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35 results on '"Tekabe, Y"'

1. Young investigator award session oral abstract session

Author: Tsukamoto, T., Morita, K., Naya, M., Katoh, C., Kuge, Y., Okamoto, H., Tsutsui, H., Tamaki, N., Namdar, M., Siegrist, P., Koepfli, P., Tschuetscher, P., Hany, T., Wyss, C., Kaufmann, P., Lautamäki, R., Airaksinen, K., Seppänen, M., Toikka, J., Luotolahti, M., Ball, E., Härkönen, R., Knuuti, J., Stewart, M., Nuutila, P., Ghanbari, H., Hassunizadeh, B., Williams, F., Cunningham, D., Agrawal, S., Machado, C., Saba, S., Tekabe, Y., Abu-Taha, A., Johnson, L., Khaw, B., Noble, G., ElKoustaf, R., Navare, S., Lundbye, J., Katten, D., Platt, M., Ahlberg, A., and Heller, G.
Published: 2018

2. Young investigator award session oral abstract session

Author: Tsukamoto, T. Takahiro, Morita, K., Naya, M., Katoh, C., Kuge, Y., Okamoto, H., Tsutsui, H., Tamaki, N., Namdar, M. Mehdi, Siegrist, P. T., Koepfli, P., Tschuetscher, P., Hany, T. F., Wyss, C. A., Kaufmann, P. A., Lautamäki, R. Riikka, Airaksinen, K. E. J., Seppänen, M., Toikka, J., Luotolahti, M., Ball, E., Härkönen, R., Knuuti, J., Stewart, M., Nuutila, P., Ghanbari, H. Hamid, Hassunizadeh, B., Williams, F., Cunningham, D., Agrawal, S., Machado, C., Saba, S., Tekabe, Y., Abu-Taha, A., Johnson, L., Khaw, B. A. Ban-AN, Noble, G. L. Gavin, ElKoustaf, R., Navare, S. M., Lundbye, J., Katten, D., Platt, M., Ahlberg, A., and Heller, G. V.
Published: 2005
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3. Disposal of Iron by a Mutant form of Siderocalin NGAL

Author: Rupert, P.B., primary, Strong, R.K., additional, Barasch, J., additional, Hollman, M., additional, Deng, R., additional, Hod, E.A., additional, Abergel, R., additional, Allred, B., additional, Xu, K., additional, Darrah, S., additional, Tekabe, Y., additional, Perlstein, A., additional, Bruck, E., additional, Stauber, J., additional, Corbin, K., additional, Buchen, C., additional, Slavkovich, V., additional, Graziano, J., additional, Spitalnik, S., additional, and Qiu, A., additional
Published: 2016
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4. Poster Session 2 : Monday 4 May 2015, 08

Author: Bouyoucef, S E, Uusitalo, V, Kamperidis, V, De Graaf, M A, Maaniitty, T, Stenstrom, I, Broersen, A, Scholte, A J, Saraste, A, Bax, J J, Knuuti, J, Furuhashi, T, Moroi, M, Awaya, T, Masai, H, Minakawa, M, Kunimasa, T, Fukuda, H, Sugi, K, Berezin, A, Kremzer, A, Clerc, O F, Kaufmann, B, Possner, M, Liga, R, Vontobel, J, Mikulicic, F, Graeni, C, Benz, D C, Kaufmann, P A, Buechel, R B, Ferreira, Mjv, Cunha, M J, Albuquerque, A, Ramos, D, Costa, G, Lima, J, Pego, M, Peix, A, Cisneros, L, Cabrera, L O, Padron, K, Rodriguez, L, Heres, F, Carrillo, R, Mena, E, Fernandez, Y, Huizing, E D, Van Dijk, J D, Van Dalen, J A, Timmer, J R, Ottervanger, J P, Slump, C H, Jager, P L, Venuraju, S, Jeevarethinam, A, Yerramasu, A, Atwal, S, Mehta, V S, Lahiri, A, Arjonilla Lopez, A, Calero Rueda, M J, Gallardo, G, Fernandez-Cuadrado, J, Hernandez Aceituno, D, Sanchez Hernandez, J, Yoshida, H, Mizukami, A, Matsumura, A, Smettei, O, Abazid, R, Sayed, S, Mlynarska, A, Mlynarski, R, Golba, K, Sosnowski, M, Winther, S, Svensson, M, Jorgensen, H S, Bouchelouche, K, Gormsen, L C, Holm, N R, Botker, H E, Ivarsen, P R, Bottcher, M, Cortes, C M, Aramayo G, E N, Daicz, M, Casuscelli, J F, Alaguibe, E D, Neira Sepulveda, A, Cerda, M, Ganum, G E, Embon, M, Vigne, J, Enilorac, B, Lebasnier, A, Valancogne, L, Peyronnet, D, Manrique, A, Agostini, D, Menendez, D, Rajpal, S, Kocherla, C, Acharya, M, Reddy, P, Sazonova, I, Ilushenkova, Yun, Batalov, R E, Rogovskaya, Y V, Lishmanov, Y B, Popov, S V, Varlamova, N V, Prado Diaz, S, Jimenez Rubio, C, Gemma, D, Refoyo Salicio, E, Valbuena Lopez, S C, Moreno Yanguela, M, Torres, M, Fernandez-Velilla, M, Lopez-Sendon, J L, Guzman Martinez, G, Puente, A, Rosales, S, Martinez, C, Cabada, M, Melendez, G M, Ferreira, R, Gonzaga, A, Santos, J, Vijayan, S, Smith, Smg, Smith, M, Muthusamy, R, Takeishi, Y, Oikawa, M, Goral, J L, Napoli, J, Montana, O R, Damico, A C, Quiroz, M C, Damico, A E, Forcada, P J, Schmidberg, J M, Zucchiatti, N E, Olivieri, D B, Dumo, A, Ruano, S, Rakhit, R, Davar, J, Nair, D, Cohen, M, Darko, D, Yokota, S, Maas, Ahe, Mouden, M, Knollema, S, Sanja Mazic, S M, Lazovic, B, Marina Djelic, Mdj, Jelena Suzic Lazic, J S, Tijana Acimovic, T A, Milica Deleva, M D, Vesnina, Z H, Zafrir, N, Bental, T, Mats, I, Solodky, A, Gutstein, A, Hasid, Y, Belzer, D, Kornowski, R, Ben Said, Rim, Ben Mansour, N, Ibn Haj Amor, H, Chourabi, C, Hagui, A, Fehri, W, Hawala, H, Shugushev, Z, Patrikeev, A, Maximkin, D, Chepurnoy, A, Kallianpur, V, Mambetov, A, Dokshokov, G, Teresinska, A, Wozniak, O, Maciag, A, Wnuk, J, Dabrowski, A, Czerwiec, A, Jezierski, J, Biernacka, K, Robinson, J, Prosser, J, Cheung, Gsm, Allan, S, Mcmaster, G, Reid, S, Tarbuck, A, Martin, W, Queiroz, R C, Falcao, A, Giorgi, McP, Imada, R, Nogueira, S A, Chalela, W A, Kalil Filho, R, Meneghetti, W A, Matveev, V V, Bubyenov, A S, Podzolkov, V I, Baranovich, V, Faibushevich, A, Kolzhecova, Y, Volkova, O, Fernandez, J, Lopez, G, Dondi, M, Paez, D, Butcher, Cjt, Reyes, E, Al-Housni, M B, Green, R, Santiago, H, Ghiotto, F, Hinton-Taylor, S, Pottle, A, Mason, M, Underwood, S R, Casans Tormo, I, Diaz-Exposito, R, Plancha-Burguera, E, Elsaban, K, Alsakhri, Hijji, Yoshinaga, K, Ochi, N, Tomiyama, Y, Katoh, C, Inoue, M, Nishida, M, Suzuki, E, Manabe, O, Ito, Y M, Tamaki, N, Tahilyani, A, Jafary, Fahim, Ho Hee Hwa, H H, Ozdemir, S, Kirilmaz, B, Barutcu, A, Tan, Y Z, Celik, F, Sakgoz, S, Cabada Gamboa, M, Puente Barragan, A, Morales Vitorino, N, Medina Servin, M A, Hindorf, C, Akil, S, Hedeer, F, Jogi, J, Engblom, H, Martire, V D, Pis Diez, E R, Martire, M V, Portillo, D O, Hoff, C M, Balche, A, Majgaard, J, Tolbod, L P, Harms, H J, Soerensen, J, Froekiaer, J, Nudi, F, Neri, G, Procaccini, E, Pinto, A, Vetere, M, Biondi-Zoccai, G, Soares, J, Do Val, R, Oliveira, M A, Meneghetti, J C, Tekabe, Y, Anthony, T, Li, Q, Schmidt, A M, Johnson, L, Groenman, M, Tarkia, M, Kakela, M, Halonen, P, Kiviniemi, T, Pietila, M, Yla-Herttuala, S, Roivainen, A, Nekolla, S, Swirzek, S, Higuchi, T, Reder, S, Schachoff, S, Bschorner, M, Laitinen, I, Robinson, S, Yousefi, B, Schwaiger, M, Kero, Tanja, Lindsjo, L, Antoni, Gunnar, Westermark, P, Carlson, K, Wikstrom, G, Sörensen, Jens, Lubberink, Mark, Rouzet, F, Cognet, T, Guedj, K, Morvan, M, El Shoukr, F, Louedec, L, Choqueux, C, Nicoletti, A, Le Guludec, D, Jimenez-Heffernan, A, Munoz-Beamud, F, Sanchez De Mora, E, Borrachero, C, Salgado, C, Ramos-Font, C, Lopez-Martin, J, Hidalgo, M L, Lopez-Aguilar, R, Soriano, E, Okizaki, A, Nakayama, M, Ishitoya, S, Sato, J, Takahashi, K, Burchert, I, Caobelli, F, Wollenweber, T, Nierada, M, Fulsche, J, Dieckmann, C, Bengel, F M, Shuaib, S, Mahlum, D, Port, S, Refoyo, E, Cuesta, E, Guzman, G, Lopez, T, Valbuena, S, Del Prado, S, Moreno, M, Harbinson, M, Donnelly, L, Einstein, A J, Johnson, L L, Deluca, A J, Kontak, A C, Groves, D W, Stant, J, Pozniakoff, T, Cheng, B, Rabbani, L E, Bokhari, S, Schuetze, C, Aguade-Bruix, S, Pizzi, M N, Romero-Farina, G, Terricabras, M, Villasboas, D, Castell-Conesa, J, Candell-Riera, J, Brunner, S, Gross, L, Todica, A, Lehner, S, Di Palo, A, Niccoli Asabella, A, Magarelli, C, Notaristefano, A, Ferrari, C, Rubini, G, Sellem, A, Melki, S, Elajmi, W, Hammami, H, Ziadi, M C, Montero, J, Ameriso, J L, Villavicencio, R L, Benito Gonzalez, T F, Mayorga Bajo, A, Gutierrez Caro, R, Rodriguez Santamarta, M, Alvarez Roy, L, Martinez Paz, E, Barinaga Martin, C, Martin Fernandez, J, Alonso Rodriguez, D, Iglesias Garriz, I, Rosillo, S, Taleb, S, Cherkaoui Salhi, G, Regbaoui, Y, Ait Idir, M, Guensi, A, Martin Lopez, C E, Castano Ruiz, M, Bouyoucef, S E, Uusitalo, V, Kamperidis, V, De Graaf, M A, Maaniitty, T, Stenstrom, I, Broersen, A, Scholte, A J, Saraste, A, Bax, J J, Knuuti, J, Furuhashi, T, Moroi, M, Awaya, T, Masai, H, Minakawa, M, Kunimasa, T, Fukuda, H, Sugi, K, Berezin, A, Kremzer, A, Clerc, O F, Kaufmann, B, Possner, M, Liga, R, Vontobel, J, Mikulicic, F, Graeni, C, Benz, D C, Kaufmann, P A, Buechel, R B, Ferreira, Mjv, Cunha, M J, Albuquerque, A, Ramos, D, Costa, G, Lima, J, Pego, M, Peix, A, Cisneros, L, Cabrera, L O, Padron, K, Rodriguez, L, Heres, F, Carrillo, R, Mena, E, Fernandez, Y, Huizing, E D, Van Dijk, J D, Van Dalen, J A, Timmer, J R, Ottervanger, J P, Slump, C H, Jager, P L, Venuraju, S, Jeevarethinam, A, Yerramasu, A, Atwal, S, Mehta, V S, Lahiri, A, Arjonilla Lopez, A, Calero Rueda, M J, Gallardo, G, Fernandez-Cuadrado, J, Hernandez Aceituno, D, Sanchez Hernandez, J, Yoshida, H, Mizukami, A, Matsumura, A, Smettei, O, Abazid, R, Sayed, S, Mlynarska, A, Mlynarski, R, Golba, K, Sosnowski, M, Winther, S, Svensson, M, Jorgensen, H S, Bouchelouche, K, Gormsen, L C, Holm, N R, Botker, H E, Ivarsen, P R, Bottcher, M, Cortes, C M, Aramayo G, E N, Daicz, M, Casuscelli, J F, Alaguibe, E D, Neira Sepulveda, A, Cerda, M, Ganum, G E, Embon, M, Vigne, J, Enilorac, B, Lebasnier, A, Valancogne, L, Peyronnet, D, Manrique, A, Agostini, D, Menendez, D, Rajpal, S, Kocherla, C, Acharya, M, Reddy, P, Sazonova, I, Ilushenkova, Yun, Batalov, R E, Rogovskaya, Y V, Lishmanov, Y B, Popov, S V, Varlamova, N V, Prado Diaz, S, Jimenez Rubio, C, Gemma, D, Refoyo Salicio, E, Valbuena Lopez, S C, Moreno Yanguela, M, Torres, M, Fernandez-Velilla, M, Lopez-Sendon, J L, Guzman Martinez, G, Puente, A, Rosales, S, Martinez, C, Cabada, M, Melendez, G M, Ferreira, R, Gonzaga, A, Santos, J, Vijayan, S, Smith, Smg, Smith, M, Muthusamy, R, Takeishi, Y, Oikawa, M, Goral, J L, Napoli, J, Montana, O R, Damico, A C, Quiroz, M C, Damico, A E, Forcada, P J, Schmidberg, J M, Zucchiatti, N E, Olivieri, D B, Dumo, A, Ruano, S, Rakhit, R, Davar, J, Nair, D, Cohen, M, Darko, D, Yokota, S, Maas, Ahe, Mouden, M, Knollema, S, Sanja Mazic, S M, Lazovic, B, Marina Djelic, Mdj, Jelena Suzic Lazic, J S, Tijana Acimovic, T A, Milica Deleva, M D, Vesnina, Z H, Zafrir, N, Bental, T, Mats, I, Solodky, A, Gutstein, A, Hasid, Y, Belzer, D, Kornowski, R, Ben Said, Rim, Ben Mansour, N, Ibn Haj Amor, H, Chourabi, C, Hagui, A, Fehri, W, Hawala, H, Shugushev, Z, Patrikeev, A, Maximkin, D, Chepurnoy, A, Kallianpur, V, Mambetov, A, Dokshokov, G, Teresinska, A, Wozniak, O, Maciag, A, Wnuk, J, Dabrowski, A, Czerwiec, A, Jezierski, J, Biernacka, K, Robinson, J, Prosser, J, Cheung, Gsm, Allan, S, Mcmaster, G, Reid, S, Tarbuck, A, Martin, W, Queiroz, R C, Falcao, A, Giorgi, McP, Imada, R, Nogueira, S A, Chalela, W A, Kalil Filho, R, Meneghetti, W A, Matveev, V V, Bubyenov, A S, Podzolkov, V I, Baranovich, V, Faibushevich, A, Kolzhecova, Y, Volkova, O, Fernandez, J, Lopez, G, Dondi, M, Paez, D, Butcher, Cjt, Reyes, E, Al-Housni, M B, Green, R, Santiago, H, Ghiotto, F, Hinton-Taylor, S, Pottle, A, Mason, M, Underwood, S R, Casans Tormo, I, Diaz-Exposito, R, Plancha-Burguera, E, Elsaban, K, Alsakhri, Hijji, Yoshinaga, K, Ochi, N, Tomiyama, Y, Katoh, C, Inoue, M, Nishida, M, Suzuki, E, Manabe, O, Ito, Y M, Tamaki, N, Tahilyani, A, Jafary, Fahim, Ho Hee Hwa, H H, Ozdemir, S, Kirilmaz, B, Barutcu, A, Tan, Y Z, Celik, F, Sakgoz, S, Cabada Gamboa, M, Puente Barragan, A, Morales Vitorino, N, Medina Servin, M A, Hindorf, C, Akil, S, Hedeer, F, Jogi, J, Engblom, H, Martire, V D, Pis Diez, E R, Martire, M V, Portillo, D O, Hoff, C M, Balche, A, Majgaard, J, Tolbod, L P, Harms, H J, Soerensen, J, Froekiaer, J, Nudi, F, Neri, G, Procaccini, E, Pinto, A, Vetere, M, Biondi-Zoccai, G, Soares, J, Do Val, R, Oliveira, M A, Meneghetti, J C, Tekabe, Y, Anthony, T, Li, Q, Schmidt, A M, Johnson, L, Groenman, M, Tarkia, M, Kakela, M, Halonen, P, Kiviniemi, T, Pietila, M, Yla-Herttuala, S, Roivainen, A, Nekolla, S, Swirzek, S, Higuchi, T, Reder, S, Schachoff, S, Bschorner, M, Laitinen, I, Robinson, S, Yousefi, B, Schwaiger, M, Kero, Tanja, Lindsjo, L, Antoni, Gunnar, Westermark, P, Carlson, K, Wikstrom, G, Sörensen, Jens, Lubberink, Mark, Rouzet, F, Cognet, T, Guedj, K, Morvan, M, El Shoukr, F, Louedec, L, Choqueux, C, Nicoletti, A, Le Guludec, D, Jimenez-Heffernan, A, Munoz-Beamud, F, Sanchez De Mora, E, Borrachero, C, Salgado, C, Ramos-Font, C, Lopez-Martin, J, Hidalgo, M L, Lopez-Aguilar, R, Soriano, E, Okizaki, A, Nakayama, M, Ishitoya, S, Sato, J, Takahashi, K, Burchert, I, Caobelli, F, Wollenweber, T, Nierada, M, Fulsche, J, Dieckmann, C, Bengel, F M, Shuaib, S, Mahlum, D, Port, S, Refoyo, E, Cuesta, E, Guzman, G, Lopez, T, Valbuena, S, Del Prado, S, Moreno, M, Harbinson, M, Donnelly, L, Einstein, A J, Johnson, L L, Deluca, A J, Kontak, A C, Groves, D W, Stant, J, Pozniakoff, T, Cheng, B, Rabbani, L E, Bokhari, S, Schuetze, C, Aguade-Bruix, S, Pizzi, M N, Romero-Farina, G, Terricabras, M, Villasboas, D, Castell-Conesa, J, Candell-Riera, J, Brunner, S, Gross, L, Todica, A, Lehner, S, Di Palo, A, Niccoli Asabella, A, Magarelli, C, Notaristefano, A, Ferrari, C, Rubini, G, Sellem, A, Melki, S, Elajmi, W, Hammami, H, Ziadi, M C, Montero, J, Ameriso, J L, Villavicencio, R L, Benito Gonzalez, T F, Mayorga Bajo, A, Gutierrez Caro, R, Rodriguez Santamarta, M, Alvarez Roy, L, Martinez Paz, E, Barinaga Martin, C, Martin Fernandez, J, Alonso Rodriguez, D, Iglesias Garriz, I, Rosillo, S, Taleb, S, Cherkaoui Salhi, G, Regbaoui, Y, Ait Idir, M, Guensi, A, Martin Lopez, C E, and Castano Ruiz, M
Published: 2015
Full Text: View/download PDF

