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210 results on '"Rohrer, D"'

1. On The Perturbations of Gibbons-Maeda Black Holes in Einstein-Maxwell-Dilaton Theories

Author

Pope, C. N., Rohrer, D. O., and Whiting, B. F.

Subjects
High Energy Physics - Theory, General Relativity and Quantum Cosmology
Abstract

The study of perturbations around black hole backgrounds in general relativity and Einstein-Maxwell theory has a long history, going back to the work of Regge and Wheeler in the 1950s. As part of a broader investigation of perturbations around black holes in supergravity, we describe here our results for the perturbations around the Gibbons-Maeda static charged black holes in a class of Einstein-Maxwell-Dilaton theories. Our analysis follows the general strategy developed by Chandrasekhar and Xanthopoulos for the perturbations of the Reissner-Nordstr\"om black hole. Here, the analysis is considerably more involved, because of the presence of the dilaton field, which couples to the other polar modes. We nonetheless find that the problem is completely solvable, in the sense that one can separate variables and eventually describe all the perturbations in terms of diagonalised second-order radial equations. We are able to prove the mode stability of all the Gibbons-Maeda black hole solutions., Comment: 43 pages

Published
2024

2. When does feedback facilitate learning of words?

Author

Pashler, Harold, Cepeda, N J, Wixted, J T, and Rohrer, D

Subjects
associative processes, feedback, learning, retention, words (phonetic units)
Abstract

Some researchers have suggested that although feedback may enhance performance during associative learning, it does so at the expense of later retention. To examine this issue, subjects (N = 258) learned Luganda-English word pairs. After 2 initial exposures to the materials, subjects were tested on each item several times, with the presence and type of feedback varying between subjects. A final test followed after I week. Supplying the correct answer after an incorrect response not only improved performance during the initial learning session-it also increased final retention by 494%. On the other hand, feedback after correct responses made little difference either immediately or at a delay, regardless of whether the subject was confident in the response. Practical and theoretical implications are discussed.

