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4. Cardiovascular Molecular Imaging With Fluorine-19 MRI: The Road to the Clinic.

Author

Heeswijk, R.B. van, Bauer, W.R., Bönner, F., Janjic, J.M., Mulder, W.J.M., Schreiber, L.M., Schwitter, J., Flögel, U., Heeswijk, R.B. van, Bauer, W.R., Bönner, F., Janjic, J.M., Mulder, W.J.M., Schreiber, L.M., Schwitter, J., and Flögel, U.

Abstract

01 september 2023, Contains fulltext : 296653.pdf (Publisher’s version ) (Closed access), Fluorine-19 ((19)F) magnetic resonance imaging is a unique quantitative molecular imaging modality that makes use of an injectable fluorine-containing tracer that generates the only visible (19)F signal in the body. This hot spot imaging technique has recently been used to characterize a wide array of cardiovascular diseases and seen a broad range of technical improvements. Concurrently, its potential to be translated to the clinical setting is being explored. This review provides an overview of this emerging field and demonstrates its diagnostic potential, which shows promise for clinical translation. We will describe (19)F magnetic resonance imaging hardware, pulse sequences, and tracers, followed by an overview of cardiovascular applications. Finally, the challenges on the road to clinical translation are discussed.

Published
2023

5. SYSTEMI - Systemic organ communication in STEMI: Design and rationale of a cohort study of patients with ST-segment elevation myocardial infarction

Author

Bönner, F, primary, Jung, C, additional, Polzin, A, additional, Erkens, R, additional, Dannenberg, L, additional, Ipek, R, additional, Kaldirim, M, additional, Cramer, M, additional, Wischmann, P, additional, Zaharia, O-P, additional, Meyer, C, additional, Flögel, U, additional, Levkau, B, additional, Gödecke, A, additional, Fischer, JW, additional, Klöcker, N, additional, Krüger, M, additional, Roden, M, additional, and Kelm, M, additional

Published
2023
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12. Poster display IV experimental and instrumentation