5. Poster Session 2: Monday 4 May 2015, 08:00-18:00 * Room: Poster Area

Author: Bouyoucef, S. E., primary, Uusitalo, V., additional, Kamperidis, V., additional, De Graaf, M., additional, Maaniitty, T., additional, Stenstrom, I., additional, Broersen, A., additional, Scholte, A., additional, Saraste, A., additional, Bax, J., additional, Knuuti, J., additional, Furuhashi, T., additional, Moroi, M., additional, Awaya, T., additional, Masai, H., additional, Minakawa, M., additional, Kunimasa, T., additional, Fukuda, H., additional, Sugi, K., additional, Berezin, A., additional, Kremzer, A., additional, Clerc, O., additional, Kaufmann, B., additional, Possner, M., additional, Liga, R., additional, Vontobel, J., additional, Mikulicic, F., additional, Graeni, C., additional, Benz, D., additional, Kaufmann, P., additional, Buechel, R., additional, Ferreira, M., additional, Cunha, M., additional, Albuquerque, A., additional, Ramos, D., additional, Costa, G., additional, Lima, J., additional, Pego, M., additional, Peix, A., additional, Cisneros, L., additional, Cabrera, L., additional, Padron, K., additional, Rodriguez, L., additional, Heres, F., additional, Carrillo, R., additional, Mena, E., additional, Fernandez, Y., additional, Huizing, E., additional, Van Dijk, J., additional, Van Dalen, J., additional, Timmer, J., additional, Ottervanger, J., additional, Slump, C., additional, Jager, P., additional, Venuraju, S., additional, Jeevarethinam, A., additional, Yerramasu, A., additional, Atwal, S., additional, Mehta, V., additional, Lahiri, A., additional, Arjonilla Lopez, A., additional, Calero Rueda, M. J., additional, Gallardo, G., additional, Fernandez-Cuadrado, J., additional, Hernandez Aceituno, D., additional, Sanchez Hernandez, J., additional, Yoshida, H., additional, Mizukami, A., additional, Matsumura, A., additional, Smettei, O., additional, Abazid, R., additional, Sayed, S., additional, Mlynarska, A., additional, Mlynarski, R., additional, Golba, K., additional, Sosnowski, M., additional, Winther, S., additional, Svensson, M., additional, Jorgensen, H., additional, Bouchelouche, K., additional, Gormsen, L., additional, Holm, N., additional, Botker, H., additional, Ivarsen, P., additional, Bottcher, M., additional, Cortes, C. M., additional, Aramayo G, E., additional, Daicz, M., additional, Casuscelli, J., additional, Alaguibe, E., additional, Neira Sepulveda, A., additional, Cerda, M., additional, Ganum, G., additional, Embon, M., additional, Vigne, J., additional, Enilorac, B., additional, Lebasnier, A., additional, Valancogne, L., additional, Peyronnet, D., additional, Manrique, A., additional, Agostini, D., additional, Menendez, D., additional, Rajpal, S., additional, Kocherla, C., additional, Acharya, M., additional, Reddy, P., additional, Sazonova, I., additional, Ilushenkova, Y., additional, Batalov, R., additional, Rogovskaya, Y., additional, Lishmanov, Y., additional, Popov, S., additional, Varlamova, N., additional, Prado Diaz, S., additional, Jimenez Rubio, C., additional, Gemma, D., additional, Refoyo Salicio, E., additional, Valbuena Lopez, S., additional, Moreno Yanguela, M., additional, Torres, M., additional, Fernandez-Velilla, M., additional, Lopez-Sendon, J., additional, Guzman Martinez, G., additional, Puente, A., additional, Rosales, S., additional, Martinez, C., additional, Cabada, M., additional, Melendez, G., additional, Ferreira, R., additional, Gonzaga, A., additional, Santos, J., additional, Vijayan, S., additional, Smith, S., additional, Smith, M., additional, Muthusamy, R., additional, Takeishi, Y., additional, Oikawa, M., additional, Goral, J. L., additional, Napoli, J., additional, Montana, O., additional, Damico, A., additional, Quiroz, M., additional, Forcada, P., additional, Schmidberg, J., additional, Zucchiatti, N., additional, Olivieri, D., additional, Dumo, A., additional, Ruano, S., additional, Rakhit, R., additional, Davar, J., additional, Nair, D., additional, Cohen, M., additional, Darko, D., additional, Yokota, S., additional, Maas, A., additional, Mouden, M., additional, Knollema, S., additional, Sanja Mazic, S., additional, Lazovic, B., additional, Marina Djelic, M., additional, Jelena Suzic Lazic, J., additional, Tijana Acimovic, T., additional, Milica Deleva, M., additional, Vesnina, Z., additional, Zafrir, N., additional, Bental, T., additional, Mats, I., additional, Solodky, A., additional, Gutstein, A., additional, Hasid, Y., additional, Belzer, D., additional, Kornowski, R., additional, Ben Said, R., additional, Ben Mansour, N., additional, Ibn Haj Amor, H., additional, Chourabi, C., additional, Hagui, A., additional, Fehri, W., additional, Hawala, H., additional, Shugushev, Z., additional, Patrikeev, A., additional, Maximkin, D., additional, Chepurnoy, A., additional, Kallianpur, V., additional, Mambetov, A., additional, Dokshokov, G., additional, Teresinska, A., additional, Wozniak, O., additional, Maciag, A., additional, Wnuk, J., additional, Dabrowski, A., additional, Czerwiec, A., additional, Jezierski, J., additional, Biernacka, K., additional, Robinson, J., additional, Prosser, J., additional, Cheung, G., additional, Allan, S., additional, Mcmaster, G., additional, Reid, S., additional, Tarbuck, A., additional, Martin, W., additional, Queiroz, R., additional, Falcao, A., additional, Giorgi, M., additional, Imada, R., additional, Nogueira, S., additional, Chalela, W., additional, Kalil Filho, R., additional, Meneghetti, W., additional, Matveev, V., additional, Bubyenov, A., additional, Podzolkov, V., additional, Baranovich, V., additional, Faibushevich, A., additional, Kolzhecova, Y., additional, Volkova, O., additional, Fernandez, J., additional, Lopez, G., additional, Dondi, M., additional, Paez, D., additional, Butcher, C., additional, Reyes, E., additional, Al-Housni, M., additional, Green, R., additional, Santiago, H., additional, Ghiotto, F., additional, Hinton-Taylor, S., additional, Pottle, A., additional, Mason, M., additional, Underwood, S., additional, Casans Tormo, I., additional, Diaz-Exposito, R., additional, Plancha-Burguera, E., additional, Elsaban, K., additional, Alsakhri, H., additional, Yoshinaga, K., additional, Ochi, N., additional, Tomiyama, Y., additional, Katoh, C., additional, Inoue, M., additional, Nishida, M., additional, Suzuki, E., additional, Manabe, O., additional, Ito, Y., additional, Tamaki, N., additional, Tahilyani, A., additional, Jafary, F., additional, Ho Hee Hwa, H., additional, Ozdemir, S., additional, Kirilmaz, B., additional, Barutcu, A., additional, Tan, Y., additional, Celik, F., additional, Sakgoz, S., additional, Cabada Gamboa, M., additional, Puente Barragan, A., additional, Morales Vitorino, N., additional, Medina Servin, M., additional, Hindorf, C., additional, Akil, S., additional, Hedeer, F., additional, Jogi, J., additional, Engblom, H., additional, Martire, V., additional, Pis Diez, E., additional, Martire, M., additional, Portillo, D., additional, Hoff, C., additional, Balche, A., additional, Majgaard, J., additional, Tolbod, L., additional, Harms, H., additional, Soerensen, J., additional, Froekiaer, J., additional, Nudi, F., additional, Neri, G., additional, Procaccini, E., additional, Pinto, A., additional, Vetere, M., additional, Biondi-Zoccai, G., additional, Soares, J., additional, Do Val, R., additional, Oliveira, M., additional, Meneghetti, J., additional, Tekabe, Y., additional, Anthony, T., additional, Li, Q., additional, Schmidt, A., additional, Johnson, L., additional, Groenman, M., additional, Tarkia, M., additional, Kakela, M., additional, Halonen, P., additional, Kiviniemi, T., additional, Pietila, M., additional, Yla-Herttuala, S., additional, Roivainen, A., additional, Nekolla, S., additional, Swirzek, S., additional, Higuchi, T., additional, Reder, S., additional, Schachoff, S., additional, Bschorner, M., additional, Laitinen, I., additional, Robinson, S., additional, Yousefi, B., additional, Schwaiger, M., additional, Kero, T., additional, Lindsjo, L., additional, Antoni, G., additional, Westermark, P., additional, Carlson, K., additional, Wikstrom, G., additional, Sorensen, J., additional, Lubberink, M., additional, Rouzet, F., additional, Cognet, T., additional, Guedj, K., additional, Morvan, M., additional, El Shoukr, F., additional, Louedec, L., additional, Choqueux, C., additional, Nicoletti, A., additional, Le Guludec, D., additional, Jimenez-Heffernan, A., additional, Munoz-Beamud, F., additional, Sanchez De Mora, E., additional, Borrachero, C., additional, Salgado, C., additional, Ramos-Font, C., additional, Lopez-Martin, J., additional, Hidalgo, M., additional, Lopez-Aguilar, R., additional, Soriano, E., additional, Okizaki, A., additional, Nakayama, M., additional, Ishitoya, S., additional, Sato, J., additional, Takahashi, K., additional, Burchert, I., additional, Caobelli, F., additional, Wollenweber, T., additional, Nierada, M., additional, Fulsche, J., additional, Dieckmann, C., additional, Bengel, F., additional, Shuaib, S., additional, Mahlum, D., additional, Port, S., additional, Refoyo, E., additional, Cuesta, E., additional, Guzman, G., additional, Lopez, T., additional, Valbuena, S., additional, Del Prado, S., additional, Moreno, M., additional, Harbinson, M., additional, Donnelly, L., additional, Einstein, A. J., additional, Johnson, L. L., additional, Deluca, A. J., additional, Kontak, A. C., additional, Groves, D. W., additional, Stant, J., additional, Pozniakoff, T., additional, Cheng, B., additional, Rabbani, L. E., additional, Bokhari, S., additional, Schuetze, C., additional, Aguade-Bruix, S., additional, Pizzi, M., additional, Romero-Farina, G., additional, Terricabras, M., additional, Villasboas, D., additional, Castell-Conesa, J., additional, Candell-Riera, J., additional, Brunner, S., additional, Gross, L., additional, Todica, A., additional, Lehner, S., additional, Di Palo, A., additional, Niccoli Asabella, A., additional, Magarelli, C., additional, Notaristefano, A., additional, Ferrari, C., additional, Rubini, G., additional, Sellem, A., additional, Melki, S., additional, Elajmi, W., additional, Hammami, H., additional, Ziadi, M., additional, Montero, J., additional, Ameriso, J., additional, Villavicencio, R., additional, Benito Gonzalez, T. F., additional, Mayorga Bajo, A., additional, Gutierrez Caro, R., additional, Rodriguez Santamarta, M., additional, Alvarez Roy, L., additional, Martinez Paz, E., additional, Barinaga Martin, C., additional, Martin Fernandez, J., additional, Alonso Rodriguez, D., additional, Iglesias Garriz, I., additional, Rosillo, S., additional, Taleb, S., additional, Cherkaoui Salhi, G., additional, Regbaoui, Y., additional, Ait Idir, M., additional, Guensi, A., additional, Martin Lopez, C. E., additional, and Castano Ruiz, M., additional
Published: 2015
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6. Abstracts

