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73 results on '"Polimeno, M."'

1. Variation in the regime : the struggle for internal political legitimacy in Egypt, 2013-2019

Author

Polimeno, M. G., Githens-Mazer, Jonathan, and Gao, Eleanor

Subjects
Authoritarianism, Political Legitimacy, Political Economy of Development, Islamist Politics, Egypt, Political Economy
Abstract

This study centres on the July 2013 coup in Egypt, framed by the Supreme Council of Armed Forces as a popularly-supported counter-revolution which overthrew the government of the Freedom and Justice Party, accused of having attempted to impose religious authoritarianism. The coup has been approached in this work both as a critical juncture and a moment of structural departure which created a legitimacy crisis. This thesis aims to document the ensuing struggle for internal political legitimacy in Egypt from 2013 until 2019. The work has been driven by the need to fill a two-fold gap, both in the existing academic literature on non-democratic regimes, and in the transformation of Egyptian politics. It therefore proposes a re-engagement with theories of authoritarianism and studies on Egyptian politics, in order to understand how the collapse of pre-existing political-institutional structures and the consequent need of establishing bases of legitimacy, may also ultimately determine a variation in the regime in a country undergoing social, structural and political transformation, such as Egypt after 2013. This study does not take a standpoint as to the political legitimacy of the post-2013 authorities, but rather intends to achieve an independent and scholarly historical-political understanding of the process of legitimation, approached as a transformative activity in a fixed and concluded timeframe. The breakdown of Egypt's former state structures as result of the 2011 uprising, and then the 2013 coup, has indirectly impacted on the mechanisms of legitimation and relations between domestic actors (e.g. Salafis, the Muslim Brotherhood, and the army). This research posits that the absence of scholarly contributions investigating transformations in leadership and the struggle for legitimation, constitutes a gap in the growing body of academic literature on authoritarianisms and sub-transformations of states and institutions in the Middle East. Therefore, this thesis seeks to capture Abdel Fattah al-Sisi's contested struggle for internal legitimacy against a background of political and economic change. The theoretical framework is situated in a modified Weberian conception of political legitimacy in combination of the theory of omnibalancing (David, 1991), an adaptation of Waltz's (1979) balance of power theory on internal realignments, plus Easton's (1975) and Gerschewski's (2013) theories explaining the dynamics of specific and internal support as basis for political legitimacy. This provides a proper intellectual approach for understanding the internal legitimation of political authority, and how this can determine internal variation within a political system. The combination of omnibalancing with theories of specific and internal support enables an understanding of domestic political behaviour, and why a political authority may decide to realign with and gain the specific support of what it perceives as a second-class internal threat, to counter what is perceived as the main domestic threat towards its authority and legitimacy. Methodologically, the work is based on a themes-based discourse analysis, combined with a framing analysis of primary sources. The methodology of this work lies in capturing and contextualising, from a political and state-structural perspective, the frames emerging from the analysis: the rule of law, charisma, internal religious alliances, and performance, identified as the four phases of legitimation in the 2013-2019 timeframe. The work additionally combines quantitative secondary sources and (to bypass the limitations posed by written texts), selected integrative interviews. Through this, new empirical data has been provided. The findings will prove a valuable addition to the broader existing literature on theories of political legitimacy and the functioning of upgraded regimes with specific focus on personalist regimes, which remain an understudied sub-category in the field of non-democratic regime types. In addition, findings from this study will prove valuable to scholars and international political state and non-state actors concerned with the state of democracy and stability in the Mediterranean region. The findings emerging from this work thus go beyond the case study of Egyptian politics, and may be introduced into new venues of research more oriented towards questioning democratisation. In addition, the study's findings may serve as stepping-stones for future research on the functioning of regimes, and military and diplomatic cooperation, as well as having implications for the study of elites and democratisation in the Mediterranean area.

Published
2021

3. Poster display II clinical general

Author

Gurgenyan, S. V. Svetlana, Vatinyan, S. K. H., Nikogosyan, K. G., Edilyan, L. B., Chobanyan, B. G., Lacourcière, Y., Marcel Dumont, M., Lefebvre, J., Poirier, L., Côté, C., Peix, A. Amalia, Alonso, O., Chae, I. H., Chung, J. K., Gutierrez, C., Kropp, J., Onsel, C., Silvasi, I., Llerena, L., Padhy, A. K., Garcia-Barreto, D., Trapaga, A., Asen, L., Infante, O., Ponce, F., Cabrera, L. O., Valiente, J., Tornes, F., Guerrero, I., Zayas, R., ones, M. A. Quin, Castro, J., Fayad, Y., Carrillo, R., Paz, A. De, Mehlsen, J. Jesper, Hædersdal, C., Daou, D. Doumit, Benada, A., Lebtahi, R., Idy-Peretti, I., Guludec, D. Le, Coaguila, C., Vilain, D., Leenhardt, A., Heinicke, N. Norbert, Benesch, B., Kaiser, T., Seegmüller, M., Schönberger, J., Eilles, C., Riegger, G. A. J., Holmer, S., Luchner, A., Kouris, N. T. Nikos, Kontogianni, D. D., Goranitou, G. S., Sifaki, M. D., Kalkandi, E. M., Grassos, H. E., Papoulia, E., Babalis, D. K., Moralidis, E. Efstratios, Spyridonidis, T., Arsos, G., Karakatsanis, K., Karatzas, N., Parameswaran, R. V. Ramanathapuram, Sundaram, P. S. Palaniswamy Shanmuga, Padma, S., Haridas, K. K., Zachariah, M., Kumar, S., Feola, M. Mauro, Leonardi, G., Peano, S., Bianchi, A., Dutto, P., Guala, E., Biggi, A., Uslenghi, E., Filardi, P. Pasquale Perrone, Pace, L., Dellegrottaglie, S., Corrado, L., Cafiero, M., Camerino, R., Maglione, A., Polimeno, M., Zarrilli, A., Chiariello, M., Giorgetti, A. Assuero, Gimelli, A., Marini, C., Schluter, M., Kusch, A., D’Aragona, I., Marzullo, P., Gimelli, A. Alessia, Stanislao, M., Zanco, P., Inglese, E., Bertelli, P., Valle, G., Tassone, F., Pepino, R., Francini, A., Garrone, O., Occelli, M., Merlano, M., Florimonte, L. Luigia, Pagani, L., Piatti, L., Butti, I., Maffioli, L. S., Casorelli, E., Dottore, F. Del, Gentili, G., Agostini, M., Pieri, P. L. Pierluigi, Milan, E., Giubbini, R. Raffaele, Mazzanti, M. Marco, Serenelli, M., Perna, G. P., Ferro, A., Duilio, C., Santomauro, M., Salvatore, M., Cuocolo, A. Alberto, Bertagna, F., Bosio, G., Terzi, A., Paghera, B., Kaneta, T. Tomohiro, Otani, H., Hakamatsuka, T., Fukuda, H., Nakazato, R. Ryo, Moroi, M., Kunimasa, T., Furuhashi, T., Sugi, K., Yasuhi, W. Watanabe, Akihiro, S., Yukawa, A., Ryu, K., Kimio, T., Yasuhiko, T., Nariaki, E., Yasunori, W., Akashi, Y. J. Yoshihiro, Musha, H., Kida, K., Itoh, K., Inoue, K., Kawasaki, K., Hashimoto, N., Nakazawa, K., Miyake, F., Fukuzawa, S. Shigeru, Ozawa, S., Inagaki, M., Sugioka, J., Okino, S., Matsuo, S. Shinro, Matsumoto, T., Nakae, I., Masuda, D., Horie, M., Mori, Y. Yoshitomo, Takahashi, K., Masai, M., Kawasaki, D., Kanemori, T., Okuda, S., Tanabe, K., Ohyanagi, M., Takahashi, K. Keiko, Masai, M., Mori, Y., Tanabe, K., OKuda, S., Toyama, T. Takuji, Hoshizaki, H., Seki, R., Isobe, N., Kawaguchi, R., Oshima, S., Taniguchi, K., Nakagawa, K. Keiichi, Sekine, T., Yamazaki, M., Komuro, I., Kim, K. M. Kyeong Min, Teramoto, N., Jino, H., Ohta, Y., Watabe, H., Hayashi, T., Iida, H., Nishimura, T. Tohru, Nagae, A., Morishima, K., Shigeyama, T., Shimoyama, K., Yoshino, H., Kawai, Y. Yuko, Jeong, S. Y., Lee, J. Jae-Tae, Seo, J. H., Bae, J. H., Ahn, B. C., Chae, S. C., Lee, K. B., Cho, I. Ihnho, Chun, K., Won, K., Lee, H., Hong, G., Park, J., Shin, D., Kim, Y., Shim, B., Pavlovic, J. Maksimovic, Peovska, I. Irena, Vavlukis, M., Gorceva, D. Pop, Majstorov, V., Alexanderson, E. Erick, Meave, A., Ricalde, A., Teresinska, A. Anna, Sliwinski, M., Konieczna, S., Szymanska, M., Hendzel, P., Juraszynski, Z., Debski, A., Szumilak, B., Kostkiewicz, M. Magdalena, Wilkolek, P., Pasowicz, M., Klimeczek, P., Pieniazek, P., Przewlocki, T., Pieculewicz, M., Tracz, W., Szot, W., Trebacz, J., Zmudka, K., Podolec, P., Dziuk, M. Miroslaw, Kazmierczak, A., Kot, E., Pietrzykowski, J., Cholewa, M., Coutinho, M. C. Maria Azevedo, Correia, M. J., Cantinho, G., Conceição, I., Bernardes, A., Silva, A., Gaspar, F., Cunha, J. A. Correia da, Lourenço, C. Cândida, Roque, C., Ferrer-Antunes, A., Ferreira, M., Providência, L. A., Lima, J., Abreu, A. Ana, Castillejos, L., Henriksson, I., Oliveira, L., Rosário, L., Geão, A., Pereira, E., Colarinha, P., Romero-Farina, G., Candell-Riera, J., Aguadé-Bruix, S. Santiago, Leon, G. De, Caresia, A. P., Mila-Lopez, M., Garcia-Alonso, C., Pifarre-Montaner, P., Negre-Buso, M., Castell-Conesa, J., Mestre-Fusco, A., Porta-Biosca, F., Aguadé-Bruix, S. Santiago, Muxi, A. Africa, Paredes, P., Ortin, J., Duch, J., Diaz-Infante, E., Fuertes, S., Orus, J., Mont, L. L., Pons, F., Pollack, C., Hellermann, J. P., Namdar, M., Siegrist, P. T. Patrick, Koepfli, P., Bartenstein, N., Schurr, U., Jenni, R., Kaufmann, P. A., Hassad, R. Rim, Hamami, H., Sellem, A., Brahim, H. Ben, Caglar, M. Meltem, Mahmoudian, B., Aytemir, K., Kahraman, S., Arýcý, M., Kabakcý, G., Karabulut, E., Akincioglu, C. Cigdem, Berman, D. S., Nishina, H., Hayes, S. W., Kavanagh, P. B., Friedman, J. D., Slomka, P. J., Germano, G., Entok, E. Emre, Cavusoglu, Y., Vardareli, E., Timuralp, B., Cheetham, A., Naylor, V., Ghiotto, F., McGhie, J., Al-Housni, M. B., Kelion, A. D. Andrew, Hutchings, F., Hinton-Taylor, S., Birkbeck, P., Thatikonda, S., Feldkamp, M., Rosamond, T. Thomas, Raza, M., Panjrath, G. S. Gurusher, Haider, A., Jain, D., Yang, A., Schumacher, R., Reynolds, J., Clark, E., Speiser, D., Schindel, M., Hackney, T., Vacek, J., Jindal, V. Vikas, Dim, U. Uzodinma, Hamburg, L. M., Mouradian, V., Nichols, K. J., Akinboboye, O. O., Snyder, K., Polepalle, D., DePuey, G. Gordon, Khattak, H., Friedman, M., Thompson, L., Thompson, R. C. Randall, McGhie, A. I., Moser, K., O’Keefe, J. H., Fritsch, N., Bateman, T. M., Mut, F., Vidal, I., Rener, A., Nuñez, M., Alvarez, B., and Beretta, M. Mario