Author

Masoli, O. Osvaldo, Redruello, M., Ogresta, F., Collaud, C., Koslowski, P., Baliño, N. Perez, Eleta, M., Arce, P., Vidal, L., Kardash, O., Maroz-Vadalajskaya, N. Natalia, Vanhove, C. Christian, Lahoutte, T., Defrise, M., Andreyev, A., Bossuyt, A., Franken, P. R., Franken, P. R. Philippe, Lahoutte, T., Maskali, F., Vanhove, C., Nloga, J., Tran, N., Marie, P. Y., Peix, A. Amalia, Garcia-Barreto, D., Ponce, F., Cabrera, L. O., Valiente, J., Tornes, F., Guerrero, I., Heres, F., Garcia, E. J., Cabale, B., Bindslev, L. Lene, Bisgaard, K. B. Kirsten, Haack-Soerensen, M. H. S. Mandana, Mortensen, S. M. Steen, Kragh, L. K. Linda, Kjaer, A. K. Andreas, Kastrup, J. K. Jens, Hesse, B. H. Birger, Aboul-Enein, F. Fatma, Battah, A., Fattah, A. Abdel, Atty, A. Abdel, Allam, A., Riou, L. Laurent, Broisat, A., Ghezzi, C., Lartizien, C., Berthonneche, C., Toufektsian, M. C., Maitrejean, S., Janier, M., Vanzetto, G., Fagret, D., Rouzet, F. Francois, Daou, D., Lebtahi, R., Frank, R., Leenhardt, A., Slama, M., Guludec, D. Le, Sarda-Mantel, L. Laure, Michel, J. B., Rouzet, F., Martet, G., Meulemans, A., Vrigneaud, J. M., Guludec, D. Le, Daou, D. Doumit, Coaguila, C., Benada, A., Razzouk, M., Idy-Peretti, I., Guludec, D. Le, Vilain, D., Lebtahi, R., Guludec, D. Le, Stegger, L. Lars, Schäfers, K., Flögel, U., Schrader, J., Schober, O., Levkau, B., Schäfers, M., Kies, P. Peter, Wichter, T., Schäfers, K. P., Schäfers, M., Wielepp, J. P. Peter, Baller, D., Pulawski, E., Weise, R., Fricke, E., Horstkotte, D., Burchert, W., Eckert, S., Dongas, A., Horstkotte, D., Burchert, W., Nekolla, S. G. Stephan, Martinez, M. J., Howe, W., Kehren, F., Ziegler, S. I., Vassiliadis, I. Ioannis, Souretis, G., Komporozos, C., Fountos, A., Papademetriou, A., Spanos, A., Antoniou, A., Strembelas, P., Moralidis, E. Efstratios, Arsos, G., Boundas, D., Georga, S., Karatzas, N., Karakatsanis, K., Prassopoulos, V. Vassilios, Parthenakis, F., Patrianakos, A., Koukouraki, S., Velidaki, A., Karkavitsas, N., Vardas, P., Velidaki, A. Antigone, Perisinakis, K., Koukouraki, S., Koutsikos, J., Prassopoulos, V., Vardas, P., Karkavitsas, N., Sundaraiya, S. Sumati, Sumati, S., Sambhasivam, KA., David, S., Zakavi, S. R. Seyed Rasoul, Kakhki, V. R. Dabagh, Jabari, H., Zingerman, B., Bendayan, D., Sagie, A., Solodky, A., Mats, I., Shapira, Y., Kremer, M. R., Zafrir, N. Nili, Rimini, M. L. Maria Luisa De, Catalano, M., Bonzani, G., Scalzone, A., Merenda, R., Monteforte, I., Monda, V., Muto, P., Carboni, G. P. Gian Piero, Miglionico, M., Tavolozza, M., Marcassa, C. Claudio, Campini, R., Calza, P., Giannuzzi, P., Eleuteri, E., Marcassa, C. Claudio, Campini, R., Scapellato, F., Temporelli, P. L., Giannuzzi, P., Pellegrino, T., Storto, G., Sorrentino, A. R., Silvestri, A., Filardi, P. Perrone, Brevetti, G., Cuocolo, A. Alberto, Cho, K. Keiichi, Kumita, S., Seino, K., Nakajo, H., Toba, M., Kumazaki, T., Muramatsu, T. Toshihiro, Yamazaki, T., Seki, K., Kawanami, J., Nakajima, T., Yamada, Y., Suga, T., Matsumoto, K., Nishimura, S., Taki, J. Junichi, Higuchi, T., Kawashima, A., Nakajima, K., Muramori, A., Matsunari, I., Tait, J. F., Vanderheyden, J. L., Strauss, H. W., Tonami, N., Adachi, I. Itaru, Shimomura, H., Kintaka, T., Komori, T., Ogura, Y., Kitaura, Y., Narabayashi, I., Iida, H. Hidehiro, Zeniya, T., Kim, K. M., Watabe, H., Teramoto, N., Yamamichi, Y., Alexanderson, E. Erick, Ricalde, A., Vargas, A., Meave, A., Amigo, M. C., Misko, J., Dziuk, M. Miroslaw, Warczynska, A., Skrobowska, E., Vasconcelos, M. Mariana, Martins, E., Faria, T., Oliveira, A., Pardal, N., Macedo, F., Pereira, J., Rocha-Gonçalves, F., Cantinho, G. Guilhermina, Pena, H., Freire, L., Veiga, A., Gonçalves, P., Godinho, F., Chua, T. Terrance, Lee, C. Y., Keng, F., Ding, Z. P., Koh, T. H., Awamleh, P. Paula, Talavera, P., Torres, V., Balsa, M. A., González, O., Alberca, M. T., Miguel, R., Cosío, F. G., Lomsky, M. Milan, Richter, J., Johansson, L., El-Ali, H., Åström, K., Ljungberg, M., Edenbrandt, L., Hung, G. U. Guang-Uei, Lee, K. W., Chen, C. P., Yang, K. T., Pekindil, G., Sarikaya, A. Ali, Ege, T., Salihoglu, S., Entok, E. Emre, Cavusoglu, Y., Ak, I., Vardareli, E., Timuralp, B., Tout, D. Deborah, Loong, C. Y., Naidoo, V. V., Aswegen, A. Van, Underwood, S. R., Thorley, P. J. Penelope, Goris, M. Michael, ZHU, H. J., Clements, I. P. Ian, Mullan, B. P., O’Connor, M. K., Breen, J. F., McGregor, C. G. A., Liu, Y. H. Yi-Hwa, Li, S., Bourke, B., Weyman, C., Sinusas, A. J., Ramakrishna, G. Gautam, Miller, T. D., O’Connor, M. K., Gibbons, R. J., Tsatkin, V., Wackers, F. J. T. H., Liu, Y. H. Yi-Hwa, Tsatkin, V., Prior, J. O. John, Facta, A. D., Schindler, T. H., Oxilia-Estigarribia, M. A., Hernandez-Pampaloni, M., Campisi, R., Zhang, X., Bischof-Delaloye, A., Nathan, L., Schelbert, H. R., Gullberg, G. T. Grant, Huesman, R. H., Reutter, B. W., Sitek, A., Veress, A. I., Weiss, J. A., Qi, J., Yang, Y., Gordi, T. Toufigh, Olmsted, A., Lieu, H., and Belardinelli, L.

Published
2005
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14. Regional analysis of inflammation and contractile function in reperfused acute myocardial infarction by in vivo 19F cardiovascular magnetic resonance in pigs.