Author: Dunet, V., primary, Dabiri, A., additional, Allenbach, G., additional, Goyeneche Achigar, A., additional, Waeber, B., additional, Feihl, F., additional, Heinzer, R., additional, Prior, J. O., additional, Van Velzen, J. E., additional, Schuijf, J. D., additional, De Graaf, F. R., additional, De Graaf, M. A., additional, Schalij, M. J., additional, Kroft, L. J., additional, De Roos, A., additional, Jukema, J. W., additional, Van Der Wall, E. E., additional, Bax, J. J., additional, Lankinen, E., additional, Saraste, A., additional, Noponen, T., additional, Klen, R., additional, Teras, M., additional, Kokki, T., additional, Kajander, S., additional, Pietila, M., additional, Ukkonen, H., additional, Knuuti, J., additional, Pazhenkottil, A. P., additional, Nkoulou, R. N., additional, Ghadri, J. R., additional, Herzog, B. A., additional, Buechel, R. R., additional, Kuest, S. M., additional, Wolfrum, M., additional, Gaemperli, O., additional, Husmann, L., additional, Kaufmann, P. A., additional, Andreini, D., additional, Pontone, G., additional, Mushtaq, S., additional, Antonioli, L., additional, Bertella, E., additional, Formenti, A., additional, Cortinovis, S., additional, Ballerini, G., additional, Fiorentini, C., additional, Pepi, M., additional, Koh, A. S., additional, Flores, J. S., additional, Keng, F. Y. J., additional, Tan, R. S., additional, Chua, T. S. J., additional, Annoni, A. D., additional, Tamborini, G., additional, Fusari, M., additional, Bartorelli, A. L., additional, Ewe, S. H., additional, Ng, A. C. T., additional, Delgado, V., additional, Schuijf, J., additional, Van Der Kley, F., additional, Colli, A., additional, De Weger, A., additional, Marsan, N. A., additional, Yiu, K. H., additional, Ng, A. C., additional, Timmer, S. A. J., additional, Knaapen, P., additional, Germans, T., additional, Dijkmans, P. A., additional, Lubberink, M., additional, Ten Berg, J. M., additional, Ten Cate, F. J., additional, Russel, I. K., additional, Lammertsma, A. A., additional, Van Rossum, A. C., additional, Wong, Y. Y., additional, Ruiter, G., additional, Raijmakers, P., additional, Van Der Laarse, W. J., additional, Westerhof, N., additional, Vonk-Noordegraaf, A., additional, Youssef, G., additional, Leung, E., additional, Wisenberg, G., additional, Marriot, C., additional, Williams, K., additional, Etele, J., additional, Dekemp, R. A., additional, Dasilva, J., additional, Birnie, D., additional, Beanlands, R. S. B., additional, Thompson, R. C., additional, Allam, A. H., additional, Wann, L. S., additional, Nureldin, A. H., additional, Adelmaksoub, G., additional, Badr, I., additional, Sutherland, M. L., additional, Sutherland, J. D., additional, Miyamoto, M. I., additional, Thomas, G. S., additional, Harms, H. J., additional, De Haan, S., additional, Huisman, M. C., additional, Schuit, R. C., additional, Windhorst, A. D., additional, Allaart, C., additional, Einstein, A. J., additional, Khawaja, T., additional, Greer, C., additional, Chokshi, A., additional, Jones, M., additional, Schaefle, K., additional, Bhatia, K., additional, Shimbo, D., additional, Schulze, P. C., additional, Srivastava, A., additional, Chettiar, R., additional, Moody, J., additional, Weyman, C., additional, Natale, D., additional, Bruni, W., additional, Liu, Y., additional, Ficaro, E., additional, Sinusas, A. J., additional, Peix, A., additional, Batista, E., additional, Cabrera, L. O., additional, Padron, K., additional, Rodriguez, L., additional, Sainz, B., additional, Mendoza, V., additional, Carrillo, R., additional, Fernandez, Y., additional, Mena, E., additional, Naum, A., additional, Bach-Gansmo, T., additional, Kleven-Madsen, N., additional, Biermann, M., additional, Johnsen, B., additional, Aase Husby, J., additional, Rotevatn, S., additional, Nordrehaug, J. E., additional, Schaap, J., additional, Kauling, R. M., additional, Post, M. C., additional, Rensing, B. J. W. M., additional, Verzijlbergen, J. F., additional, Sanchez, J., additional, Giamouzis, G., additional, Tziolas, N., additional, Georgoulias, P., additional, Karayannis, G., additional, Chamaidi, A., additional, Zavos, N., additional, Koutrakis, K., additional, Sitafidis, G., additional, Skoularigis, J., additional, Triposkiadis, F., additional, Radovanovic, S., additional, Djokovic, A., additional, Simic, D. V., additional, Krotin, M., additional, Savic-Radojevic, A., additional, Pljesa-Ercegovac, M., additional, Zdravkovic, M., additional, Saponjski, J., additional, Jelic, S., additional, Simic, T., additional, Eckardt, R., additional, Kjeldsen, B. J., additional, Andersen, L. I., additional, Haghfelt, T., additional, Grupe, P., additional, Johansen, A., additional, Hesse, B., additional, Pena, H., additional, Cantinho, G., additional, Wilk, M., additional, Srour, Y., additional, Godinho, F., additional, Zafrir, N., additional, Gutstein, A., additional, Mats, I., additional, Battler, A., additional, Solodky, A., additional, Sari, E., additional, Singh, N., additional, Vara, A., additional, Peters, A. M., additional, De Belder, A., additional, Nair, S., additional, Ryan, N., additional, James, R., additional, Dizdarevic, S., additional, Depuey, G., additional, Friedman, M., additional, Wray, R., additional, Old, R., additional, Babla, H., additional, Chuanyong, B., additional, Maddahi, J., additional, Tragardh Johansson, E., additional, Sjostrand, K., additional, Edenbrandt, L., additional, Aguade-Bruix, S., additional, Cuberas-Borros, G., additional, Pizzi, M. N., additional, Sabate-Fernandez, M., additional, De Leon, G., additional, Garcia-Dorado, D., additional, Castell-Conesa, J., additional, Candell-Riera, J., additional, Casset-Senon, D., additional, Edjlali-Goujon, M., additional, Alison, D., additional, Delhommais, A., additional, Cosnay, P., additional, Low, C. S., additional, Notghi, A., additional, O'brien, J., additional, Tweddel, A. C., additional, Bingham, N., additional, O Neil, P., additional, Harbinson, M., additional, Lindner, O., additional, Burchert, W., additional, Schaefers, M., additional, Marcassa, C., additional, Campini, R., additional, Calza, P., additional, Zoccarato, O., additional, Kisko, A., additional, Kmec, J., additional, Babcak, M., additional, Vereb, M., additional, Vytykacova, M., additional, Cencarik, J., additional, Gazdic, P., additional, Stasko, J., additional, Abreu, A., additional, Pereira, E., additional, Oliveira, L., additional, Colarinha, P., additional, Veloso, V., additional, Enriksson, I., additional, Proenca, G., additional, Delgado, P., additional, Rosario, L., additional, Sequeira, J., additional, Kosa, I., additional, Vassanyi, I., additional, Egyed, C. S., additional, Kozmann, G. Y., additional, Morita, S., additional, Nanasato, M., additional, Nanbu, I., additional, Yoshida, Y., additional, Hirayama, H., additional, Allam, A., additional, Sharef, A., additional, Shawky, I., additional, Farid, M., additional, Mouden, M., additional, Ottervanger, J. P., additional, Timmer, J. R., additional, De Boer, M. J., additional, Reiffers, S., additional, Jager, P. L., additional, Knollema, S., additional, Nasr, G. M., additional, Mohy Eldin, M., additional, Ragheb, M., additional, Casans-Tormo, I., additional, Diaz-Exposito, R., additional, Hurtado-Mauricio, F. J., additional, Ruano, R., additional, Diego, M., additional, Gomez-Caminero, F., additional, Albarran, C., additional, Martin De Arriba, A., additional, Rosero, A., additional, Lopez, R., additional, Martin Luengo, C., additional, Garcia-Talavera, J. R., additional, Laitinen, I. E. K., additional, Rudelius, M., additional, Weidl, E., additional, Henriksen, G., additional, Wester, H. J., additional, Schwaiger, M., additional, Pan, X. B., additional, Schindler, T., additional, Quercioli, A., additional, Zaidi, H., additional, Ratib, O., additional, Declerck, J. M., additional, Alexanderson Rosas, E., additional, Jacome, R., additional, Jimenez-Santos, M., additional, Romero, E., additional, Pena-Cabral, M. A., additional, Meave, A., additional, Gonzalez, J., additional, Rouzet, F., additional, Bachelet, L., additional, Alsac, J. M., additional, Suzuki, M., additional, Louedec, L., additional, Petiet, A., additional, Chaubet, F., additional, Letourneur, D., additional, Michel, J. B., additional, Le Guludec, D., additional, Aktas, A., additional, Cinar, A., additional, Yaman, G., additional, Bahceci, T., additional, Kavak, K., additional, Gencoglu, A., additional, Jimenez-Heffernan, A., additional, Sanchez De Mora, E., additional, Lopez-Martin, J., additional, Lopez-Aguilar, R., additional, Ramos, C., additional, Salgado, C., additional, Ortega, A., additional, Sanchez-Gonzalez, C., additional, Roa, J., additional, Tobaruela, A., additional, Nesterov, S. V., additional, Turta, O., additional, Maki, M., additional, Han, C., additional, Daou, D., additional, Tawileh, M., additional, Chamouine, S. O., additional, Coaguila, C., additional, Mariscal-Labrador, E., additional, Kisiel-Gonzalez, N., additional, De Araujo Goncalves, P., additional, Sousa, P. J., additional, Marques, H., additional, O'neill, J., additional, Pisco, J., additional, Cale, R., additional, Brito, J., additional, Gaspar, A., additional, Machado, F. P., additional, Roquette, J., additional, Martinez, M., additional, Melendez, G., additional, Kimura, E., additional, Ochoa, J. M., additional, Alessio, A. M., additional, Patel, A., additional, Lautamaki, R., additional, Bengel, F. M., additional, Bassingthwaighte, J. B., additional, Caldwell, J. H., additional, Rahbar, K., additional, Seifarth, H., additional, Schafers, M., additional, Stegger, L., additional, Spieker, T., additional, Hoffmeier, A., additional, Maintz, D., additional, Scheld, H., additional, Schober, O., additional, Weckesser, M., additional, Aoki, H., additional, Matsunari, I., additional, Kajinami, K., additional, Martin Fernandez, M., additional, Barreiro Perez, M., additional, Fernandez Cimadevilla, O. V., additional, Leon Duran, D., additional, Velasco Alonso, E., additional, Florez Munoz, J. P., additional, Luyando, L. H., additional, Templin, C., additional, Veltman, C. E., additional, Reiber, J. H. C., additional, Venuraju, S., additional, Yerramasu, A., additional, Atwal, S., additional, Lahiri, A., additional, Kunimasa, T., additional, Shiba, M., additional, Ishii, K., additional, Aikawa, J., additional, Kroner, E. S. J., additional, Ho, K. T., additional, Yong, Q. W., additional, Chua, K. C., additional, Panknin, C., additional, Roos, C. J., additional, Van Werkhoven, J. M., additional, Witkowska-Grzeslo, A. J., additional, Boogers, M. J., additional, Anand, D. V., additional, Dey, D., additional, Berman, D., additional, Mut, F., additional, Giubbini, R., additional, Lusa, L., additional, Massardo, T., additional, Iskandrian, A., additional, Dondi, M., additional, Sato, A., additional, Kakefuda, Y., additional, Ojima, E., additional, Adachi, T., additional, Atsumi, A., additional, Ishizu, T., additional, Seo, Y., additional, Hiroe, M., additional, Aonuma, K., additional, Kruk, M., additional, Pracon, R., additional, Kepka, C., additional, Pregowski, J., additional, Kowalewska, A., additional, Pilka, M., additional, Opolski, M., additional, Michalowska, I., additional, Dzielinska, Z., additional, Demkow, M., additional, Stoll, V., additional, Sabharwal, N., additional, Chakera, A., additional, Ormerod, O., additional, Fernandes, H., additional, Bernardes, M., additional, Martins, E., additional, Oliveira, P., additional, Vieira, T., additional, Terroso, G., additional, Oliveira, A., additional, Faria, T., additional, Ventura, F., additional, Pereira, J., additional, Fukuzawa, S., additional, Inagaki, M., additional, Sugioka, J., additional, Ikeda, A., additional, Okino, S., additional, Maekawa, J., additional, Uchiyama, T., additional, Kamioka, N., additional, Ichikawa, S., additional, Afshar, M., additional, Alvi, R., additional, Aguilar, N., additional, Ippili, R., additional, Shaqra, H., additional, Bella, J., additional, Bhalodkar, N., additional, Dos Santos, A., additional, Daicz, M., additional, Cendoya, L. O., additional, Marrero, H. G., additional, Casuscelli, J., additional, Embon, M., additional, Vera Janavel, G., additional, Duronto, E., additional, Gurfinkel, E. P., additional, Cortes, C. M., additional, Takeishi, Y., additional, Nakajima, K., additional, Yamasaki, Y., additional, Nishimura, T., additional, Hayes Brown, K., additional, Collado, F., additional, Alhaji, M., additional, Green, J., additional, Alexander, S., additional, Vashistha, R., additional, Jain, S., additional, Aldaas, F., additional, Shanes, J., additional, Doukky, R., additional, Ashikaga, K., additional, Akashi, Y. J., additional, Uemarsu, M., additional, Kamijima, R., additional, Yoneyama, K., additional, Omiya, K., additional, Miyake, Y., additional, Brodov, Y., additional, Raval, U., additional, Berezin, A., additional, Seden, V., additional, Koretskaya, E., additional, Panasenko, T. A., additional, Matsuo, S., additional, Kinuya, S., additional, Chen, J., additional, Van Bommel, R. J., additional, Van Der Hiel, B., additional, Dibbets-Schneider, P., additional, Garcia, E. V., additional, Rutten-Vermeltfoort, I., additional, Gevers, M. M. J., additional, Verhoeven, B., additional, Dijk Van, A. B., additional, Raaijmakers, E., additional, Raijmakers, P. G. H. M., additional, Engvall, J. E., additional, Gjerde, M., additional, De Geer, J., additional, Olsson, E., additional, Quick, P., additional, Persson, A., additional, Mazzanti, M., additional, Marini, M., additional, Pimpini, L., additional, Perna, G. P., additional, Marciano, C., additional, Gargiulo, P., additional, Galderisi, M., additional, D'amore, C., additional, Savarese, G., additional, Casaretti, L., additional, Paolillo, S., additional, Cuocolo, A., additional, Perrone Filardi, P., additional, Al-Amoodi, M., additional, Thompson, E. C., additional, Kennedy, K., additional, Bybee, K. A., additional, Mcghie, A. I., additional, O'keefe, J. H., additional, Bateman, T. M., additional, Van Der Palen, R. L. F., additional, Mavinkurve-Groothuis, A. M., additional, Bulten, B., additional, Bellersen, L., additional, Van Laarhoven, H. W. M., additional, Kapusta, L., additional, De Geus-Oei, L. F., additional, Pollice, P. P., additional, Bonifazi, M. B., additional, Pollice, F. P., additional, Clements, I. P., additional, Hodge, D. O., additional, Scott, C. G., additional, De Ville De Goyet, M., additional, Brichard, B., additional, Pirotte, T., additional, Moniotte, S., additional, Tio, R. A., additional, Elvan, A., additional, Dierckx, R. A. I. O., additional, Slart, R. H. J. A., additional, Furuhashi, T., additional, Moroi, M., additional, Hase, H., additional, Joki, N., additional, Masai, H., additional, Nakazato, R., additional, Fukuda, H., additional, Sugi, K., additional, Kryczka, K., additional, Kaczmarska, E., additional, Petryka, J., additional, Mazurkiewicz, L., additional, Ruzyllo, W., additional, Smanio, P., additional, Vieira Segundo, E., additional, Siqueira, M., additional, Kelendjian, J., additional, Ribeiro, J., additional, Alaca, J., additional, Oliveira, M., additional, Alves, F., additional, Peovska, I., additional, Maksimovic, J., additional, Vavlukis, M., additional, Kostova, N., additional, Pop Gorceva, D., additional, Majstorov, V., additional, Zdraveska, M., additional, Hussain, S., additional, Djearaman, M., additional, Hoey, E., additional, Morus, L., additional, Erinfolami, O., additional, Macnamara, A., additional, Opolski, M. P., additional, Witkowski, A., additional, Berti, V., additional, Ricci, F., additional, Gallicchio, R., additional, Acampa, W., additional, Cerisano, G., additional, Vigorito, C., additional, Sciagra', R., additional, Pupi, A., additional, Sliem, H., additional, Collado, F. M., additional, Schmidt, S., additional, Maheshwari, A., additional, Kiriakos, R., additional, Mwansa, V., additional, Ljubojevic, S., additional, Sedej, S., additional, Holzer, M., additional, Marsche, G., additional, Marijanski, V., additional, Kockskaemper, J., additional, Pieske, B., additional, Ricalde, A., additional, Alexanderson, G., additional, Mohani, A., additional, Khanna, P., additional, Sinusas, A., additional, Lee, F., additional, Pinas, V. A., additional, Van Eck-Smit, B. L. F., additional, Verberne, H. J., additional, De Bruin, C. M., additional, Guilhermina, G., additional, Jimenez-Angeles, L., additional, Ruiz De Jesus, O., additional, Yanez-Suarez, O., additional, Vallejo, E., additional, Reyes, E., additional, Chan, M., additional, Hossen, M. L., additional, Underwood, S. R., additional, Karu, A., additional, Bokhari, S., additional, Pineda, V., additional, Gracia-Sanchez, L. M., additional, Garcia-Burillo, A., additional, Zavadovskiy, K., additional, Lishmanov, Y. U., additional, Saushkin, W., additional, Kovalev, I., additional, Chernishov, A., additional, Annoni, A., additional, Tarkia, M., additional, Saanijoki, T., additional, Oikonen, V., additional, Savunen, T., additional, Green, M. A., additional, Strandberg, M., additional, Roivainen, A., additional, Gaeta, M. C., additional, Artigas, C., additional, Deportos, J., additional, Geraldo, L., additional, Flotats, A., additional, La Delfa, V., additional, Carrio, I., additional, Laarse, W. J., additional, Izquierdo Gomez, M. 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A., additional, Boersma, E. H., additional, Krestin, G. P., additional, Purvis, J. A., additional, Sharma, D., additional, Hughes, S. M., additional, Berman, D. S., additional, Taillefer, R., additional, Udelson, J., additional, Devine, M., additional, Lazewatsky, J., additional, Bhat, G., additional, Washburn, D., additional, Patel, D., additional, Mazurek, T., additional, Tandon, S., additional, Bansal, S., additional, Inzucchi, S., additional, Staib, L., additional, Davey, J., additional, Chyun, D., additional, Young, L., additional, Wackers, F., additional, Harbinson, M. T., additional, Wells, G., additional, Dougan, J., additional, Borges-Neto, S., additional, Phillips, H., additional, Farzaneh-Far, A., additional, Starr, Z., additional, Shaw, L. K., additional, Fiuzat, M., additional, O'connor, C., additional, Henzlova, M., additional, Duvall, W. 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T., additional, Waehrens, L. N., additional, Heegaard, C. W., additional, Silvola, J. M. U., additional, Forsback, S., additional, Laine, J. O., additional, Heinonen, S., additional, Ylaherttuala, S., additional, Broisat, A., additional, Ruiz, M., additional, Goodman, N. C., additional, Dimastromatteo, J., additional, Glover, D. K., additional, Hyafil, F., additional, Blackwell, F., additional, Pavon-Djavid, G., additional, Sarda-Mantel, L., additional, Feldman, L. J., additional, Meddahi-Pelle, A., additional, Tsatkin, V., additional, Liu, Y.- H., additional, De Kemp, R., additional, Slomka, P. J., additional, Klein, R., additional, Germano, G., additional, Beanlands, R. S., additional, Rohani, A., additional, Akbari, V., additional, Groothuis, J. G. J., additional, Fransen, M., additional, Beek, A. M., additional, Brinckman, S. L., additional, Meijerink, M. R., additional, Hofman, M. B. M., additional, Van Kuijk, C., additional, Kogure, S., additional, Yamashita, E., additional, Murakami, J., additional, Kawaguchi, R., additional, Adachi, H., additional, Oshima, S., additional, Minin, S., additional, Popov, S., additional, Saushkina, Y. U., additional, Savenkova, G., additional, Lebedev, D., additional, Alexandridis, E., additional, Rovithis, D., additional, Parisis, C., additional, Sazonova, I., additional, Saushkin, V., additional, Chernov, V., additional, Zaabar, L., additional, Bahri, H., additional, Hadj Ali, S., additional, Sellem, A., additional, Slim, I., additional, El Kadri, N., additional, Slimen, H., additional, Hammami, H., additional, Lucic, S., additional, Peter, A., additional, Tadic, S., additional, Nikoletic, K., additional, Jung, R., additional, Lucic, M., additional, Tagil, K., additional, Jakobsson, D., additional, Svensson, S.- E., additional, Wollmer, P., additional, Leccisotti, L., additional, Indovina, L., additional, Paraggio, L., additional, Calcagni, M. L., additional, Giordano, A., additional, Kapitan, M., additional, Paolino, A., additional, Nunez, M., additional, Sweeny, J., additional, Kulkarni, N., additional, Guma, K., additional, Akashi, Y., additional, Takano, M., additional, Takai, M., additional, Koh, S., additional, Miyake, F., additional, Torun, N., additional, Durmus Altun, G., additional, Altun, A., additional, Kaya, E., additional, Saglam, H., additional, Matsuoka, D. T., additional, Sanchez, A., additional, Bartolozzi, C., additional, Padua, D., additional, Ponta, G., additional, Ponte, A., additional, Carneiro, A., additional, Thom, A., additional, Ashrafi, R., additional, Garg, P., additional, Davis, G., additional, Falcao, A., additional, Costa, M., additional, Bussolini, F., additional, Meneghetti, J. A. C., additional, Tobisaka, M., additional, Correia, E., additional, Jansen, J. W., additional, Van Der Vleuten, P. A., additional, Willems, T. P., additional, Zijlstra, F., additional, Sato, M., additional, Taniguchi, K., additional, Kurabayashi, M., additional, Pop Gjorcheva, D., additional, Zdraveska-Kochovska, M., additional, Moriwaki, K., additional, Kawamura, A., additional, Watanabe, K., additional, Omura, T., additional, Sakabe, S., additional, Seko, T., additional, Kasai, A., additional, Ito, M., additional, Obana, M., additional, Akasaka, T., additional, Hruska, C., additional, Truong, D., additional, Pletta, C., additional, Collins, D., additional, Tortorelli, C., additional, Rhodes, D., additional, El-Prince, M., additional, Martinez-Moeller, A., additional, Marinelli, M., additional, Weismueller, S., additional, Hillerer, C., additional, Jensen, B., additional, Nekolla, S. G., additional, Wakabayashi, H., additional, Tsukamoto, K., additional, Baker, S. M. E. A., additional, Sirajul Haque, K. M. H. S., additional, Siddique, A., additional, Krishna Banarjee, S., additional, Ahsan, A., additional, Rahman, F., additional, Mukhlesur Rahman, M., additional, Parveen, T., additional, Lutfinnessa, M., additional, Nasreen, F., additional, Sano, H., additional, Naito, S., additional, De Rimini, M. L., additional, Borrelli, G., additional, Baldascino, F., additional, Calabro, P., additional, Maiello, C., additional, Russo, A., additional, Amarelli, C., additional, Muto, P., additional, Danad, I., additional, Raijmakers, P. G., additional, Appelman, Y. E., additional, Hoekstra, O. S., additional, Marcus, J. T., additional, Boonstra, A., additional, Ryzhkova, D. V., additional, Kuzmina, T. V., additional, Borodina, O. S., additional, Trukshina, M. A., additional, Kostina, I. S., additional, Hommel, H., additional, Feuchtner, G., additional, Pachinger, O., additional, Friedrich, G., additional, Stel, A. M., additional, Deckers, J. W., additional, Gama, V., additional, Ciarka, A., additional, Neefjes, L. A., additional, Mollet, N. R., additional, Sijbrands, E. J., additional, Wilczek, J., additional, Llibre Pallares, C., additional, Abdul-Jawad Altisent, O., additional, Cuellar Calabria, H., additional, Mahia Casado, P., additional, Gonzalez-Alujas, M. T., additional, Evangelista Masip, A., additional, Garcia-Dorado Garcia, D., additional, Tekabe, Y., additional, Shen, X., additional, Li, Q., additional, Luma, J., additional, Weisenberger, D., additional, Schmidt, A. M., additional, Haubner, R., additional, Johnson, L., additional, Sleiman, L., additional, Thorn, S., additional, Hasu, M., additional, Thabet, M., additional, Dasilva, J. N., additional, Whitman, S. C., additional, Genovesi, D., additional, Giorgetti, A., additional, Gimelli, A., additional, Cannizzaro, G., additional, Bertagna, F., additional, Fagioli, G., additional, Rossi, M., additional, Bonini, R., additional, Marzullo, P., additional, Paterson, C. A., additional, Smith, S. A., additional, Small, A. D., additional, Goodfield, N. E. R., additional, Martin, W., additional, Nekolla, S., additional, Sherif, H., additional, Reder, S., additional, Yu, M., additional, Kusch, A., additional, Li, D., additional, Zou, J., additional, Lloyd, M. S., additional, Cao, K., additional, Motherwell, D. W., additional, Rice, A., additional, Mccurrach, G. M., additional, Cobbe, S. M., additional, Petrie, M. C., additional, Al Younis, I., additional, Van Der Wall, E., additional, Mirza, T., additional, Raza, M., additional, Hashemizadeh, H., additional, Santos, L., additional, Krishna, B. 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S., additional, Sattar, A., additional, Swadia, T., additional, Chattahi, J., additional, Qureshi, W., additional, Khalid, F., additional, Gonzalez, A., additional, Hechavarria, S., additional, Takamura, K., additional, Fujimoto, S., additional, Nakanishi, R., additional, Yamashina, S., additional, Namiki, A., additional, Yamazaki, J., additional, Koshino, K., additional, Hashikawa, Y., additional, Teramoto, N., additional, Hikake, M., additional, Ishikane, S., additional, Ikeda, T., additional, Iida, H., additional, Takahashi, Y., additional, Oriuchi, N., additional, Higashino, H., additional, Endo, K., additional, Mochizuki, T., additional, Murase, K., additional, Baali, A., additional, Moreno, R., additional, Chau, M., additional, Rousseau, H., additional, Nicoud, F., additional, Dolliner, P., additional, Brammen, L., additional, Steurer, G., additional, Traub-Weidinger, T., additional, Ubl, P., additional, Schaffarich, P., additional, Dobrozemsky, G., additional, Staudenherz, A., additional, Ozgen Kiratli, M., additional, Temelli, B., additional, Kanat, N. B., additional, Aksoy, T., additional, Slavich, G. A., additional, Piccoli, G., additional, Puppato, M., additional, Grillone, S., additional, Gasparini, D., additional, Dunet, V., additional, Perruchoud, S., additional, Poitry-Yamate, C., additional, Lepore, M., additional, Gruetter, R., additional, Pedrazzini, T., additional, Anselm, D., additional, Anselm, A., additional, Atkins, H., additional, Renaud, J., additional, Dekemp, R., additional, Burwash, I., additional, Guo, A., additional, Beanlands, R., additional, Glover, C., additional, Vilardi, I., additional, Zangheri, B., additional, Calabrese, L., additional, Romano, P., additional, Bruno, A., additional, Fernandez Cimadevilla, O. C., additional, Uusitalo, V. A., additional, Luotolahti, M., additional, Wendelin-Saarenhovi, M., additional, Sundell, J., additional, Raitakari, O., additional, Huidu, S., additional, Gadiraju, R., additional, Ghesani, M., additional, Uddin, Q., additional, Wosnitzer, B., additional, Takahashi, N., additional, Alhaj, E., additional, Legasto, A., additional, Abiri, B., additional, Elsaban, K., additional, El Khouly, T., additional, El Kammash, T., additional, Al Ghamdi, A., additional, Kyung Deok, B., additional, Bon Seung, K., additional, Sang Geun, Y., additional, Chang Min, D., additional, and Gwan Hong, M., additional
Published: 2011
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7. 4.9Development of anti-RAGE antibody to image atherosclerosis