Published
2005

3. Thanks to Reviewers!

Author

Adams, R, Bahnson, M, Bhaduri, S, Adams, T, Bairaktarova, D, Bielefeldt, A, Aguirre-Munoz, Z, Balakrishnan, B, Blosser, EG, Ahn, B, Beagon, U, Bodnar, C, Aleong, R, Becker, K, Borgford-Parnell, J, Amelink, C, Beddoes, K, Maura, B, Anderson, R, Bego, C, Bowe, B, Andrews, CJ, Beigpourian, B, Bowen, B, Angel, J, Bekki, J, Boyd, J, Fonseca, MA, Bennett, D, Bradburn, I, Kranov, AA, Berdanier, C, Brady, C, Bae, CL, Bernhard, J, Brawner, C, Brose, A, Case, J, Cropley, D, Brown, F, Cassady, R, Cross, K, Brown, P, Celik, S, Cunningham, P, Ben, C, Cutler, S, Brown, S, Chance, SM, Dabbagh, N, Brozina, C, Chen, H, Dallal, A, Brunhaver, S, Chen, O, Daly, S, Bryant, A, Cheville, RA, Daniel, S, Bucciarelli, L, Chiu, J, Danowitz, A, Burkholder, E, Choe, NH, Darolia, R, Burks, G, Clark, R, Davis, K, Burt, B, Clevenger, C, Davis, S, Canney, N, Cole, J, de Jong, T, Cao, Y, Coley, B, De Vries, C, Caratozzolo, P, Cooper, L, Delaine, D, Carballo, R, Cooper, M, DeMonbrun, R, Cardella, M, Craig, T, Denton, M, Di Stefano, M, Erdman, AM, Gilmartin, S, DiBiasio, D, Eris, O, Gladstone, J, Diefes-Dux, H, Evangelou, D, Glancy, A, Dika, S, Ewen, B, Godwin, A, Direito, I, Faber, C, Goldsmith, R, Dohn, N, Falconer, J, Grigg, SJ, Dolansky, M, Fantz, T, Grohs, J, Faulkner, B, Doom, D, Felder, R, Gummer, E, Douglas, E, Ferris, T, Guzey, S, Douglas, KA, Figueiredo, J, Hadgraft, R, Dounas-Frazer, D, Fiorella, L, Hammack, R, Dringenberg, E, Flores, L, Han, K, Duffy, G, Fong, C, Harding, T, Easley, D, Fowler, RR, Harper, K, Eccles, J, Friedrichsen, D, Hartmann, B, Edstrom, K, Ge, J, Hattingh, T, Ellestad, R, Gelles, L, Henderson, R, Henderson, TS, Immekus, J, Kamphorst, J, Herman, G, Inda, M, Karatas, F, Hess, J, Itabashi-Campbell, R, Kartal, O, Hieb, J, Jackson, A, Karwat, D, Higbee, S, Jankowski, N, Katz, A, Hilton, E, Javernick-Will, A, Keipi, T, Hira, A, Jensen, KJ, Kim, D, Hirshfield, L, Smith, J, Kirn, A, Knaphus-Soran, E, Holly, J, Jesiek, B, Knight, D, Horng, S-M, Johnson, A, Knott, T, Huang-Saad, A, Johnson, B, Kohl, P, Huerta, M, Johri, A, Kohtala, C, Huff, J, Jones, B, Komives, S, Hughes, B, Jones, L, Korsunskiy, E, Hughes, R, Jones, T, Kotys-Schwartz, D, Hunsu, N, Kaminski, J, Kramer, J, Hunter, C, Kampe, J-C, Inkelas, KK, Lamm, M, Lonngren, J, McCall, C, Lande, M, Lottero-Perdue, PS, McCave, E, Lappalainen, P, Aguilar, JFL, McCray, E, Lawanto, O, Lucena, J, McGee, E, Lawson, J, Luk, LYY, McGough, C, Leath, S, Lutz, B, McGowan, V, Lee, D, Ma, Y, McNair, LD, Lee, W, Madon, T, McNaughtan, J, Liberatore, M, Mamaril, N, McNeill, N, Lichtenstein, G, Mangiante, E, Mejia, J, Lima, M, Martin, B, Diaz, NM, Lima, RM, Martin, K, Menekse, M, Lin, J, Lippard, C, Mones, AM, Mesquita, DIDA, Michell, K, Litzler, E, Matthews, M, Miller, S, Lo, CK, Matusovich, H, Minichiello, A, London, J, Maynard, N, Miskioglu, EE, Longwell-Grice, R, Mazzurco, A, Yusof, KM, Mohedas, I, Nghia, TLH, Pearson, A, Monat, J, Norton, P, Pearson, N, Monteiro, F, Novoselich, BJ, Pembridge, J, Moote, J, Noy, S, Perez-Felkner, L, Mora, M, O'Hara, R, Perkins, H, O'Moore, L, Peters-Burton, E, Morgan, D, Ohland, M, Pfirman, A, Morgan, T, Okai, B, Pinto, C, Morton, T, Olds, B, Pitterson, N, Mosyjowski, E, Orr, M, Polmear, M, Murphy, T, Ortega-Alvarez, JD, Prince, T, Murray, J, Oseguera, L, Purzer, S, Murzi, H, Owen, C, Quan, GM, Nagy, G, Ozkan, DS, Quillin, K, Natarajathinam, M, Panther, G, Rayess, N, Nelson, M, Patrick, A, Reed, T, Newberry, B, Paul, K, Reeping, D, Newstetter, W, Pawley, A, Reese, M, Reid, K, Rulifson, G, Shivy, V, Renn, K, Rynearson, AM, Simpson, Z, Ricco, G, Sanchez-Pena, ML, Sitomer, A, Richards, L, Saunders-Smits, G, Siverling, E, Rios, L, Sax, L, Slaton, A, Ro, HK, Schimpf, C, Sleezer, R, Roberts, D, Rodgers, K, Schippers, M, Smith-On, C, Rodriguez, S, Schnittka, C, Schunn, C, Rogers, C, Seah, LH, Rohde, J, Rohrer, D, Secules, S, Smith, K, Smith, N, Romine, W, Seifert, C, Sochacka, N, Ross, L, Sessa, V, Stearns, E, Ross, M, Sharp, H, Steif, M, Rottmann, C, Sharp, J, Stephan, P, Rucks, L, Shaw, C, Stevens, R, Streveler, R, Tolbert, D, van Der Marel, F, Strobel, J, Toraman, S, van Hattum, N, Stump, G, Tougaw, D, Verdin, D, Su, X, Trautvetter, LC, Verleger, M, Sundararaja, N, Trenshaw, KF, Vieira, C, Trevelyan, J, Svihla, V, Troussas, C, Villanueva, I, Swan, C, Tsai, J, Vinck, D, Virguez, L, Swanson, R, Tsugawa, MA, Vitasari, P, Sweeny, K, Tuononen, T, Vossoughi, S, Swenson, J, Turner, J, Wallin, P, Talley, K, Turner, S, Tan, L, Tyson, W, Watted, A, Tang, Y, Utley, J, Webber, K, Tank, K, Vasquez, RV, Weintrop, D, Thomas, K, Valdivia, A, Weiss, E, Thompson, JD, Valentine, A, West, R, Tierney, G, Van den Bogaard, M, Wiles, D, Wilson-Lopez, AA, Xinrui, X, Zastavker, Y, Wilson, D, Xu, YJ, Zhang, G, Wolmarans, N, Yang, Y, Zhu, J, Wong, R, Yi, S, Zoltowski, CB, Woollacott, L, Yoon, SY, Adams, R, Bahnson, M, Bhaduri, S, Adams, T, Bairaktarova, D, Bielefeldt, A, Aguirre-Munoz, Z, Balakrishnan, B, Blosser, EG, Ahn, B, Beagon, U, Bodnar, C, Aleong, R, Becker, K, Borgford-Parnell, J, Amelink, C, Beddoes, K, Maura, B, Anderson, R, Bego, C, Bowe, B, Andrews, CJ, Beigpourian, B, Bowen, B, Angel, J, Bekki, J, Boyd, J, Fonseca, MA, Bennett, D, Bradburn, I, Kranov, AA, Berdanier, C, Brady, C, Bae, CL, Bernhard, J, Brawner, C, Brose, A, Case, J, Cropley, D, Brown, F, Cassady, R, Cross, K, Brown, P, Celik, S, Cunningham, P, Ben, C, Cutler, S, Brown, S, Chance, SM, Dabbagh, N, Brozina, C, Chen, H, Dallal, A, Brunhaver, S, Chen, O, Daly, S, Bryant, A, Cheville, RA, Daniel, S, Bucciarelli, L, Chiu, J, Danowitz, A, Burkholder, E, Choe, NH, Darolia, R, Burks, G, Clark, R, Davis, K, Burt, B, Clevenger, C, Davis, S, Canney, N, Cole, J, de Jong, T, Cao, Y, Coley, B, De Vries, C, Caratozzolo, P, Cooper, L, Delaine, D, Carballo, R, Cooper, M, DeMonbrun, R, Cardella, M, Craig, T, Denton, M, Di Stefano, M, Erdman, AM, Gilmartin, S, DiBiasio, D, Eris, O, Gladstone, J, Diefes-Dux, H, Evangelou, D, Glancy, A, Dika, S, Ewen, B, Godwin, A, Direito, I, Faber, C, Goldsmith, R, Dohn, N, Falconer, J, Grigg, SJ, Dolansky, M, Fantz, T, Grohs, J, Faulkner, B, Doom, D, Felder, R, Gummer, E, Douglas, E, Ferris, T, Guzey, S, Douglas, KA, Figueiredo, J, Hadgraft, R, Dounas-Frazer, D, Fiorella, L, Hammack, R, Dringenberg, E, Flores, L, Han, K, Duffy, G, Fong, C, Harding, T, Easley, D, Fowler, RR, Harper, K, Eccles, J, Friedrichsen, D, Hartmann, B, Edstrom, K, Ge, J, Hattingh, T, Ellestad