects in early hematopoiesis may contribute to poor immune responses in the elderly. Previous studies in our lab indicated that inhibition of the DNA-binding protein ARID3a in hematopoietic cultures of human cord blood led to hematopoietic developmental skewing toward myeloid lineage rather than lymphoid lineage progenitors. Furthermore, we previously reported that numbers of ARID3a-expressing hematopoietic stem cells (HSCs) can be highly variable in some patient subsets as well as in healthy individuals. ARID3a expression levels in hematopoietic progenitor cells have not previously been analyzed in relationship to age. We hypothesized that alterations in ARID3a expression levels in early hematopoietic progenitors could contribute to poor immune responses observed in elderly people. Our data suggest that hematopoietic progenitors obtained from peripheral blood of aged healthy persons show decreased frequencies of ARID3a-expressing HSCs in comparison to HSCs from young individuals. Furthermore, lineage committed progenitor numbers were also altered in aged persons compared young people. Ongoing analyses to investigate the gene expression data in young and aged HSCs in relation to ARID3a expression will assess potential genes regulated by ARID3a that contributes to lineage commitment and development.

Published
2019
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16. TO OPERATE OR NOT, WHEN, AND HOW IN A PATIENT WITH LEFT VENTRICULAR THROMBUS AND SEVERE CORONARY ARTERY DISEASE

Author

Paul Andre, Said Yassin, Carlos A. Roldan, and Michelle Ratliff

Subjects
medicine.medical_specialty, business.industry, Left ventricular thrombus, medicine.disease, Coronary revascularization, Coronary artery disease, Internal medicine, medicine, Cardiology, cardiovascular diseases, Cardiology and Cardiovascular Medicine, Clinical decision, business, Dyslipidemia
Abstract

The presence of a left ventricular thrombus in a patient with severe coronary artery disease poses a difficult clinical decision regarding safety, effectiveness, timing, and type of coronary revascularization. The patient is a 69-year-old male with a history of hypertension and dyslipidemia who

Published
2019
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17. Sudden Death in Patients With Coronary Heart Disease Without Severe Systolic Dysfunction

Author

Charles Shoultz, Henri Marais, Ellis Lader, Dhiraj Narula, Cezar Staniloae, Sam Durr, Kevin Marzo, Robert Mendelson, Bilal Malik, Suneet Mittal, Samir Saba, T. Jared Bunch, Rajul Patel, Leng Jiang, Shujahat Shah, Daniel C. Lee, Roopinder K. Sandhu, Steven Hsu, W. Kevin Tsai, Walid Saliba, Preetham Jetty, Kevin H. Silver, Frank Gredler, Zakir Sahul, James Bengston, Mark Niebauer, Neal A. Chatterjee, David B. Delurgio, Daniel G. Anderson, Scott E. Mattson, Greg C. Flaker, Daniel S. Menees, Elizabeth S Kaufman, Susan Graham, Chris Geohas, John F. Heitner, Joel Reinoehl, Otto Costantini, Pedro Colon-Hernandez, Frank McGrew, Brent McLaurin, Arthur Riba, Andre Gauri, Sung Lee, Zayd Eldadah, Nancy R. Cook, William Bugni, Gerald M. Pohost, Matthew Koshy, David E. Haines, Peter Ott, Romel Figueredo, Shelley R. Hankins, Alan H. Kadish, Christopher K. Dyke, Syed M. Mohiuddin, Kathryn Rohr, David Huneycutt, David Kraus, Marcus Averbach, Lindsey L. White, Peter Hotvedt, John McKenzie, David Sandler, Ronald Blonder, Mahmoud Atieh, Norman Erenrich, Sei Iwai, Aziz Hany, Ned Claxton, Hal Skopicki, Steven Klein, Geariod O'Neill, Sorin Danciu, Julie Pester, Diego Sadler, Robert Phang, Jay Schmidt, Udho Thadani, Azhar Aslam, M. Vinayaga Moorthy, Harischandra Karunaratne, James Baker, Jeffrey J. Goldberger, Sean Whalen, Michael Radin, Raul Garcia-Rinaldi, Ronald D. Berger, Michelle Ratliff, Steven D. Owens, Miguel Valderrábano, Christine M. Elbert, Steven Greenberg, Enrique Flores, Pablo Saavedra, Vincent See, David S. Rosenbaum, Michael Fong, Gopi Krishna Panicker, Steven Tishler, Joon Ahn, Mehmet K. Aktas, John E.A. Griffin, Edward Mostel, Stephen Hustead, Charles B. Treasure, Thomas Oliver, Terrence Hack, Talal Baki, Alexander Altschuller, Sharan Mahal, Michael Langer, Benjamin Trichon, Nadim Nasir, Juan M. Aranda, Mohit Bhasin, Patrick Simpson, David Bello, Selcuk Adabag, Kodangudi Ramanathan, Glover Johnson, William Wickemeyer, Charles Gottlieb, Jamal Islam, John Herre, David Wolinsky, Kevin Cochran, Lee Arcement, Judith A. Mackall, Gervasio Lamas, Jeffrey Shanes, Terence Ross, Mirza Baig, Joseph McGarvey, Stephanie H. Dunlap, Robert Weiss, Victoria Bernstein, Terrence X. O'Brien, Mark Myers, Benjamin Cheong, David Serfas, Robert Spencer, William Whang, Charles Gornick, Hemal M. Nayak, Andi Schaecter, J. Thomas Svinarich, Muqtada Chaudhry, P. Kasi Ramanathan, John Kazmierski, John Sobolski, Robert W Biederman, Andrew Sumner, Eve Gillespie, Christine M. Albert, Matthew Nora, and Claudio Schuger