Author: TEKABE, Y, primary, ROSARIO, R, additional, HARJA, E, additional, GUPTA, A, additional, SEDLAR, M, additional, SCHMIDT, A, additional, and JOHNSON, L, additional
Published: 2007
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8. Enhanced imaging of very small experimental atherosclerotic lesions in ApoE−/− mice: Use of bispecific antibody and Tc-99m-labeled polymeric probes

Author: TEKABE, Y, primary, ABUTAHA, A, additional, JOHNSON, L, additional, and KHAW, B, additional
Published: 2005
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9. 4.9: Development of anti-RAGE antibody to image atherosclerosis

Author: Tekabe, Y. Yared, Rosario, R., Harja, E., Gupta, A., Sedlar, M., Schmidt, A.M., and Johnson, L.L.
Published: 2007
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10. Young investigator award session oral abstract session

Author: Tsukamoto, T., Morita, K., Naya, M., Katoh, C., Kuge, Y., Okamoto, H., Tsutsui, H., Tamaki, N., Namdar, M., Siegrist, P., Koepfli, P., Tschuetscher, P., Hany, T., Wyss, C., Kaufmann, P., Lautamäki, R., Airaksinen, K., Seppänen, M., Toikka, J., Luotolahti, M., Ball, E., Härkönen, R., Knuuti, J., Stewart, M., Nuutila, P., Ghanbari, H., Hassunizadeh, B., Williams, F., Cunningham, D., Agrawal, S., Machado, C., Saba, S., Tekabe, Y., Abu-Taha, A., Johnson, L., Khaw, B., Noble, G., ElKoustaf, R., Navare, S., Lundbye, J., Katten, D., Platt, M., Ahlberg, A., Heller, G., Tsukamoto, T., Morita, K., Naya, M., Katoh, C., Kuge, Y., Okamoto, H., Tsutsui, H., Tamaki, N., Namdar, M., Siegrist, P., Koepfli, P., Tschuetscher, P., Hany, T., Wyss, C., Kaufmann, P., Lautamäki, R., Airaksinen, K., Seppänen, M., Toikka, J., Luotolahti, M., Ball, E., Härkönen, R., Knuuti, J., Stewart, M., Nuutila, P., Ghanbari, H., Hassunizadeh, B., Williams, F., Cunningham, D., Agrawal, S., Machado, C., Saba, S., Tekabe, Y., Abu-Taha, A., Johnson, L., Khaw, B., Noble, G., ElKoustaf, R., Navare, S., Lundbye, J., Katten, D., Platt, M., Ahlberg, A., and Heller, G.

11. Blocking RAGE expression after injury reduces inflammation in mouse model of acute lung injury.

Author: Johnson LL, Tekabe Y, Zelonina T, Ma X, Zhang G, Goldklang M, and D'Armiento J
Subjects: Female, Male, Animals, Mice, Lipopolysaccharides toxicity, Fluorescein-5-isothiocyanate metabolism, Mice, Inbred C57BL, Lung metabolism, Inflammation metabolism, Immunoglobulin G metabolism, Acute Lung Injury drug therapy, Pneumonia chemically induced, Pneumonia metabolism
Abstract: Background: Receptor for Advanced Glycated Endproducts (RAGE) plays a major role in the inflammatory response to infectious and toxin induced acute lung injury. We tested the hypothesis that a RAGE blocking antibody when administered after the onset of injury can reduce lung inflammation compared to control antibody., Methods: Male and female C57BL/6 (WT) mice were used. Forty-six received lipopolysaccharide (LPS) and 26 PBS by nasal instillation on day one, repeated on day three. On day 2, 36 mice receiving LPS were divided into two groups of 18, one treated with 200 μg of non-immune isotype control IgG and the second group treated with 200 μg of anti-RAGE Ab, each dose divided between IV and IP. Ten of the 46 were not treated. On day 4, before euthanasia, mice were injected with fluorescein isothiocyanate (FITC) labelled albumen. BALF and serum samples were collected as well as lung tissue for immunohistochemistry (IHC). BALF was analyzed for cell (leukocyte) counts, for FITC BALF/serum ratios indicating pulmonary vascular leak, and for cytokines/chemokines using bead based multiplex assays. Quantitative IHC was performed for MPO and RAGE., Results: Ten LPS mice showed minimal inflammation by all measures indicating poor delivery of LPS and were excluded from analysis leaving n = 11 in the LPS + IgG group and n = 12 in the LPS + anti-RAGE group. BALF cell counts were low in the PBS administered mice (4.9 ± 2.1 × 10 5 /ml) and high in the LPS injured untreated mice (109 ± 34) and in the LPS + IgG mice (91 ± 54) while in comparison, LPS + anti-RAGE ab mice counts were significantly lower (51.3 ± 18 vs. LPS + IgG, P = 0.03). The BALF/serum FITC ratios were lower for the LPS + anti-RAGE mice than for the LPS + IgG mice indicating less capillary leakiness. Quantitative IHC RAGE staining was lower in the LPS + anti-RAGE ab mice than in the LPS + IgG treated mice (P = 0.02)., Conclusions: These results describe a four-day LPS protocol to sustain lung injury and allow for treatment and suggests that treatment aimed at blocking RAGE when given after onset of injury can reduce lung inflammation., (© 2023. The Author(s).)
Published: 2023
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12. Novel Receptor for Advanced Glycation End Products-Blocking Antibody to Treat Diabetic Peripheral Artery Disease.