Published
2005
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4. Posters display III clinical outcome and PET

Author

Baliño, N. Nestor Perez, Masoli, O., Traverso, S., Grynberg, L., Rappallo, C., Redruello, M., Rosa, D., Cragnolino, D., Meretta, A., Vidal, L., Graf, S., Khorsand, A. Aliasghar, Gyongyosi, M., Karanikas, G., Eidherr, H., Kletter, K., Porenta, G., Glogar, D., Sochor, H., Beheshti, M., Poetzi, C., Wadsak, W., Porenta, G., Maurer, G., Wolfram, J., Winter, O. Olivier De, Velghe, A., Veire, N. Van de, Bondt, P. De, Buyzere, M. De, Wiele, C. Van de, Backer, G. De, Gillebert, T. C., Dierckx, R. A., Sutter, J. De, Bernard, D., Langlois, M., Duarte, P. S. Paulo, Mastrocolla, L. E., Sampaio, C. R. E., Rossi, J. M., Smanio, P. E., Lima, E. V., Oliveira, C. A. R., Pereira, J. C. R., Smanio, P. Paola, Beraldo, P., Rodrigues, F., Thom, A., Yoshinaga, K. Keiichiro, Ukkonen, H., Burwash, I., DeKemp, R., Dafoe, W., Davies, R., Haddad, H., Ruddy, T., DaSilva, J., Beanlands, R., Chow, B., Williams, K., Garrard, L., Szeto, A., Aung, M., Sondergaard, H. Hanne, Bottcher, M., Madsen, M. M., Schmitz, O., Nielsen, T. T., Botker, H. E., Høilund-Carlsen, P. F. Poul F., Johansen, A., Christensen, H. W., Vach, W., Møldrup, M., Haghfelt, T., Johansen, A. Allan, Høilund-Carlsen, P. F., Christensen, H. W., Møldrup, M., Kristensen, J. Jens Hedega, Maeng, M., Mortensen, U. M., Berg, J. S., Rehling, M., Nielsen, T. T., Elsaban, K. Khaled, El-Kady, T., El-Gabaly, M., Yehia, A., El-Sayed, M., Naum, A. Alexandru, Laaksonen, M. S., Tuunanen, H., Oikonen, V., Kemppainen, J., Järvisalo, M. J., Nuutila, P., Knuuti, J., Vanzetto, G. Gerald, Jacon, P., Fagret, D., Machecourt, J., Lindner, O. Oliver, Vogt, J., Kammeier, A., Fricke, E., Wielepp, P., Baller, D., Lamp, B., Holzinger, J., Horstkotte, D., Burchert, W., Nekolla, S. G. Stephan, Souvatzoglou, M., Hausleiter, J., Henke, N., Kruschke, K., Bengel, F., Schwaiger, M., Sundaram, P. S. Palaniswamy Shanmuga, Padma, S., Haridas, K. K., Kumar, S., Zachariah, M., Livschitz, S. Shay, Zornitzki, T., Vered, S., Oettinger, M., Levy, R., Caspi, A., Faraggi, D., Knobler, H., Mats, I., Solodky, A., Ben-Gal, T., Battler, A., Zafrir, N. Nili, Varani, E. Elisabetta, Balducelli, M., Severi, S., Patroncini, A. L., Vecchi, G., Gatti, C., Corbelli, C., Casanova, R., Maresta, A., Cittanti, C. Corrado, Valgimigli, M., Giganti, M., Malagutti, P., Percoco, G., Bagatin, E., Panareo, S., Avigni, N., Ferrari, R., Feggi, L., Filardi, P. Pasquale Perrone, Cuocolo, A., Storto, G., Brevetti, G., Dellegrottaglie, S., Corrado, L., Cafiero, M., Polimeno, M., Zarrilli, A., Chiariello, M., Marcassa, C. Claudio, Campini, R., Calza, P., Giannuzzi, P., Galassi, A. R. Alfredo, Grasso, C., Azzarelli, S., Leotta, E., Moshiri, S., Tamburino, C., Acampa, W., Ferro, A., Petretta, M., Salvatore, M., Cuocolo, A. Alberto, Pieri, P. L. Pierluigi, Berta, R., Moscatelli, G., Buccoliero, F., Inglese, E., Marcassa, C. Claudio, Medolago, G., Imperiale, A., Rimini, M. L. De, Bertagna, F., Sullo, P., Lupo, M., Cappagli, M., Fukuda, H. Hiroshi, Kunimasa, T., Furuhashi, T., Moroi, M., Yasuhi, W. Watanabe, Akihiro, S., Akio, Y., Ryou, K., Kimio, T., Yasunori, W., Yasuhiko, T., Nariaki, E., Watabe, H. Hiroshi, Teramoto, N., Ohta, Y., Kou, Y., Hayashi, T., Iida, H., Bom, H. S. Hee-Seung, Song, H. C., Min, J. J., Heo, Y. J., Seo, J. H., Lee, J. Jae-Tae, Bae, J. H., Jeong, S. Y., Ahn, B. C., Chae, S. C., Lee, K. B., Popiel, M. Malgorzata, Grajek, S., Czepczynski, R., Breborowicz, P., Lesiak, M., Czyz, A., Sawinski, K., Komarnicki, M., Cieslinski, A., Sowinski, J., Ferreira, A. António, Ventosa, A., Gil, V., Calqueiro, J., Lima, S., Aguiar, C., Couto, R., Raposo, L., Seabra-Gomes, R., Vasconcelos, M. Mariana, Martins, E., Faria, T., Oliveira, A., Garcia, M., Pereira, J., Rocha-Gonçalves, F., Lourenço, C. Cândida, Roque, C., Ferrer-Antunes, A., Ferreira, M., Providência, L. A., Lima, J., Medrea, C. Claudia, Bogdan, R., Lazar, A., Mot, S., Capilneanu, R., Kozulin, V. Vickenty, Berkovich, O., Ivashchenko, T., Larionova, V., Esipovich, I., Gordeev, M., Panov, A., Shlyakhto, E., Burova, N., Baranov, D., Timoshin, V., Chuprova, S., Shkolnikova, M., Zaklyazminskaya, E., Poliakov, A., Sazonova, S. Svetlana, Romero-Farina, G., Arenillas, J. F., Candell-Riera, J., Aguadè-Bruix, S. Santiago, Leon, G. De, Molina, C. A., Chacon, P., Montaner, J., Rovira, A., Alvarez-Sabin, J., Namdar, M. Mehdi, Siegrist, P. T., Grathwohl, R., Delaloye, R., Koepfli, P., Wyss, C. A., Kaufmann, P. A., Bartenstein, N., Hellermann, J., Siegrist, P. T. Patrick, Namdar, M., Pollack, C., Schurr, U., Kaufmann, P. A., Zellweger, M. J. Michael, Burger, P. C., Mueller-Brand, J., Pfisterer, M. E., Gordon, L. Leonie, Epps, A., Chiarameda, S., Navare, S. Sachin, Ahlberg, A., Cyr, G., Katten, D., Ausef, A., Heller, G., Darrow, B. Bruce, Thomas, G. S. Gregory, Ip, T. K., Thompson, R. C., Kramer, D. B., Rice, D. L., Thomas, J. J., Miyamoto, M. I., Druz, R. S. Regina, Nichols, K. J., Akinboboye, O. O., Reichek, N., Podrasky, E. Ernest, Tuttle, R. T. Robert, Shaw, L. S. Linda, Hanson, M. W. H. Michael, Borges-Neto, S. Salvador, Lundbye, J. Justin, Werden, S., Kazi, F., Whalen, A., Noble, G. L., O’Sullivan, D., Boden, W. E., Heller, G. V., Ausef, A. Amir, Ahlberg, A. W., Danias, P. G., Papaioannou, G. I., Leka, I. A., Boden, W. E., Heller, G. V., Beretta, M. Mario, Viňas, S., Gonzalez, A., Vidal, I., and Rener, A.