Subjects
medicine.medical_specialty, medicine.medical_treatment, Population, Coronary Disease, 030204 cardiovascular system & hematology, behavioral disciplines and activities, Sudden death, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, mental disorders, Humans, Medicine, Cumulative incidence, 030212 general & internal medicine, education, Prospective cohort study, Original Investigation, education.field_of_study, Ejection fraction, business.industry, Implantable cardioverter-defibrillator, medicine.disease, Death, Sudden, Cardiac, Heart failure, Cardiology, Cardiomyopathies, Cardiology and Cardiovascular Medicine, business, Cohort study
Abstract

Importance The majority of sudden and/or arrhythmic deaths (SAD) in patients with coronary heart disease occur in those without severe systolic dysfunction, for whom strategies for sudden death prevention are lacking. Objective To provide contemporary estimates of SAD vs other competing causes of death in patients with coronary heart disease without severe systolic dysfunction to search for high-risk subgroups that might be targeted in future trials of SAD prevention. Design, Setting, and Participants This prospective observational cohort study included 135 clinical sites in the United States and Canada. A total of 5761 participants with coronary heart disease who did not qualify for primary prevention implantable cardioverter defibrillator therapy based on left ventricular ejection fraction (LVEF) of more than 35% or New York Heart Association (NYHA) heart failure class (LVEF >30%, NYHA I). Exposures Clinical risk factors measured at baseline including age, LVEF, and NYHA heart failure class. Main Outcomes and Measures Primary outcome of SAD, which is a composite of SAD and resuscitated ventricular fibrillation arrest. Results The mean (SD) age of the cohort was 64 (11) years. During a median of 3.9 years, the cumulative incidence of SAD and non-SAD was 2.1% and 7.7%, respectively. Sudden and/or arrhythmic death was the most common mode of cardiovascular death accounting for 114 of 202 cardiac deaths (56%), although noncardiac death was the primary mode of death in this population. The 4-year cumulative incidence of SAD was lowest in those with an LVEF of more than 60% (1.0%) and highest among those with LVEF of 30% to 40% (4.9%) and class III/IV heart failure (5.1%); however, the cumulative incidence of non-SAD was similarly elevated in these latter high-risk subgroups. Patients with a moderately reduced LVEF (40%-49%) were more likely to die of SAD, whereas those with class II heart failure and advancing age were more likely to die of non-SAD. The proportion of deaths due to SAD varied widely, from 14% (18 of 131 deaths) in patients with NYHA II to 49% (37 of 76 deaths) in those younger than 60 years. Conclusions and Relevance In a contemporary population of patients with coronary heart disease without severe systolic dysfunction, SAD accounts for a significant proportion of overall mortality. Moderately reduced LVEF, age, and NYHA class distinguished SAD and non-SAD, whereas other markers were equally associated with both modes of death. Absolute and proportional risk of SAD varied significantly across clinical subgroups, and both will need to be maximized in future risk stratification efforts.

Published
2018
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18. Genes associated with ARID3a expression in B Lymphocytes from Systemic Lupus Erythematosus patients

Author

Joshua W. Garton, Richard Pelikan, Michelle Ratliff, Judith A. James, Patrick Gaffney, and Carol F. Webb

Subjects
Immunology, Immunology and Allergy
Abstract

Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease characterized by overproduction of autoantibodies by B cells and the loss of tolerance to nucleic acids. Our previous studies demonstrated that AT-rich interacting domain 3a (ARID3a), a DNA-binding protein associated with immunoglobulin transcription, is more abundant in SLE B lymphocytes than in healthy control B cells. ARID3a expression in SLE patient blood occurred in naïve B cell subsets which do not express ARID3a in healthy controls. Importantly, increased numbers of ARID3a+ B cells in SLE correlated with increased disease activity in patients. Our recent data indicated that ARID3a is critical for the expression of the key inflammatory cytokine, interferon-alpha (IFNa), in B cells and other blood cells. ARID3a+ B cells appear to denote a new kind of B effector cell that can induce IFNa expression in other cell types. We hypothesize that ARID3a is an important contributor to increased disease activity in SLE patients. Therefore, it is important to better define the characteristics of these cells. ARID3a is bimodally expressed, such that only a fraction of the cells within any B cell subset express ARID3a at a given time. Our current studies took advantage of this bimodal expression using single-cell technology to perform RNA-seq analyses of ARID3a+ and ARID3a− SLE B cells to identify differentially expressed genes associated with ARID3a. To date, ARID3a expression is correlated with innate immune response genes and epigenetic regulators. We predict these studies will be informative regarding how ARID3a expression contributes to disease pathogenesis in patients with SLE, and will provide novel information defining a new subset of effector B cells.