Author: Johnson LL, Johnson J, Ober R, Holland A, Zhang G, Backer M, Backer J, Ali Z, and Tekabe Y
Subjects: Angiography methods, Animals, Diabetes Mellitus, Experimental blood, Diabetes Mellitus, Experimental metabolism, Drug Discovery methods, Glycation End Products, Advanced metabolism, Hindlimb blood supply, Muscle, Skeletal blood supply, Swine, Swine, Miniature, Treatment Outcome, Angiogenesis Inducing Agents pharmacology, Antibodies, Monoclonal pharmacology, Diabetic Angiopathies drug therapy, Diabetic Angiopathies metabolism, Peripheral Arterial Disease drug therapy, Peripheral Arterial Disease etiology, Peripheral Arterial Disease metabolism, Receptor for Advanced Glycation End Products antagonists & inhibitors, Receptor for Advanced Glycation End Products immunology
Abstract: Background Expression of receptor for advanced glycation end products (RAGE) plays an important role in diabetic peripheral artery disease. We proposed to show that treatment with an antibody blocking RAGE would improve hind limb perfusion and muscle viability in diabetic pig with femoral artery (FA) ligation. Methods and Results Purpose-bred diabetic Yucatan minipigs with average fasting blood sugar of 357 mg/dL on insulin to maintain a glucose range of 300 to 500 mg/dL were treated with either a humanized monoclonal anti-RAGE antibody (CR-3) or nonimmune IgG. All pigs underwent intravascular occlusion of the anterior FA. Animals underwent ( 201 Tl) single-photon emission computed tomography/x-ray computed tomography imaging on days 1 and 28 after FA occlusion, angiogenesis imaging with [ 99m Tc]dodecane tetra-acetic acid-polyethylene glycol-single chain vascular endothelial growth factor (scVEGF), muscle biopsies on day 7, and contrast angiogram day 28. Results showed greater increases in perfusion to the gastrocnemius from day 1 to day 28 in CR-3 compared with IgG treated pigs ( P =0.0024), greater uptake of [99mTc]dodecane tetra-acetic acid-polyethylene glycol-scVEGF (scV/Tc) in the proximal gastrocnemius at day 7, confirmed by tissue staining for capillaries and vascular endothelial growth factor A, and less muscle loss and fibrosis at day 28. Contrast angiograms showed better reconstitution of the distal FA from collaterals in the CR-3 versus IgG treated diabetic pigs ( P =0.01). The gastrocnemius on nonoccluded limb at necropsy had higher 201 Tl uptake (percentage injected dose per gram) and reduced RAGE staining in arterioles in CR-3 treated compared with IgG treated animals ( P =0.04). Conclusions A novel RAGE-blocking antibody improved hind limb perfusion and angiogenesis in diabetic pigs with FA occlusion. Contributing factors are increased collaterals and reduced vascular RAGE expression. CR-3 shows promise for clinical treatment in diabetic peripheral artery disease.
Published: 2021
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13. VEGF receptor targeted imaging of angiogenic response to limb ischemia in diabetic vs. non-diabetic Yucatan minipigs.

Author: Johnson LL, Johnson J, Ali Z, Tekabe Y, Ober R, Geist G, McLuckie A, Safarov A, Holland A, Zhang G, Backer M, and Backer J
Abstract: Background: New therapies to treat diabetic peripheral artery disease (PAD) require target-specific non-invasive imaging modalities to follow efficacy. As a translational study, we performed targeted imaging of receptors for vascular endothelial growth factor (VEGF) in response to anterior femoral artery occlusion (FAO) in Yucatan minipigs and compare the normal response to response in diabetic Yucatan minipigs., Methods: Eleven Yucatan minipigs, 6 non-diabetic (non-D) and 5 purpose bred diabetic (D) (Sinclair, Auxvasse MO), underwent intravascular total occlusion of the anterior femoral artery (FA). At days 1 and 28, pigs underwent SPECT/CT 201 Tl hindlimb perfusion imaging and at day 7 were injected with [ 99m Tc]DOTA-PEG-scVEGF (scV/Tc) tracer targeting VEGF receptor, and underwent biopsies of the hindlimb muscles for gamma counting and histology, followed by imaging. One day after the final scan, pigs underwent contrast angiography of the lower extremities. Counts from scans were converted to percentage injected activity (%IA)., Results: Perfusion was lower in the occluded hindlimb compared to non-occluded on day 1 in both the D and non-D pigs. At day 7, scV/Tc count ratio of counts from ROIs drawn in proximal gastrocnemius muscle for the occluded over non-occluded limb was significantly higher in non-D vs. D pigs (1.32 ± 0.06 vs. 1.04 ± 0.13, P = 0.02) reflecting higher level of angiogenesis. Perfusion increased between days 1 and 28 in the muscles in the occluded limb for the non-diabetic pigs while the diabetic pig showed no increase (+ 0.13 ± 0.08 %IA vs. - 0.13 ± 0.11, P = 0.003). The anterior FA showed poor contrast filling beyond occluder and qualitatively fewer bridging collaterals compared to non-D pigs at 28 days., Conclusion: VEGF receptor targeted imaging showed the effects of diabetes to suppress angiogenesis in response to occlusion of the anterior femoral artery of purpose bred diabetic Yucatan minipigs and indicates potential applicability as a marker to follow efficacy of novel therapies to improve blood flow by stimulating angiogenesis in diabetic PAD.
Published: 2020
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14. Single-photon emission computed tomography/computed tomography imaging of RAGE in smoking-induced lung injury.

Author: Goldklang MP, Tekabe Y, Zelonina T, Trischler J, Xiao R, Stearns K, Rodriguez K, Shields A, Romanov A, D'Armiento JM, and Johnson LL
Subjects: Animals, Female, Rabbits, Smoking, Tobacco Smoking pathology, Disease Models, Animal, Lung diagnostic imaging, Lung metabolism, Receptor for Advanced Glycation End Products metabolism, Single Photon Emission Computed Tomography Computed Tomography methods, Tobacco Smoking metabolism
Abstract: Background: Expression of the Receptor for Advanced Glycation Endproducts (RAGE) initiates pro-inflammatory pathways resulting in lung destruction. We hypothesized that RAGE directed imaging demonstrates increased lung uptake in smoke-exposure., Methods: After exposure to room air or to cigarette smoke for 4-weeks or 16-weeks, rabbits were injected with 99m Tc-anti-RAGE F(ab') 2 and underwent Single-Photon Emission Computed Tomography/Computed Tomography (SPECT/CT) imaging. Lung radiotracer uptake was calculated as percent injected dose (%ID). Lungs were dissected for gamma well counting and histological analysis., Results: 99m Tc-anti-RAGE F(ab') 2 SPECT/CT imaging demonstrated increased lung expression of RAGE with smoke exposure compared to room air control at 4-weeks: Room air right (R) 0.75 ± 0.38%ID, left (L) 0.62 ± 0.32%ID vs. Smoke exposed R 0.17 ± 0.03, L 0.17 ± 0.02%ID (p = 0.02 and 0.028, respectively). By 16-weeks of smoke exposure, the uptake decreased to 0.19 ± 0.05%ID R and 0.17 ± 0.05%ID L, significantly lower than 4-week imaging (p = 0.0076 and 0.0129 respectively). Staining for RAGE confirmed SPECT results, with the RAGE ligand HMGB1 upregulated in the macrophages of 4-week smoke-exposed rabbits., Conclusions: RAGE-directed imaging identified pulmonary RAGE expression acutely in vivo in an animal model of emphysema early after smoke exposure, with diminution over time. These studies document the extent and time course of RAGE expression under smoke exposure conditions and could be utilized for disease monitoring and examining response to future RAGE-targeted therapies.
Published: 2019
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15. Imaging VEGF Receptors and α v β 3 Integrins in a Mouse Hindlimb Ischemia Model of Peripheral Arterial Disease.

Author: Tekabe Y, Li Q, Zhang G, Johnson J, Schmidt AM, Backer M, Backer J, and Johnson LL
Subjects: Animals, Biomarkers metabolism, Disease Models, Animal, Endothelial Cells metabolism, Hindlimb pathology, Ischemia pathology, Male, Mice, Inbred C57BL, Peripheral Arterial Disease metabolism, Peripheral Arterial Disease pathology, Hindlimb blood supply, Integrin alphaVbeta3 metabolism, Ischemia diagnostic imaging, Ischemia metabolism, Molecular Imaging methods, Peripheral Arterial Disease diagnostic imaging, Receptors, Vascular Endothelial Growth Factor metabolism
Abstract: Purpose: To compare targeted imaging of vascular endothelial growth factor (VEGF) receptors vs. α v β 3 integrins in a mouse hindlimb ischemia model of peripheral artery disease., Procedures: Male wild-type (WT) C57BL/6 mice (8- to 10-week old) (n = 24) underwent left femoral artery ligation. The right leg served as control. Five days later, mice were injected with either VEGF receptor targeting [ 99m Tc]DOTA-PEG-scVEGF ([ 99m Tc]scV) (n = 8) or with α v β 3 -targeting tracer [ 99m Tc]HYNIC-cycloRGD ([ 99m Tc]RGD) (n = 8) and underwent single photon emission computed tomography (SPECT) x-ray computed tomography imaging. To assess non-specific [ 99m Tc]scV uptake, six additional mice received a mixture of [ 99m Tc]scV and 30-fold excess of targeting protein, scVEGF. Tracer uptake as %ID was measured using volumetric regions encompassing the hindlimb muscles and as %ID/g from harvested limb muscles. Double and triple immunofluorescent analysis on tissue sections established localization of α v β 3 , VEGFR-1, VEGFR-2, as well as certain cell lineage markers., Results: Tracer uptake, as %ID/g, was higher in ligated limbs of mice injected with [ 99m Tc]scV compared to ligated hindlimbs in mice injected with [ 99m Tc]RGD (p = 0.02). The ratio of tracer uptake for ligated/control hindlimb was borderline higher for [ 99m Tc]scV than for [ 99m Tc]RGD (p = 0.06). Immunofluorescent analysis showed higher prevalence of VEGFR-1, VEGFR-2, and α v β 3 , in damaged vs. undamaged hindlimb tissue, but with little co-localization of these markers. Double immunofluorescent staining showed partial co-localization of VEGFR-1, VEGFR-2, and α v β 3, with endothelial cell marker FVIII, but not with CD31. Immunostaining for VEGFR-1 and VEGFR-2 additionally co-localized with lineage markers for endothelial progenitor cell and monocytes/macrophages, with a more diverse pattern of co-localization for VEGFR-2., Conclusion: In a mouse hindlimb ischemia model of peripheral artery disease, [ 99m Tc]scV SPECT tracer-targeting VEGF receptors showed a more robust signal than [ 99m Tc]RGD tracer-targeting α v β 3 . Immunofluorescent analysis suggests that uptake of [ 99m Tc]scV and [ 99m Tc]RGD in damaged tissue is due to non-overlapping cell populations and reflects different dynamic processes and that enhanced uptake of [ 99m Tc]scV may be due to the presence of VEGF receptors on additional cell types.
Published: 2018
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16. Selective Imaging of Vascular Endothelial Growth Factor Receptor-1 and Receptor-2 in Atherosclerotic Lesions in Diabetic and Non-diabetic ApoE -/- Mice.

Author: Tekabe Y, Johnson LL, Rodriquez K, Li Q, Backer M, and Backer JM
Subjects: Animals, Apolipoproteins E metabolism, Atherosclerosis complications, Atherosclerosis pathology, Blood Glucose metabolism, Diabetes Mellitus, Experimental blood, Diabetes Mellitus, Experimental complications, Male, Mice, Polyethylene Glycols chemistry, Single-Chain Antibodies, Tissue Distribution, Tomography, Emission-Computed, Single-Photon, Apolipoproteins E deficiency, Atherosclerosis diagnosis, Atherosclerosis metabolism, Diabetes Mellitus, Experimental diagnosis, Diabetes Mellitus, Experimental metabolism, Molecular Imaging methods, Vascular Endothelial Growth Factor Receptor-1 metabolism, Vascular Endothelial Growth Factor Receptor-2 metabolism
Abstract: Purpose: Plaque vulnerability is associated with inflammation and angiogenesis, processes that rely on vascular endothelial growth factor (VEGF) signaling via two receptors, VEGFR-1 and VEGFR-2. We have recently reported that enhanced uptake of scVEGF-PEG-DOTA/Tc-99m (scV/Tc) single photon emission computed tomography (SPECT) tracer that targets both VEGFR-1 and VEGFR-2, identifies accelerated atherosclerosis in diabetic relative to non-diabetic ApoE -/- mice. Since VEGFR-1 and VEGFR-2 may play different roles in atherosclerotic plaques, we reasoned that selective imaging of each receptor can provide more detailed information on plaque biology., Procedures: Recently described VEGFR-1 and VEGFR-2 selective mutants of scVEGF, named scVR1 and scVR2, were site-specifically derivatized with Tc-99m chelator DOTA via 3.4 kDa PEG linker, and their selectivity to the cognate receptors was confirmed in vitro. scVR1 and scVR2 conjugates were radiolabeled with Tc-99m to specific activity of 110 ± 11 MBq/nmol, yielding tracers named scVR1/Tc and scVR2/Tc. 34-40 week old diabetic and age-matched non-diabetic ApoE -/- mice were injected with tracers, 2-3 h later injected with x-ray computed tomography (CT) contrast agent and underwent hybrid SPECT/CT imaging. Tracer uptake, localized to proximal aorta and brachiocephalic vessels, was quantified as %ID from. Tracer uptake was also quantified as %ID/g from gamma counting of harvested plaques. Harvested atherosclerotic arterial tissue was used for immunofluorescent analyses of VEGFR-1 and VEGFR-2 and various lineage-specific markers., Results: Focal, receptor-mediated uptake in proximal aorta and brachiocephalic vessels was detected for both scVR1/Tc and scVR2/Tc tracers. Uptake of scVR1/Tc and scVR2/Tc was efficiently inhibited only by "cold" proteins of the same receptor selectivity. Tracer uptake in this area, expressed as %ID, was higher in diabetic vs. non- diabetic mice for scVR1/Tc (p = 0.01) but not for scVR2/Tc. Immunofluorescent analysis revealed enhanced VEGFR-1 prevalence in and around plaque area in diabetic mice., Conclusions: Selective VEGFR-1 and VEGFR-2 imaging of atherosclerotic lesions may be useful to explore plaque biology and identify vulnerability.
Published: 2018
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17. Single-Photon Emission Computed Tomography/Computed Tomography Imaging in a Rabbit Model of Emphysema Reveals Ongoing Apoptosis In Vivo.

Author: Goldklang MP, Tekabe Y, Zelonina T, Trischler J, Xiao R, Stearns K, Romanov A, Muzio V, Shiomi T, Johnson LL, and D'Armiento JM
Subjects: Animals, Annexin A5 metabolism, Compliance, Disease Models, Animal, Female, Humans, Lung diagnostic imaging, Lung pathology, Lung physiopathology, Pneumonia complications, Pneumonia diagnostic imaging, Pneumonia pathology, Pneumonia physiopathology, Pulmonary Emphysema complications, Pulmonary Emphysema physiopathology, Rabbits, Smoke, Technetium metabolism, Time Factors, Apoptosis, Pulmonary Emphysema diagnostic imaging, Pulmonary Emphysema pathology, Single Photon Emission Computed Tomography Computed Tomography
Abstract: Evaluation of lung disease is limited by the inability to visualize ongoing pathological processes. Molecular imaging that targets cellular processes related to disease pathogenesis has the potential to assess disease activity over time to allow intervention before lung destruction. Because apoptosis is a critical component of lung damage in emphysema, a functional imaging approach was taken to determine if targeting apoptosis in a smoke exposure model would allow the quantification of early lung damage in vivo. Rabbits were exposed to cigarette smoke for 4 or 16 weeks and underwent single-photon emission computed tomography/computed tomography scanning using technetium-99m-rhAnnexin V-128. Imaging results were correlated with ex vivo tissue analysis to validate the presence of lung destruction and apoptosis. Lung computed tomography scans of long-term smoke-exposed rabbits exhibit anatomical similarities to human emphysema, with increased lung volumes compared with controls. Morphometry on lung tissue confirmed increased mean linear intercept and destructive index at 16 weeks of smoke exposure and compliance measurements documented physiological changes of emphysema. Tissue and lavage analysis displayed the hallmarks of smoke exposure, including increased tissue cellularity and protease activity. Technetium-99m-rhAnnexin V-128 single-photon emission computed tomography signal was increased after smoke exposure at 4 and 16 weeks, with confirmation of increased apoptosis through terminal deoxynucleotidyl transferase dUTP nick end labeling staining and increased tissue neutral sphingomyelinase activity in the tissue. These studies not only describe a novel emphysema model for use with future therapeutic applications, but, most importantly, also characterize a promising imaging modality that identifies ongoing destructive cellular processes within the lung.
Published: 2016
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18. Disposal of iron by a mutant form of lipocalin 2.

