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2. Contributors

Author

Abramson, Steven, primary, An, KaiNan, additional, Andrade, Felipe, additional, Ardoin, Stacy P., additional, Barton, Anne, additional, Baughman, Robert P., additional, Beaton, Dorcas E., additional, Beere, Helen M., additional, Beltran, Javier, additional, Bending, David, additional, Bennett, Robert M., additional, Bermas, Bonnie L., additional, Bertsias, George, additional, Bhardwaj, Nina, additional, Bijlsma, Johannes W.J., additional, Bockenstedt, Linda K., additional, Boers, Maarten, additional, Boilard, Eric, additional, Boin, Francesco, additional, Boumpas, Dimitrios T., additional, Boyle, David L., additional, Bradley, Sean, additional, Brown, Matthew, additional, Buch, Maya, additional, Buckley, Christopher D., additional, Budd, Ralph C., additional, Burg, Nathalie, additional, Burns, Christopher M., additional, Cannella, Amy C., additional, Carter, John D., additional, Chakravarty, Eliza F., additional, Chakravarty, Soumya D., additional, Chang, Christopher, additional, Cheng, Joseph S., additional, Chiodo, Christopher P., additional, Chung, Sharon, additional, Cleland, Leslie G., additional, Cohen, Stanley, additional, Colbert, Robert A., additional, Cook, Paul P., additional, Craft, Joseph E., additional, Crofford, Leslie J., additional, Cronstein, Bruce N., additional, Crow, Mary K., additional, Crowson, Cynthia S., additional, Culley, Kirsty L., additional, Cunnane, Gaye, additional, Dall'Era, Maria, additional, Darrah, Erika, additional, Davis, John M., additional, Bari, Cosimo De, additional, Dell'Accio, Francesco, additional, Diamond, Betty, additional, Di Cesare, Paul E., additional, Dixit, Rajiv, additional, Drenth, Joost P.H., additional, Dustin, Michael L., additional, El-Gabalawy, Hani S., additional, Elmamoun, Musaab, additional, Erickson, Alan R., additional, Erkan, Doruk, additional, Eyre, Stephen, additional, Fanouriakis, Antonis, additional, Felson, David T., additional, Field, Max, additional, Filer, Andrew, additional, Firestein, Gary S., additional, Fishman, Felicity G., additional, FitzGerald, Oliver, additional, Flaherty, John P., additional, Fors, César E., additional, Fortner, Karen A., additional, Gabriel, Sherine E., additional, Gasque, Philippe, additional, Gershwin, M. Eric, additional, Gladue, Heather S., additional, Goldring, Mary B., additional, Goldring, Steven R., additional, Golightly, Yvonne M., additional, Goodman, Stuart, additional, Gordon, Siamon, additional, Grassi, Walter, additional, Green, Douglas R., additional, Greenspan, Adam, additional, Gregersen, Peter, additional, Grimaldi, Christine, additional, Guilherme, Luiza, additional, Hajj-Ali, Rula A., additional, Haudenschild, Dominik R., additional, Hellmann, David B., additional, Holmdahl, Rikard, additional, Hsu, Joyce J., additional, Huddleston, James I., additional, Hudson, Alan P., additional, Huizinga, Thomas W.J., additional, Hunder, Gene G., additional, Iversen, Maura D., additional, Jacobs, Johannes W.G., additional, Jen, Ho, additional, Jordan, Joanne M., additional, Jorizzo, Joseph L., additional, Kalil, Jorge, additional, Kaufman, Kenton, additional, Kaufman, William S., additional, Kavanaugh, Arthur, additional, Keenan, Robert T., additional, Kenna, Tony, additional, Kerr, Darcy A., additional, Koch, Alisa E., additional, Kono, Dwight H., additional, Korsten, Peter, additional, Krakow, Deborah, additional, Krasnokutsky, Svetlana, additional, Lafeber, Floris P.J.G., additional, Lambert, Robert G.W., additional, Lane, Nancy E., additional, Langford, Carol A., additional, Laskin, Daniel M., additional, Layh-Schmitt, Gerlinde, additional, Lee, Lela A., additional, Lee, Tzielan C., additional, Lockshin, Michael D., additional, Lozada, Carlos J., additional, Lundberg, Ingrid E., additional, Luqmani, Raashid, additional, Luyten, Frank P., additional, Mader, Reuven, additional, Maksymowych, Walter, additional, Markenson, Joseph A., additional, Martin, Scott David, additional, Matteson, Eric L., additional, McGregor, Laura, additional, McInnes, Iain B., additional, McNamara, Elizabeth K., additional, Mikuls, Ted R., additional, Miller, Mark S., additional, Ming, Pedro Azevedo, additional, Moder, Kevin G., additional, Monach, Paul A., additional, Moulton, Vaishali R., additional, Nagaraju, Kanneboyina, additional, Nelson, Amanda E., additional, Nigrovic, Peter A., additional, Nistala, Kiran, additional, O'Dell, James R., additional, Okada, Yasunori, additional, Østergaard, Mikkel, additional, Otero, Miguel, additional, Palmer, Bradley M., additional, Panush, Richard S., additional, Peng, Stanford L., additional, Pillai, Shiv, additional, Pillinger, Michael H., additional, Plüddemann, Annette, additional, Polston, Gregory R., additional, Porcelli, Steven A., additional, Price, Mark D., additional, Reed, Ann M., additional, Reveille, John D., additional, Robinson, Angela B., additional, Robinson, Philip, additional, Robinson, William H., additional, Roosendaal, Goris, additional, Rosen, Antony, additional, Rosenbaum, James T., additional, Rosenberg, Andrew E., additional, Ruderman, Eric M., additional, Saag, Kenneth G., additional, Salmon, Jane E., additional, Sammaritano, Lisa R., additional, Samuels, Jonathan, additional, Sandborg, Christy I., additional, Sawalha, Amr H., additional, Saxena, Amit, additional, Schett, Georg, additional, Schutgens, Roger E.G., additional, Seldin, David C., additional, Shah, Binita, additional, Sikora, Keith A., additional, Simon, Anna, additional, Siraj, Dawd S., additional, Sorkin, Linda S., additional, St. Clair, E. William, additional, Stamp, Lisa K., additional, Stone, John H., additional, Suarez-Fueyo, Abel, additional, Svensson, Camilla I., additional, Sweiss, Nadera J., additional, Swigart, Carrie R., additional, Szekanecz, Zoltán, additional, Tait, Stephen, additional, Tanne, Antoine, additional, Taylor, Peter C., additional, Terkeltaub, Robert, additional, Theofilopoulos, Argyrios N., additional, Thornhill, Thomas S., additional, Torok, Kathryn S., additional, Toth, Michael J., additional, Tozman, Elaine C., additional, Trouw, Leendert A., additional, Tsokos, George C., additional, Tugwell, Peter, additional, Tutuncu, Zuhre, additional, Upadhyaya, Shivam, additional, Van, Annette H.M., additional, van der Linden, Sjef, additional, Van, Jos W.M., additional, Van, Jacob M., additional, Meter, Heather Van, additional, van Vollenhoven, Ronald F., additional, van Vulpen, Lize F.D., additional, Varga, John, additional, Vaseer, Samera, additional, Vasquez-Castellanos, Raul, additional, Veale, Douglas J., additional, Wakefield, Richard J., additional, Wallace, Mark S., additional, Wang, Ruoning, additional, Wang, Tingting, additional, Warshaw, David M., additional, Wedderburn, Lucy R., additional, Werth, Victoria P., additional, Wigley, Fredrick M., additional, Wofsy, David, additional, Wollheim, Frank A., additional, Wondimu, Elisabeth, additional, Wong, Cyrus, additional, Wortmann, Robert L., additional, Yelin, Edward, additional, Zayat, Ahmed, additional, Zou, Yong-Rui, additional, and Zurier, Robert B., additional