Published
2005
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5. Poster display II clinical general

Author

Gurgenyan, S., Vatinyan, S., Nikogosyan, K., Edilyan, L., Chobanyan, B., Lacourcière, Y., Marcel Dumont, M., Lefebvre, J., Poirier, L., Côté, C., Peix, A., Alonso, O., Chae, I., Chung, J., Gutierrez, C., Kropp, J., Onsel, C., Silvasi, I., Llerena, L., Padhy, A., Garcia-Barreto, D., Trapaga, A., Asen, L., Infante, O., Ponce, F., Cabrera, L., Valiente, J., Tornes, F., Guerrero, I., Zayas, R., ones, M., Castro, J., Fayad, Y., Carrillo, R., Paz, A., Mehlsen, J., Hædersdal, C., Daou, D., Benada, A., Lebtahi, R., Idy-Peretti, I., Guludec, D., Coaguila, C., Vilain, D., Leenhardt, A., Heinicke, N., Benesch, B., Kaiser, T., Seegmüller, M., Schönberger, J., Eilles, C., Riegger, G., Holmer, S., Luchner, A., Kouris, N., Kontogianni, D., Goranitou, G., Sifaki, M., Kalkandi, E., Grassos, H., Papoulia, E., Babalis, D., Moralidis, E., Spyridonidis, T., Arsos, G., Karakatsanis, K., Karatzas, N., Parameswaran, R., Sundaram, P., Padma, S., Haridas, K., Zachariah, M., Kumar, S., Feola, M., Leonardi, G., Peano, S., Bianchi, A., Dutto, P., Guala, E., Biggi, A., Uslenghi, E., Filardi, P., Pace, L., Dellegrottaglie, S., Corrado, L., Cafiero, M., Camerino, R., Maglione, A., Polimeno, M., Zarrilli, A., Chiariello, M., Giorgetti, A., Gimelli, A., Marini, C., Schluter, M., Kusch, A., D'Aragona, I., Marzullo, P., Stanislao, M., Zanco, P., Inglese, E., Bertelli, P., Valle, G., Tassone, F., Pepino, R., Francini, A., Garrone, O., Occelli, M., Merlano, M., Florimonte, L., Pagani, L., Piatti, L., Butti, I., Maffioli, L., Casorelli, E., Dottore, F., Gentili, G., Agostini, M., Pieri, P., Milan, E., Giubbini, R., Mazzanti, M., Serenelli, M., Perna, G., Ferro, A., Duilio, C., Santomauro, M., Salvatore, M., Cuocolo, A., Bertagna, F., Bosio, G., Terzi, A., Paghera, B., Kaneta, T., Otani, H., Hakamatsuka, T., Fukuda, H., Nakazato, R., Moroi, M., Kunimasa, T., Furuhashi, T., Sugi, K., Yasuhi, W., Akihiro, S., Yukawa, A., Ryu, K., Kimio, T., Yasuhiko, T., Nariaki, E., Yasunori, W., Akashi, Y., Musha, H., Kida, K., Itoh, K., Inoue, K., Kawasaki, K., Hashimoto, N., Nakazawa, K., Miyake, F., Fukuzawa, S., Ozawa, S., Inagaki, M., Sugioka, J., Okino, S., Matsuo, S., Matsumoto, T., Nakae, I., Masuda, D., Horie, M., Mori, Y., Takahashi, K., Masai, M., Kawasaki, D., Kanemori, T., Okuda, S., Tanabe, K., Ohyanagi, M., OKuda, S., Toyama, T., Hoshizaki, H., Seki, R., Isobe, N., Kawaguchi, R., Oshima, S., Taniguchi, K., Nakagawa, K., Sekine, T., Yamazaki, M., Komuro, I., Kim, K., Teramoto, N., Jino, H., Ohta, Y., Watabe, H., Hayashi, T., Iida, H., Nishimura, T., Nagae, A., Morishima, K., Shigeyama, T., Shimoyama, K., Yoshino, H., Kawai, Y., Jeong, S., Lee, J., Seo, J., Bae, J., Ahn, B., Chae, S., Lee, K., Cho, I., Chun, K., Won, K., Lee, H., Hong, G., Park, J., Shin, D., Kim, Y., Shim, B., Pavlovic, J., Peovska, I., Vavlukis, M., Gorceva, D., Majstorov, V., Alexanderson, E., Meave, A., Ricalde, A., Teresinska, A., Sliwinski, M., Konieczna, S., Szymanska, M., Hendzel, P., Juraszynski, Z., Debski, A., Szumilak, B., Kostkiewicz, M., Wilkolek, P., Pasowicz, M., Klimeczek, P., Pieniazek, P., Przewlocki, T., Pieculewicz, M., Tracz, W., Szot, W., Trebacz, J., Zmudka, K., Podolec, P., Dziuk, M., Kazmierczak, A., Kot, E., Pietrzykowski, J., Cholewa, M., Coutinho, M., Correia, M., Cantinho, G., Conceição, I., Bernardes, A., Silva, A., Gaspar, F., Cunha, J., Lourenço, C., Roque, C., Ferrer-Antunes, A., Ferreira, M., Providência, L., Lima, J., Abreu, A., Castillejos, L., Henriksson, I., Oliveira, L., Rosário, L., Geão, A., Pereira, E., Colarinha, P., Romero-Farina, G., Candell-Riera, J., Aguadé-Bruix, S., Leon, G., Caresia, A., Mila-Lopez, M., Garcia-Alonso, C., Pifarre-Montaner, P., Negre-Buso, M., Castell-Conesa, J., Mestre-Fusco, A., Porta-Biosca, F., Muxi, A., Paredes, P., Ortin, J., Duch, J., Diaz-Infante, E., Fuertes, S., Orus, J., Mont, L., Pons, F., Pollack, C., Hellermann, J., Namdar, M., Siegrist, P., Koepfli, P., Bartenstein, N., Schurr, U., Jenni, R., Kaufmann, P., Hassad, R., Hamami, H., Sellem, A., Brahim, H., Caglar, M., Mahmoudian, B., Aytemir, K., Kahraman, S., Arýcý, M., Kabakcý, G., Karabulut, E., Akincioglu, C., Berman, D., Nishina, H., Hayes, S., Kavanagh, P., Friedman, J., Slomka, P., Germano, G., Entok, E., Cavusoglu, Y., Vardareli, E., Timuralp, B., Cheetham, A., Naylor, V., Ghiotto, F., McGhie, J., Al-Housni, M., Kelion, A., Hutchings, F., Hinton-Taylor, S., Birkbeck, P., Thatikonda, S., Feldkamp, M., Rosamond, T., Raza, M., Panjrath, G., Haider, A., Jain, D., Yang, A., Schumacher, R., Reynolds, J., Clark, E., Speiser, D., Schindel, M., Hackney, T., Vacek, J., Jindal, V., Dim, U., Hamburg, L., Mouradian, V., Nichols, K., Akinboboye, O., Snyder, K., Polepalle, D., DePuey, G., Khattak, H., Friedman, M., Thompson, L., Thompson, R., McGhie, A., Moser, K., O'Keefe, J., Fritsch, N., Bateman, T., Mut, F., Vidal, I., Rener, A., Nuñez, M., Alvarez, B., and Beretta, M.