, R, Gelles, L, Henderson, R, Henderson, TS, Immekus, J, Kamphorst, J, Herman, G, Inda, M, Karatas, F, Hess, J, Itabashi-Campbell, R, Kartal, O, Hieb, J, Jackson, A, Karwat, D, Higbee, S, Jankowski, N, Katz, A, Hilton, E, Javernick-Will, A, Keipi, T, Hira, A, Jensen, KJ, Kim, D, Hirshfield, L, Smith, J, Kirn, A, Knaphus-Soran, E, Holly, J, Jesiek, B, Knight, D, Horng, S-M, Johnson, A, Knott, T, Huang-Saad, A, Johnson, B, Kohl, P, Huerta, M, Johri, A, Kohtala, C, Huff, J, Jones, B, Komives, S, Hughes, B, Jones, L, Korsunskiy, E, Hughes, R, Jones, T, Kotys-Schwartz, D, Hunsu, N, Kaminski, J, Kramer, J, Hunter, C, Kampe, J-C, Inkelas, KK, Lamm, M, Lonngren, J, McCall, C, Lande, M, Lottero-Perdue, PS, McCave, E, Lappalainen, P, Aguilar, JFL, McCray, E, Lawanto, O, Lucena, J, McGee, E, Lawson, J, Luk, LYY, McGough, C, Leath, S, Lutz, B, McGowan, V, Lee, D, Ma, Y, McNair, LD, Lee, W, Madon, T, McNaughtan, J, Liberatore, M, Mamaril, N, McNeill, N, Lichtenstein, G, Mangiante, E, Mejia, J, Lima, M, Martin, B, Diaz, NM, Lima, RM, Martin, K, Menekse, M, Lin, J, Lippard, C, Mones, AM, Mesquita, DIDA, Michell, K, Litzler, E, Matthews, M, Miller, S, Lo, CK, Matusovich, H, Minichiello, A, London, J, Maynard, N, Miskioglu, EE, Longwell-Grice, R, Mazzurco, A, Yusof, KM, Mohedas, I, Nghia, TLH, Pearson, A, Monat, J, Norton, P, Pearson, N, Monteiro, F, Novoselich, BJ, Pembridge, J, Moote, J, Noy, S, Perez-Felkner, L, Mora, M, O'Hara, R, Perkins, H, O'Moore, L, Peters-Burton, E, Morgan, D, Ohland, M, Pfirman, A, Morgan, T, Okai, B, Pinto, C, Morton, T, Olds, B, Pitterson, N, Mosyjowski, E, Orr, M, Polmear, M, Murphy, T, Ortega-Alvarez, JD, Prince, T, Murray, J, Oseguera, L, Purzer, S, Murzi, H, Owen, C, Quan, GM, Nagy, G, Ozkan, DS, Quillin, K, Natarajathinam, M, Panther, G, Rayess, N, Nelson, M, Patrick, A, Reed, T, Newberry, B, Paul, K, Reeping, D, Newstetter, W, Pawley, A, Reese, M, Reid, K, Rulifson, G, Shivy, V, Renn, K, Rynearson, AM, Simpson, Z, Ricco, G, Sanchez-Pena, ML, Sitomer, A, Richards, L, Saunders-Smits, G, Siverling, E, Rios, L, Sax, L, Slaton, A, Ro, HK, Schimpf, C, Sleezer, R, Roberts, D, Rodgers, K, Schippers, M, Smith-On, C, Rodriguez, S, Schnittka, C, Schunn, C, Rogers, C, Seah, LH, Rohde, J, Rohrer, D, Secules, S, Smith, K, Smith, N, Romine, W, Seifert, C, Sochacka, N, Ross, L, Sessa, V, Stearns, E, Ross, M, Sharp, H, Steif, M, Rottmann, C, Sharp, J, Stephan, P, Rucks, L, Shaw, C, Stevens, R, Streveler, R, Tolbert, D, van Der Marel, F, Strobel, J, Toraman, S, van Hattum, N, Stump, G, Tougaw, D, Verdin, D, Su, X, Trautvetter, LC, Verleger, M, Sundararaja, N, Trenshaw, KF, Vieira, C, Trevelyan, J, Svihla, V, Troussas, C, Villanueva, I, Swan, C, Tsai, J, Vinck, D, Virguez, L, Swanson, R, Tsugawa, MA, Vitasari, P, Sweeny, K, Tuononen, T, Vossoughi, S, Swenson, J, Turner, J, Wallin, P, Talley, K, Turner, S, Tan, L, Tyson, W, Watted, A, Tang, Y, Utley, J, Webber, K, Tank, K, Vasquez, RV, Weintrop, D, Thomas, K, Valdivia, A, Weiss, E, Thompson, JD, Valentine, A, West, R, Tierney, G, Van den Bogaard, M, Wiles, D, Wilson-Lopez, AA, Xinrui, X, Zastavker, Y, Wilson, D, Xu, YJ, Zhang, G, Wolmarans, N, Yang, Y, Zhu, J, Wong, R, Yi, S, Zoltowski, CB, Woollacott, L, and Yoon, SY