Published
2017
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5. List of Contributors

Author

Aliprantis, Antonios O., primary, Bello-Irizarry, Sheila N., additional, Berry, Ryan, additional, Briot, Karine, additional, Charles, Julia F., additional, Choi, Yongwon, additional, Daiss, John L., additional, Dayer, Jean-Michel, additional, de Mesy Bentley, Karen L., additional, Einhorn, Thomas A., additional, Faccio, Roberta, additional, Fretz, Jackie A., additional, Garlet, Gustavo P., additional, Gerstenfeld, Louis C., additional, Geusens, Piet, additional, Goldring, Mary B., additional, Goldring, Steven R., additional, Gravallese, Ellen M., additional, Graves, Dana T., additional, Grčević, Danka, additional, Horowitz, Mark C., additional, Ishii, Masaru, additional, Kayal, Rayyan A., additional, Kikuta, Junichi, additional, Klibansky, Anne, additional, Kovačić, Natasa, additional, Kronenberg, Henry M., additional, Lee, Sun-Kyeong, additional, Lorenzo, Joseph, additional, MacDougald, Ormond, additional, Martin, T. John, additional, Nakamura, Mary C., additional, Nanes, Mark S., additional, Nevius, Erin, additional, Nishitani, Kohei, additional, O’Brien, Charles A., additional, Oates, Thomas, additional, Penninger, Josef Martin, additional, Pereira, João P., additional, Quinn, Julian M.W., additional, Rodeheffer, Matthew S., additional, Roodman, Garson David, additional, Rosen, Clifford J., additional, Roux, Christian, additional, Schett, Georg, additional, Schwarz, Edward M., additional, Sigl, Verena, additional, Silbermann, Rebecca, additional, Sims, Natalie A., additional, Steen, Brandon M., additional, Sylvester, Francisco A., additional, Takayanagi, Hiroshi, additional, Teitelbaum, Steven L., additional, Vella, Anthony T., additional, and Wu, Joy Y., additional

Published
2016
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9. Contributors