Published
2018

6. Posters display III clinical outcome and PET

Author

Baliño, N., Masoli, O., Traverso, S., Grynberg, L., Rappallo, C., Redruello, M., Rosa, D., Cragnolino, D., Meretta, A., Vidal, L., Graf, S., Khorsand, A., Gyongyosi, M., Karanikas, G., Eidherr, H., Kletter, K., Porenta, G., Glogar, D., Sochor, H., Beheshti, M., Poetzi, C., Wadsak, W., Maurer, G., Wolfram, J., Winter, O., Velghe, A., Veire, N., Bondt, P., Buyzere, M., Wiele, C., Backer, G., Gillebert, T., Dierckx, R., Sutter, J., Bernard, D., Langlois, M., Duarte, P., Mastrocolla, L., Sampaio, C., Rossi, J., Smanio, P., Lima, E., Oliveira, C., Pereira, J., Beraldo, P., Rodrigues, F., Thom, A., Yoshinaga, K., Ukkonen, H., Burwash, I., DeKemp, R., Dafoe, W., Davies, R., Haddad, H., Ruddy, T., DaSilva, J., Beanlands, R., Chow, B., Williams, K., Garrard, L., Szeto, A., Aung, M., Sondergaard, H., Bottcher, M., Madsen, M., Schmitz, O., Nielsen, T., Botker, H., Høilund-Carlsen, P., Johansen, A., Christensen, H., Vach, W., Møldrup, M., Haghfelt, T., Kristensen, J., Maeng, M., Mortensen, U., Berg, J., Rehling, M., Elsaban, K., El-Kady, T., El-Gabaly, M., Yehia, A., El-Sayed, M., Naum, A., Laaksonen, M., Tuunanen, H., Oikonen, V., Kemppainen, J., Järvisalo, M., Nuutila, P., Knuuti, J., Vanzetto, G., Jacon, P., Fagret, D., Machecourt, J., Lindner, O., Vogt, J., Kammeier, A., Fricke, E., Wielepp, P., Baller, D., Lamp, B., Holzinger, J., Horstkotte, D., Burchert, W., Nekolla, S., Souvatzoglou, M., Hausleiter, J., Henke, N., Kruschke, K., Bengel, F., Schwaiger, M., Sundaram, P., Padma, S., Haridas, K., Kumar, S., Zachariah, M., Livschitz, S., Zornitzki, T., Vered, S., Oettinger, M., Levy, R., Caspi, A., Faraggi, D., Knobler, H., Mats, I., Solodky, A., Ben-Gal, T., Battler, A., Zafrir, N., Varani, E., Balducelli, M., Severi, S., Patroncini, A., Vecchi, G., Gatti, C., Corbelli, C., Casanova, R., Maresta, A., Cittanti, C., Valgimigli, M., Giganti, M., Malagutti, P., Percoco, G., Bagatin, E., Panareo, S., Avigni, N., Ferrari, R., Feggi, L., Filardi, P., Cuocolo, A., Storto, G., Brevetti, G., Dellegrottaglie, S., Corrado, L., Cafiero, M., Polimeno, M., Zarrilli, A., Chiariello, M., Marcassa, C., Campini, R., Calza, P., Giannuzzi, P., Galassi, A., Grasso, C., Azzarelli, S., Leotta, E., Moshiri, S., Tamburino, C., Acampa, W., Ferro, A., Petretta, M., Salvatore, M., Pieri, P., Berta, R., Moscatelli, G., Buccoliero, F., Inglese, E., Medolago, G., Imperiale, A., Rimini, M., Bertagna, F., Sullo, P., Lupo, M., Cappagli, M., Fukuda, H., Kunimasa, T., Furuhashi, T., Moroi, M., Yasuhi, W., Akihiro, S., Akio, Y., Ryou, K., Kimio, T., Yasunori, W., Yasuhiko, T., Nariaki, E., Watabe, H., Teramoto, N., Ohta, Y., Kou, Y., Hayashi, T., Iida, H., Bom, H., Song, H., Min, J., Heo, Y., Seo, J., Lee, J., Bae, J., Jeong, S., Ahn, B., Chae, S., Lee, K., Popiel, M., Grajek, S., Czepczynski, R., Breborowicz, P., Lesiak, M., Czyz, A., Sawinski, K., Komarnicki, M., Cieslinski, A., Sowinski, J., Ferreira, A., Ventosa, A., Gil, V., Calqueiro, J., Lima, S., Aguiar, C., Couto, R., Raposo, L., Seabra-Gomes, R., Vasconcelos, M., Martins, E., Faria, T., Oliveira, A., Garcia, M., Rocha-Gonçalves, F., Lourenço, C., Roque, C., Ferrer-Antunes, A., Ferreira, M., Providência, L., Lima, J., Medrea, C., Bogdan, R., Lazar, A., Mot, S., Capilneanu, R., Kozulin, V., Berkovich, O., Ivashchenko, T., Larionova, V., Esipovich, I., Gordeev, M., Panov, A., Shlyakhto, E., Burova, N., Baranov, D., Timoshin, V., Chuprova, S., Shkolnikova, M., Zaklyazminskaya, E., Poliakov, A., Sazonova, S., Romero-Farina, G., Arenillas, J., Candell-Riera, J., Aguadè-Bruix, S., Leon, G., Molina, C., Chacon, P., Montaner, J., Rovira, A., Alvarez-Sabin, J., Namdar, M., Siegrist, P., Grathwohl, R., Delaloye, R., Koepfli, P., Wyss, C., Kaufmann, P., Bartenstein, N., Hellermann, J., Pollack, C., Schurr, U., Zellweger, M., Burger, P., Mueller-Brand, J., Pfisterer, M., Gordon, L., Epps, A., Chiarameda, S., Navare, S., Ahlberg, A., Cyr, G., Katten, D., Ausef, A., Heller, G., Darrow, B., Thomas, G., Ip, T., Thompson, R., Kramer, D., Rice, D., Thomas, J., Miyamoto, M., Druz, R., Nichols, K., Akinboboye, O., Reichek, N., Podrasky, E., Tuttle, R., Shaw, L., Hanson, M., Borges-Neto, S., Lundbye, J., Werden, S., Kazi, F., Whalen, A., Noble, G., O'Sullivan, D., Boden, W., Danias, P., Papaioannou, G., Leka, I., Beretta, M., Viňas, S., Gonzalez, A., Vidal, I., and Rener, A.

Published
2018

7. Non-imaging nuclear monitoring of left ventricular function: twenty-five years of technical development and clinical experience

Author

Dellegrottaglie, S., Filardi, P. P., Leonardo Pace, Ponticelli, M. P., Corrado, L., Cafiero, M., Polimeno, M., Camerino, R., Chiariello, M., Dellegrottaglie, S., Filardi, P. P., Pace, L., Ponticelli, M. P., Corrado, L., Cafiero, M., Polimeno, M., Camerino, R., Chiariello, Massimo, Dellegrottaglie, S, PERRONE FILARDI, Pasquale, Pace, Leonardo, Ponticelli, Mp, Corrado, L, Cafiero, M, Polimeno, M, Camerino, R, and Chiariello, M.

Subjects
Ventricular Dysfunction, Left, Point-of-Care Systems, Heart Function Tests, Humans, Monitoring, Ambulatory, Cardiovascular Agents, Heart, Radionuclide Ventriculography, Ventricular Function, Left, Monitoring, Physiologic
Abstract

Although the first non-imaging nuclear probe for clinical application was already available 25 years ago, this technique is still underused for the assessment of ventricular function. Over the years substantial technological progress rendered nuclear probes more accurate and easier to use, and so far the applicability of these devices has been evaluated in several experimental and clinical contexts. Bedside devices can be used in the evaluation of hemodynamically unstable patients and of drug therapy. In patients with several heart diseases, particularly with ischemic cardiomyopathy, accurate information on the changes in ventricular function occurring during routine activities, as well as during structured activities, can be provided using the ambulatory probes. This review will focus on the development and clinical application of these diagnostic tools.

Published
2002

8. Differential role of CD133 and CXCR4 in renal cellcarcinoma

Author

D'Alterio C, Cindolo L, Portella L, Polimeno M, Consales C, Riccio A, Cioffi M, Franco R, Chiodini P, Cartenì G, Mirone V, Longo N, Marra L, Perdonà S, Claudio L, Falsaperla M, Puglisi M, Martignoni G, Ficarra V, Castello G, Scala S., MASCOLO, MASSIMO, STAIBANO, STEFANIA, D'Alterio, C, Cindolo, L, Portella, L, Polimeno, M, Consales, C, Riccio, A, Cioffi, M, Franco, R, Chiodini, P, Cartenì, G, Mirone, V, Longo, N, Marra, L, Perdonà, S, Claudio, L, Mascolo, Massimo, Staibano, Stefania, Falsaperla, M, Puglisi, M, Martignoni, G, Ficarra, V, Castello, G, and Scala, S.