Published
2018
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19. Inhibitor of MyoD Family A (I-mfa) regulates HSPC and myeloid differentiation

Author

Jeremy S. Houser, Marta Onopiuk, Michelle Ratliff, Peter Ngo, Carol Webb, Leonidas Tsiokas, and Mary Beth Humphrey

Subjects
Immunology, Immunology and Allergy
Abstract

Hematopoietic stem and progenitor cell (HSPC) populations are capable of expanding in response to immunological insult or homeostatic turnover. Regulation of the fate decision between self-renewal and differentiation allows for both maintenance of blood cell populations and sustained hematopoiesis across the entire life-span. I-mfa, a small cytosolic protein, has been shown to inhibit lineage-specific transcription factors as well as regulate β-catenin/Wnt signaling. We have previously shown that I-mfa-null mice have increased myeloid cells resulting in increased osteoclasts and hypothesized that I-mfa regulates myeloid lineage differentiation and may affect HSPC populations. In order to test this, bone marrow (BM) from I-mfa−/− mice was analyzed by flow cytometry, showing increases in both long-term and short-term hematopoietic stem cells compared to WT controls, an effect which increased with age. Additionally, both common myeloid precursors (CMP) and granulocyte-macrophage precursors (GMP) were increased in I-mfa−/− mice. Conditional knockout of I-mfa in all hematopoietic lineages using Vav1-Cre lead to similar findings, while conditional knockout in myeloid cells with LysM-Cre showed only increases in myeloid progenitors. These data indicate that I-mfa has separate roles in regulating HSPC expansion and myeloid cell differentiation. Mechanistically, M-CSF-stimulated I-mfa−/− BM had significantly increased transcription of β-catenin signaling target genes Ccnd1, Axin2, and Myc, as well as myelopoietic transcription factors Spi1, Irf8, and Klf4, compared to WT. Further studies are being conducted to determine the effect of I-mfa on quiescence, Wnt ligand sensitivity, and BM reconstitution capacity.

Published
2018
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20. Imprinting the Fate of Antigen-Reactive B Cells through the Affinity of the B Cell Receptor

Author

Randolph J. Noelle, Weijun Zhang, William M. Loo, Michelle Ratliff, Danielle Shnider, Evan F. Lind, Brian P. O'Connor, Laura A. Vogel, and Loren D. Erickson

Subjects
Cellular differentiation, Immunology, B-cell receptor, Naive B cell, Antibody Affinity, Receptors, Antigen, B-Cell, Enzyme-Linked Immunosorbent Assay, Mice, Transgenic, Biology, Article, Mice, Immune system, Antigen, Image Processing, Computer-Assisted, Animals, Immunology and Allergy, B-Lymphocytes, Microscopy, Confocal, Reverse Transcriptase Polymerase Chain Reaction, breakpoint cluster region, Germinal center, Cell Differentiation, Germinal Center, Adoptive Transfer, Molecular biology, humanities, Humoral immunity
Abstract

Long-lived plasma cells (PCs) and memory B cells (Bmem) constitute the cellular components of enduring humoral immunity, whereas short-lived PCs that rapidly produce Ig correspond to the host’s need for immediate protection against pathogens. In this study we show that the innate affinity of the BCR for Ag imprints upon naive B cells their differentiation fate to become short- or long-lived PCs and Bmem. Using BCR transgenic mice with varying affinities for Ag, naive B cells with high affinity lose their capacity to form germinal centers (GCs), develop neither Bmem nor long-lived PCs, and are destined to a short-lived PC fate. Moderate affinity interactions result in hastened GC responses, and differentiation to long-lived PCs, but Bmem remain extinct. In contrast, lower affinity interactions show tempered GCs, producing Bmem and affinity-matured, long-lived PCs. Thus, a continuum of elementary to comprehensive humoral immune responses exists that is controlled by inherent BCR affinity.