Author

Abramson, Steven B., primary, An, Kai-Nan, additional, Andrade, Felipe, additional, Atkinson, John P., additional, Baeten, Dominique, additional, Baughman, Robert P., additional, Beaton, Dorcas E., additional, Bennett, Robert, additional, Benseler, Susanne M., additional, Bertsias, George, additional, Bhardwaj, Nina, additional, Bijlsma, Johannes W.J., additional, Bockenstedt, Linda K., additional, Boers, Maarten, additional, Boin, Francesco, additional, Boumpas, Dimitrios T., additional, Bresnihan, Barry, additional, Brettler, Doreen B., additional, Buckley, Christopher D., additional, Budd, Ralph C., additional, Burns, Christopher M., additional, Cannella, Amy C., additional, Chakravarty, Eliza F., additional, Chang, Christopher, additional, Cheng, Joseph S., additional, Chiodo, Christopher P., additional, Cleland, Leslie G., additional, Clowse, Megan E., additional, Cook, Paul P., additional, Craft, Joseph E., additional, Crofford, Leslie J., additional, Cronstein, Bruce N., additional, Crow, Mary K., additional, Cunnane, Gaye, additional, Cush, John J., additional, Cutolo, Maurizio, additional, Dall'Era, Maria, additional, Dao, Kathryn H., additional, Darrah, Erika, additional, Davis, John M., additional, DeGroot, Jeroen, additional, Devin, Clint, additional, Diamond, Betty, additional, Díaz-González, Federico, additional, Di Cesare, Paul E., additional, Dixit, Rajiv, additional, Drenth, Joost P.H., additional, Dustin, Michael L., additional, El-Gabalawy, Hani S., additional, Elkon, Keith B., additional, Erkan, Doruk, additional, Fanouriakis, Antonios, additional, Field, Max, additional, Filer, Andrew, additional, Firestein, Gary S., additional, Fitzgerald, Oliver, additional, Flaherty, John P., additional, Flanagan, Adrienne M., additional, Fortner, Karen A., additional, Gabriel, Sherine E., additional, Gaston, J.S. Hill, additional, Gay, Steffen, additional, Gershwin, M. Eric, additional, Gibofsky, Allan, additional, Ginsberg, Mark H., additional, Goldring, Mary B., additional, Goldring, Steven R., additional, Golightly, Yvonne M., additional, Goodman, Stuart, additional, Gordon, Siamon, additional, Grassi, Walter, additional, Greenspan, Adam, additional, Gregersen, Peter K., additional, Grimaldi, Christine, additional, Hajj-Ali, Rula A., additional, Harper, Lorraine, additional, Harris, Edward D., additional, Haudenschild, Dominik R., additional, Hellmann, David B., additional, Holmdahl, Rikard, additional, Hsu, Joyce J., additional, Huddleston, James I., additional, Huizinga, Thomas W.J., additional, Hunder, Gene G., additional, Hung, Emily W., additional, Inman, Robert D., additional, Iversen, Maura Daly, additional, Jacobs, Johannes W.G., additional, Jordan, Joanne M., additional, Jorizzo, Joseph L., additional, Kaufman, Kenton R., additional, Kaufman, William S., additional, Kavanaugh, Arthur, additional, Keenan, Robert T., additional, Khan, Shaukat, additional, Koch, Alisa E., additional, Kono, Dwight H., additional, Krakow, Deborah, additional, Lambert, Robert G.W., additional, Landewé, Robert B.M., additional, Lane, Nancy E., additional, Langford, Carol A., additional, Laskin, Daniel M., additional, Laxer, Ronald M., additional, Lee, David M., additional, Lee, Lela A., additional, Lee, Tzielan Chang, additional, Lockshin, Michael D., additional, Lories, Rik, additional, Lozada, Carlos J., additional, Lundberg, Ingrid E., additional, Luqmani, Raashid, additional, Luyten, Frank P., additional, Mader, Reuven, additional, Maksymowych, Walter P., additional, Mandell, Brian, additional, Martin, Scott David, additional, Matteson, Eric L., additional, McGirt, Matthew J., additional, McInnes, Iain B., additional, McNamara, Elizabeth Kaufman, additional, Mikuls, Ted R., additional, Miller, Mark S., additional, Moder, Kevin G., additional, Nagaraju, Kanneboyina, additional, Naides, Stanley J., additional, Nelson, Amanda E., additional, Nigrovic, Peter A., additional, Nistala, Kiran, additional, Nowatzky, Johannes, additional, O'Dell, James R., additional, Okada, Yasunori, additional, Orduño, Nataly Manjarrez, additional, Ospelt, Caroline, additional, Østergaard, Mikkel, additional, Palmer, Bradley M., additional, Panush, Richard S., additional, Peng, Stanford L., additional, Pillinger, Michael H., additional, Polston, Gregory R., additional, Porcelli, Steven A., additional, Price, Mark D., additional, Rasker, Johannes J., additional, Reveille, John D., additional, Roberts, W. Neal, additional, Ronneberger, Monika, additional, Rosen, Antony, additional, Rosenbaum, James T., additional, Rosenberg, Andrew E., additional, Ruderman, Eric M., additional, Ruutu, Merja, additional, Salmon, Jane E., additional, Samuels, Jonathan, additional, Sandborg, Christy I., additional, Savage, Caroline O.S., additional, Saxena, Amit, additional, Scher, Jose U., additional, Schett, Georg, additional, Seldin, David C., additional, Simon, Anna, additional, Siraj, Dawd S., additional, Skinner, Martha, additional, St. Clair, E. William, additional, Stamp, Lisa K., additional, Stone, John H., additional, Straub, Rainer H., additional, Sweeney, Susan E., additional, Sweiss, Nadera J., additional, Swigart, Carrie R., additional, Symmons, Deborah, additional, Szekanecz, Zoltan, additional, Tak, Paul-Peter, additional, Taylor, Peter C., additional, Terkeltaub, Robert, additional, Theofilopoulos, Argyrios N., additional, Thomas, Ranjeny, additional, Thornhill, Thomas S., additional, Torralba, Karina D., additional, Toth, Michael J., additional, Tugwell, Peter, additional, Tutuncu, Zuhre, additional, Upchurch, Katherine S., additional, van der Heijde, Désirée M.F.M., additional, van der Helm-van Mil, Annette H.M., additional, van der Linden, Sjef M., additional, van der Meer, Jos W.M., additional, van Laar, Jacob M., additional, Varga, John, additional, Wallace, Mark S., additional, Warshaw, David M., additional, Wedderburn, Lucy R., additional, Werth, Victoria P., additional, Wigley, Fredrick M., additional, Wise, Christopher M., additional, Wofsy, David, additional, Wolfe, Frederick, additional, Wollheim, Frank A., additional, Wortmann, Robert L., additional, Yelin, Edward, additional, Yu, David, additional, Zabriskie, John B., additional, Zurier, Robert B., additional, and Zuurmond, Anne-Marie, additional

Published
2013
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10. Contributors