Published
2021

6. Abstracts

Author

Rosen, L., Reed, J., Ufberg, D., Thorburn, H., Carter, K., Goldberg, J., Finlay, I. G., Church, J. M., Hill, G. L., Carter, F. M., Cohen, Z., McLeod, R. S., Bauer, J. J., Sher, M. E., Gelernt, I. M., Crim, R. W., Fazio, V. W., Lavery, I. C., Williams, J. G., Nemer, F. D., Rothenberger, D. A., Goldberg, S. M., Hyman, N. H., Tuckson, W. B., Deutsch, A. A., Gregoire, R., Cullen, J., Johnson, G. P., Wolff, B. G., Koltun, W., Schoetz, Jr., D. J., Roberts, P. L., Murray, J. J., Coller, J. A., Veidenheimer, M. C., Keighley, M. R. B., Hosie, K., Sakaguchi, M., Tudor, R., Kmiot, W., Ambroze, Jr., W. L., Dozois, R. R., Pemberton, J. H., Kelly, K. A., Wiltz, O., Hashmi, H., Fucini, C., Thayer, M. L., Madoff, R. D., Jacobs, D. M., Bubrick, M. P., Galandiuk, S., Tsao, J., Ilstrup, D. M., Duthie, G. S., Bartolo, D. C. C., Miller, R., Pinho, M., Kunin, J. D., Fleshman, J. W., Kodner, I. J., Fry, R. D., Wexner, S. D., Jagelman, D. G., Corredor, C., Salanga, V., Scholefield, J. H., Whatrup, C., Talbot, I. C., Northover, J. M. A., Sonnex, C., Safavi, A., Gottesman, L., Dailey, T., Moenning, S., Nightengale, S., Simonton, T., Huber, P., Odom, C., Kaplan, E., Strong, S. A., Milsom, J. W., Taylor, C. W., Cho, C. C., Stewart, W. R. C., Hartmann, R. F., Khanduja, K. S., Aguilar, P. S., Rahman, S. M., Arnold, M. W., Caushaj, P., Viratyosin, S., French, T., Madoff, R., Karamjit, S., Meesig, D. M., Macleod, C. A. H., Balcos, E. G., Buls, J. G., Nelson, H., Donohue, J. H., McKean, D. J., Leu, S. Y., Wang, S. R., Hsu, H., Ramanujam, P. S., Alberts, D. S., Clark, L., Ritenbaugh, C., Rowley, S., Kane, N., Jones, C., Davies, A., Baker, P., Neoptolemos, J. P., Devereux, D. F., Robertson, F. M., Spain, D. A., Cance, W. G., Cohen, A. M., Sigurdson, E. R., Enker, W. E., Konishi, F., Yasuda, Y., Ochiai, S., Kanazawa, K., Davis, M., Medina, V., Miller, D., Fielding, L. P., Prats, I., Berman, M., West, B., Savoca, P. E., Ballantyne, G. H., Flannery, J. T., Modlin, I. M., Tsukada, K., Jagelman, D. A., McGannon, E. M., Schroeder, T., Sakamoto, G. D., MacKeigan, J. M., Opelka, F., Timmcke, A., Gathright, J. B., Hicks, T., Ray, J., McKee, C. C., Ragland, J. J., Myers, J. O., Christie, J. P., Marrazzo, III, J., Flemming, F. X., Longo, W. E., Pollard, C. W., Nivatvongs, S., Rojanasakul, A., Jetmore, A. B., Baker, J., Wiltz, O. H., McKee, R. F., Lauder, J., Poon, F., Aitchison, M., Fleshman, James W., Dreznik, Zeev, Kodner, Ira J., Fry, Robert D., Kerner, B. A., Labow, S., Hoexter, B., Moseson, M., Cheape, J. D., Bowinkelman, K., Dziki, A. J., Malthaner, R. A., Harmon, J. W., Saini, N., Duncan, M. D., Fernicola, M. T., Fischer, B. A., Hakki, F. Z., Trad, K. S., Ugarte, R., Senagore, A. J., Mazier, W. P., Kilbride, M., Herrera, L., Goumas, W., Petrelli, N., Bailey, H. R., Huval, W. V., Max, E., Smith, K. W., Marks, G., Mohiuddin, M., Basile, M., Eitan, A., Wolff, B., Dozois, R., Devine, R., Beart, R., Kelly, A., Unti, J. A., Orsay, C. P., Pearl, R. K., Nelson, R. L., Duarte, B., Prasad, M. L., Abcarian, H., Senagore, A., Milson, J. W., Strong, S., Walshaw, R. K., Chaudry, I. H., Hojo, K., Sugihara, K., Katunuma, K., Vernava, A., Beart, R. W., Stewart, J., Diament, R. H., Salter, M., Brennan, T. G., Sheikh, F., Khubchandani, I. T., Miyajima, N., Uematsu, Y., Kodaira, S., Teramoto, T., Orrom, W. J., Duthie, G., Corne, H., Blatchford, G. J., Perry, R. E., Christensen, M. A., Thorson, A. G., Dreznik, Zeev, Wong, W. D., Jensen, L. L., Lee, K. H., Yoon, Choong, Joo, H. Z., Levien, D. H., Gibbons, S., Begos, D., Byrne, D. W., Gordon, P. H., Bégin, L. R., Mitmaker, B., Saclarides, T., Bhattacharyya, A., Britton, C., Stone, J. M., Lowry, A. C., Moran, M., Launer, D. P., McReynolds, D. G., Eastman, A. B., Peck, J. J., Rozycki, G. S., Ramanujam, Paravasthu S., Bellapravalu, Sharad, Venkatesh, Kurakurachi S., Griffin, Kathleen M., Vernava, A. M., Beckman, R., Andrus, C., Johnson, F., Herrmann, V., Kaminski, D. L., Wetter, L. A., Dinneen, M., Levitt, M., Motson, R. W., Rohrer, D. A., Bapna, M. S., Rotstein, L. E., Radhakrishnan, Jayant, Shrader, Charisse, Ravo, B., Frattaroli, F. M., Reggio, D., Litchy, W. J., Hanson, R. B., Morgado, Pedro J., Alfaro, Rodrigo, Alfonzo, Rafael, Vachon, D. A., Oliver, G. C., Eisenstat, T. E., Salvati, E. P., Rubin, R. J., Clay, R. P., Kumar, Sanath, Guillem, J. G., Levy, M. F., Hsieh, L. L., Johnson, M. D., Forde, K. A., Weinstein, I. B., Bilchik, A. J., Fleming, F. X., Pernikoff, B. J., Goldenring, J. R., Fozard, J. B., Lowndes, R. H., Young, H. L., Sackier, J., Leite, J. F. M. S., Fausto-Pontes, Martins, M. I., Kmiot, W. A., Youngs, D. J., Harding, L. K., Hesselwood, S. R., Smith, N., Hartley, M. G., Hudson, M. J., Hill, M. J., Gent, A. E., Grace, R. H., Swarbrick, E. T., Hellier, M. D., Procaccino, J. A., Oakley, J. R., Flanagan, Jr., R. A., Lapos, L., Riether, R. D., Stasik, J. J., Trostle, D. R., Sheets, J. A., Ferrara, A., Armstrong, D. N., Bjorck, S., McMillen, M. A., Nicholson, J. D., Halleran, D. R., Trivisonno, D. P., Ziegler, J. A., Lott, J., Saleeby, R., Sullivan, T., and Nelson, R.

Published
1990
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9. Do subtle reminders of money change people's political views?

Author

Rohrer, D, Pashler, H, and Harris, CR

Abstract

© 2015 American Psychological Association. A number of researchers have reported studies showing that subtle reminders of money can alter behaviors and beliefs that are seemingly unrelated to money. In 1 set of studies published in this journal, Caruso, Vohs, Baxter, and Waytz (2013) found that incidental exposures to money led subjects to indicate greater support for inequality, socioeconomic differences, group-based discrimination, and free market economies. We conducted high-powered replication attempts of these 4 money priming effects and found no evidence of priming (weighted Cohen's d = 0.03). We later learned that Caruso et al. also found several null effects in their line of research that were not reported in the original article. In addition, the money priming effect observed in the first study of Caruso et al. was included in the Many Labs Replication Project (Klein et al., 2014), and only 1 of the 36 labs was able to find the effect.