Author

Bönner, Florian, Gastl, M., Nienhaus, F., Rothe, M., Jahn, A., Pfeiler, S., Gross, U., Schultheiss, H.-P., Ibanez, B., Kozerke, S., Szendroedi, J., Roden, M., Westenfeld, R., Schrader, J., Flögel, U., Heusch, G., and Kelm, M.

Abstract

Inflammatory cell infiltration is central to healing after acute myocardial infarction (AMI). The relation of regional inflammation to edema, infarct size (IS), microvascular obstruction (MVO), intramyocardial hemorrhage (IMH), and regional and global LV function is not clear. Here we noninvasively characterized regional inflammation and contractile function in reperfused AMI in pigs using fluorine (19F) cardiovascular magnetic resonance (CMR). Adult anesthetized pigs underwent left anterior descending coronary artery instrumentation with either 90 min occlusion (n = 17) or without occlusion (sham, n = 5). After 3 days, in surviving animals a perfluorooctyl bromide nanoemulsion was infused intravenously to label monocytes/macrophages. At day 6, in vivo 1H-CMR was performed with cine, T2 and T2* weighted imaging, T2 and T1 mapping, perfusion and late gadolinium enhancement followed by 19F-CMR. Pigs were sacrificed for subsequent ex vivo scans and histology. Edema extent was 35 ± 8% and IS was 22 ± 6% of LV mass. Six of ten surviving AMI animals displayed both MVO and IMH (3.3 ± 1.6% and 1.9 ± 0.8% of LV mass). The 19F signal, reflecting the presence and density of monocytes/macrophages, was consistently smaller than edema volume or IS and not apparent in remote areas. The 19F signal-to-noise ratio (SNR) > 8 in the infarct border zone was associated with impaired remote systolic wall thickening. A whole heart value of 19F integral (19F SNR × milliliter) > 200 was related to initial LV remodeling independently of edema, IS, MVO, and IMH. Thus, 19F-CMR quantitatively characterizes regional inflammation after AMI and its relation to edema, IS, MVO, IMH and regional and global LV function and remodeling. [ABSTRACT FROM AUTHOR]

Published
2022
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24. Poster display IV experimental and instrumentation