Author

Aletaha, Daniel, primary, Alfredsson, Lars, additional, Backhaus, Marina, additional, Bathon, Joan M., additional, Bijlsma, Johannes W.J., additional, Boers, Maarten, additional, Breedveld, Ferdinand C., additional, Burmester, Gerd R., additional, Bushar, Nicholas D., additional, Buttgereit, Frank, additional, Conaghan, Philip G., additional, Dass, Shouvik, additional, Deane, Kevin D., additional, Dörner, Thomas, additional, Emery, Paul, additional, Esdaile, John M., additional, Farber, Donna L., additional, Freeston, Jane E., additional, Gay, Steffen, additional, Gerlag, Daniëlle M., additional, Goldring, Mary B., additional, Goycochea, Mavis, additional, van der Heijde, Désirée, additional, Hochberg, Marc C., additional, Holers, V. Michael, additional, Hueber, Axel J., additional, Huizinga, Tom W.J., additional, Johnsen, Alyssa K., additional, Kavanaugh, Arthur, additional, Keystone, Edward, additional, Kiener, Hans P., additional, Kinne, Raimund W., additional, Klareskog, Lars, additional, Kobelt, Gisela, additional, Koch, Alisa E., additional, Kremer, Joel, additional, Kvien, Tore K., additional, Lacaille, Diane, additional, Landewe, Robert, additional, Lee, David M., additional, Lipsky, Peter E., additional, Machold, Klaus P., additional, MacKenzie, C. Ronald, additional, Matteson, Eric L., additional, McInnes, Iain B., additional, Meyer, Christopher G., additional, Mima, Toru, additional, Mirjafari, Hoda, additional, Moreland, Larry W., additional, Moudgil, Kamal D., additional, Nigrovic, Peter A., additional, Nishimoto, Norihiro, additional, Okada, Sarah, additional, Okoye, Francesca I., additional, Oliver, Jacqueline E., additional, Ospelt, Caroline, additional, Paget, Stephen A., additional, Pai, Saparna, additional, Pap, Thomas, additional, Pappas, Dimitrios A., additional, Kaprove Penn, Sarah, additional, Plenge, Robert M., additional, Posalski, Jana, additional, Rajaiah, Rajesh, additional, Redlich, Kurt, additional, Rönnelid, Johan, additional, Scheinecker, Clemens, additional, Schett, Georg, additional, Scott, David L., additional, Siegel, Jeffrey N., additional, Silman, Alan J., additional, Simon, Lee S., additional, Singh, Jasvinder A., additional, Smolen, Josef S., additional, Solomon, Daniel H., additional, St. Clair, E. William, additional, Steiner, Günter, additional, Strand, Vibeke, additional, Stuhlmüller, Bruno, additional, Symmons, Deborah, additional, Szekanecz, Zoltán, additional, Tak, Paul Peter, additional, Taylor, Peter C., additional, Thomas, Ranjeny, additional, Turesson, Carl, additional, Vital, Edward M., additional, Ward, Michael M., additional, Weber, Deborah, additional, Weinblatt, Michael E., additional, Weisman, Michael H., additional, West, Sterling G., additional, Winthrop, Kevin L., additional, Zink, Angela, additional, and Zvaifler, Nathan J., additional

Published
2009
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14. Contributors

Author

Bennell, Kim, primary, Berenbaum, Francis, additional, Chen, Lan X., additional, Dougados, Maxime, additional, Garnero, Patrick, additional, Goldring, Mary B., additional, Goodson, Nicola J., additional, Hinman, Rana S., additional, Lajeunesse, Daniel, additional, and Le Graverand, Marie-Pierre Hellio, additional

Published
2007
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17. Contributors

Author

Åkesson, Kristina, primary, Alatalo, Sari L., additional, Allison, Susan J., additional, Aly, Ziyad Al, additional, Baldock, Paul A., additional, Bilezikian, John P., additional, Binkley, Neil, additional, Body, Jean-Jacques, additional, Bonjour, Jean-Philippe, additional, Boskey, Adele L., additional, Bouillon, Roger, additional, Brixen, Kim, additional, Bruckner, Peter, additional, Carmeliet, Geert, additional, Clark, Ian M, additional, Croucher, Peter, additional, Delmas, Pierre D., additional, Dempster, David W., additional, Devogelaer, Jean-Pierre, additional, Drezner, Marc K., additional, Eastell, Richard, additional, Eelen, Guy, additional, Eriksen, Erik Fink, additional, Fitzpatrick, Lorraine A., additional, Fuleihan, Ghada El-Hajj, additional, Gardiner, Edith M., additional, Garnero, Patrick, additional, Gay, Renate E., additional, Gay, Steffen, additional, Glorieux, Francis H., additional, Goldring, Mary B., additional, Goldring, Steven R., additional, Goltzman, David, additional, González, Esther A., additional, Grauer, Andreas, additional, Gundberg, Caren M., additional, Hardingham, Tim, additional, Harrison, John R., additional, Heinegård, Dick, additional, Helfrich, M.H., additional, Herzog, Herbert, additional, Horton, M.A., additional, Hulley, Philippa, additional, Jüppner, Harald, additional, Kaija, Helena, additional, Khosla, S., additional, Kraenzlin, Marius E., additional, Kream, Barbara E., additional, Kulak, Carolina A. Moreira, additional, van Leeuwen, Johannes P.T.M., additional, Lensmeyer, Gary L., additional, Lian, Jane B., additional, Lorenzo, Joseph A., additional, Lorenzo, Pilar, additional, Maes, Christa, additional, Manicourt, Daniel-Henri, additional, von der Mark, Klaus, additional, Martin, Kevin J., additional, Martin, T. John, additional, Meier, Christian, additional, van Meurs, Joyce B.J., additional, Millán, José Luis, additional, Monroe, David G., additional, Mulder, Jean E., additional, Murphy, Gillian, additional, Naylor, Kim E., additional, Neidhart, Michel, additional, Nguyen, Tuan V., additional, Nishimoto, Satoru K., additional, Patrikainen, Lila O.T., additional, Pols, Huibert A.P., additional, Raisz, Lawrence G., additional, Ralston, Stuart, additional, Rauch, Frank, additional, Reid, Ian R., additional, Risteli, Juha, additional, Risteli, Leila, additional, Rivadeneira, Fernando, additional, Rizzoli, René, additional, Robins, Simon P., additional, Rosen, Clifford J., additional, Rubin, Mishaela R., additional, Russell, Graham, additional, Saxne, Tore, additional, Schmidt-Gayk, Heinrich, additional, Seeman, Ego, additional, Seibel, Markus J., additional, Shane, Elizabeth, additional, Silverberg, Shonni J., additional, Simkin, Peter A., additional, Sims, Natalie A., additional, Siris, Ethel, additional, Spelsberg, Thomas C., additional, Stein, Gary S., additional, Thonar, Eugene J.-M. A., additional, Uitterlinden, André G., additional, Väänänen, H. Kalervo, additional, Verstuyf, Annemieke, additional, Vihko, Pirkko T., additional, Whyte, Michael P., additional, and Zhou, Hua, additional

Published
2006
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18. Identification of formulation parameters that affect the analgesic efficacy of ProGel-Dex - A thermoresponsive polymeric dexamethasone prodrug for chronic arthritis pain relief.