Published
2015
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11. Interim Analysis of the MMRF CoMMpass Study: Comprehensive Characterization of Multiple Myeloma Patients at Diagnosis Reveals Distinct Molecular Subtypes and Clinical Outcomes

Author

Keats, J., primary, Speyer, G., additional, Christofferson, A., additional, Stephenson, K., additional, Kurdoglu, A., additional, Russell, M., additional, Aldrich, J., additional, Legendre, C., additional, Cuyugan, L., additional, Adkins, J., additional, McDonald, J., additional, Helland, A., additional, Blanski, A., additional, Hodges, M., additional, Rohrer, D., additional, Jagannath, S., additional, Siegel, D., additional, Vij, R., additional, Orloff, G., additional, Zimmerman, T., additional, Niesvizky, R., additional, Liles, D., additional, Fay, J., additional, Wolf, J., additional, Rifkin, R., additional, Derome, M., additional, Auclair, D., additional, Liang, W., additional, Kim, S., additional, Gutierrez, N., additional, Kidd, P., additional, Jewell, S., additional, Craig, D., additional, Carpten, J., additional, and Lonial, S., additional

Published
2015
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13. Camera and film processor

Author

Rohrer, D. J

Subjects
Instrumentation And Photography
Abstract

Camera and photographic film processor

Published
1966

18. Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans.

Author

Dulloo AG, Duret C, Rohrer D, Girardier L, Mensi N, Fathi M, Chantre P, and Vandermander J

Abstract

Background: Current interest in the role of functional foods in weight control has focused on plant ingredients capable of interfering with the sympathoadrenal system. Objective: We investigated whether a green tea extract, by virtue of its high content of caffeine and catechin polyphenols, could increase 24-h energy expenditure (EE) and fat oxidation in humans. Design: Twenty-four-hour EE, the respiratory quotient (RQ), and the urinary excretion of nitrogen and catecholamines were measured in a respiratory chamber in 10 healthy men. On 3 separate occasions, subjects were randomly assigned among 3 treatments: green tea extract (50 mg caffeine and 90 mg epigallocatechin gallate), caffeine (50 mg), and placebo, which they ingested at breakfast, lunch, and dinner. Results: Relative to placebo, treatment with the green tea extract resulted in a significant increase in 24-h EE (4%; P < 0.01) and a significant decrease in 24-h RQ (from 0.88 to 0.85; P < 0.001) without any change in urinary nitrogen. Twenty-four-hour urinary norepinephrine excretion was higher during treatment with the green tea extract than with the placebo (40%, P < 0.05). Treatment with caffeine in amounts equivalent to those found in the green tea extract had no effect on EE and RQ nor on urinary nitrogen or catecholamines. Conclusions: Green tea has thermogenic properties and promotes fat oxidation beyond that explained by its caffeine content per se. The green tea extract may play a role in the control of body composition via sympathetic activation of thermogenesis, fat oxidation, or both. Copyright (c) 1999 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]

Published
1999
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19. On the relative and absolute strength of a memory trace.

Author

Rohrer D

Abstract

Subjects studied either an 8- or 16-word list and later recalled the items while a voice key recorded each response latency. The trials were partitioned by recall total in order to examine the means and distributions of both latencies and interresponse times as a function of recall total. Each analysis was consistent with the view that an item's absolute strength determines whether it is recalled whereas an item's relative strength determines when it is recalled. In addition, mean latency was effectively proportional to study list length yet independent of recall total. All of the analyses were consistent with the view that the set of study items is sampled according to a relative-strength rule until all items are found and that a sampled item is recovered into consciousness only when its absolute strength exceeds a fixed threshold. [ABSTRACT FROM AUTHOR]

Published
1996
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25. Spontaneous activation of beta(2)- but not beta(1)-adrenoceptors expressed in cardiac myocytes from beta(1)beta(2) double knockout mice.

Author

Y, Zhou Y, D, Yang, Z, Zhu W, J, Zhang S, J, Wang D, K, Rohrer D, E, Devic, K, Kobilka B, G, Lakatta E, H, Cheng, and P, Xiao R

Abstract

Although ligand-free, constitutive beta(2)-adrenergic receptor (AR) signaling has been demonstrated in naive cell lines and in transgenic mice overexpressing cardiac beta(2)-AR, it is unclear whether the dominant cardiac beta-AR subtype, beta(1)-AR, shares the ability of spontaneous activation. In the present study, we expressed human beta(1)- or beta(2)-AR via recombinant adenoviral infection in ventricular myocytes isolated from beta(1)beta(2)-AR double knockout mice, creating pure beta(1)-AR and beta(2)-AR systems with variable receptor densities. A contractile response to a nonselective beta-AR agonist, isoproterenol, was absent in double knockout mouse myocytes but was fully restored after adenoviral beta(1)-AR or adenoviral beta(2)-AR infection. Increasing the titer of adenoviral vectors (multiplicity of infection 10-1000) led to a dose-dependent expression of beta(1)- or beta(2)-AR with a maximal density of 1207 +/- 173 (36-fold over the wild-type control value) and 821+/-38 fmol/mg protein (69-fold), respectively. Using confocal immunohistochemistry, we directly visualized the cellular distribution of beta(1)-AR and beta(2)-AR and found that both subtypes were distributed on the cell surface membrane and transverse tubules, resulting in a striated pattern. In the absence of ligand, beta(2)-AR expression resulted in graded increases in baseline cAMP and contractility up to 428% and 233% of control, respectively, at the maximal beta(2)-AR density. These effects were specifically reversed by a beta(2)-AR inverse agonist, ICI 118,551 (10(-7) M). In contrast, overexpression of beta(1)-AR, even at a greater density, failed to enhance either basal cAMP or contractility; the alleged beta(1)-AR inverse agonist, CGP 20712A (10(-6) M), had no significant effect on basal contraction in these cells. Thus, we conclude that acute beta(2)-AR overexpression in cardiac myocytes elicits significant physiological responses due to spontaneous receptor activation; however, this property is beta-AR subtype specific because beta(1)-AR does not exhibit agonist-independent spontaneous activation.