Published
2006
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21. Differential expression of the transcription factor ARID3a in lupus patient hematopoietic progenitor cells

Author

Michelle Ratliff, Judith A. James, Carol F. Webb, Joan T. Merrill, and Julie M. Ward

Subjects
Adult, Immunology, Population, CD34, Gene Expression, Mice, SCID, Biology, Article, Immunophenotyping, Mice, Young Adult, Mice, Inbred NOD, medicine, Immunology and Allergy, Animals, Humans, Lupus Erythematosus, Systemic, Progenitor cell, education, B cell, Aged, Mice, Knockout, education.field_of_study, B-Lymphocytes, Middle Aged, Hematopoietic Stem Cells, Transplantation, DNA-Binding Proteins, Haematopoiesis, medicine.anatomical_structure, Gene Expression Regulation, Antibodies, Antinuclear, Case-Control Studies, Antibody Formation, Antigens, Surface, Stem cell, Transcription Factors
Abstract

Although hematopoietic stem/progenitor cells (HSPCs) are used for transplantation, characterization of the multiple subsets within this population in humans has lagged behind similar studies in mice. We found that expression of the DNA-binding protein, ARID3a, in mouse stem cells was important for normal development of hematopoietic lineages; however, progenitors expressing ARID3a in humans have not been defined. We previously showed increased numbers of ARID3a+ B cells in nearly half of systemic lupus erythematosus (SLE) patients, and total numbers of ARID3a+ B cells were associated with increased disease severity. Because expression of ARID3a in those SLE patients occurred throughout all B cell subsets, we hypothesized that ARID3a expression in patient HSPCs might also be increased relative to expression in healthy controls. Our data now show that ARID3a expression is not limited to any defined subset of HSPCs in either healthy controls or SLE patients. Numbers of ARID3a+ HSPCs in SLE patients were increased over numbers of ARID3a+ cells in healthy controls. Although all SLE-derived HSPCs exhibited poor colony formation in vitro compared with controls, SLE HSPCs with high numbers of ARID3a+ cells yielded increased numbers of cells expressing the early progenitor marker, CD34. SLE HSPCs with high numbers of ARID3a+ cells also more readily generated autoantibody-producing cells than HSPCs with lower levels of ARID3a in a humanized mouse model. These data reveal new functions for ARID3a in early hematopoiesis and suggest that knowledge regarding ARID3a levels in HSPCs could be informative for applications requiring transplantation of those cells.

Published
2014

22. Abstract 19026: Libman-sacks Endocarditis: Can It Be Clinically Predicted?

Author

Leonardo Macias, Richard Snider, Michelle Ratliff, Paola Roldan, Rodrigo Rodriguez, Clifford Qualls, Wilmer Sibbitt, and Carlos A Roldan

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Background: Libman-Sacks endocarditis, characterized by Libman-Sacks vegetations (LSV), is common in patients with systemic lupus erythematosus (SLE) and is a strong predictor of stroke and transient ischemic attacks (TIA), cognitive dysfunction, and increased mortality. Accurate detection of LSV may lead to early therapy and prevention of development or progression of embolic cerebrovascular disease. TEE is accurate for detecting LSV, but is semi-invasive. Thus, there is a need for identifying clinical variables with a high predictive value for LSV on TEE. Methods: 76 SLE patients (69 women, 38 ± 12 years old) and 26 age-and sex-matched healthy controls underwent TEE and assessment of demographics, atherogenic risk factors, and parameters of inflammation, platelet activity, coagulation, and fibrinolysis. Patients were also assessed for SLE duration, activity, injury, therapy, and autoantibodies including antiphospholipid antibodies. Multivariate regression and optimal receiver operator curve by Neyman-Pearson lemma were used to determine the best clinical predictors of LSV on TEE. Results: 39 (51%) SLE patients vs 2 (8%) controls had LSV on TEE (p LSV on TEE ( Figure 1 ). Conclusion: In SLE patients, acute stroke/TIA, or SLE duration ≥12 years, or SLE duration ≥5 years and age ≥32 provide a high diagnostic yield for detecting LSV on TEE.

Published
2014
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23. In aged mice, low surrogate light chain promotes pro-B-cell apoptotic resistance, compromises the PreBCR checkpoint, and favors generation of autoreactive, phosphorylcholine-specific B cells

Author

Michelle, Ratliff, Sarah, Alter, Kelly, McAvoy, Daniela, Frasca, Jacqueline A, Wright, Sandra S, Zinkel, Wasif N, Khan, Bonnie B, Blomberg, and Richard L, Riley

Subjects
B cells, phosphorylcholine, senescence, Immunoglobulin Light Chains, Surrogate, Precursor Cells, B-Lymphoid, aging, Apoptosis, Cell Differentiation, Cell Cycle Checkpoints, Original Articles, Lymphocyte Activation, Mice, Inbred C57BL, B lymphopoeisis, inflammation, Animals, TNF alpha, autoreactivity
Abstract