Abstract

The chemokine receptor CXCR4 and CD133, putative stem cell markers, were previously described in renal cancer (RCC). To evaluate the biological and prognostic role of CD133 and CXCR4 in RCC the expression was evaluated through qPCR and immunoblotting in human renal cancer cell lines (786-O, A498, ACHN, CAKI-1, SN12C, TK10, UO31) and patients biopsies. Renal cancer cells and surgical biopsies expressed functional CXCR4 while CD133 was not detectable. CXCR4 and CD133 expression was then evaluated in 240 renal cancer patients through immunohistochemistry. CXCR4 and CD133 were low in 19.1% and 59.6%; intermediate in 20% and 17.9%; high in 60.8% and 22.5% of the cases, respectively. CXCR4 was overexpressed in tumours (p= 0.02), while CD133 was over expressed in healthy tissues (p= 0.04). Disease free survival Kaplan Meier plots suggest that prognosis is unfavourable for patients whose primary tumours express CXCR4 (p= 0.0199) but nor CD133 (p= 0.151) neither the concomitant CXCR4-CD133 (p=0.848) high expression affected prognosis. Analysis of prognostic factors suggests that age, clinical presentation, AJCC stage and CXCR4 had a significant prognostic value at the univariate analysis. The CXCR4 predictive ability was confirmed at the multivariate analysis while no prognostic role was identified for CD133.Thus concomitant CD133 and CXCR4 evaluation is not worth in RCC patient while the CXCR4 prognostic role encourage CXCR4 antagonists as promising therapeutic option.

Published
2010

9. AT-1 receptor antagonism with candesartan cilexitil improves endothelial function in patients with hypertension and coronary artery disease: A double-blind, randomized, placebo-controlled trial

Author

PERRONE FILARDI, PASQUALE, Brevetti G, Silvestro A, Corrado L, Cafiero M, Petretta A, Caiazzo G, Polimeno M, Zarrilli A, Camerino R, Maglione A., PERRONE FILARDI, Pasquale, Brevetti, G, Silvestro, A, Corrado, L, Cafiero, M, Petretta, A, Caiazzo, G, Polimeno, M, Zarrilli, A, Camerino, R, and Maglione, A.

Published
2005

10. Relation of brachial artery flow-mediated vasodilation to significant coronary artery disease in patients with peripheral arterial disease

Author

PERRONE FILARDI, PASQUALE, CUOCOLO, ALBERTO, Brevetti G, Silvestro A, Storto G, Dellegrottaglie S, Corrado L, Cafiero M, Camerino R, Polimeno M, Zarrilli A, Caiazzo G, Maglione A, Petretta A, Chiariello M., PERRONE FILARDI, Pasquale, Cuocolo, Alberto, Brevetti, G, Silvestro, A, Storto, G, Dellegrottaglie, S, Corrado, L, Cafiero, M, Camerino, R, Polimeno, M, Zarrilli, A, Caiazzo, G, Maglione, A, Petretta, A, and Chiariello, M.

Published
2005

12. At-1 receptor antagonism with candesartan cilexitil improves endothelial function in patients with hypertension and coronary artery disease: A double-blind, randomized, placebo-controlled trial

Author

Corrado L, Brevetti G, Silvestro A, Cafiero M, Caiazzo G, Petretta A, Polimeno M, Zarrilli A, Camerino R, Maglione A, Monda C, Guerra G, Fiumara G, Chiariello M., PERRONE FILARDI, PASQUALE, Corrado, L, PERRONE FILARDI, Pasquale, Brevetti, G, Silvestro, A, Cafiero, M, Caiazzo, G, Petretta, A, Polimeno, M, Zarrilli, A, Camerino, R, Maglione, A, Monda, C, Guerra, G, Fiumara, G, and Chiariello, M.

Published
2005

14. La dilatazione dell’arteria brachiale flusso-mediata esclude l’arteropatia coronarica nei pazienti con arteropatia periferica

Author

Cafiero M, Cuocolo A, Storto G, Corrado L, Dellegrottaglie S, Camerino R, Zarrilli A, Polimeno M, Petretta A, Pucciarelli A, Caiazzo G, Chiariello M., PERRONE FILARDI, PASQUALE, Cafiero, M, PERRONE FILARDI, Pasquale, Cuocolo, A, Storto, G, Corrado, L, Dellegrottaglie, S, Camerino, R, Zarrilli, A, Polimeno, M, Petretta, A, Pucciarelli, A, Caiazzo, G, and Chiariello, M.

Published
2004

15. Il Candesartan Cilextil migliora la funzione endoteliale in pazienti con ipertensione arteriosa ed aterosclerosi coronarica

Author

PERRONE FILARDI, PASQUALE, Brevetti G, Silvestro A, Corrado L, Cafiero M, Zarrilli A, Camerino R, Polimeno M, Maglione A, Pucciarelli A, Caiazzo G, Petretta A, Chiariello M., PERRONE FILARDI, Pasquale, Brevetti, G, Silvestro, A, Corrado, L, Cafiero, M, Zarrilli, A, Camerino, R, Polimeno, M, Maglione, A, Pucciarelli, A, Caiazzo, G, Petretta, A, and Chiariello, M.

Published
2004

18. Prefazione

Author

RULLI, GIUSEPPE, POLIMENO, M. ALESSANDRA, De Natale, Maria Luisa (ORCID:0000-0002-4217-0820), RULLI, GIUSEPPE, POLIMENO, M. ALESSANDRA, and De Natale, Maria Luisa (ORCID:0000-0002-4217-0820)

Abstract

Questo manuale fornisce indicazioni per promuovere lo sviluppo del turismo sociale, inteso come servizio sociale, in favore delle persone con bisogni specifici (disabili, anziani, emodializzati, malati oncologici, cardiopatici, ecc.). In particolare è descritta una metodologia per finalizzare pacchetti turistici ad una utenza disabile, sono delineati gli elementi per organizzare un sistema di informazioni sul turismo sociale accessibile a tutti, i comportamenti del personale addetto all'accoglienza e all'accompagnamento del turista disabile e il percorso per far cooperare i servizi sociosanitari con i servizi turistici al fine di sostenere il processo di formazione della cultura che consideri la vacanza un "diritto di tutti".

Published
2008

19. Concomitant CXCR4 and CXCR7 Expression Predicts Poor Prognosis in Renal Cancer

Author

D'Alterio, C., primary, Consales, C., additional, Polimeno, M., additional, Franco, R., additional, Cindolo, L., additional, Portella, L., additional, Cioffi, M., additional, Calemma, R., additional, Marra, L., additional, Claudio, L., additional, Perdona, S., additional, Pignata, S., additional, Facchini, G., additional, Carteni, G., additional, Longo, N., additional, Pucci, L., additional, Ottaiano, A., additional, Costantini, S., additional, Castello, G., additional, and Scala, S., additional

Published
2010
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21. Peripheral diagnostic and interventional procedures using an automated injection system for carbon dioxide (C02): case series and learning curve.

Author

Giordano, A., Messina, S., Polimeno, M., Corcione, N., Ferraro, P., Biondi-Zoccai, G., and Giordano, G.

Subjects
ANGIOGRAPHY, CARBON dioxide, CHI-squared test, CLINICAL pathology, FISHER exact test, CASE studies, SCIENTIFIC observation, KIDNEY failure, CONTRAST media, RETROSPECTIVE studies, DATA analysis software, DESCRIPTIVE statistics, MANN Whitney U Test, DISEASE complications
Published
2015

26. Concomitant CXCR4 and CXCR7 Expression Predicts Poor Prognosis in Renal Cancer

Author

DAlterio, C., Consales, C., Polimeno, M., Franco, R., Cindolo, L., Portella, L., Cioffi, M., Calemma, R., Marra, L., Claudio, L., Perdona, S., Pignata, S., Facchini, G., Carteni, G., Longo, N., Pucci, L., Ottaiano, A., Costantini, S., Castello, G., and Scala, S.