Author: Barasch J, Hollmen M, Deng R, Hod EA, Rupert PB, Abergel RJ, Allred BE, Xu K, Darrah SF, Tekabe Y, Perlstein A, Wax R, Bruck E, Stauber J, Corbin KA, Buchen C, Slavkovich V, Graziano J, Spitalnik SL, Bao G, Strong RK, and Qiu A
Subjects: Animals, Disease Models, Animal, Humans, Inflammation, Iron Chelating Agents, Iron Overload genetics, Kidney metabolism, Ligands, Mice, Mice, Transgenic, Mutation, Oxidation-Reduction, Protein Binding, Siderophores, Transferrin metabolism, Iron metabolism, Iron Overload metabolism, Lipocalin-2 genetics, Lipocalin-2 physiology
Abstract: Iron overload damages many organs. Unfortunately, therapeutic iron chelators also have undesired toxicity and may deliver iron to microbes. Here we show that a mutant form (K3Cys) of endogenous lipocalin 2 (LCN2) is filtered by the kidney but can bypass sites of megalin-dependent recapture, resulting in urinary excretion. Because K3Cys maintains recognition of its cognate ligand, the iron siderophore enterochelin, this protein can capture and transport iron even in the acidic conditions of urine. Mutant LCN2 strips iron from transferrin and citrate, and delivers it into the urine. In addition, it removes iron from iron overloaded mice, including models of acquired (iron-dextran or stored red blood cells) and primary (Hfe -/- ) iron overload. In each case, the mutants reduce redox activity typical of non-transferrin-bound iron. In summary, we present a non-toxic strategy for iron chelation and urinary elimination, based on manipulating an endogenous protein:siderophore:iron clearance pathway., Competing Interests: J.B. and A.Q. declare patent applications with Columbia University for the use of LCN2 (Scn or NGAL). R.K.S., P.B.R. and R.J.A. declare patent applications with Fred Hutchinson Cancer Research Center for the use of Scn (NGAL). All the other authors declare no competing financial interest.
Published: 2016
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19. Treatment effect with anti-RAGE F(ab')2 antibody improves hind limb angiogenesis and blood flow in Type 1 diabetic mice with left femoral artery ligation.

Author: Tekabe Y, Anthony T, Li Q, Ray R, Rai V, Zhang G, Schmidt AM, and Johnson LL
Subjects: Animals, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 1 complications, Diabetic Angiopathies drug therapy, Diabetic Angiopathies etiology, Femoral Artery, Ligation, Male, Mice, Mice, Inbred C57BL, Antibodies therapeutic use, Hindlimb blood supply, Ischemia drug therapy, Neovascularization, Physiologic drug effects, Receptor for Advanced Glycation End Products immunology
Abstract: We investigated treatment with a receptor for advanced glycation endproduct (RAGE) blocking antibody on angiogenic response to hind limb ischemia in diabetic mice. Streptozotocin treated C57BL/6 mice received either murine monoclonal anti-RAGE F(ab')2 intraperitoneally (n=10) or saline (n=9) for 9 weeks. Diabetic plus 10 non-diabetic C57BL/6 mice underwent left femoral artery ligation and 5 days later angiogenesis imaging with (99m)Tc-Arg-Gly-Asp (RGD) nanoSPECT/CT. Twenty-four days later, hind limb blood flow was measured with ultrasound, the mice were euthanized, and tissue was taken for immunohistochemistry. The angiogenic imaging signal in ischemic limbs was higher in RAGE-ab treated versus saline treated mice at day 5 (3.1±1.4 vs 1.68±0.35, p=0.02) and blood flow was higher at day 24 (1.49±0.5 vs 0.61±0.39, p=0.04). Immunohistochemistry of ischemic muscles showed greater capillary density in the RAGE-ab treated group versus the vehicle-treated group (p<0.001) (NS from non-diabetic mice). In conclusion, treatment with anti-RAGE F(ab')2 in diabetic mice improves neovascularization in the ischemic leg., (© The Author(s) 2015.)
Published: 2015
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20. Imaging VEGF receptor expression to identify accelerated atherosclerosis.

Author: Tekabe Y, Kollaros M, Zerihoun A, Zhang G, Backer MV, Backer JM, and Johnson LL
Abstract: Background: The biology of the vulnerable plaque includes increased inflammation and rapid growth of vasa vasorum, processes that are associated with enhanced vascular endothelial growth factor (VEGF)/ imaging receptors for VEGF (VEGFR) signaling and are accelerated in diabetes. This study was designed to test the hypothesis that VEGFRs in atherosclerotic plaques with a SPECT tracer scVEGF-PEG-DOTA/(99m)Tc (scV/Tc) can identify accelerated atherosclerosis in diabetes., Methods: Male apolipoprotein E null (ApoE(-/-)) mice (6 weeks of age) were made diabetic (n = 10) or left as non-diabetic (n = 13). At 26 to 28 weeks of age, 5 non-diabetic mice were injected with functionally inactivated scV/Tc (in-scV/Tc) that does not bind to VEGF receptors, while 8 non-diabetic and 10 diabetic mice were injected with scV/Tc. After blood pool clearance, at 3 to 4 h post-injection, mice were injected with CT contrast agent and underwent SPECT/CT imaging. From the scans, regions of interest (ROI) were drawn on serial transverse sections comprising the proximal aorta and the percentage of injected dose (%ID) in ROIs was calculated. At the completion of imaging, mice were euthanized, proximal aorta explanted for gamma well counting to determine the percentage of injected dose per gram (%ID/g) uptake and immunohistochemical characterization., Results: The uptake of scV/Tc in the proximal aorta, calculated from SPECT/CT co-registered scans as %ID, was significantly higher in the diabetic mice (0.036 ± 0.017%ID) compared to non-diabetic mice (0.017 ± 0.005%ID; P < 0.01), as was uptake measured as %ID/g in harvested aorta, 1.81 ± 0.50%ID/g in the diabetic group vs. 0.98 ± 0.25%ID/g in the non-diabetic group (P < 0.01). The nonspecific uptake of in-scV/Tc in proximal aorta was significantly lower than the uptake of functionally active scV/Tc. Immunostaining of the atherosclerotic lesions showed higher expression of VEGFR-1 and VEGFR-2 in the diabetic mice., Conclusion: These initial results suggest that imaging VEGFR with scV/Tc shows promise as a non-invasive approach to identify accelerated atherosclerosis.
Published: 2014
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21. Imaging RAGE expression in atherosclerotic plaques in hyperlipidemic pigs.

Author: Johnson LL, Tekabe Y, Kollaros M, Eng G, Bhatia K, Li C, Krueger CG, Shanmuganayagam D, and Schmidt AM
Abstract: Background: Receptor for advanced glycated end product (RAGE) expression is a prominent feature of atherosclerosis. We have previously shown in apoE null mice uptake of a radiolabeled anti-RAGE antibody in atherosclerotic plaque and now evaluate RAGE-directed imaging to identify advanced plaques in a large animal model., Methods: Nine hyperlipidemic (HL) pigs were injected with 603.1 ± 129.5 MBq of (99m)Tc-anti-RAGE F(ab')2, and after 6 h (blood pool clearance), they underwent single-photon emission computed tomography/computed tomography (SPECT/CT) imaging of the neck, thorax, and hind limbs. Two HL pigs received (99m)Tc non-immune IgG F(ab')2, and three farm pigs were injected with (99m)Tc-anti-RAGE F(ab')2. After imaging, the pigs were euthanized. The aorta from the root to bifurcation was dissected, and the innominates, proximal carotids, and coronaries were dissected and counted, stained for H&E and RAGE, and AHA-classified., Results: On pathology, 24% of the arterial segments showed AHA class III or IV lesions, and these lesions were confined almost exclusively to coronaries and carotids with % stenosis from 15% to 65%. Scatter plots of %ID/g for class III/IV vs. I/II lesions showed almost complete separation. Focal vascular uptake of tracer visualized on SPECT scans corresponded to class III/IV lesions in the coronary and carotid vessels. In addition, uptake in the hind limbs was noted in the HL pigs and corresponded to RAGE staining of small arteries in the muscle sections. Correlations for the vascular lesions were r = 0.747, P = 0.001 for %ID vs. %ID/g and r = 0.83, P = 0.002 for %ID/g vs. % RAGE staining., Conclusions: Uptake of radiolabeled anti-RAGE antibody in coronary and carotid fibroatheroma and in the small arteries of the hind limbs in a relevant large animal model of atherosclerosis supports the important role of RAGE in atherosclerosis and peripheral artery disease as a target for imaging and treatment.
Published: 2014
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22. Beneficial Effect of Glucose Control on Atherosclerosis Progression in Diabetic ApoE(-/-) Mice: Shown by Rage Directed Imaging.

Author: Tekabe Y, Kollaros M, Li Q, Zhang G, Li C, Schmidt AM, and Johnson LL
Abstract: Objective. Receptor for advanced glycated endproducts (RAGE) plays an important role in atherogenesis in diabetes. We imaged RAGE to investigate the effect of glucose control to suppress RAGE and reduce atherosclerosis in apolipoprotein E null (apoE(-/-)) diabetic mice. Methods and Results. Thirty-three apoE(-/-) mice received streptozotocin and 6 weeks later 15 began treatment with insulin implants. Blood glucose measurements during study averaged: 140 ± 23 mg/dL (treated) and 354 ± 14 mg/dL (untreated). After 15 wk 30 mice were injected with (99m)Tc-anti-RAGE F(ab')2, 3 with (99m)Tc-nonimmune IgG F(ab')2, and all with CT contrast agent and underwent SPECT/CT imaging. At necropsy, the proximal aorta was weighed, counted, and sectioned and the % injected dose per gram (%ID/g) was calculated. From the merged SPECT/CT scans, tracer uptake localized to arteries was lower in the treated mice: 3.15 ± 1.82 × 10(-3) versus 8.69 ± 4.58 × 10(-3)%ID (P = 0.001). Percent cross-sectional lesion area was smaller in the treated (14.3 ± 7.8% versus 29.5 ± 10.9%) (P = 0.03). RAGE uptake on scans (%ID) correlated with quantitative RAGE staining in the atheroma and with %ID/g (R = 0.6887; P = 0.01). Lesion size as percent cross-sectional area was smaller in the treated (14.3 ± 7.8% versus 29.5 ± 10.9%) (P = 0.03). RAGE uptake on scans (%ID) correlated with quantitative RAGE staining in the atheroma and with %ID/g (R = 0.6887; P = 0.01). Conclusions. These results support the importance of suppressing RAGE to reduce atherosclerotic complications of diabetes and value of molecular imaging to assess treatment effect.
Published: 2014
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23. In vitro demonstration of enhanced prostate cancer toxicity: pretargeting with Bombesin bispecific complexes and targeting with polymer-drug-conjugates.

Author: Patil V, Gada K, Panwar R, Majewski S, Tekabe Y, Varvarigou A, and Khaw BA
Subjects: Animals, Antibiotics, Antineoplastic administration & dosage, Antibiotics, Antineoplastic pharmacology, Antibiotics, Antineoplastic toxicity, Antibodies, Bispecific immunology, Bombesin administration & dosage, Cell Line, Cell Line, Tumor, Doxorubicin administration & dosage, Doxorubicin toxicity, Drug Carriers chemistry, Humans, Inhibitory Concentration 50, Male, Myocytes, Cardiac drug effects, Myocytes, Cardiac metabolism, Pentetic Acid immunology, Polyglutamic Acid chemistry, Prostatic Neoplasms pathology, Rats, Receptors, Bombesin metabolism, Bombesin pharmacology, Doxorubicin pharmacology, Drug Delivery Systems, Prostatic Neoplasms drug therapy
Abstract: Background: Bombesin has been used to target Bombesin receptor, a growth receptor, which is over-expressed in many cancers, including prostate cancer. Polymer-anti-neoplastic-drug-conjugates (PDC) were also developed to reduce non-specific toxicity and increase tumor toxicity utilizing the enhanced permeability and retention effect, benefitting treatment of large tumors with well-established vasculature., Purpose: If PDCs were delivered by targeted delivery to cancer cells, tumor toxicity would be enhanced and non-specific toxicity decreased., Methods: Cardiocyte toxicity was assessed in H9c2 cardiocytes with doxorubicin (Dox) or N-terminal DTPA-modified-Doxorubicin-loaded-polyglutamic acid polymers (D-Dox-PGA). Therapeutic efficacy of targeted D-Dox-PGA after pretargeting with Bombesin-conjugated anti-DTPA-antibody Bispecific Complexes (Bom-BiSpCx) was compared to that of Dox in PC3 cells. Bom-BiSpCx was generated by thioether bond between Bombesin to Anti-DTPA antibody., Results: D-Dox-PGA was demonstrated to have less cardiocyte toxicity (IC50 = 20 µg/ml) than free Dox (1.55 µg/ml, p < 0.001). However, after pre-targeting of human prostate cancer PC3 cells with Bom-BiSpCx and targeting with D-Dox-PGA, IC50 (13.2 µg/ml) was about two times less than that of Dox (28.5 µg/ml, p < 0.0001)., Discussion: Targeted delivery of PDCs having lower cardiocyte toxicity enabled higher efficiency cancer cell therapy., Conclusion: This study may allow development of very efficient targeted prostate cancer pro-drug therapy.
Published: 2013
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24. Noninvasive imaging of myocyte apoptosis following application of a stem cell-engineered delivery platform to acutely infarcted myocardium.

Author: Godier-Furnémont AF, Tekabe Y, Kollaros M, Eng G, Morales A, Vunjak-Novakovic G, and Johnson LL
Subjects: Acute Disease, Animals, Annexin A5, Heart Ventricles diagnostic imaging, Heart Ventricles pathology, Humans, Ischemic Preconditioning, Myocardial, Male, Myocardial Infarction therapy, Organ Size, Organotechnetium Compounds, Rats, Rats, Nude, Apoptosis, Mesenchymal Stem Cells cytology, Multimodal Imaging, Myocardial Infarction diagnostic imaging, Myocardial Infarction pathology, Myocytes, Cardiac pathology, Positron-Emission Tomography, Tissue Engineering methods, Tomography, X-Ray Computed
Abstract: Unlabelled: The cardioprotective effects of mesenchymal stem cells (MSCs) include reducing myocyte apoptosis, and this effect can be enhanced by preconditioning and encapsulation in a fibrin scaffold. This study aimed to test the hypothesis that apoptosis imaging can detect the cardioprotective effects of a conditioned MSC patch grafted in a rat model of acute myocardial infarction., Methods: Cell culture experiments simulating engraftment of fibrin patches onto beating rat ventricular myocytes exposed to hypoxia showed an effect of conditioned cells to reduce apoptosis. Twenty-three nude rats underwent successful left anterior descending coronary artery occlusion and were divided into 3 groups: transforming growth factor β1-conditioned human MSC-laden patches (CP), infarct alone without patch (no patch [NP]), and patch alone (patch only [PO]). Twenty-four hours after myocardial infarction, all rats were injected with (99m)Tc-hydrazinonicotinamide ((99m)Tc-HYNIC) annexin V and (201)Tl and underwent dual-isotope SPECT/CT imaging. Six rats were sacrificed for histology and counting. The remaining rats (n = 17; 1 rat was eliminated) were injected and imaged on day 7; of those, 3 rats were sacrificed for histology and counting, and the remaining 13 rats survived to day 21, when they were sacrificed for histology. Numbers of rats imaged on day 7 in the 3 groups were 7 in the CP group, 5 in the NP, and 5 in the PO. Perfused myocardium, infarct size, and (99m)Tc-HYNIC annexin V uptake were quantified from the scans from days 1 and 7. (99m)Tc-HYNIC annexin V uptake was correlated with quantitative caspase staining, and infarct size as percentage fibrosis was quantified at day 21., Results: (99m)Tc-HYNIC annexin V uptake as percentage injected dose (×10(-4)) decreased between days 1 and 7 by 1.04 ± 0.28 in the CP group, 0.44 ± 0.17 in the NP group, and 0.34 ± 0.27 in the PO group (P = 0.003 for NP vs. CP, P = 0.005 for PO vs. CP, and P = 0.5 for NP vs. CP). The changes in defect size as percentage myocardium between days 1 and 7 were -8.83 ± 4.40 in the CP group, +1.00 ± 2.24 in the NP group, and -0.50 ± 4.20 in the PO group (P = 0.003 for NP vs. CP, P = 0.005 for PO vs. CP, and P = 0.50 for NP vs. PO). (99m)Tc-HYNIC annexin V uptake as percentage left ventricle by scanning correlated with caspase staining (r = 0.931, P = 0.002)., Conclusion: Transforming growth factor β1-conditioned human MSC-laden patches reduce myocyte apoptosis in the setting of acute infarction, and this effect can be detected by in vivo imaging with (99m)Tc-HYNIC annexin V.
Published: 2013
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25. Imaging receptor for advanced glycation end product expression in mouse model of hind limb ischemia.