In aged mice, new B-cell development is diminished and the antibody repertoire becomes more autoreactive. Our studies suggest that (i) apoptosis contributes to reduced B lymphopoiesis in old age and preferentially eliminates those B-cell precursors with higher levels of the surrogate light chain (SLC) proteins (λ5/VpreB) and (ii) λ5(low) B-cell precursors generate new B cells which show increased reactivity to the self-antigen/bacterial antigen phosphorylcholine (PC). Pro-B cells in old bone marrow as well as pro-B cells from young adult λ5-deficient mice are resistant to cytokine-induced apoptosis (TNFα; TGFβ), indicating that low λ5 expression in pro-B cells is sufficient to cause increased survival. Transfer of TNFα-producing 'age-associated B cells' (ABC; CD21/35(-) CD23(-)) or follicular (FO) B cells from aged mice into RAG-2 KO recipients led to preferential loss of λ5(high) pro-B cells, but retention of λ5(low), apoptosis-resistant pro-B cells. In old mice, there is increased reactivity to PC in both immature bone marrow B cells and mature splenic FO B cells. In young mice, absence of λ5 expression led to a similar increase in PC reactivity among bone marrow and splenic B cells. We propose that in old age, increased apoptosis, mediated in part by TNFα-producing B cells, results in preferential loss of SLC(high) pro-B cells within the bone marrow. Further B-cell development then occurs via an 'SLC(low)' pathway that not only impairs B-cell generation, but promotes autoreactivity within the naïve antibody repertoires in the bone marrow and periphery.

Published
2014

24. Oxidative stress indices in IDDM subjects with and without long-term diabetic complications

Author

D. Michelle Ratliff, Lucy A. Hunsaker, Jason M Harrison, David L. Vander Jagt, and Dorothy J. VanderJagt

Subjects
Adult, Male, medicine.medical_specialty, Time Factors, medicine.medical_treatment, Clinical Biochemistry, Population, Ascorbic Acid, Glucosephosphate Dehydrogenase, medicine.disease_cause, Thiobarbituric Acid Reactive Substances, Antioxidants, chemistry.chemical_compound, Internal medicine, Diabetes mellitus, medicine, TBARS, Humans, Vitamin E, education, Chromatography, High Pressure Liquid, Aged, Glutathione Transferase, Glutathione Peroxidase, education.field_of_study, Chemistry, General Medicine, Glutathione, Middle Aged, Malondialdehyde, Ascorbic acid, medicine.disease, Oxidative Stress, Diabetes Mellitus, Type 1, Endocrinology, Models, Chemical, Case-Control Studies, Female, Biomarkers, Oxidative stress
Abstract

Background: Numerous animal and population studies of diabetes have identified markers of oxidative stress. However, for most markers that have been measured the results are not consistent. In addition, it is less clear whether oxidative stress is related to the development of diabetic complications. The objective of this study was to evaluate a series of plasma markers and leukocyte markers to test the hypothesis that type 1 Insulin Dependent Diabetes Mellitus (IDDM) subjects experience oxidative stress. A related question was whether markers of oxidative stress are higher in IDDM subjects who have developed long-term complications. Methods: The study population consisted of 22 IDDM subjects with diabetic complications and 22 IDDM subjects without complications, both groups matched by age and gender and with similar HbA1c levels, and 16 nondiabetic control subjects. Plasma levels of organoperoxides were determined by the ferrous oxidation/xylenol orange (FOX) assay, malondialdehyde by the thiobarbituric acid (TBARS) assay, and vitamin E by HPLC. Mononuclear cells and polymorphonuclear cells were analyzed for ascorbic acid by HPLC and for glutathione (GSH) by enzymatic recycling. In addition, GSH peroxidase, GSH transferase and glucose-6-phosphate dehydrogenase levels were determined in both cell fractions. Results: Plasma organoperoxides were significantly elevated in the IDDM subjects compared to controls (p = 0.02) while TBARS and vitamin E levels were not significantly different. In the IDDM subjects, mononuclear cell levels of ascorbic acid were significantly lower (p < 0.02) and levels of GSH were lower, approaching significance (p = 0.07), compared to controls. Ascorbic acid and GSH levels in polymorphonuclear cells were not significantly different between IDDM subjects and controls, nor were enzyme levels different. In addition, the plasma and intracellular indices of oxidative status in IDDM subjects were not different when IDDM subjects with complications were compared to IDDM subjects without complications. Conclusion: Demonstration of oxidative stress in IDDM subjects depends upon which markers are measured. This is in agreement with previous studies of oxidative stress in various disease states including diabetes. Plasma levels of organoperoxides may be the most reliable indicators of oxidative stress. However, it is unclear whether elevated plasma organoperoxides indicate a generalized systemic stress or are produced in localized areas. By comparison, oxidative stress indices determined with isolated blood cells may provide a clearer picture. Depressed levels of ascorbic acid and GSH were observed only in mononuclear cells, which are mainly long-lived T lymphocytes. Mononuclear cells antioxidant status may reflect systemic oxidative stress. In this study, neither plasma markers nor intracellular markers of oxidative stress were different in IDDM subjects with long-term diabetic complications compared to subjects without complications.