Abstract

CXCR4 is a chemokine receptor implicated in the metastatic process. The CXCR4 ligand, CXCL12, was shown to bind the CXCR7 receptor also, a recently deorphanized chemokine receptor whose signalling pathway and function are still controversial. This study was conducted to determine patients clinic-pathological factors and outcome according to the expressions of CXCR4 and CXCR7 in renal cell carcinoma (RCC). CXCR4 and CXCR7 expression were evaluated in 223 RCC patients through immunohistochemistry; moreover CXCR4 and CXCR7 were detected in 49 other consecutive RCC patients through RT- PCR. CXCR4 expression was low in 42/223 RCC (18,8), intermediate in 71/223 (31,9) and high in 110/223 (49,3). CXCR7 expression was low in 44/223 RCC patients (19,8), intermediate in 65/223 (29,1) and high in 114/223 (51,1). High CXCR4 and high CXCR7 expression predicted shorter disease free survival. In multivariate analysis, high CXCR4 expression (p 0.0061), high CXCR7 (p 0.0194) expression and the concomitant high expression of CXCR4 and CXCR7 (p 0.0235) are independent prognosis factors. Through RT-PCR, CXCR4 was overexpressed in 36/49 and CXCR7 in 33/49 samples correlating with symptoms at diagnosis and lymph nodes status. So we can hypothesize that CXCR4 and CXCR7, singularly evaluated and in combination, are valuable prognostic factors in RCC patients.

Published
2010

28. Poster display II clinical general

Author

Gurgenyan, S., Vatinyan, S., Nikogosyan, K., Edilyan, L., Chobanyan, B., Lacourcière, Y., Marcel Dumont, M., Lefebvre, J., Poirier, L., Côté, C., Peix, A., Alonso, O., Chae, I., Chung, J., Gutierrez, C., Kropp, J., Onsel, C., Silvasi, I., Llerena, L., Padhy, A., Garcia-Barreto, D., Trapaga, A., Asen, L., Infante, O., Ponce, F., Cabrera, L., Valiente, J., Tornes, F., Guerrero, I., Zayas, R., ones, M., Castro, J., Fayad, Y., Carrillo, R., Paz, A., Mehlsen, J., Hædersdal, C., Daou, D., Benada, A., Lebtahi, R., Idy-Peretti, I., Guludec, D., Coaguila, C., Vilain, D., Leenhardt, A., Heinicke, N., Benesch, B., Kaiser, T., Seegmüller, M., Schönberger, J., Eilles, C., Riegger, G., Holmer, S., Luchner, A., Kouris, N., Kontogianni, D., Goranitou, G., Sifaki, M., Kalkandi, E., Grassos, H., Papoulia, E., Babalis, D., Moralidis, E., Spyridonidis, T., Arsos, G., Karakatsanis, K., Karatzas, N., Parameswaran, R., Sundaram, P., Padma, S., Haridas, K., Zachariah, M., Kumar, S., Feola, M., Leonardi, G., Peano, S., Bianchi, A., Dutto, P., Guala, E., Biggi, A., Uslenghi, E., Filardi, P., Pace, L., Dellegrottaglie, S., Corrado, L., Cafiero, M., Camerino, R., Maglione, A., Polimeno, M., Zarrilli, A., Chiariello, M., Giorgetti, A., Gimelli, A., Marini, C., Schluter, M., Kusch, A., D'Aragona, I., Marzullo, P., Stanislao, M., Zanco, P., Inglese, E., Bertelli, P., Valle, G., Tassone, F., Pepino, R., Francini, A., Garrone, O., Occelli, M., Merlano, M., Florimonte, L., Pagani, L., Piatti, L., Butti, I., Maffioli, L., Casorelli, E., Dottore, F., Gentili, G., Agostini, M., Pieri, P., Milan, E., Giubbini, R., Mazzanti, M., Serenelli, M., Perna, G., Ferro, A., Duilio, C., Santomauro, M., Salvatore, M., Cuocolo, A., Bertagna, F., Bosio, G., Terzi, A., Paghera, B., Kaneta, T., Otani, H., Hakamatsuka, T., Fukuda, H., Nakazato, R., Moroi, M., Kunimasa, T., Furuhashi, T., Sugi, K., Yasuhi, W., Akihiro, S., Yukawa, A., Ryu, K., Kimio, T., Yasuhiko, T., Nariaki, E., Yasunori, W., Akashi, Y., Musha, H., Kida, K., Itoh, K., Inoue, K., Kawasaki, K., Hashimoto, N., Nakazawa, K., Miyake, F., Fukuzawa, S., Ozawa, S., Inagaki, M., Sugioka, J., Okino, S., Matsuo, S., Matsumoto, T., Nakae, I., Masuda, D., Horie, M., Mori, Y., Takahashi, K., Masai, M., Kawasaki, D., Kanemori, T., Okuda, S., Tanabe, K., Ohyanagi, M., OKuda, S., Toyama, T., Hoshizaki, H., Seki, R., Isobe, N., Kawaguchi, R., Oshima, S., Taniguchi, K., Nakagawa, K., Sekine, T., Yamazaki, M., Komuro, I., Kim, K., Teramoto, N., Jino, H., Ohta, Y., Watabe, H., Hayashi, T., Iida, H., Nishimura, T., Nagae, A., Morishima, K., Shigeyama, T., Shimoyama, K., Yoshino, H., Kawai, Y., Jeong, S., Lee, J., Seo, J., Bae, J., Ahn, B., Chae, S., Lee, K., Cho, I., Chun, K., Won, K., Lee, H., Hong, G., Park, J., Shin, D., Kim, Y., Shim, B., Pavlovic, J., Peovska, I., Vavlukis, M., Gorceva, D., Majstorov, V., Alexanderson, E., Meave, A., Ricalde, A., Teresinska, A., Sliwinski, M., Konieczna, S., Szymanska, M., Hendzel, P., Juraszynski, Z., Debski, A., Szumilak, B., Kostkiewicz, M., Wilkolek, P., Pasowicz, M., Klimeczek, P., Pieniazek, P., Przewlocki, T., Pieculewicz, M., Tracz, W., Szot, W., Trebacz, J., Zmudka, K., Podolec, P., Dziuk, M., Kazmierczak, A., Kot, E., Pietrzykowski, J., Cholewa, M., Coutinho, M., Correia, M., Cantinho, G., Conceição, I., Bernardes, A., Silva, A., Gaspar, F., Cunha, J., Lourenço, C., Roque, C., Ferrer-Antunes, A., Ferreira, M., Providência, L., Lima, J., Abreu, A., Castillejos, L., Henriksson, I., Oliveira, L., Rosário, L., Geão, A., Pereira, E., Colarinha, P., Romero-Farina, G., Candell-Riera, J., Aguadé-Bruix, S., Leon, G., Caresia, A., Mila-Lopez, M., Garcia-Alonso, C., Pifarre-Montaner, P., Negre-Buso, M., Castell-Conesa, J., Mestre-Fusco, A., Porta-Biosca, F., Muxi, A., Paredes, P., Ortin, J., Duch, J., Diaz-Infante, E., Fuertes, S., Orus, J., Mont, L., Pons, F., Pollack, C., Hellermann, J., Namdar, M., Siegrist, P., Koepfli, P., Bartenstein, N., Schurr, U., Jenni, R., Kaufmann, P., Hassad, R., Hamami, H., Sellem, A., Brahim, H., Caglar, M., Mahmoudian, B., Aytemir, K., Kahraman, S., Arýcý, M., Kabakcý, G., Karabulut, E., Akincioglu, C., Berman, D., Nishina, H., Hayes, S., Kavanagh, P., Friedman, J., Slomka, P., Germano, G., Entok, E., Cavusoglu, Y., Vardareli, E., Timuralp, B., Cheetham, A., Naylor, V., Ghiotto, F., McGhie, J., Al-Housni, M., Kelion, A., Hutchings, F., Hinton-Taylor, S., Birkbeck, P., Thatikonda, S., Feldkamp, M., Rosamond, T., Raza, M., Panjrath, G., Haider, A., Jain, D., Yang, A., Schumacher, R., Reynolds, J., Clark, E., Speiser, D., Schindel, M., Hackney, T., Vacek, J., Jindal, V., Dim, U., Hamburg, L., Mouradian, V., Nichols, K., Akinboboye, O., Snyder, K., Polepalle, D., DePuey, G., Khattak, H., Friedman, M., Thompson, L., Thompson, R., McGhie, A., Moser, K., O'Keefe, J., Fritsch, N., Bateman, T., Mut, F., Vidal, I., Rener, A., Nuñez, M., Alvarez, B., Beretta, M., Gurgenyan, S., Vatinyan, S., Nikogosyan, K., Edilyan, L., Chobanyan, B., Lacourcière, Y., Marcel