Author

Masoli, O., Redruello, M., Ogresta, F., Collaud, C., Koslowski, P., Baliño, N., Eleta, M., Arce, P., Vidal, L., Kardash, O., Maroz-Vadalajskaya, N., Vanhove, C., Lahoutte, T., Defrise, M., Andreyev, A., Bossuyt, A., Franken, P., Maskali, F., Nloga, J., Tran, N., Marie, P., Peix, A., Garcia-Barreto, D., Ponce, F., Cabrera, L., Valiente, J., Tornes, F., Guerrero, I., Heres, F., Garcia, E., Cabale, B., Bindslev, L., Bisgaard, K., Haack-Soerensen, M., Mortensen, S., Kragh, L., Kjaer, A., Kastrup, J., Hesse, B., Aboul-Enein, F., Battah, A., Fattah, A., Atty, A., Allam, A., Riou, L., Broisat, A., Ghezzi, C., Lartizien, C., Berthonneche, C., Toufektsian, M., Maitrejean, S., Janier, M., Vanzetto, G., Fagret, D., Rouzet, F., Daou, D., Lebtahi, R., Frank, R., Leenhardt, A., Slama, M., Guludec, D., Sarda-Mantel, L., Michel, J., Martet, G., Meulemans, A., Vrigneaud, J., Coaguila, C., Benada, A., Razzouk, M., Idy-Peretti, I., Vilain, D., Stegger, L., Schäfers, K., Flögel, U., Schrader, J., Schober, O., Levkau, B., Schäfers, M., Kies, P., Wichter, T., Wielepp, J., Baller, D., Pulawski, E., Weise, R., Fricke, E., Horstkotte, D., Burchert, W., Eckert, S., Dongas, A., Nekolla, S., Martinez, M., Howe, W., Kehren, F., Ziegler, S., Vassiliadis, I., Souretis, G., Komporozos, C., Fountos, A., Papademetriou, A., Spanos, A., Antoniou, A., Strembelas, P., Moralidis, E., Arsos, G., Boundas, D., Georga, S., Karatzas, N., Karakatsanis, K., Prassopoulos, V., Parthenakis, F., Patrianakos, A., Koukouraki, S., Velidaki, A., Karkavitsas, N., Vardas, P., Perisinakis, K., Koutsikos, J., Sundaraiya, S., Sumati, S., Sambhasivam, KA, David, S., Zakavi, S., Kakhki, V., Jabari, H., Zingerman, B., Bendayan, D., Sagie, A., Solodky, A., Mats, I., Shapira, Y., Kremer, M., Zafrir, N., Rimini, M., Catalano, M., Bonzani, G., Scalzone, A., Merenda, R., Monteforte, I., Monda, V., Muto, P., Carboni, G., Miglionico, M., Tavolozza, M., Marcassa, C., Campini, R., Calza, P., Giannuzzi, P., Eleuteri, E., Scapellato, F., Temporelli, P., Pellegrino, T., Storto, G., Sorrentino, A., Silvestri, A., Filardi, P., Brevetti, G., Cuocolo, A., Cho, K., Kumita, S., Seino, K., Nakajo, H., Toba, M., Kumazaki, T., Muramatsu, T., Yamazaki, T., Seki, K., Kawanami, J., Nakajima, T., Yamada, Y., Suga, T., Matsumoto, K., Nishimura, S., Taki, J., Higuchi, T., Kawashima, A., Nakajima, K., Muramori, A., Matsunari, I., Tait, J., Vanderheyden, J., Strauss, H., Tonami, N., Adachi, I., Shimomura, H., Kintaka, T., Komori, T., Ogura, Y., Kitaura, Y., Narabayashi, I., Iida, H., Zeniya, T., Kim, K., Watabe, H., Teramoto, N., Yamamichi, Y., Alexanderson, E., Ricalde, A., Vargas, A., Meave, A., Amigo, M., Misko, J., Dziuk, M., Warczynska, A., Skrobowska, E., Vasconcelos, M., Martins, E., Faria, T., Oliveira, A., Pardal, N., Macedo, F., Pereira, J., Rocha-Gonçalves, F., Cantinho, G., Pena, H., Freire, L., Veiga, A., Gonçalves, P., Godinho, F., Chua, T., Lee, C., Keng, F., Ding, Z., Koh, T., Awamleh, P., Talavera, P., Torres, V., Balsa, M., González, O., Alberca, M., Miguel, R., Cosío, F., Lomsky, M., Richter, J., Johansson, L., El-Ali, H., Åström, K., Ljungberg, M., Edenbrandt, L., Hung, G., Lee, K., Chen, C., Yang, K., Pekindil, G., Sarikaya, A., Ege, T., Salihoglu, S., Entok, E., Cavusoglu, Y., Ak, I., Vardareli, E., Timuralp, B., Tout, D., Loong, C., Naidoo, V., Aswegen, A., Underwood, S., Thorley, P., Goris, M., ZHU, H., Clements, I., Mullan, B., O'Connor, M., Breen, J., McGregor, C., Liu, Y., Li, S., Bourke, B., Weyman, C., Sinusas, A., Ramakrishna, G., Miller, T., Gibbons, R., Tsatkin, V., Wackers, F., Prior, J., Facta, A., Schindler, T., Oxilia-Estigarribia, M., Hernandez-Pampaloni, M., Campisi, R., Zhang, X., Bischof-Delaloye, A., Nathan, L., Schelbert, H., Gullberg, G., Huesman, R., Reutter, B., Sitek, A., Veress, A., Weiss, J., Qi, J., Yang, Y., Gordi, T., Olmsted, A., Lieu, H., Belardinelli, L., Masoli, O., Redruello, M., Ogresta, F., Collaud, C., Koslowski, P., Baliño, N., Eleta, M., Arce, P., Vidal, L., Kardash, O., Maroz-Vadalajskaya, N., Vanhove, C., Lahoutte, T., Defrise, M., Andreyev, A., Bossuyt, A., Franken, P., Maskali, F., Nloga, J., Tran, N., Marie, P., Peix, A., Garcia-Barreto, D., Ponce, F., Cabrera, L., Valiente, J., Tornes, F., Guerrero, I., Heres, F., Garcia, E., Cabale, B., Bindslev, L., Bisgaard, K., Haack-Soerensen, M., Mortensen, S., Kragh, L., Kjaer, A., Kastrup, J., Hesse, B., Aboul-Enein, F., Battah, A., Fattah, A., Atty, A., Allam, A., Riou, L., Broisat, A., Ghezzi, C., Lartizien, C., Berthonneche, C., Toufektsian, M., Maitrejean, S., Janier, M., Vanzetto, G., Fagret, D., Rouzet, F., Daou, D., Lebtahi, R., Frank, R., Leenhardt, A., Slama, M., Guludec, D., Sarda-Mantel, L., Michel, J., Martet, G., Meulemans, A., Vrigneaud, J., Coaguila, C., Benada, A., Razzouk, M., Idy-Peretti, I., Vilain, D., Stegger, L., Schäfers, K., Flögel, U., Schrader, J., Schober, O., Levkau, B., Schäfers, M., Kies, P., Wichter, T., Wielepp, J., Baller, D., Pulawski, E., Weise, R., Fricke, E., Horstkotte, D., Burchert, W., Eckert, S., Dongas, A., Nekolla, S., Martinez, M., Howe, W., Kehren, F., Ziegler, S., Vassiliadis, I., Souretis, G., Komporozos, C., Fountos, A., Papademetriou, A., Spanos, A., Antoniou, A., Strembelas, P., Moralidis, E., Arsos, G., Boundas, D., Georga, S., Karatzas, N., Karakatsanis, K., Prassopoulos, V., Parthenakis, F., Patrianakos, A., Koukouraki, S., Velidaki, A., Karkavitsas, N., Vardas, P., Perisinakis, K., Koutsikos, J., Sundaraiya, S., Sumati, S., Sambhasivam, KA, David, S., Zakavi, S., Kakhki, V., Jabari, H., Zingerman, B., Bendayan, D., Sagie, A., Solodky, A., Mats, I., Shapira, Y., Kremer, M., Zafrir, N., Rimini, M., Catalano, M., Bonzani, G., Scalzone, A., Merenda, R., Monteforte, I., Monda, V., Muto, P., Carboni, G., Miglionico, M., Tavolozza, M., Marcassa, C., Campini, R., Calza, P., Giannuzzi, P., Eleuteri, E., Scapellato, F., Temporelli, P., Pellegrino, T., Storto, G., Sorrentino, A., Silvestri, A., Filardi, P., Brevetti, G., Cuocolo, A., Cho, K., Kumita, S., Seino, K., Nakajo, H., Toba, M., Kumazaki, T., Muramatsu, T., Yamazaki, T., Seki, K., Kawanami, J., Nakajima, T., Yamada, Y., Suga, T., Matsumoto, K., Nishimura, S., Taki, J., Higuchi, T., Kawashima, A., Nakajima, K., Muramori, A., Matsunari, I., Tait, J., Vanderheyden, J., Strauss, H., Tonami, N., Adachi, I., Shimomura, H., Kintaka, T., Komori, T., Ogura, Y., Kitaura, Y., Narabayashi, I., Iida, H., Zeniya, T., Kim, K., Watabe, H., Teramoto, N., Yamamichi, Y., Alexanderson, E., Ricalde, A., Vargas, A., Meave, A., Amigo, M., Misko, J., Dziuk, M., Warczynska, A., Skrobowska, E., Vasconcelos, M., Martins, E., Faria, T., Oliveira, A., Pardal, N., Macedo, F., Pereira, J., Rocha-Gonçalves, F., Cantinho, G., Pena, H., Freire, L., Veiga, A., Gonçalves, P., Godinho, F., Chua, T., Lee, C., Keng, F., Ding, Z., Koh, T., Awamleh, P., Talavera, P., Torres, V., Balsa, M., González, O., Alberca, M., Miguel, R., Cosío, F., Lomsky, M., Richter, J., Johansson, L., El-Ali, H., Åström, K., Ljungberg, M., Edenbrandt, L., Hung, G., Lee, K., Chen, C., Yang, K., Pekindil, G., Sarikaya, A., Ege, T., Salihoglu, S., Entok, E., Cavusoglu, Y., Ak, I., Vardareli, E., Timuralp, B., Tout, D., Loong, C., Naidoo, V., Aswegen, A., Underwood, S., Thorley, P., Goris, M., ZHU, H., Clements, I., Mullan, B., O'Connor, M., Breen, J., McGregor, C., Liu, Y., Li, S., Bourke, B., Weyman, C., Sinusas, A., Ramakrishna, G., Miller, T., Gibbons, R., Tsatkin, V., Wackers, F., Prior, J., Facta, A., Schindler, T., Oxilia-Estigarribia, M., Hernandez-Pampaloni, M., Campisi, R., Zhang, X., Bischof-Delaloye, A., Nathan, L., Schelbert, H., Gullberg, G., Huesman, R., Reutter, B., Sitek, A., Veress, A., Weiss, J., Qi, J., Yang, Y., Gordi, T., Olmsted, A., Lieu, H., and Belardinelli, L.