Author

Wei X, Zhao G, Chen N, Xu X, Jiang H, Tran D, Glissmeyer E, Goldring MB, Goldring SR, and Wang D

Subjects
Animals, Analgesics chemistry, Analgesics pharmacology, Analgesics therapeutic use, Male, Rats, Polymers chemistry, Osteoarthritis drug therapy, Osteoarthritis pathology, Arthritis, Experimental drug therapy, Arthritis, Experimental pathology, Hydrogels chemistry, Humans, Chronic Pain drug therapy, Mice, Dexamethasone therapeutic use, Dexamethasone administration & dosage, Dexamethasone pharmacology, Dexamethasone chemistry, Prodrugs chemistry, Prodrugs pharmacology
Abstract

The relief of joint pain is one of the main objectives in the clinical management of arthritis. Although significant strides have been made in improving management of rheumatoid and related forms of inflammatory arthritis, there are still major unmet needs for therapies that selectively provide potent, sustained and safe joint pain relief, especially among patients with osteoarthritis (OA), the most common form of arthritis. We have recently developed ProGel-Dex, an N-(2-hydroxypropyl) methacrylamide (HPMA) copolymer-based thermoresponsive dexamethasone (Dex) prodrug, which forms a hydrogel upon intra-articular administration and provides sustained improvement in pain-related behavior and inflammation in rodent models of arthritis. The focus of the present study was to investigate the impact of ProGel-Dex formulation parameters on its physicochemical properties and in vivo efficacy. The results of this study provide essential knowledge for the future design of ProGel-Dex that can provide more effective, sustained and safe relief of joint pain and inflammation., Competing Interests: Declaration of competing interest D. Wang, S. R. Goldring, G. Zhao, and X. Wei are co-inventors of a PCT patent application covering ProGel technology. D. Wang and S. R. Goldring hold equity positions in Ensign Pharmaceutical, Inc., a start-up company which has licensed ProGel technology for further preclinical and translational development. The other coauthors declare no competing interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Published
2024
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19. Single dose thermoresponsive dexamethasone prodrug completely mitigates joint pain for 15 weeks in a murine model of osteoarthritis.

Author

Chen N, Wei X, Zhao G, Jia Z, Fu X, Jiang H, Xu X, Zhao Z, Singh P, Lessard S, Otero M, Goldring MB, Goldring SR, and Wang D

Subjects
Mice, Animals, Dexamethasone pharmacology, Dexamethasone therapeutic use, Disease Models, Animal, Arthralgia chemically induced, Arthralgia drug therapy, Analgesics pharmacology, Analgesics therapeutic use, Prodrugs pharmacology, Prodrugs therapeutic use, Osteoarthritis drug therapy
Abstract

In this study, we aimed to assess the analgesic efficacy of a thermoresponsive polymeric dexamethasone (Dex) prodrug (ProGel-Dex) in a mouse model of osteoarthritis (OA). At 12 weeks post model establishment, the OA mice received a single intra-articular (IA) injection of ProGel-Dex, dose-equivalent Dex, or Saline. Comparing to Saline and Dex controls, ProGel-Dex provided complete and sustained pain relief for >15 weeks according to incapacitance tests. In vivo optical imaging confirmed the continuous presence of ProGel-Dex in joints for 15 weeks post-injection. According to micro-CT analysis, ProGel-Dex treated mice had significantly lower subchondral bone thickness and medial meniscus bone volume than Dex and Saline controls. Except for a transient delay of body weight increase and slightly lower endpoint liver and spleen weights, no other adverse effect was observed after ProGel-Dex treatment. These findings support ProGel-Dex's potential as a potent and safe analgesic candidate for management of OA pain., Competing Interests: Declaration of competing interest D. Wang, S.R. Goldring, G. Zhao, and X. Wei are co-inventors of a PCT patent application covering ProGel technology. D. Wang, S.R. Goldring and G. Zhao hold equity positions in Ensign Pharmaceutical, Inc., a start-up company which has licensed ProGel technology for further preclinical and translational development. M. Otero owns shares in Jannu Therapeutics, LLC. The rest of the coauthors declare no competing interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Published
2024
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20. Laminins and Nidogens in the Pericellular Matrix of Chondrocytes: Their Role in Osteoarthritis and Chondrogenic Differentiation.

Author

Schminke B, Frese J, Bode C, Goldring MB, and Miosge N

Subjects
Adult, Aged, Aged, 80 and over, Calcium-Binding Proteins, Chondrogenesis physiology, Collagen Type II metabolism, Female, Humans, Male, Middle Aged, Stem Cells metabolism, Cell Adhesion Molecules metabolism, Cell Differentiation physiology, Chondrocytes metabolism, Extracellular Matrix metabolism, Laminin metabolism, Osteoarthritis, Knee metabolism
Abstract

The aim of this study was to investigate the role of laminins and nidogen-2 in osteoarthritis (OA) and their potential to support chondrogenic differentiation. We applied immunohistochemistry, electron microscopy, siRNA, quantitative RT-PCR, Western blot, and proteome analysis for the investigation of cartilage tissue and isolated chondrocytes in three-dimensional culture obtained from patients with late-stage knee OA and nidogen-2 knockout mice. We demonstrate that subunits of laminins appear in OA cartilage and that nidogen-2-null mice exhibit typical osteoarthritic features. Chondrogenic progenitor cells (CPCs) produced high levels of laminin-α1, laminin-α5, and nidogen-2 in their pericellular matrix, and laminin-α1 enhanced collagen type II and reduced collagen type I expression by cultured CPCs. Nidogen-2 increased SOX9 gene expression. Knockdown of nidogen-2 reduced SOX9 expression, whereas it up-regulated RUNX2 expression. This study reveals that the influence of the pericellular matrix on CPCs is important for the expression of the major regulator transcription factors, SOX9 and RUNX2. Our novel findings that laminins and nidogen-2 drive CPCs toward chondrogenesis may help in the elucidation of new treatment strategies for cartilage tissue regeneration., (Copyright © 2016 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Published
2016
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21. Intact pericellular matrix of articular cartilage is required for unactivated discoidin domain receptor 2 in the mouse model.