Dumont, M., Lefebvre, J., Poirier, L., Côté, C., Peix, A., Alonso, O., Chae, I., Chung, J., Gutierrez, C., Kropp, J., Onsel, C., Silvasi, I., Llerena, L., Padhy, A., Garcia-Barreto, D., Trapaga, A., Asen, L., Infante, O., Ponce, F., Cabrera, L., Valiente, J., Tornes, F., Guerrero, I., Zayas, R., ones, M., Castro, J., Fayad, Y., Carrillo, R., Paz, A., Mehlsen, J., Hædersdal, C., Daou, D., Benada, A., Lebtahi, R., Idy-Peretti, I., Guludec, D., Coaguila, C., Vilain, D., Leenhardt, A., Heinicke, N., Benesch, B., Kaiser, T., Seegmüller, M., Schönberger, J., Eilles, C., Riegger, G., Holmer, S., Luchner, A., Kouris, N., Kontogianni, D., Goranitou, G., Sifaki, M., Kalkandi, E., Grassos, H., Papoulia, E., Babalis, D., Moralidis, E., Spyridonidis, T., Arsos, G., Karakatsanis, K., Karatzas, N., Parameswaran, R., Sundaram, P., Padma, S., Haridas, K., Zachariah, M., Kumar, S., Feola, M., Leonardi, G., Peano, S., Bianchi, A., Dutto, P., Guala, E., Biggi, A., Uslenghi, E., Filardi, P., Pace, L., Dellegrottaglie, S., Corrado, L., Cafiero, M., Camerino, R., Maglione, A., Polimeno, M., Zarrilli, A., Chiariello, M., Giorgetti, A., Gimelli, A., Marini, C., Schluter, M., Kusch, A., D'Aragona, I., Marzullo, P., Stanislao, M., Zanco, P., Inglese, E., Bertelli, P., Valle, G., Tassone, F., Pepino, R., Francini, A., Garrone, O., Occelli, M., Merlano, M., Florimonte, L., Pagani, L., Piatti, L., Butti, I., Maffioli, L., Casorelli, E., Dottore, F., Gentili, G., Agostini, M., Pieri, P., Milan, E., Giubbini, R., Mazzanti, M., Serenelli, M., Perna, G., Ferro, A., Duilio, C., Santomauro, M., Salvatore, M., Cuocolo, A., Bertagna, F., Bosio, G., Terzi, A., Paghera, B., Kaneta, T., Otani, H., Hakamatsuka, T., Fukuda, H., Nakazato, R., Moroi, M., Kunimasa, T., Furuhashi, T., Sugi, K., Yasuhi, W., Akihiro, S., Yukawa, A., Ryu, K., Kimio, T., Yasuhiko, T., Nariaki, E., Yasunori, W., Akashi, Y., Musha, H., Kida, K., Itoh, K., Inoue, K., Kawasaki, K., Hashimoto, N., Nakazawa, K., Miyake, F., Fukuzawa, S., Ozawa, S., Inagaki, M., Sugioka, J., Okino, S., Matsuo, S., Matsumoto, T., Nakae, I., Masuda, D., Horie, M., Mori, Y., Takahashi, K., Masai, M., Kawasaki, D., Kanemori, T., Okuda, S., Tanabe, K., Ohyanagi, M., OKuda, S., Toyama, T., Hoshizaki, H., Seki, R., Isobe, N., Kawaguchi, R., Oshima, S., Taniguchi, K., Nakagawa, K., Sekine, T., Yamazaki, M., Komuro, I., Kim, K., Teramoto, N., Jino, H., Ohta, Y., Watabe, H., Hayashi, T., Iida, H., Nishimura, T., Nagae, A., Morishima, K., Shigeyama, T., Shimoyama, K., Yoshino, H., Kawai, Y., Jeong, S., Lee, J., Seo, J., Bae, J., Ahn, B., Chae, S., Lee, K., Cho, I., Chun, K., Won, K., Lee, H., Hong, G., Park, J., Shin, D., Kim, Y., Shim, B., Pavlovic, J., Peovska, I., Vavlukis, M., Gorceva, D., Majstorov, V., Alexanderson, E., Meave, A., Ricalde, A., Teresinska, A., Sliwinski, M., Konieczna, S., Szymanska, M., Hendzel, P., Juraszynski, Z., Debski, A., Szumilak, B., Kostkiewicz, M., Wilkolek, P., Pasowicz, M., Klimeczek, P., Pieniazek, P., Przewlocki, T., Pieculewicz, M., Tracz, W., Szot, W., Trebacz, J., Zmudka, K., Podolec, P., Dziuk, M., Kazmierczak, A., Kot, E., Pietrzykowski, J., Cholewa, M., Coutinho, M., Correia, M., Cantinho, G., Conceição, I., Bernardes, A., Silva, A., Gaspar, F., Cunha, J., Lourenço, C., Roque, C., Ferrer-Antunes, A., Ferreira, M., Providência, L., Lima, J., Abreu, A., Castillejos, L., Henriksson, I., Oliveira, L., Rosário, L., Geão, A., Pereira, E., Colarinha, P., Romero-Farina, G., Candell-Riera, J., Aguadé-Bruix, S., Leon, G., Caresia, A., Mila-Lopez, M., Garcia-Alonso, C., Pifarre-Montaner, P., Negre-Buso, M., Castell-Conesa, J., Mestre-Fusco, A., Porta-Biosca, F., Muxi, A., Paredes, P., Ortin, J., Duch, J., Diaz-Infante, E., Fuertes, S., Orus, J., Mont, L., Pons, F., Pollack, C., Hellermann, J., Namdar, M., Siegrist, P., Koepfli, P., Bartenstein, N., Schurr, U., Jenni, R., Kaufmann, P., Hassad, R., Hamami, H., Sellem, A., Brahim, H., Caglar, M., Mahmoudian, B., Aytemir, K., Kahraman, S., Arýcý, M., Kabakcý, G., Karabulut, E., Akincioglu, C., Berman, D., Nishina, H., Hayes, S., Kavanagh, P., Friedman, J., Slomka, P., Germano, G., Entok, E., Cavusoglu, Y., Vardareli, E., Timuralp, B., Cheetham, A., Naylor, V., Ghiotto, F., McGhie, J., Al-Housni, M., Kelion, A., Hutchings, F., Hinton-Taylor, S., Birkbeck, P., Thatikonda, S., Feldkamp, M., Rosamond, T., Raza, M., Panjrath, G., Haider, A., Jain, D., Yang, A., Schumacher, R., Reynolds, J., Clark, E., Speiser, D., Schindel, M., Hackney, T., Vacek, J., Jindal, V., Dim, U., Hamburg, L., Mouradian, V., Nichols, K., Akinboboye, O., Snyder, K., Polepalle, D., DePuey, G., Khattak, H., Friedman, M., Thompson, L., Thompson, R., McGhie, A., Moser, K., O'Keefe, J., Fritsch, N., Bateman, T., Mut, F., Vidal, I., Rener, A., Nuñez, M., Alvarez, B., and Beretta, M.