Author: Tekabe Y, Kollaros M, Li C, Zhang G, Schmidt AM, and Johnson L
Abstract: Background: The purpose of this study is to image the effect of diabetes on expression of receptor for advanced glycation endproducts (RAGE) in limb ischemia in live animals., Methods: Male wild-type C57BL/6 mice were either made diabetic or left as control. Two months later, diabetic and non-diabetic mice underwent left femoral artery ligation. The right leg served as lesion control. Five days later, mice were injected with 15.1 ± 4.4 MBq 99mTc-anti-RAGE F(ab')2 and 4 to 5 h later (blood pool clearance) underwent SPECT/CT imaging. At the completion of imaging, mice were euthanized, hind limbs counted and sectioned, and scans reconstructed. Regions of interest were drawn on serial transverse sections comprising the hind limbs and activity in millicuries summed and divided by the injected dose (ID). Quantitative histology was performed for RAGE staining and angiogenesis., Results: Uptake of 99mTc-anti-RAGE F(ab')2 as %ID × 10-3 was higher in the left (ischemic) limbs for the diabetic mice (n = 8) compared to non-diabetic mice (n = 8) (1.20 ± 0.44% vs. 0.49 ± 0.40%; P = 0.0007) and corresponded to less angiogenesis in the diabetic mice. Uptake was also higher in the right limbs of diabetic compared to non-diabetic animals (0.82 ± 0.33% vs. 0.40 ± 0.14%; P = 0.0004)., Conclusions: These data show the feasibility of imaging and quantifying the effect of diabetes on RAGE expression in limb ischemia.
Published: 2013
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26. Imaging small human prostate cancer xenografts after pretargeting with bispecific bombesin-antibody complexes and targeting with high specific radioactivity labeled polymer-drug conjugates.

Author: Patil V, Gada K, Panwar R, Varvarigou A, Majewski S, Weisenberger A, Ferris C, Tekabe Y, and Khaw BA
Subjects: Animals, Antibodies, Bispecific chemistry, Antibodies, Bispecific immunology, Antibodies, Monoclonal immunology, Antineoplastic Agents chemistry, Cell Line, Tumor, Humans, Immunoglobulin Fab Fragments immunology, Indium Radioisotopes, Isotope Labeling, Male, Mice, Mice, Inbred C57BL, Organotechnetium Compounds, Pentetic Acid immunology, Sulfides chemistry, Antibodies, Bispecific metabolism, Bombesin immunology, Cell Transformation, Neoplastic, Molecular Imaging methods, Polylysine chemistry, Prostatic Neoplasms pathology, Tumor Burden
Abstract: Purpose: Pretargeting with bispecific monoclonal antibodies (bsMAb) for tumor imaging was developed to enhance target to background activity ratios. Visualization of tumors was achieved by the delivery of mono- and divalent radiolabeled haptens. To improve the ability to image tumors with bsMAb, we have combined the pretargeting approach with targeting of high specific activity radiotracer labeled negatively charged polymers. The tumor antigen-specific antibody was replaced with bombesin (Bom), a ligand that binds specifically to the growth receptors that are overexpressed by many tumors including prostate cancer. Bomanti- diethylenetriaminepentaacetic acid (DTPA) bispecific antibody complexes were used to demonstrate pretargeting and imaging of very small human prostate cancer xenografts targeted with high specific activity ¹¹¹In- or ⁹⁹mTc-labeled negatively charged polymers., Methods: Bispecific antibody complexes consisting of intact anti-DTPA antibody or Fab′ linked to Bom via thioether bonds (Bom-bsCx or Bom-bsFCx, respectively) were used to pretarget PC-3 human prostate cancer xenografts in SCID mice. Negative control mice were pretargeted with Bom or anti-DTPA Ab. 111In-Labeled DTPA-succinyl polylysine (DSPL) was injected intravenously at 24 h (7.03 ± 1.74 or 6.88 ± 1.89 MBq ¹¹¹In-DSPL) after Bom-bsCx or 50 ± 5.34 MBq of ⁹⁹mTc-DSPL after Bom-bsFCx pretargeting, respectively. Planar or single photon emission computed tomography (SPECT)/CT gamma images were obtained for up to 3 h and only planar images at 24 h. After imaging, all mice were killed and biodistribution of 111In or 99mTc activities were determined by scintillation counting., Results: Both planar and SPECT/CT imaging enabled detection of PC-3 prostate cancer lesions less than 1-2 mm in diameter in 1-3 h post 111In-DSPL injection. No lesions were visualized in Bom or anti-DTPA Ab pretargeted controls. 111In-DSPL activity in Bom-bsCx pretargeted tumors (1.21 ± 0.36 %ID/g) was 5.4 times that in tumors pretargeted with Bom or anti-DTPA alone (0.22 ± 0.08, p = 0.001). PC-3 xenografts pretargeted with Bom-bsFCx and targeted with ⁹⁹mTc-DSPL were visualizable by 1-3 h. Exquisite tumor uptake at 24 h (6.54 ± 1.58 %ID/g) was about 15 times greater than that of Bom pretargeted controls (0.44 ± 0.17, p = 0.002)., Conclusion: Pretargeting prostate cancer with Bom-bsCx or Bom-bsFCx enabled fast delivery of high specific radioactivity ¹¹¹In- or ⁹⁹mTc-labeled polymer-drug conjugates resulting in visualization of lesions smaller than 1- 2 mm in diameter within 3 h.
Published: 2012
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27. Imaging of receptors for advanced glycation end products in experimental myocardial ischemia and reperfusion injury.

Author: Tekabe Y, Luma J, Li Q, Schmidt AM, Ramasamy R, and Johnson LL
Subjects: Animals, Apoptosis, Disease Models, Animal, Fluorescent Antibody Technique, Male, Mice, Mice, Inbred C57BL, Myocardial Reperfusion Injury immunology, Myocardial Reperfusion Injury metabolism, Myocardium immunology, Receptor for Advanced Glycation End Products, Receptors, Immunologic immunology, Time Factors, Immunoglobulin Fab Fragments, Molecular Imaging methods, Multimodal Imaging, Myocardial Reperfusion Injury diagnostic imaging, Myocardium metabolism, Positron-Emission Tomography, Receptors, Immunologic metabolism, Technetium, Tomography, X-Ray Computed
Abstract: Objectives: The aim of this study was to image expression of receptor for advanced glycation end products (RAGE) in a mouse model of myocardial reperfusion injury., Background: RAGE and its ligands are implicated in the pathogenesis of ischemia/reperfusion injury and infarction. We hypothesized that RAGE-directed quantitative imaging of myocardial uptake of technetium-99m ((99m)Tc)-anti-RAGE F(ab')(2) in a mouse model of myocardial ischemic injury can detect RAGE expression and show quantitative differences between early (18 to 20 h) and later times (48 h) after reperfusion., Methods: Twenty-five wild-type (WT) mice underwent left anterior descending coronary artery occlusion for 30 min. Mice were injected with 19.98 ± 1.78 MBq of (99m)Tc anti-RAGE F(ab')(2) at 2 time points after reperfusion (at 18 to 20 h [n = 8] and at 48 h [n = 12]) and 5 h later with 6.14 ± 2.0 MBq of thallium-201 ((201)Tl). Five WT mice were injected with nonspecific F(ab')(2) and (201)Tl 18 to 20 h after reperfusion. Six WT mice underwent sham operation without coronary intervention. After injection with (201)Tl, all mice immediately underwent dual isotope single-photon emission computed tomography/computed tomography. At completion of imaging, hearts were counted and sectioned., Results: The uptake of (99m)Tc-anti-RAGE F(ab')(2) in the ischemic zone from the scans as mean percentage injected dose was significantly greater at 18 to 20 h (5.7 ± 2.1 × 10(-3)%) as compared with at 48 h (1.4 ± 1.1 × 10(-3)%; p < 0.001) after reperfusion. Disease and antibody controls showed no focal uptake in the infarct. Gamma well counting of the myocardium supported the quantitative scan data. By immunohistochemical staining there was greater caspase-3 and RAGE staining at 18 to 20 h versus at 48 h (p = 0.04 and p = 0.01, respectively). On dual immunofluorescence, RAGE colocalized mainly with injured cardiomyocytes undergoing apoptosis., Conclusions: RAGE expression in myocardial ischemic injury can be imaged in vivo using a novel (99m)Tc-anti-RAGE F(ab')(2). RAGE plays a role in several cardiovascular diseases and is a potential target for clinical imaging., (Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)
Published: 2012
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28. Pretargeted gamma imaging of murine metastatic melanoma lung lesions with bispecific antibody and radiolabeled polymer drug conjugates.

Author: Gada KS, Patil V, Panwar R, Majewski S, Tekabe Y, and Khaw BA
Subjects: Animals, Antigens, Neoplasm immunology, Feasibility Studies, Lung Neoplasms secondary, Male, Melanoma secondary, Mice, Mice, Inbred C57BL, Pentetic Acid, Radiopharmaceuticals, Technetium, Technetium Compounds, Tomography, Emission-Computed, Single-Photon methods, Antibodies, Bispecific, Lung Neoplasms diagnostic imaging, Melanoma diagnostic imaging, Polymers, Skin Neoplasms diagnostic imaging
Abstract: Introduction: Bispecific monoclonal antibodies (bsMAbs) have been developed as a pretargeting tool to reduce background activity, thereby increasing target to background (T : B) ratios. To enhance visualization of small lesions in vivo, we have used the pretargeting approach of bsMAb and negatively charged polymers radiolabeled with high-specific radioactivity., Methods: Imaging of metastatic melanoma lesions localized in lung tissues pretargeted with bsMAb and targeted with high-specific radioactivity polymers was carried out. The bsMAb was prepared by covalent conjugation of an antinucleosomal antibody (2C5) recognizing a nucleosomal pan cancer antigen and an anti-diethylene triaminepentaacetic acid antibody (6C31H3) by means of thioether linkage. BsMAb was injected intravenously 10 days after the initiation of the induction of murine melanoma metastasized to the lungs. The next day, 37 MBq ⁹⁹mTc-diethylene triaminepentaacetic acid-succinylated polylysine were injected intravenously and in-vivo imaging was carried out after the injection. In-vivo and ex-vivo target (T) to background (B) activity ratios were assessed by computer planimetry and biodistribution studies., Results: Lesions were visualized unequivocally in 3 h by gamma scintigraphy. Ex-vivo gamma-scintillation counting corrected for the lesion mass showed that the mean lesion activity was 24.85 ± 13.53 percent injected dose per gram when pretargeted with bsMAb, whereas it was 0.977 ± 0.465 percent injected dose per gram (P<0.01) in the control group injected only with radioactive polymers also corrected similarly., Conclusion: The use of bsMAb complexes and ⁹⁹mTc-diethylene triaminepentaacetic acid-succinylated polylysine enabled early in-vivo visualization of small metastatic melanoma lesions in the lungs.
Published: 2011
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29. New application of optical agent to image angiogenesis in hindlimb ischemia.

Author: Tekabe Y, Klose A, Nizami S, Luma J, Lee FY, and Johnson L
Subjects: Animals, Capillaries metabolism, Femoral Artery surgery, Hindlimb metabolism, Hindlimb pathology, Integrin alphaV metabolism, Integrin alphaVbeta3 antagonists & inhibitors, Integrin alphaVbeta3 metabolism, Ligation, Male, Mice, Mice, Inbred Strains, Microscopy, Fluorescence, Plant Lectins metabolism, Platelet Endothelial Cell Adhesion Molecule-1 metabolism, Sensitivity and Specificity, Diagnostic Imaging methods, Fluorescent Dyes metabolism, Hindlimb blood supply, Ischemia pathology, Neovascularization, Physiologic
Abstract: Optical agents targeting α(v)β₃ are potential tools to image the angiogenic response to limb ischemia. The left (L) femoral artery was ligated in 17 mice and sham surgery performed on the contralateral right (R) hindlimb. Seven days later, IntegriSense (2 nmol) was injected into 11 mice and 6 were probe controls. Six hours later, mice underwent optical imaging. Ratios of photon flux in the L/R limbs were calculated. Tissue was stained for α(v) , CD31, and lectin. The signal was increased in the ischemic limbs compared to contralateral legs and ratio of photon flux in L/R limb averaged 2.37. Control probe showed no hindlimb signal. IntegriSense colocalized with CD31 by dual fluorescent staining. Ratios for L/R hindlimbs correlated with quantitative lectin staining (r = 0.88, p = 0.003). Optical imaging can identify and quantify angiogenic response to hindlimb ischemia., (Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)
Published: 2011
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30. Imaging the effect of receptor for advanced glycation endproducts on angiogenic response to hindlimb ischemia in diabetes.

Author: Tekabe Y, Shen X, Luma J, Weisenberger D, Yan SF, Haubner R, Schmidt AM, and Johnson L
Abstract: Background: Receptor for advanced glycation endproducts (RAGE) expression contributes to the impaired angiogenic response to limb ischemia in diabetes. The aim of this study was to detect the effect of increased expression of RAGE on the angiogenic response to limb ischemia in diabetes by targeting αvβ3 integrin with 99mTc-labeled Arg-Gly-Asp (RGD)., Methods: Male wild-type (WT) C57BL/6 mice were either made diabetic or left as control for 2 months when they underwent femoral artery ligation. Four groups were studied at days 3 to 7 after ligation: WT without diabetes (NDM) (n = 14), WT with diabetes (DM) (n = 14), RAGE-/- NDM (n = 16), and RAGE-/- DM (n = 14). Mice were injected with 99mTc-HYNIC-RGD and imaged. Count ratios for ischemic/non-ischemic limbs were measured. Muscle was stained for RAGE, αvβ3, and lectins., Results: There was no difference in count ratio between RAGE-/- and WT NDM groups. Mean count ratio was lower for WT DM (1.38 ± 0.26) vs. WT NDM (1.91 ± 0.34) (P<0.001). Mean count ratio was lower for the RAGE-/- DM group than for RAGE-/- NDM group (1.75 ± 0.22 vs. 2.02 ± 0.29) (P<0.001) and higher than for the WT DM group (P<0.001). Immunohistopathology supported the scan findings., Conclusions: In vivo imaging of αvβ3 integrin can detect the effect of RAGE on the angiogenic response to limb ischemia in diabetes.
Published: 2011
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31. Noninvasive monitoring the biology of atherosclerotic plaque development with radiolabeled annexin V and matrix metalloproteinase inhibitor in spontaneous atherosclerotic mice.