Author

Xu L, Polur I, Servais JM, Hsieh S, Lee PL, Goldring MB, and Li Y

Subjects
Animals, Collagen Type II metabolism, Collagen Type IV, Discoidin Domain Receptors, Doxycycline pharmacology, Immunohistochemistry, Mice, Mice, Transgenic, Osteoarthritis, Knee etiology, Osteoarthritis, Knee metabolism, RNA, Messenger metabolism, Transgenes, Cartilage, Articular metabolism, Matrix Metalloproteinase 13 metabolism, Receptor Protein-Tyrosine Kinases metabolism, Receptors, Mitogen metabolism, Stifle metabolism
Abstract

Increased expression of the discoidin domain receptor 2 (DDR2) results from its interaction with collagen type II. This induces expression of matrix metalloproteinase (MMP)-13, leading to osteoarthritis (OA). To investigate the impact of the pericellular matrix of chondrocytes on DDR2, we generated a mouse model with inducible overexpression of DDR2 in cartilage. Conditional overexpression of DDR2 in mature mouse articular cartilage was controlled via the cartilage oligomeric matrix protein promoter using the Tet-Off-inducible system. Doxycycline was withdrawn at 1 month of age, and knee joints were examined at 2, 3, and 4 months of age. Microsurgery was performed on 3-month-old transgenic mice overexpressing DDR2 to destabilize the medial meniscus, and serial paraffin sections were examined at 2, 4, 8, and 12 weeks after surgery. DDR2 expression increased in the knee joints of transgenic mice. However, the increased DDR2 did not induce MMP-13 expression. No OA-like changes were observed in the transgenic mice at the age of 4 months. When transgenic mice were subjected to destabilizing of the medial meniscus, we observed accelerated progression to OA, which was associated with DDR2 activation. Therefore, conditionally overexpressing DDR2 in the mature articular cartilage of mouse knee joints requires activation to induce OA, and altered biomechanical stress can accelerate the onset of cartilage loss and progression to OA in transgenic mice., (Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Published
2011
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22. Suppressors of cytokine signalling (SOCS) are reduced in osteoarthritis.

Author

de Andrés MC, Imagawa K, Hashimoto K, Gonzalez A, Goldring MB, Roach HI, and Oreffo RO

Subjects
Cells, Cultured, DNA Methylation, Gene Expression Regulation, Humans, Osteoarthritis genetics, Promoter Regions, Genetic, Protein Biosynthesis, RNA, Messenger biosynthesis, RNA, Messenger genetics, Suppressor of Cytokine Signaling Proteins genetics, Cartilage, Articular metabolism, Chondrocytes metabolism, Osteoarthritis metabolism, Suppressor of Cytokine Signaling Proteins biosynthesis
Abstract

Objectives: Suppressor of cytokine signalling (SOCS) proteins are inhibitors of cytokine signalling that function via the JAK/STAT pathway (Janus kinase/signal transducers and activators of transcription). Eight SOCS proteins, SOCS1-SOCS7 and CIS-1 (cytokine-inducible SH2-domain, with similar structure to the other SOCS proteins) have been identified, of which SOCS1, 2, and 3 and CIS-1 are the best characterised. A characteristic feature of osteoarthritis (OA) is increased production by articular chondrocytes of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNFα), which may be induced by mechanotransduction and contribute to cartilage destruction. In this study, we have compared the gene expression of SOCS1, 2, 3 and CIS-1 in healthy and OA human chondrocytes, and also analyzed the effects of IL-1β and TNFα on the levels of mRNA encoding these SOCS family members. In addition, SOCS2 protein production was assessed and the CpG methylation status of the SOCS2 promoter was analyzed to determine the role of epigenetics in its regulation., Methods: Femoral heads were obtained after joint replacement surgery for late stage OA and hemiarthroplasty following a fracture of the neck of femur (#NOF). Chondrocytes from the superficial layer of OA cartilage and the deep zone of #NOF cartilage were isolated by sequential treatment with trypsin, hyaluronidase and collagenase B. Total DNA and RNA were extracted from the same chondrocytes, and the levels of SOCS1, 2, 3 and CIS-1 mRNA were determined by qRT-PCR. The percentage of methylation in the CpG sites of the SOCS2 proximal promoter was quantified by pyrosequencing. Alternatively, healthy chondrocytes were isolated from #NOF cartilage and cultured with and without a mixture of IL-1β and oncostatin M (OSM, both 2.5ng/ml) or TNFα (10ng/ml). The short-term cultures with single cytokine treatment were harvested 24 and 72h after treatment, and the long-term cultures were maintained for 4-5 weeks until confluent with periodical cytokine stimulation. Total RNA was extracted and mRNA levels were determined by qRT-PCR., Results: The SOCS2 and CIS-1 mRNA levels were reduced by approximately 10-fold in OA samples compared to control samples, while SOCS1 and SOCS3 showed similar expression patterns in OA and control chondrocytes. The SOCS2 and CIS-1 mRNA levels declined by 6-fold and 3-fold with long-term treatment with IL-1β and OSM in combination and TNFα, respectively. There was no significant difference in the CpG methylation status of the SOCS2 promoter between healthy and OA chondrocytes. Similarly, cytokine stimulation did not change the CpG methylation status of the SOCS2 promoter., Conclusions: This study demonstrates the reduced expression of SOCS2 and CIS-1 in OA, while SOCS1 and SOCS3 were unaffected. The observation that long-term treatment with inflammatory cytokines attenuated the expression of SOCS2 and CIS-1 suggests a potential positive feedback mechanism, and a role of SOCS in the pathology of OA., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Published
2011
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23. The epigenetic effect of glucosamine and a nuclear factor-kappa B (NF-kB) inhibitor on primary human chondrocytes--implications for osteoarthritis.