Published
2001
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25. In senescence, age-associated B cells secrete TNFα and inhibit survival of B-cell precursors

Author

Richard L. Riley, Bonnie B. Blomberg, Michelle Ratliff, Sarah Alter, and Daniela Frasca

Subjects
medicine.medical_specialty, Adoptive cell transfer, Aging, Cell Survival, medicine.medical_treatment, B-Lymphocyte Subsets, Apoptosis, Biology, Lymphocyte Activation, Article, Immunophenotyping, Mice, Antigens, CD, Bone Marrow, Internal medicine, medicine, Animals, Lymphopoiesis, B cell, Cells, Cultured, Mice, Knockout, Tumor Necrosis Factor-alpha, Precursor Cells, B-Lymphoid, CD23, Cell Differentiation, Cell Biology, Adoptive Transfer, Interleukin-10, DNA-Binding Proteins, Interleukin 10, medicine.anatomical_structure, Endocrinology, Cytokine, Bone marrow, Spleen
Abstract

Aged mice exhibit ~ 5-10-fold increases in an ordinarily minor CD21/35(-) CD23(-) mature B-cell subset termed age-associated B cells (ABCs). ABCs from old, but not young, mice induce apoptosis in pro-B cells directly through secretion of TNFα. In addition, aged ABCs, via TNFα, stimulate bone marrow cells to suppress pro-B-cell growth. ABC effects can be prevented by the anti-inflammatory cytokine IL-10. Notably, CD21/35(+) CD23(+) follicular (FO) splenic and FO-like recirculating bone marrow B cells in both young and aged mice contain a subpopulation that produces IL-10. Unlike young adult FO B cells, old FO B cells also produce TNFα; however, secretion of IL-10 within this B-cell population ameliorates the TNFα-mediated effects on B-cell precursors. Loss of B-cell precursors in the bone marrow of old mice in vivo was significantly associated with increased ABC relative to recirculating FO-like B cells. Adoptive transfer of aged ABC into RAG-2 KO recipients resulted in significant losses of pro-B cells within the bone marrow. These results suggest that alterations in B-cell composition during old age, in particular, the increase in ABC within the B-cell compartments, contribute to a pro-inflammatory environment within the bone marrow. This provides a mechanism of inappropriate B-cell 'feedback' that promotes down-regulation of B lymphopoiesis in old age.

Published
2013

26. A molecular mechanism for TNF-α-mediated downregulation of B cell responses

Author

Ana Marie Landin, Daniela Frasca, Maria Romero, Richard L. Riley, Alain Diaz, Sarah Alter-Wolf, Bonnie B. Blomberg, and Michelle Ratliff

Subjects
Lipopolysaccharides, Male, medicine.medical_specialty, Aging, RNA Stability, Immunology, Down-Regulation, Stimulation, Biology, Article, Proinflammatory cytokine, Mice, Transcription Factor 3, Downregulation and upregulation, Tristetraprolin, Internal medicine, Cytidine Deaminase, medicine, Immunology and Allergy, Animals, RNA, Messenger, Autocrine signalling, B cell, Cells, Cultured, B-Lymphocytes, Mice, Inbred BALB C, Tumor Necrosis Factor-alpha, Cytidine deaminase, Immunoglobulin Class Switching, Cell biology, Autocrine Communication, Endocrinology, medicine.anatomical_structure, Immunoglobulin class switching, Tumor necrosis factor alpha, Female
Abstract

B cell function with age is decreased in class switch recombination (CSR), activation-induced cytidine deaminase (AID), and stability of E47 mRNA. The latter is regulated, at least in part, by tristetraprolin (TTP), which is increased in aged B cells and also negatively regulates TNF-α. In this study, we investigated whether B cells produce TNF-α, whether this changes with age, and how this affects their function upon stimulation. Our hypothesis is that in aging there is a feedback mechanism of autocrine inflammatory cytokines (TNF-α) that lowers the expression of AID and CSR. Our results showed that unstimulated B cells from old BALB/c mice make significantly more TNF-α mRNA and protein than do B cells from young mice, but after stimulation the old make less than the young; thus, they are refractory to stimulation. The increase in TNF-α made by old B cells is primarily due to follicular, but not minor, subsets of B cells. Incubation of B cells with TNF-α before LPS stimulation decreased both young and old B cell responses. Importantly, B cell function was restored by adding anti–TNF-α Ab to cultured B cells. To address a molecular mechanism, we found that incubation of B cells with TNF-α before LPS stimulation induced TTP, a physiological regulator of mRNA stability of the transcription factor E47, which is crucial for CSR. Finally, anti–TNF-α given in vivo increased B cell function in old, but not in young, follicular B cells. These results suggest new molecular mechanisms that contribute to reduced Ab responses in aging.