Published
2018

25. Genetic immunization with mouse thyrotropin hormone receptor plasmid breaks self-tolerance for a murine model of autoimmune thyroid disease and Graves' orbitopathy

Author

Schlüter A, Horstmann M, Diaz-Cano, Salvador J., Plöhn S, Stähr K, Mattheis S, Oeverhaus M, S, Lang, Flögel U, Berchner-Pfannschmidt U, Eckstein A, and JP, Banga

Subjects
endocrine system, endocrine system diseases, eye diseases
Abstract

Experimental models of Graves' hyperthyroid disease accompanied by Graves' orbitopathy (GO) can be efficiently induced in susceptible inbred strains of mice by immunization by electroporation of heterologous human TSH receptor (TSHR) A-subunit plasmid. In this study, we report on the development of a bona fide murine model of autoimmune Graves' disease induced with homologous mouse TSHR A-subunit plasmid. Autoimmune thyroid disease in the self-antigen model was accompanied by GO and characterized by histopathology of hyperplastic glands with large thyroid follicular cells. Examination of orbital tissues showed significant inflammation in extraocular muscle with an accumulation of T cells and macrophages together with the substantial deposition of adipose tissue. Notably, increased levels of brown adipose tissue were present in the orbital tissue of animals undergoing experimental GO. Further analysis of inflammatory loci by ¹⁹F-magnetic resonance imaging showed inflammation to be confined to orbital muscle and optic nerve, but orbital fat showed no difference in inflammatory signs in comparison to control ß-Gal immunized animals. Pathogenic antibodies induced to mouse TSHR were specific for the self-antigen, with minimal cross-reactivity to human TSHR. Moreover, compared to other self-antigen models of murine Graves' disease induced in TSHR knock out mice, the repertoire of autoantibodies to mouse TSHR generated following the breakdown of thymic self-tolerance is different to those that arise when tolerance is not immunologically breached as in the knock out models. Overall, we show mouse TSHR A-subunit plasmid immunization by electroporation overcomes tolerance to self-antigen to provide a faithful model of Graves' disease and GO. This article is protected by copyright. All rights reserved.

Published
2017
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26. Fluorine Magnetic Resonance Imaging of Inflammation in Atherosclerotic Plaque In Vivo

Author

van Heeswijk R, Pellegrin M., Flögel U., Gonzales C., Aubert J-F., Mazzolai L., Schwitter J., and Stuber M.

Abstract

PURPOSE: To preliminarily test the hypothesis that fluorine 19 ((19)F) magnetic resonance (MR) imaging enables the noninvasive in vivo identification of plaque inflammation in a mouse model of atherosclerosis with histologic findings as the reference standard. MATERIALS AND METHODS: The animal studies were approved by the local animal ethics committee. Perfluorocarbon (PFC) emulsions were injected intravenously in a mouse model of atherosclerosis (n = 13) after which (19)F and anatomic MR imaging were performed at the level of the thoracic aorta and its branches at 9.4 T. Four of these animals were imaged repeatedly (at 2 14 days) to determine the optimal detection time. Repeated measures analysis of variance with a Tukey test was applied to determine if there was a significant change in (19)F signal to noise ratio (SNR) of the plaques and liver between the time points. Six animals were injected with a PFC emulsion that also contained a fluorophore. As a control against false positive results wild type mice (n = 3) were injected with a PFC emulsion and atherosclerotic mice were injected with a saline solution (n = 2). The animals were sacrificed after the last MR imaging examination after which high spatial resolution ex vivo MR imaging and bright field and immunofluorescent histologic examination were performed. RESULTS: (19)F MR signal was detected in vivo in plaques in the aortic arch and its branches. The SNR was found to significantly increase up to day 6 (P < .001) and the SNR of all mice at this time point was 13.4 ± 3.3. The presence of PFC and plaque in the excised vessels was then confirmed both through ex vivo (19)F MR imaging and histologic examination while no signal was detected in the control animals. Immunofluorescent histologic findings confirmed the presence of PFC in plaque macrophages. CONCLUSION: (19)F MR imaging allows the noninvasive in vivo detection of inflammation in atherosclerotic plaques in a mouse model of atherosclerosis and opens up new avenues for both the early detection of vulnerable atherosclerosis and the elucidation of inflammation mechanisms in atherosclerosis.

Published
2014
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27. PET and molecular imaging oral abstract session

Author

Levkau, B., Hermann, S. Sven, Baba, H., Stegger, L., Flögel, U., Schrader, J., Schäfers, K., Schober, O., Schäfers, M., Koutelou, M. Maria, Kollaros, N., Theodorakos, A., Manginas, A., Peristeri, I., Tsapaki, V., Kouzoumi, A., Cokkinos, D., Hosokawa, R. Ryohei, Ohba, M., Kambara, N., Tadamura, E., Kimura, T., Nohara, R., Kita, T., Panjrath, G. S. Gurusher, Patel, V., Narula, N., Narula, J., Jain, D., Dobrucki, L. W. Wawrzyniec, Lindsey, M. L., Song, J., Escobar, G. P., Su, H., Bourke, B., Mendizabal, M., Spinale, F. G., Sinusas, A. J., Herrero, P. Pilar, Kisrieva-Ware, Z., Dence, C. S., Coggan, A. R., Eisenbeis, P., Scott, S. R. W., Welch, M. J., and Gropler, R. J.