Published
2000

26. Cardiovascular and metabolic alterations in mice lacking both beta1- and beta2-adrenergic receptors.

Author

Rohrer, D K, Chruscinski, A, Schauble, E H, Bernstein, D, and Kobilka, B K

Abstract

The activation state of beta-adrenergic receptors (beta-ARs) in vivo is an important determinant of hemodynamic status, cardiac performance, and metabolic rate. In order to achieve homeostasis in vivo, the cellular signals generated by beta-AR activation are integrated with signals from a number of other distinct receptors and signaling pathways. We have utilized genetic knockout models to test directly the role of beta1- and/or beta2-AR expression on these homeostatic control mechanisms. Despite total absence of beta1- and beta2-ARs, the predominant cardiovascular beta-adrenergic subtypes, basal heart rate, blood pressure, and metabolic rate do not differ from wild type controls. However, stimulation of beta-AR function by beta-AR agonists or exercise reveals significant impairments in chronotropic range, vascular reactivity, and metabolic rate. Surprisingly, the blunted chronotropic and metabolic response to exercise seen in beta1/beta2-AR double knockouts fails to impact maximal exercise capacity. Integrating the results from single beta1- and beta2-AR knockouts as well as the beta1-/beta2-AR double knock-out suggest that in the mouse, beta-AR stimulation of cardiac inotropy and chronotropy is mediated almost exclusively by the beta1-AR, whereas vascular relaxation and metabolic rate are controlled by all three beta-ARs (beta1-, beta2-, and beta3-AR). Compensatory alterations in cardiac muscarinic receptor density and vascular beta3-AR responsiveness are also observed in beta1-/beta2-AR double knockouts. In addition to its ability to define beta-AR subtype-specific functions, this genetic approach is also useful in identifying adaptive alterations that serve to maintain critical physiological setpoints such as heart rate, blood pressure, and metabolic rate when cellular signaling mechanisms are perturbed.

Published
1999

27. Targeted disruption of the beta2 adrenergic receptor gene.

Author

Chruscinski, A J, Rohrer, D K, Schauble, E, Desai, K H, Bernstein, D, and Kobilka, B K

Abstract

beta-Adrenergic receptors (beta-ARs) are members of the superfamily of G-protein-coupled receptors that mediate the effects of catecholamines in the sympathetic nervous system. Three distinct beta-AR subtypes have been identified (beta1-AR, beta2-AR, and beta3-AR). In order to define further the role of the different beta-AR subtypes, we have used gene targeting to inactivate selectively the beta2-AR gene in mice. Based on intercrosses of heterozygous knockout (beta2-AR +/-) mice, there is no prenatal lethality associated with this mutation. Adult knockout mice (beta2-AR -/-) appear grossly normal and are fertile. Their resting heart rate and blood pressure are normal, and they have a normal chronotropic response to the beta-AR agonist isoproterenol. The hypotensive response to isoproterenol, however, is significantly blunted compared with wild type mice. Despite this defect in vasodilation, beta2-AR -/- mice can still exercise normally and actually have a greater total exercise capacity than wild type mice. At comparable workloads, beta2-AR -/- mice had a lower respiratory exchange ratio than wild type mice suggesting a difference in energy metabolism. beta2-AR -/- mice become hypertensive during exercise and exhibit a greater hypertensive response to epinephrine compared with wild type mice. In summary, the primary physiologic consequences of the beta2-AR gene disruption are observed only during the stress of exercise and are the result of alterations in both vascular tone and energy metabolism.

Published
1999

29. Thyroid hormone markedly increases the mRNA coding for sarcoplasmic reticulum Ca2+-ATPase in the rat heart.

Author

Rohrer, D and Dillmann, W H

Abstract

Previous findings have shown that thyroid hormone markedly increases the speed of diastolic relaxation in the heart. This thyroid hormone-dependent change is also accompanied by an increased Ca2+ pumping ability in the sarcoplasmic reticulum. In an effort to determine the underlying cause of improved Ca2+ transport, mRNA levels of the slow Ca2+-ATPase of the sarcoplasmic reticulum were quantified on Northern blots. In hypothyroid rat hearts, the steady state level of Ca2+-ATPase mRNA was only 36% of control levels, whereas hyperthyroid rat heart mRNA levels were 136% of control. Ca2+-ATPase mRNA responded rapidly to T3, as the mRNA level was significantly increased by 2 h and normalized by 5 h after T3 injection into hypothyroid rats. The well established effect of thyroid hormone on improved myocardial contractility and increased speed of diastolic relaxation may in part relate to specific alterations in the level of the mRNA coding for Ca2+-ATPase, resulting in increased pump units.