Author: Tekabe Y, Li Q, Luma J, Weisenberger D, Sedlar M, Harja E, Narula J, and Johnson LL
Subjects: Animals, Annexin A5 metabolism, Apolipoproteins E genetics, Apoptosis, Disease Models, Animal, Enzyme Inhibitors pharmacology, Image Processing, Computer-Assisted, Immunohistochemistry methods, Male, Mice, Mice, Knockout, Technetium pharmacology, Time Factors, Annexin A5 pharmacology, Atherosclerosis diagnosis, Atherosclerosis pathology, Matrix Metalloproteinase Inhibitors, Plaque, Atherosclerotic pathology
Abstract: Objectives: To compare the ability of (99m)Tc-labeled broad-based matrix metalloproteinase inhibitor (RP805) (MPI) and (99m)Tc-annexin V to identify more advanced atherosclerotic disease in apolipoprotein E-null (apoE(-/-)) mice., Background: Both MMP expression and apoptotic cell death occur in both early and in advanced atherosclerotic plaques., Methods: Eight 6-9-week-old apoE(-/-) mice, 10 apoE(-/-) mice at 20 weeks, and 12 apoE(-/-) at 40 weeks were injected with both tracers in alternating sequence separated by 48 h, underwent planar imaging and were killed. Radiotracer uptake was quantified from the scans as percent whole body and from tissue as percent injected dose per gram (%ID/g). Quantitative immunohistopathology of the aorta and carotids for macrophages, MMPs, and caspase was performed., Results: At 6 weeks, mice showed no tracer uptake in the chest or neck and had minimal lesion. At 20 weeks, uptake of annexin V as %ID was borderline higher than MPI (1.10 ± .48% vs .77 ± .31%, P = .09), between 20 and 40 weeks aortic lesion area increased from 37.4 ± 12.0% to 46.2 ± 7.4% and at 40 weeks MPI was significantly greater than annexin V uptake (1.11 ± .66% vs .70 ± .16%, P = .05). On histology there were greater increases in % MMP-2 and -9 than % caspase positive cells. Carotid uptake of MPI was greater than annexin V at both 20 and 40 weeks (1.25 ± .48% vs .78 ± .25%, P = .02 and 3.70 ± 1.45% vs 2.25 ± .66%, P = .005). The carotid lesion area at 40 weeks was 74 ± 9% with greater % cells positive for MMP's than caspase. %ID/g annexin V correlated significantly with % macrophages and with caspase-3 positive cells and %ID/g MPI correlated significantly with % macrophages and with MMP-2 and -9 positive cells., Conclusions: In apoE(-/-) mice, MMP expression is greater than apoptosis as the disease progresses and MPI may be a better imaging agent for more advanced disease.
Published: 2010
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32. Targeting very small model lesions pretargeted with bispecific antibody with 99mTc-labeled high-specific radioactivity polymers.

Author: Tekabe Y, Einstein AJ, Johnson LL, and Khaw BA
Subjects: Animals, Antibody Affinity, Antibody Specificity, Antigens administration & dosage, Antigens chemistry, Antigens immunology, Endothelial Cells pathology, Femoral Artery pathology, Humans, Injections, Intramuscular, Molecular Probes administration & dosage, Molecular Probes pharmacokinetics, Pentetic Acid chemistry, Polystyrenes administration & dosage, Polystyrenes pharmacokinetics, Rats, Antibodies, Bispecific immunology, Molecular Imaging methods, Molecular Probes chemistry, Molecular Probes immunology, Polystyrenes chemistry, Polystyrenes immunology, Technetium chemistry
Abstract: Background: Two-step targeting with bispecific antibody and Tc-labeled high-specific radioactivity polymers was used for molecular imaging of two very small model lesions in rats., Methods and Results: Sprague-Dawley rats (group I) were injected with surrogate antigen-coated beads (SA beads) in the right hind leg or unmodified beads in the contralateral hind leg. In group II, femoral artery de-endothelialization was induced in the left hind leg and sham operation was performed in the contralateral hind leg. Bispecific antibody Z2D3 F(ab')2-anti-DTPA F(ab')2 was injected intravenously 24 h after SAB injection or 1 week after endothelial denudation. Tc-labeled polymers were injected intravenously 24 h later and gamma-images obtained at 2 and 24 h in group I or approximately 2.5 h in group II. Lesions were visualized by 2 h. In group I, SA beads-specific uptake in muscles was significantly greater than with unmodified beads (P<0.015). In group II, lesions were visualized by 2.5 h after radiopolymer injection with uptake activity 2.1+/-0.6 times greater than in the contralateral side from in-vivo images (P<0.004) and 1.8+/-0.7 times by gamma-scintillation counting (P<0.04)., Conclusion: Pretargeting with Z2D3 bispecific antibody for the localization of radiolabeled polymers enabled successful in-vivo gamma-imaging of very small lesions in two rat models of extravascular and intravascular targets. Biodistribution data confirmed that pretargeting with bispecific antibody enabled targeted visualization of two different very small model lesions by in-vivo gamma-imaging.
Published: 2010
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33. A novel monoclonal antibody for RAGE-directed imaging identifies accelerated atherosclerosis in diabetes.

Author: Tekabe Y, Luma J, Einstein AJ, Sedlar M, Li Q, Schmidt AM, and Johnson LL
Subjects: Amino Acid Sequence, Animals, Apolipoproteins E genetics, Apolipoproteins E physiology, Atherosclerosis pathology, Chelating Agents, Diabetes Complications pathology, Image Processing, Computer-Assisted, Immunoglobulin Fab Fragments immunology, Isotope Labeling, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Pentetic Acid, Receptor for Advanced Glycation End Products, Regression Analysis, Tomography, Emission-Computed, Single-Photon, Antibodies, Monoclonal, Atherosclerosis diagnostic imaging, Atherosclerosis etiology, Diabetes Complications diagnostic imaging, Radiopharmaceuticals, Receptors, Immunologic immunology
Abstract: Unlabelled: Receptor for advanced glycation end products (RAGE) binds advanced glycation end products and other inflammatory ligands and is expressed in atherosclerotic plaques in diabetic and nondiabetic subjects. The higher expression in diabetes mellitus corresponds to the accelerated course of the atherosclerosis. This study was designed to test the hypothesis that the level of RAGE expression in atherosclerosis can be detected by quantitative in vivo SPECT and that counts in the target will correlate with the strength of the biologic signal., Methods: A monoclonal murine antibody was developed against the V-domain of RAGE, fragmented into F(ab')(2) and labeled with (99m)Tc, and injected at a dose of 15.14 +/- 1.23 MBq into 24-wk-old male apolipoprotein E null (ApoE(-/-)) mice (n = 22), including mice with streptozotocin-induced diabetes mellitus (n = 8), nondiabetic mice (n = 8), and control ApoE(-/-)/RAGE(-/-) double-knock-out mice (n = 6). Four hours later (allowing for blood-pool clearance), the mice were imaged and sacrificed, and the proximal aorta was removed and counted to calculate the percentage injected dose of RAGE per gram of tissue, followed by histologic and immunohistochemical characterization., Results: Radiotracer uptake in the aortic lesions was clearly visualized noninvasively by SPECT. RAGE uptake as percentage injected dose in diabetic ApoE(-/-) mice (1.39 +/- 0.16 x 10(-2)) was significantly higher than that in nondiabetic ApoE(-/-) mice (0.48 +/- 0.27 x 10(-2)) (P < 0.0001). The radiotracer uptake was highly correlated with RAGE expression by quantitative immunohistomorphometry (r = 0.82, P = 0.002) and with percentage of macrophages (r = 0.86, P < 0.0001)., Conclusion: In this study, (99m)Tc-labeled anti-RAGE F(ab')(2) SPECT successfully identified early accelerated disease in diabetes mellitus for age-matched ApoE(-/-) mice and quantified RAGE expression over a range of lesion severities.
Published: 2010
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34. Development of receptor for advanced glycation end products-directed imaging of atherosclerotic plaque in a murine model of spontaneous atherosclerosis.

Author: Tekabe Y, Li Q, Rosario R, Sedlar M, Majewski S, Hudson BI, Einstein AJ, Schmidt AM, and Johnson LL
Subjects: Animals, Gamma Cameras, Immunoglobulin Fab Fragments immunology, Immunohistochemistry, Mice, Mice, Inbred C57BL, Mice, Knockout, Microscopy, Confocal, Receptor for Advanced Glycation End Products, Receptors, Immunologic immunology, Technetium, Antibodies, Monoclonal, Atherosclerosis diagnosis, Atherosclerosis metabolism, Glycation End Products, Advanced, Receptors, Immunologic analysis
Abstract: Background: The receptor for advanced glycation end products (RAGE) is implicated in the development and progression of atherosclerosis. We tested the hypothesis that (99m)Tc-labeled anti-RAGE F(ab')(2) can be used as a noninvasive tool to image atherosclerotic lesions in apolipoprotein E-deficient (apoE(-/-)) mice., Methods and Results: A sequence in the V-type Ig extracellular domain of RAGE was used to develop a peptide injected into rabbits; serum was retrieved, IgG prepared and affinity-purified, and pepsin-digested into F(ab')(2). Thirteen 6-week apoE(-/-) mice were fed a Western diet. At 20 weeks, 6 were injected with 15.2+/-1.9 MBq (350 to 411 microCi) (99m)Tc-labeled anti-RAGE F(ab')(2), 6 were injected with (99m)Tc-labeled control nonspecific IgG F(ab')(2), and 1 was injected with dual-labeled (99m)Tc and rhodamine anti-RAGE F(ab')(2). Four 20-week C57BL/6 mice were injected with (99m)Tc-labeled anti-RAGE F(ab')(2). All mice were imaged on a high resolution mini-gamma camera 4 hours after injection and euthanized. The aortic tree was dissected and photographed, and the proximal aorta was sectioned for staining after gamma scintillation counting. All 6 apoE(-/-) mice injected with (99m)Tc-labeled anti-RAGE F(ab')(2) fragments showed focal tracer uptake in the proximal aorta (mean %ID/g, 1.98%). Disease and antibody controls showed no focal tracer uptake in the thorax (%ID/g, <1.0%). Histological sections of the proximal aorta showed American Heart Association class III lesions with lipid laden macrophages, smooth muscle cells, and positive staining for RAGE. On immunofluorescence, RAGE colocalized with macrophages., Conclusions: These data show the feasibility of noninvasively imaging RAGE in atherosclerotic lesions in a murine model and confirm levels of RAGE expression sufficient to allow detection on in vivo imaging.
Published: 2008
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35. Imaging experimental atherosclerotic lesions in ApoE knockout mice: enhanced targeting with Z2D3-anti-DTPA bispecific antibody and 99mTc-labeled negatively charged polymers.

Author: Khaw BA, Tekabe Y, and Johnson LL
Subjects: Animals, Antibodies, Bispecific chemistry, Atherosclerosis diagnostic imaging, Chelating Agents pharmacology, Cross-Linking Reagents pharmacology, Female, Femoral Artery pathology, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Muscle, Smooth, Vascular cytology, Polymers chemistry, Radionuclide Imaging, Tissue Distribution, Apolipoproteins E genetics, Atherosclerosis genetics, Atherosclerosis pathology, Pentetic Acid pharmacology, Technetium metabolism
Abstract: Unlabelled: In vivo molecular imaging may be improved if specific radioactivity at the target site could be increased while maintaining low background activity. Bispecific antibody complexes and (99m)Tc-labeled negatively charged chelating polymers that react specifically with the capture arm of the bispecific antibody complex were used to demonstrate the feasibility of imaging very small atherosclerotic lesions in ApoE knockout mice., Methods: Left femoral artery denudation in ApoE(-/-) mice on a hyperlipidemic diet was used to induce accelerated atherosclerotic lesions. Approximately 40 microg of bispecific antibodies were injected intravenously after 2 wk of endothelial denudation. The next day, approximately 15.0 MBq (99m)Tc-DTPA-succinyl-polylysine (2 microg; DTPA is diethylenetriaminepentaacetic acid) were injected intravenously., Results: In vivo gamma-images showed that lesions were observed unequivocally by 2-3 h. Sham-operated right femoral regions showed no radiotracer accumulation. Ex vivo gamma-scintillation counting corrected for sham-operated nonspecific activity and lesion mass showed that the mean lesion activity was 10.10 +/- 6.76 %ID/g (percentage injected dose per gram), whereas nonspecific human IgG bispecific control (NSB control) also corrected similarly was 0.939 +/- 0.877 %ID/g (P < 0.03). Atherosclerotic lesions were confirmed by immunohistochemical staining. Computer planimetry of immunohistograms showed the mean lesion size to be 2.64 +/- 2.46 mg., Conclusion: Use of bispecific antibody complexes and (99m)Tc-DTPA-succinyl-polylysine enabled in vivo visualization of very small atherosclerotic lesions in ApoE knockout mice.
Published: 2006

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35 results on '"Tekabe, Y"'

1. Young investigator award session oral abstract session

2. Young investigator award session oral abstract session

3. Disposal of Iron by a Mutant form of Siderocalin NGAL

4. Poster Session 2 : Monday 4 May 2015, 08

5. Poster Session 2: Monday 4 May 2015, 08:00-18:00 * Room: Poster Area

6. Abstracts

7. 4.9Development of anti-RAGE antibody to image atherosclerosis

8. Enhanced imaging of very small experimental atherosclerotic lesions in ApoE−/− mice: Use of bispecific antibody and Tc-99m-labeled polymeric probes

9. 4.9: Development of anti-RAGE antibody to image atherosclerosis

10. Young investigator award session oral abstract session

11. Blocking RAGE expression after injury reduces inflammation in mouse model of acute lung injury.

12. Novel Receptor for Advanced Glycation End Products-Blocking Antibody to Treat Diabetic Peripheral Artery Disease.

13. VEGF receptor targeted imaging of angiogenic response to limb ischemia in diabetic vs. non-diabetic Yucatan minipigs.

14. Single-photon emission computed tomography/computed tomography imaging of RAGE in smoking-induced lung injury.

15. Imaging VEGF Receptors and α v β 3 Integrins in a Mouse Hindlimb Ischemia Model of Peripheral Arterial Disease.

16. Selective Imaging of Vascular Endothelial Growth Factor Receptor-1 and Receptor-2 in Atherosclerotic Lesions in Diabetic and Non-diabetic ApoE -/- Mice.

17. Single-Photon Emission Computed Tomography/Computed Tomography Imaging in a Rabbit Model of Emphysema Reveals Ongoing Apoptosis In Vivo.

18. Disposal of iron by a mutant form of lipocalin 2.

19. Treatment effect with anti-RAGE F(ab')2 antibody improves hind limb angiogenesis and blood flow in Type 1 diabetic mice with left femoral artery ligation.

20. Imaging VEGF receptor expression to identify accelerated atherosclerosis.

21. Imaging RAGE expression in atherosclerotic plaques in hyperlipidemic pigs.

22. Beneficial Effect of Glucose Control on Atherosclerosis Progression in Diabetic ApoE(-/-) Mice: Shown by Rage Directed Imaging.

23. In vitro demonstration of enhanced prostate cancer toxicity: pretargeting with Bombesin bispecific complexes and targeting with polymer-drug-conjugates.

24. Noninvasive imaging of myocyte apoptosis following application of a stem cell-engineered delivery platform to acutely infarcted myocardium.

25. Imaging receptor for advanced glycation end product expression in mouse model of hind limb ischemia.

26. Imaging small human prostate cancer xenografts after pretargeting with bispecific bombesin-antibody complexes and targeting with high specific radioactivity labeled polymer-drug conjugates.

27. Imaging of receptors for advanced glycation end products in experimental myocardial ischemia and reperfusion injury.

28. Pretargeted gamma imaging of murine metastatic melanoma lung lesions with bispecific antibody and radiolabeled polymer drug conjugates.

29. New application of optical agent to image angiogenesis in hindlimb ischemia.

30. Imaging the effect of receptor for advanced glycation endproducts on angiogenic response to hindlimb ischemia in diabetes.

31. Noninvasive monitoring the biology of atherosclerotic plaque development with radiolabeled annexin V and matrix metalloproteinase inhibitor in spontaneous atherosclerotic mice.

32. Targeting very small model lesions pretargeted with bispecific antibody with 99mTc-labeled high-specific radioactivity polymers.

33. A novel monoclonal antibody for RAGE-directed imaging identifies accelerated atherosclerosis in diabetes.

34. Development of receptor for advanced glycation end products-directed imaging of atherosclerotic plaque in a murine model of spontaneous atherosclerosis.

35. Imaging experimental atherosclerotic lesions in ApoE knockout mice: enhanced targeting with Z2D3-anti-DTPA bispecific antibody and 99mTc-labeled negatively charged polymers.

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35 results on '"Tekabe, Y"'

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