Published
2005
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31. Genetic immunization with mouse thyrotrophin hormone receptor plasmid breaks self-tolerance for a murine model of autoimmune thyroid disease and Graves' orbitopathy

Author

Schlüter, A, primary, Horstmann, M, additional, Diaz-Cano, S, additional, Plöhn, S, additional, Stähr, K, additional, Mattheis, S, additional, Oeverhaus, M, additional, Lang, S, additional, Flögel, U, additional, Berchner-Pfannschmidt, U, additional, Eckstein, A, additional, and Banga, J P, additional

Published
2017
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35. Genetic immunization with mouse thyrotrophin hormone receptor plasmid breaks self‐tolerance for a murine model of autoimmune thyroid disease and Graves' orbitopathy.

Author

Schlüter, A., Horstmann, M., Diaz‐Cano, S., Plöhn, S., Stähr, K., Mattheis, S., Oeverhaus, M., Lang, S., Flögel, U., Berchner‐Pfannschmidt, U., Eckstein, A., and Banga, J. P.

Subjects
GRAVES' disease, THYROTROPIN receptors, LABORATORY mice, AUTOIMMUNE diseases, THYROID diseases
Abstract

Summary: Experimental models of Graves' hyperthyroid disease accompanied by Graves' orbitopathy (GO) can be induced efficiently in susceptible inbred strains of mice by immunization by electroporation of heterologous human TSH receptor (TSHR) A‐subunit plasmid. In this study, we report on the development of a bona fide murine model of autoimmune Graves' disease induced with homologous mouse TSHR A‐subunit plasmid. Autoimmune thyroid disease in the self‐antigen model was accompanied by GO and characterized by histopathology of hyperplastic glands with large thyroid follicular cells. Examination of orbital tissues showed significant inflammation in extra‐ocular muscle with accumulation of T cells and macrophages together with substantial deposition of adipose tissue. Notably, increased levels of brown adipose tissue were present in the orbital tissue of animals undergoing experimental GO. Further analysis of inflammatory loci by 19F‐magnetic resonance imaging showed inflammation to be confined to orbital muscle and optic nerve, but orbital fat showed no difference in inflammatory signs in comparison to control β‐Gal‐immunized animals. Pathogenic antibodies induced to mouse TSHR were specific for the self‐antigen, with minimal cross‐reactivity to human TSHR. Moreover, compared to other self‐antigen models of murine Graves' disease induced in TSHR knock‐out mice, the repertoire of autoantibodies to mouse TSHR generated following the breakdown of thymic self‐tolerance is different to those that arise when tolerance is not breached immunologically, as in the knock‐out models. Overall, we show that mouse TSHR A‐subunit plasmid immunization by electroporation overcomes tolerance to self‐antigen to provide a faithful model of Graves' disease and GO. [ABSTRACT FROM AUTHOR]

Published
2018
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41. Monocyte imaging after myocardial infarction with 19F MRI at 3 T: a pilot study in explanted porcine hearts.

Author

Bönner, F., Merx, M. W., Klingel, K., Begovatz, P., Flögel, U., Sager, M., Temme, S., Jacoby, C., Ravesh, M. Salehi, Grapentin, C., Schubert, R., Bunke, J., Roden, M., Kelm, M., and Schrader, J.

Subjects
INFLAMMATION, ANIMAL experimentation, DIAGNOSTIC imaging, FLUORINE compounds, FLUOROCARBONS, MACROPHAGES, MAGNETIC resonance imaging, MONOCYTES, MYOCARDIAL infarction, MYOCARDIUM, PHAGOCYTOSIS, SWINE, PILOT projects, DIAGNOSIS
Abstract

Aim Inflammation is a hallmark of cardiac healing after myocardial infarction and it determines subsequent cardiovascular morbidity and mortality. The aim of the present study was to explore whether inflammation imaging with two perfluor-ocarbon (PFC)nanoemulsions and fluorine magnetic resonance imaging (19F MRI) is feasible at 3.0 T with sufficient signal-to-noise ratio (SNR) using explanted hearts, an 19F surface coil and dedicated MR sequences. Methods and results Acute myocardial infarction (AMI) was induced by balloon angioplasty (50 min) of the distal left anterior descending artery in 12 pigs. One day thereafter, PFCs were injected intravenously to label circulating monocytes. Either emulsified perfluoro-15-crown-5 ether or already clinically applied perfluorooctyl bromide (PFOB) was applied. Four days after AM I and immediately after gadolinium administration, hearts were explanted and imaged with a 3.0 T Achieva MRI scanner. 19F MRI could be acquired with an SNR of >15 using an in-plane resolution of 2 x 2 mm² within <20 min for both agents. Combined late gadolinium enhancement (LGE) and 19F MRI revealed that 19F signal was inhomogenously distributed across LGE myocardium reflecting patchy macrophage infiltration as confirmed by histology. In whole hearts, we found an apico-basal 19F gradient within LGE-positive myocardium. The 19F-positive volume was always smaller than LGE volume. Ex vivo experiments on isolated monocytes revealed that pig and human cells phagocytize PFCs even more avidly than mouse monocytes. Conclusion This pilot study demonstrates that 19F MRI at 3.0 T with clinically applicable PFOB is feasible, thus highlighting the potential of 19F MRI to monitor the inflammatory response after AMI. [ABSTRACT FROM AUTHOR]

Published
2015
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44. Unmasking the Janus face of myoglobin in health and disease.