Published
2011

27. Low surrogate light chain in pro-B cells from old mice suppresses apoptosis and alters the idiotypes and proportions of phosphorylcholine reactive B cells (LYM6P.718)

Author

Richard Riley, Kelly McAvoy, Michelle Ratliff, Sarah Alter, Daniela Frasca, Wasif Khan, and Bonnie Blomberg

Subjects
Immunology, Immunology and Allergy
Abstract

The generation of new B cells is substantially decreased in old mice (>2 years). Early B cell precursors (pro-B cells) are reduced in old mice and exhibit a reduction in the surrogate light chain (SLC) protein λ5. We hypothesize that this alters the expression and function of the pre-B cell receptor and influences the “read-out” of antibody specificities in the B cell repertoire. In old mice, the remaining pro-B cells, low in SLC, are resistant to apoptotic stimuli (TNFα), in contrast to young adult pro-B cells. Apoptotic sensitivity reflects levels of the SLC, since young pro-B cells partially or completely deficient in λ5 are also resistant to apoptosis. Age-associated B cells (ABC) represent a B cell subset which expands in old mice; ABC are pro-inflammatory and secrete TNFα. Adoptive transfer of ABC into young RAG-2 KO recipients results in partial loss of pro-B cells and, in particular, loss of pro-B cells with higher levels of SLC λ5. Anti-phosphorylcholine (PC) reactive B cells, especially those of the T15 idiotype, are important in defense against pneumococci. In old age, the proportion of PC reactive B cells, particularly with less protective T15 negative idiotypes, increases. Low SLC promotes both increased PC reactivity and T15 negative idiotypes. These studies suggest that ABC promote an “SLClow” B cell pathway that alters antibody specificities in old age.

Published
2015
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28. Age-associated B cells (ABC) cause reduced surrogate light chain expression and loss of B cell precursors in old age (HEM2P.269)

Author

Richard Riley, Michelle Ratliff, Sarah Alter, Daniela Frasca, Jacqueline Wright, Wasif Khan, and Bonnie Blomberg

Subjects
Immunology, Immunology and Allergy
Abstract

Age-associated B cells (ABC, CD21/35- CD23-) accumulate in spleen and bone marrow of ~2 yrs. old mice and induce TNF-α-dependent apoptosis of pro-B cells. The remaining B cell precursors in aged mice exhibit reductions in surrogate light chain (SLC) and compromise of the preBCR checkpoint. Notably, the residual pro-B cells in aged bone marrow are resistant to ABC/TNF-α-mediated apoptosis. SLC is associated with cadherin 17 on the surface of pro-B cells. Like SLC-low aged pro-B cells, pro-B cells from λ5 SLC-deficient young adult mice were also resistant to TNF-α-induced apoptosis. This implies that expression of the SLC/cadherin 17 complex is required for normal susceptibility to apoptosis in pro-B cells. Resistance to apoptosis in aged pro-B cells and λ5-deficient young pro-B cells coincided with increased phosphorylation of the pro-apoptotic protein Bim, a modification that tags Bim for degradation. We hypothesize that, in old mice, expanded pro-inflammatory ABC within the bone marrow cause apoptosis of pro-B cells. However, this cell death occurs preferentially in pro-B cells which express relatively high levels of SLC. The remaining pro-B cells in aged mice are consequently skewed to lower SLC expression. We suggest that ABC, by inducing the loss of “high SLC” pro-B cells, deviate B lymphopoiesis into an ”SLC low pathway” with inefficient B cell production and altered B cell antibody repertoire.

Published
2014
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29. Differential expression of the transcription factor ARID3a in lupus patient hematopoietic progenitors may affect function (BA12P.101)

Author

Michelle Ratliff, Julie Ward, Judith James, and Carol Webb

Subjects
Immunology, Immunology and Allergy
Abstract

Autologous hematopoietic stem cell (HSC) transplants have been used for severe cases of autoimmune disease, but success rates for systemic lupus erythrematosus (SLE) patients are less than for other autoimmune diseases. We recently found >40% of SLE patients had increased numbers of peripheral B lymphocytes that express the DNA-binding protein ARID3a, and that numbers of ARID3a+ B cells were associated with increased disease activity. Because ARID3a is also expressed in HSCs, we queried if SLE CD34+ cells abnormally express ARID3a. Indeed, nearly 40% of SLE patients had increased numbers of CD34+ cells with higher expression of ARID3a compared to healthy controls. Progenitors with increased ARID3a expression showed enhanced proliferation in vitro relative to other SLE cultures, and those progenitors generated increased numbers of cells that retained CD34 expression. We hypothesize that variation in ARID3a expression in hematopoietic progenitors contributes to variability in engraftment and are testing that hypothesis using humanized mice. Together, these data suggest new functions for ARID3a in HSCs and autoimmunity.

Published
2014
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30. Inhibition of Human Aldose and Aldehyde Reductases by Non-Steroidal Anti-Inflammatory Drugs

Author

David L. Vander Jagt, Francella J. Martinez, Christina M. Schimandle, B Robinson, D. Michelle Ratliff, Lucy A. Hunsaker, and Timothy J. Van der Jagt

Subjects
chemistry.chemical_classification, Aldose reductase, Chemistry, Aldose reductase inhibitor, Molecular biology, Aldehyde, chemistry.chemical_compound, Polyol pathway, Aldose, Oxidoreductase, medicine, Sorbitol, Aldehyde Reductase, medicine.drug
Abstract