Published
1988
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30. The effect of 16 beta-substitution on the structure and activity of digitoxigenin: is there an additional binding interaction with Na+,K+-ATPase?

Author

Griffin, J F, Rohrer, D C, Ahmed, K, From, A H, Hashimoto, T, Rathore, H, and Fullerton, D S

Abstract

We have studied the basis of the effect of 16 beta-substitution on the structure and activity of digitoxigenin derivatives by examining the crystal structures of these compounds and their inhibitory activity toward the receptor for these drugs, Na+,K+-ATPase. To understand the increase in inhibitory activity of the 16 beta-ester compounds and the decrease in activity of gitoxigenin (16 beta-hydroxydigitoxigenin), both with respect to digitoxigenin, we have compared the observed conformations of gitoxigenin, gitoxigenin 16 beta-formate, and other 16 beta-esters to that of digitoxigenin. Our data do not support the possibility of hydrogen bonding between the 16 beta-hydroxyl of gitoxigenin and the lactone ring, previously suggested to account for the decreased activity of gitoxigenin vis à vis digitoxigenin, but, rather, suggest that the decreased activity may be due to an intramolecular hydrogen bond between the hydroxyls on C-14 and C-16 and an unusual D-ring conformation which combine to alter the carbonyl oxygen of the lactone ring away from the putative active position. In contrast, the 16 beta-ester moiety has a preferred conformation which may serve to fix the lactone ring in the active conformation. Thus, the increased activity of the 16 beta-esters cannot be explained by altered carbonyl oxygen position and may be related to an additional receptor binding site for the ester moiety.

Published
1986

31. Interaction of (Na+,K+)-ATPases and digitalis genins. A general model for inhibitory activity.

Author

Ahmed, K, Rohrer, D C, Fullerton, D S, Deffo, T, Kitatsuji, E, and From, A H

Abstract

Previous models of digitalis genin interaction with the (Na+,K+)-ATPase system (the putative receptor for such drugs) were deficient in explaining the (Na+,K+)-ATPase inhibitory activity of a number of digitalis genin analogues. With rat brain (Na+,K+)-ATPase we observed that the C-17 side chain carbonyl (C = O) oxygen distance of a given genin in relation to its position in the reference compound digitoxigenin was the primary determinant of its biological activity. With a number of genin analogues, we observed a strict correlation of this structural parameter with its binding site compatibility as well as inhibitory potency with respect to the (Na+,K+)-ATPase. In every case the correlation to inhibition data was obtained using a minimum energy conformation for the genin structure. The general applicability of that model is now proposed based on the following observations. The carbonyl oxygen position versus the biological activity relationship fully holds with (Na+,K+)-ATPase preparations from other tissues and species and also when different binding conditions are used for the enzyme genin interaction. The relationship is equally valid for the K+-p-nitrophenyl phosphatase activity. Correlations of the data obtained under these various conditions provide further support for this relationship and for the concept that altered affinities of the enzyme for a given genin under different binding conditions reflect conformational variations of a single binding site.

Published
1983
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34. Comparison of formalin-free tissue fixatives a proteomic study testing their application for routine pathology and research

Author

Kothmaier, H., Rohrer, D., Stacher, E., Quehenberger, F., Karl-Friedrich Becker, and Popper, H. H.

Subjects
Proteomics, Lung Neoplasms, Paraffin Embedding, Tissue Fixation, Pathology, Surgical, Blotting, Western, General Medicine, Immunohistochemistry, Pathology and Forensic Medicine, Neoplasm Proteins, ErbB Receptors, Medical Laboratory Technology, Fixatives, Formaldehyde, Biomarkers, Tumor, Frozen Sections, Humans
Abstract

Context.—Formalin-fixed, paraffin-embedded tissue is the routine processing method for diagnostics practiced in pathology departments worldwide. Objective.—To determine the potential value of non–cross-linking, formalin-free tissue fixation for diagnostics in pathology and proteomic investigations. Design.—We tested 3 commercially available, formalin-free tissue fixatives—FineFIX, RCL2, and HOPE—in lung cancer specimens from 10 patients. The fixatives were evaluated for their effects on tissue morphology, protein recovery, and immunoreactivity for a selected panel of proteins differently expressed in lung cancer, using immunohistochemistry and Western blotting. Results.—Tumor-cell analysis with hematoxylin-eosin worked equally well for all tested fixatives when compared with the standard formalin-fixed, paraffin-embedded procedure. Movat pentachrome stains showed comparable results for the different matrices and cellular proteins analyzed. The RCL2 (P = .01) and HOPE fixatives (P = .03) improved protein recovery when compared with formalin-fixed, paraffin-embedded or frozen tissues. Our data clearly show that the fixatives evaluated influenced immunoreactivity to matched, formalin-fixed, paraffin-embedded lung cancer tissue. In particular, membrane-bound proteins, such as epidermal growth factor receptor EGFR, can be detected more efficiently by immunohistochemistry and Western blotting. Conclusion.—We have demonstrated that formalin-free fixatives have the potential in routine pathology and research to replace formalin in histomorphology and protein preservation.

43. Bufalin

Author

Rohrer, D. C., primary, Fullerton, D. S., additional, Kitatsuji, E., additional, Nambara, T., additional, and Yoshii, E., additional

Published
1982
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