Author

Imagawa K, de Andrés MC, Hashimoto K, Pitt D, Itoi E, Goldring MB, Roach HI, and Oreffo RO

Subjects
Cells, Cultured, DNA (Cytosine-5-)-Methyltransferase 1, DNA (Cytosine-5-)-Methyltransferases antagonists & inhibitors, DNA (Cytosine-5-)-Methyltransferases biosynthesis, DNA (Cytosine-5-)-Methyltransferases genetics, DNA Methylation drug effects, Down-Regulation, Humans, Interleukin-1beta genetics, Interleukin-1beta metabolism, Matrix Metalloproteinase 13 genetics, Matrix Metalloproteinase 13 metabolism, Osteoarthritis genetics, Promoter Regions, Genetic drug effects, Chondrocytes drug effects, Epigenesis, Genetic drug effects, Glucosamine pharmacology, NF-kappa B antagonists & inhibitors, Nitriles pharmacology, Osteoarthritis metabolism, Sulfones pharmacology
Abstract

Objective: Idiopathic osteoarthritis is the most common form of osteoarthritis (OA) world-wide and remains the leading cause of disability and the associated socio-economic burden in an increasing aging population. Traditionally, OA has been viewed as a degenerative joint disease characterized by progressive destruction of the articular cartilage and changes in the subchondral bone culminating in joint failure. However, the etiology of OA is multifactorial involving genetic, mechanical and environmental factors. Treatment modalities include analgesia, joint injection with steroids or hyaluronic acid, oral supplements including glucosamine and chondroitin sulfate, as well as physiotherapy. Thus, there is significant interest in the discovery of disease modifying agents. One such agent, glucosamine (GlcN) is commonly prescribed even though the therapeutic efficacy and mechanism of action remain controversial. Inflammatory cytokines, including IL-1β, and proteinases such as MMP-13 have been implicated in the pathogenesis and progression of OA together with an associated CpG demethylation in their promoters. We have investigated the potential of GlcN to modulate NF-kB activity and cytokine-induced abnormal gene expression in articular chondrocytes and, critically, whether this is associated with an epigenetic process., Method: Human chondrocytes were isolated from the articular cartilage of femoral heads, obtained with ethical permission, following fractured neck of femur surgery. Chondrocytes were cultured for 5 weeks in six separate groups; (i) control culture, (ii) cultured with a mixture of 2.5 ng/ml IL-1β and 2.5 ng/ml oncostatin M (OSM), (iii) cultured with 2mM N-acetyl GlcN (Sigma-Aldrich), (iv) cultured with a mixture of 2.5 ng/ml IL-1β, 2.5 ng/ml OSM and 2mM GlcN, (v) cultured with 1.0 μM BAY 11-7082 (BAY; NF-kB inhibitor: Calbiochem, Darmstadt, Germany) and, (vi) cultured with a mixture of 2.5 ng/ml IL-1β, 2.5 ng/ml OSM and 1.0 μM BAY. The levels of IL1B and MMP13 mRNA were examined using qRT-PCR. The percentage DNA methylation in the CpG sites of the IL1β and MMP13 proximal promoter were quantified by pyrosequencing., Result: IL1β expression was enhanced over 580-fold in articular chondrocytes treated with IL-1β and OSM. GlcN dramatically ameliorated the cytokine-induced expression by 4-fold. BAY alone increased IL1β expression by 3-fold. In the presence of BAY, IL-1β induced IL1B mRNA levels were decreased by 6-fold. The observed average percentage methylation of the -256 CpG site in the IL1β promoter was 65% in control cultures and decreased to 36% in the presence of IL-1β/OSM. GlcN and BAY alone had a negligible effect on the methylation status of the IL1B promoter. The cytokine-induced loss of methylation status in the IL1B promoter was ameliorated by both GlcN and BAY to 44% and 53%, respectively. IL-1β/OSM treatment increased MMP13 mRNA levels independently of either GlcN or BAY and no change in the methylation status of the MMP13 promoter was observed., Conclusion: We demonstrate for the first time that GlcN and BAY can prevent cytokine-induced demethylation of a specific CpG site in the IL1β promoter and this was associated with decreased expression of IL1β. These studies provide a potential mechanism of action for OA disease modifying agents via NF-kB and, critically, demonstrate the need for further studies to elucidate the role that NF-kB may play in DNA demethylation in human chondrocytes., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Published
2011
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24. Characterization and regulation of ADAMTS-16.

Author

Surridge AK, Rodgers UR, Swingler TE, Davidson RK, Kevorkian L, Norton R, Waters JG, Goldring MB, Parker AE, and Clark IM

Subjects
ADAMTS Proteins, Amino Acid Sequence, Animals, Cell Line, Chondrocytes cytology, Chondrocytes metabolism, Chondrosarcoma metabolism, Gene Expression Regulation, Humans, Male, Molecular Sequence Data, Phenotype, Promoter Regions, Genetic, RNA, Messenger genetics, RNA, Messenger metabolism, Sequence Alignment, Transcription Initiation Site, ADAM Proteins genetics, ADAM Proteins metabolism
Abstract

The ADAMTS (a disintegrin and metalloproteinase domain with thrombospondin motifs) family includes 19 secreted proteinases in man. ADAMTS16 is a recently cloned gene expressed at high levels in fetal lung and kidney and adult brain and ovary. The ADAMTS-16 protein currently has no known function. ADAMTS16 is also expressed in human cartilage and synovium where its expression is increased in tissues from osteoarthritis patients compared to normal tissues. In this study, we ascertained that the full length ADAMTS16 mRNA was expressed in chondrocytes and cloned the appropriate cDNA. Stable over-expression of ADAMTS16 in chondrosarcoma cells led to a decrease in cell proliferation and migration, though not adhesion, as well as a decrease in the expression of matrix metalloproteinase-13 (MMP13). The transcription start point of the human ADAMTS16 gene was experimentally identified as 138 bp upstream of the translation start ATG and the basal promoter was mapped out to -1802 bp. Overexpression of Egr1 induced ADAMTS16 promoter constructs of -157/+138 or longer whilst Sp1 induced all ADAMTS16 promoter constructs. Transforming growth factor beta (TGFbeta) stimulated expression of endogenous ADAMTS16 gene expression in chondrocyte cell lines.

Published
2009
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25. Update on the biology of the chondrocyte and new approaches to treating cartilage diseases.