Aldose reductase (EC 1.1.1.21; alditol:NAD(P)+oxidoreductase; ALR2), a member of the multi gene family of NADPH-dependent aldo-keto reductases, is one of the major enzymes implicated in the intracellular events leading to the development of diabetic complications. ALR2 catalyzes the reduction of glucose to sorbitol in the first reaction of the polyol pathway which may be important under conditions of hyperglycemia (Kador and Kinoshita, 1985). There have been a number of reports that some non-steroidal anti-inflammatory drugs (NSAIDs) can delay the development of diabetic complications. These reports include in vitro studies with isolated lens or nerve tissue (Chaudhry et al., 1983; Sharma and Cotlier, 1982; Crabbe et al., 1985; Jacobson et al., 1983), animal studies (Gupta and Joshi, 1991a; Blakytny and Harding, 1992; Gupta and Joshi, 1991b; Mansour et al., 1990; Sharma et al., 1989a), and clinical studies (Sharma et al., 1989b; Cunha-Vaz et al., 1985; Cohen and Harris, 1987). Several NSAIDs have been shown to be inhibitors of ALR2 (Chaudhry et al., 1983; Sharma and Cotlier, 1982; Crabbe et al., 1985; Gupta and Joshi, 1991a; Gupta and Joshi, 1991b). Most studies of inhibition of ALR2 by NSAIDs have used either animal ALR2 or crude homogenates of human tissues (Sharma and Cotlier, 1982; Crabbe et al., 1985; Gupta and Joshi, 1991a; Gupta and Joshi, 1991b). There are marked differences in the inhibitor-binding properties of ALR2 from various sources (Kador et al., 1980). In addition, we have shown that human ALR2 can be oxidized easily, resulting in the formation of a form of ALR2 with markedly altered kinetic properties (Vander Jagt et al., 1990a). There is also the problem that crude homogenates generally contain a mixture of ALR2 and the immunochemically distinct, but kinetically related, aldehyde reductase, ALR1 (Vander Jagt et al., 1990b).

Published
1999
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31. Radial Artery Grafts vs Saphenous Vein Grafts in Coronary Artery Bypass Surgery

Author

Mei Chiung Shih, William L. Holman, Kelvin K. Lee, Miguel Haime, Gulshan K. Sethi, Steven Goldman, Ernesto R. Soltero, Stephen E. Fremes, Donald Thomas, Sandra Kreamer, Thomas E. Moritz, Vigneshwar Kasirajan, Douglass A. Morrison, Lori Planting, Meredith Miller, Stewart Pett, Birger Rhenman, Lynn Harrison, Mohammed M. Moursi, Yajie Wang, Hoang Thai, Yvette Rodriguez, Rosemary F. Kelly, Anand Irimpen, Domenic J. Reda, Gareth H. Tobler, Joseph Huh, Edward O. McFalls, Michelle Ratliff, Herbert B. Ward, Faisal G. Bakaeen, Michael D. Crittenden, Elizabeth Juneman, William Gunnar, Todd H. Wagner, and Mary Kaye Pierce

Subjects
medicine.medical_specialty, business.industry, General Medicine, Anterior Descending Coronary Artery, medicine.disease, Surgery, Coronary artery disease, Coronary artery bypass surgery, surgical procedures, operative, medicine.anatomical_structure, medicine.artery, Internal medicine, medicine, Cardiology, Vascular Patency, Myocardial infarction, Radial artery, Vein, business, Artery
Abstract

Context Arterial grafts are thought to be better conduits than saphenous vein grafts for coronary artery bypass grafting (CABG) based on experience with using the left internal mammary artery to bypass the left anterior descending coronary artery. The efficacy of the radial artery graft is less clear. Objective To compare 1-year angiographic patency of radial artery grafts vs saphenous vein grafts in patients undergoing elective CABG. Design, Setting, and Participants Multicenter, randomized controlled trial conducted from February 2003 to February 2009 at 11 Veterans Affairs medical centers among 757 participants (99% men) undergoing first-time elective CABG. Interventions The left internal mammary artery was used to preferentially graft the left anterior descending coronary artery whenever possible; the best remaining recipient vessel was randomized to radial artery vs saphenous vein graft. Main Outcome Measures The primary end point was angiographic graft patency at 1 year after CABG. Secondary end points included angiographic graft patency at 1 week after CABG, myocardial infarction, stroke, repeat revascularization, and death. Results Analysis included 733 patients (366 in the radial artery group, 367 in the saphenous vein group). There was no significant difference in study graft patency at 1 year after CABG (radial artery, 238/266; 89%; 95% confidence interval [CI], 86%-93%; saphenous vein, 239/269; 89%; 95% CI, 85%-93%; adjusted OR, 0.99; 95% CI, 0.56-1.74; P = .98). There were no significant differences in the secondary end points. Conclusion Among Veterans Affairs patients undergoing first-time elective CABG, the use of a radial artery graft compared with saphenous vein graft did not result in greater 1-year patency. Trial Registration clinicaltrials.gov Identifier: NCT00054847

Published
2011
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