Author

Hendgen-Cotta, U. B., Flögel, U., Kelm, M., and Rassaf, T.

Subjects
*MYOGLOBIN, *NITRIC oxide, *HEART physiology, *RHABDOMYOLYSIS, *TUMOR growth, *NITRITES
Abstract

For more than 100 years, myoglobin has been among the most extensively studied proteins. Since the first comprehensive review on myoglobin function as a dioxygen store by Millikan in 1939 and the discovery of its structure 50 years ago, multiple studies have extended our understanding of its occurrence, properties and functions. Beyond the two major roles, the storage and the facilitation of dioxygen diffusion, recent physiological studies have revealed that myoglobin acts as a potent scavenger of nitric oxide (NO*) representing a control system that preserves mitochondrial respiration. In addition, myoglobin may also protect the heart against reactive oxygen species (ROS), and, under hypoxic conditions, deoxygenated myoglobin is able to reduce Aitrite to NO* leading to a downregulation of the cardiac energy status and to a decreased heart injury after reoxygenation. Thus, by controlling the NO* bioavailability via scavenging or formation, myoglobin serves as part of a sensitive dioxygen sensory system. In this review, the physiological relevance of these recent findings are delineated for pathological states where NO* and ROS bioavailability are known to be critical determinants for the outcome of the disease, e.g. ischemia/reperfusion injury. Detrimental and beneficial effects of the presence of myoglobin are discussed for various states of tissue oxygen tension within the heart and skeletal muscle. Furthermore, the impact of myoglobin on parasite infection, rhabdomyolysis, hindlimb and liver ischemia, angiogenesis and tumor growth are considered. [ABSTRACT FROM AUTHOR]

Published
2010
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45. Targeting murine heart and brain: visualisation conditions for multi-pinhole SPECT with 99mTc- and 123I-labelled probes.

Author

Pissarek, M., Meyer-Kirchrath, J., Hohlfeld, T., Vollmar, S., Oros-Peusquens, A. M., Flögel, U., Jacoby, C., Krügel, U., and Schramm, N.

Subjects
SINGLE-photon emission computed tomography, IMAGING systems, COLLIMATORS, CARDIAC imaging, BRAIN imaging, LABORATORY mice
Abstract

The study serves to optimise conditions for multi-pinhole SPECT small animal imaging of 123I- and 99mTc-labelled radiopharmaceuticals with different distributions in murine heart and brain and to investigate detection and dose range thresholds for verification of differences in tracer uptake. A Triad 88/Trionix system with three 6-pinhole collimators was used for investigation of dose requirements for imaging of the dopamine D2 receptor ligand [123I]IBZM and the cerebral perfusion tracer [99mTc]HMPAO (1.2–0.4 MBq/g body weight) in healthy mice. The fatty acid [123I]IPPA (0.94 ± 0.05 MBq/g body weight) and the perfusion tracer [99mTc]sestamibi (3.8 ± 0.45 MBq/g body weight) were applied to cardiomyopathic mice overexpressing the prostaglandin EP3 receptor. In vivo imaging and in vitro data revealed 45 kBq total cerebral uptake and 201 kBq cardiac uptake as thresholds for visualisation of striatal [123I]IBZM and of cardiac [99mTc]sestamibi using 100 and 150 s acquisition time, respectively. Alterations of maximal cerebral uptake of [123I]IBZM by >20% (116 kBq) were verified with the prerequisite of 50% striatal of total uptake. The labelling with [99mTc]sestamibi revealed a 30% lower uptake in cardiomyopathic hearts compared to wild types. [123I]IPPA uptake could be visualised at activity doses of 0.8 MBq/g body weight. Multi-pinhole SPECT enables detection of alterations of the cerebral uptake of 123I- and 99mTc-labelled tracers in an appropriate dose range in murine models targeting physiological processes in brain and heart. The thresholds of detection for differences in the tracer uptake determined under the conditions of our experiments well reflect distinctions in molar activity and uptake characteristics of the tracers. [ABSTRACT FROM AUTHOR]

Published
2009
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