Author

Goldring MB

Subjects
Animals, Bone Morphogenetic Proteins physiology, Cartilage Diseases metabolism, Cartilage, Articular metabolism, Cartilage, Articular pathology, Chondrocytes drug effects, Chondrocytes pathology, Disease Progression, Extracellular Matrix physiology, Genetic Therapy, Humans, Matrix Metalloproteinases metabolism, Osteoarthritis metabolism, Risk Factors, Signal Transduction drug effects, Signal Transduction physiology, Tissue Engineering, Transcriptional Activation physiology, Cartilage Diseases physiopathology, Chondrocytes physiology, Osteoarthritis physiopathology, Osteoarthritis therapy
Abstract

Osteoarthritis (OA) is a joint disease that involves degeneration of articular cartilage, limited intraarticular inflammation manifested by synovitis and changes in the subchondral bone. The aetiology of OA is largely unknown, but since it may involve multiple factors, including mechanical, biochemical and genetic factors, it has been difficult to identify unique targets for therapy. Chondrocytes, which are the unique cellular component of adult articular cartilage, are capable of responding to structural changes in the surrounding cartilage matrix. Since the initial stages of OA involve increased cell proliferation and synthesis of matrix proteins, proteinases and cytokines in the cartilage, laboratory investigations have focused on the chondrocyte as a target for therapeutic intervention. The capacity of the adult articular chondrocyte to regenerate the normal cartilage matrix architecture is limited, however, and the damage becomes irreversible unless the destructive process is interrupted. Current pharmacological interventions that address chronic pain are insufficient and no proven disease-modifying therapy is available. Identification of methods for early diagnosis is of key importance, since therapeutic interventions aimed at blocking or reversing structural damage will be more effective when there is the possibility of preserving normal homeostasis. At later stages, cartilage tissue engineering with or without gene therapy with anabolic factors will also require therapy to inhibit inflammation and block damage to newly repaired cartilage. This review will focus on experimental approaches currently under study that may lead to elucidation of effective strategies for therapy in OA, with emphasis on mediators that affect the function of chondrocytes and interactions with surrounding tissues.

Published
2006
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26. Endostatin/collagen XVIII--an inhibitor of angiogenesis--is expressed in cartilage and fibrocartilage.

Author

Pufe T, Petersen WJ, Miosge N, Goldring MB, Mentlein R, Varoga DJ, and Tillmann BN

Subjects
Aging metabolism, Animals, Cartilage, Articular metabolism, Cells, Cultured, Chondrocytes metabolism, Collagen Type XVIII genetics, Endostatins pharmacology, Extracellular Signal-Regulated MAP Kinases metabolism, Fetus, Humans, Menisci, Tibial metabolism, Nitric Oxide biosynthesis, Osmolar Concentration, Phosphorylation drug effects, RNA, Messenger metabolism, Rats, Rats, Wistar, Vascular Endothelial Growth Factor A pharmacology, Angiogenesis Inhibitors metabolism, Cartilage metabolism, Collagen Type XVIII metabolism, Endostatins metabolism
Abstract

Unlabelled: Aim of the study was to get a deeper insight in the mechanisms regulating avascularity of cartilaginious tissues. In the center of our interest was the expression of the anti-angiogenic fragment of collagen XVIII and its potency to inhibit angiogenesis. We observed a strong endostatin/collagen XVIII production in articular and fibrocartilage and an inhibitory potency concerning the VEGF-signalling pathway., Introduction: Cartilaginous tissue is mainly avascular and shows a limited intrinsic capacity for healing. Aim of this study was to investigate the expression of the antiangiogenic peptide endostatin/collagen XVIII in cartilage and fibrocartilage., Results: In fetal epiphyseal cartilage of humans high endostatin/collagen XVIII levels could be detected by ELISA whereas significantly lower levels were found in articular cartilage of adults. In the fibrocartilaginous tissue of the menisci, there was no significant difference in the endostatin/collagen XVIII concentrations between samples of fetuses and adults. But in the menisci of adults, endostatin/collagen XVIII concentrations were higher in the internal avascular two thirds of the meniscus whereas in the fetal menisci higher endostatin/collagen XVIII concentrations were found in the external third. Endostatin/collagen XVIII immunostaining of rat articular cartilage shows that endostatin/collagen XVIII downregulation starts soon after birth. In fetal cartilage and fibrocartilage of rats and humans, endostatin/collagen XVIII could be immunostained in the extracellular matrix and in the pericellular matrix of endothelial cells, fibrochondrocytes and chondrocytes. In adult cells, weak endostatin/collagen XVIII immunostaining was restricted to the pericellular matrix of fibrochondrocytes and chondrocytes. The detection of endostatin/collagen XVIII could be verified by in situ hybridization. Chondrocytes in vitro released measurable amounts of endostatin/collagen XVIII into culture supernatants. Stimulation of chondrocytes with EGF, as an example of a growth factor, or dexamethasone had no influence on endostatin/collagen XVIII expression. Endostatin inhibited VEGF-induced phosphorylation of MAPK in chondrocytes., Conclusions: The spatial and temporal expression of endostatin/collagen XVIII in cartilaginous tissue and its potency regarding inactivation of VEGF signalling suggests that this antiangiogenic factor is important not only for the development but also for the maintenance of avascular zones in cartilage and fibrocartilage., Experimental Procedures: We analyzed the spatial and temporal expression of endostatin/collagen XVIII--an endogenous angiogenesis inhibiting factor--in cartilage and fibrocartilage of humans and rats by immunohistochemical and biochemical (ELISA) methods and by in situ hybridization. To elucidate possible factors responsible for the induction or suppression of endostatin/collagen XVIII in cartilaginous tissues, chondrocytes (cell line C28/I2) were exposed to EGF and dexamethason. To study the possible interaction of endostatin/collagen XVIII with angiogenic factors, the immortalized human chondrocytes (C28/I2) have been incubated with VEGF and the phosphorylation of the MAPK Erk 1/2 (extracellular-regulated kinases), a known signal transduction pathway for VEGF has been determined under the influence of endostatin.

Published
2004
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