29. Posters display III clinical outcome and PET

Author

Baliño, N., Masoli, O., Traverso, S., Grynberg, L., Rappallo, C., Redruello, M., Rosa, D., Cragnolino, D., Meretta, A., Vidal, L., Graf, S., Khorsand, A., Gyongyosi, M., Karanikas, G., Eidherr, H., Kletter, K., Porenta, G., Glogar, D., Sochor, H., Beheshti, M., Poetzi, C., Wadsak, W., Maurer, G., Wolfram, J., Winter, O., Velghe, A., Veire, N., Bondt, P., Buyzere, M., Wiele, C., Backer, G., Gillebert, T., Dierckx, R., Sutter, J., Bernard, D., Langlois, M., Duarte, P., Mastrocolla, L., Sampaio, C., Rossi, J., Smanio, P., Lima, E., Oliveira, C., Pereira, J., Beraldo, P., Rodrigues, F., Thom, A., Yoshinaga, K., Ukkonen, H., Burwash, I., DeKemp, R., Dafoe, W., Davies, R., Haddad, H., Ruddy, T., DaSilva, J., Beanlands, R., Chow, B., Williams, K., Garrard, L., Szeto, A., Aung, M., Sondergaard, H., Bottcher, M., Madsen, M., Schmitz, O., Nielsen, T., Botker, H., Høilund-Carlsen, P., Johansen, A., Christensen, H., Vach, W., Møldrup, M., Haghfelt, T., Kristensen, J., Maeng, M., Mortensen, U., Berg, J., Rehling, M., Elsaban, K., El-Kady, T., El-Gabaly, M., Yehia, A., El-Sayed, M., Naum, A., Laaksonen, M., Tuunanen, H., Oikonen, V., Kemppainen, J., Järvisalo, M., Nuutila, P., Knuuti, J., Vanzetto, G., Jacon, P., Fagret, D., Machecourt, J., Lindner, O., Vogt, J., Kammeier, A., Fricke, E., Wielepp, P., Baller, D., Lamp, B., Holzinger, J., Horstkotte, D., Burchert, W., Nekolla, S., Souvatzoglou, M., Hausleiter, J., Henke, N., Kruschke, K., Bengel, F., Schwaiger, M., Sundaram, P., Padma, S., Haridas, K., Kumar, S., Zachariah, M., Livschitz, S., Zornitzki, T., Vered, S., Oettinger, M., Levy, R., Caspi, A., Faraggi, D., Knobler, H., Mats, I., Solodky, A., Ben-Gal, T., Battler, A., Zafrir, N., Varani, E., Balducelli, M., Severi, S., Patroncini, A., Vecchi, G., Gatti, C., Corbelli, C., Casanova, R., Maresta, A., Cittanti, C., Valgimigli, M., Giganti, M., Malagutti, P., Percoco, G., Bagatin, E., Panareo, S., Avigni, N., Ferrari, R., Feggi, L., Filardi, P., Cuocolo, A., Storto, G., Brevetti, G., Dellegrottaglie, S., Corrado, L., Cafiero, M., Polimeno, M., Zarrilli, A., Chiariello, M., Marcassa, C., Campini, R., Calza, P., Giannuzzi, P., Galassi, A., Grasso, C., Azzarelli, S., Leotta, E., Moshiri, S., Tamburino, C., Acampa, W., Ferro, A., Petretta, M., Salvatore, M., Pieri, P., Berta, R., Moscatelli, G., Buccoliero, F., Inglese, E., Medolago, G., Imperiale, A., Rimini, M., Bertagna, F., Sullo, P., Lupo, M., Cappagli, M., Fukuda, H., Kunimasa, T., Furuhashi, T., Moroi, M., Yasuhi, W., Akihiro, S., Akio, Y., Ryou, K., Kimio, T., Yasunori, W., Yasuhiko, T., Nariaki, E., Watabe, H., Teramoto, N., Ohta, Y., Kou, Y., Hayashi, T., Iida, H., Bom, H., Song, H., Min, J., Heo, Y., Seo, J., Lee, J., Bae, J., Jeong, S., Ahn, B., Chae, S., Lee, K., Popiel, M., Grajek, S., Czepczynski, R., Breborowicz, P., Lesiak, M., Czyz, A., Sawinski, K., Komarnicki, M., Cieslinski, A., Sowinski, J., Ferreira, A., Ventosa, A., Gil, V., Calqueiro, J., Lima, S., Aguiar, C., Couto, R., Raposo, L., Seabra-Gomes, R., Vasconcelos, M., Martins, E., Faria, T., Oliveira, A., Garcia, M., Rocha-Gonçalves, F., Lourenço, C., Roque, C., Ferrer-Antunes, A., Ferreira, M., Providência, L., Lima, J., Medrea, C., Bogdan, R., Lazar, A., Mot, S., Capilneanu, R., Kozulin, V., Berkovich, O., Ivashchenko, T., Larionova, V., Esipovich, I., Gordeev, M., Panov, A., Shlyakhto, E., Burova, N., Baranov, D., Timoshin, V., Chuprova, S., Shkolnikova, M., Zaklyazminskaya, E., Poliakov, A., Sazonova, S., Romero-Farina, G., Arenillas, J., Candell-Riera, J., Aguadè-Bruix, S., Leon, G., Molina, C., Chacon, P., Montaner, J., Rovira, A., Alvarez-Sabin, J., Namdar, M., Siegrist, P., Grathwohl, R., Delaloye, R., Koepfli, P., Wyss, C., Kaufmann, P., Bartenstein, N., Hellermann, J., Pollack, C., Schurr, U., Zellweger, M., Burger, P., Mueller-Brand, J., Pfisterer, M., Gordon, L., Epps, A., Chiarameda, S., Navare, S., Ahlberg, A., Cyr, G., Katten, D., Ausef, A., Heller, G., Darrow, B., Thomas, G., Ip, T., Thompson, R., Kramer, D., Rice, D., Thomas, J., Miyamoto, M., Druz, R., Nichols, K., Akinboboye, O., Reichek, N., Podrasky, E., Tuttle, R., Shaw, L., Hanson, M., Borges-Neto, S., Lundbye, J., Werden, S., Kazi, F., Whalen, A., Noble, G., O'Sullivan, D., Boden, W., Danias, P., Papaioannou, G., Leka, I., Beretta, M., Viňas, S., Gonzalez, A., Vidal, I., Rener, A., Baliño, N., Masoli, O., Traverso, S., Grynberg, L., Rappallo, C., Redruello, M., Rosa, D., Cragnolino, D., Meretta, A., Vidal, L., Graf, S., Khorsand, A., Gyongyosi, M., Karanikas, G., Eidherr, H., Kletter, K., Porenta, G., Glogar, D., Sochor, H., Beheshti, M., Poetzi, C., Wadsak, W., Maurer, G., Wolfram, J., Winter, O., Velghe, A., Veire, N., Bondt, P., Buyzere, M., Wiele, C., Backer, G., Gillebert, T., Dierckx, R., Sutter, J., Bernard, D., Langlois, M., Duarte, P., Mastrocolla, L., Sampaio, C., Rossi, J., Smanio, P., Lima, E., Oliveira, C., Pereira, J., Beraldo, P., Rodrigues, F., Thom, A., Yoshinaga, K., Ukkonen, H., Burwash, I., DeKemp, R., Dafoe, W., Davies, R., Haddad, H., Ruddy, T., DaSilva, J., Beanlands, R., Chow, B., Williams, K., Garrard, L., Szeto, A., Aung, M., Sondergaard, H., Bottcher, M., Madsen, M., Schmitz, O., Nielsen, T., Botker, H., Høilund-Carlsen, P., Johansen, A., Christensen, H., Vach, W., Møldrup, M., Haghfelt, T., Kristensen, J., Maeng, M., Mortensen, U., Berg, J., Rehling, M., Elsaban, K., El-Kady, T., El-Gabaly, M., Yehia, A., El-Sayed, M., Naum, A., Laaksonen, M., Tuunanen, H., Oikonen, V., Kemppainen, J., Järvisalo, M., Nuutila, P., Knuuti, J., Vanzetto, G., Jacon, P., Fagret, D., Machecourt, J., Lindner, O., Vogt, J., Kammeier, A., Fricke, E., Wielepp, P., Baller, D., Lamp, B., Holzinger, J., Horstkotte, D., Burchert, W., Nekolla, S., Souvatzoglou, M., Hausleiter, J., Henke, N., Kruschke, K., Bengel, F., Schwaiger, M., Sundaram, P., Padma, S., Haridas, K., Kumar, S., Zachariah, M., Livschitz, S., Zornitzki, T., Vered, S., Oettinger, M., Levy, R., Caspi, A., Faraggi, D., Knobler, H., Mats, I., Solodky, A., Ben-Gal, T., Battler, A., Zafrir, N., Varani, E., Balducelli, M., Severi, S., Patroncini, A., Vecchi, G., Gatti, C., Corbelli, C., Casanova, R., Maresta, A., Cittanti, C., Valgimigli, M., Giganti, M., Malagutti, P., Percoco, G., Bagatin, E., Panareo, S., Avigni, N., Ferrari, R., Feggi, L., Filardi, P., Cuocolo, A., Storto, G., Brevetti, G., Dellegrottaglie, S., Corrado, L., Cafiero, M., Polimeno, M., Zarrilli, A., Chiariello, M., Marcassa, C., Campini, R., Calza, P., Giannuzzi, P., Galassi, A., Grasso, C., Azzarelli, S., Leotta, E., Moshiri, S., Tamburino, C., Acampa, W., Ferro, A., Petretta, M., Salvatore, M., Pieri, P., Berta, R., Moscatelli, G., Buccoliero, F., Inglese, E., Medolago, G., Imperiale, A., Rimini, M., Bertagna, F., Sullo, P., Lupo, M., Cappagli, M., Fukuda, H., Kunimasa, T., Furuhashi, T., Moroi, M., Yasuhi, W., Akihiro, S., Akio, Y., Ryou, K., Kimio, T., Yasunori, W., Yasuhiko, T., Nariaki, E., Watabe, H., Teramoto, N., Ohta, Y., Kou, Y., Hayashi, T., Iida, H., Bom, H., Song, H., Min, J., Heo, Y., Seo, J., Lee, J., Bae, J., Jeong, S., Ahn, B., Chae, S., Lee, K., Popiel, M., Grajek, S., Czepczynski, R., Breborowicz, P., Lesiak, M., Czyz, A., Sawinski, K., Komarnicki, M., Cieslinski, A., Sowinski, J., Ferreira, A., Ventosa, A., Gil, V., Calqueiro, J., Lima, S., Aguiar, C., Couto, R., Raposo, L., Seabra-Gomes, R., Vasconcelos, M., Martins, E., Faria, T., Oliveira, A., Garcia, M., Rocha-Gonçalves, F., Lourenço, C., Roque, C., Ferrer-Antunes, A., Ferreira, M., Providência, L., Lima, J., Medrea, C., Bogdan, R., Lazar, A., Mot, S., Capilneanu, R., Kozulin, V., Berkovich, O., Ivashchenko, T., Larionova, V., Esipovich, I., Gordeev, M., Panov, A., Shlyakhto, E., Burova, N., Baranov, D., Timoshin, V., Chuprova, S., Shkolnikova, M., Zaklyazminskaya, E., Poliakov, A., Sazonova, S., Romero-Farina, G., Arenillas, J., Candell-Riera, J., Aguadè-Bruix, S., Leon, G., Molina, C., Chacon, P., Montaner, J., Rovira, A., Alvarez-Sabin, J., Namdar, M., Siegrist, P., Grathwohl, R., Delaloye, R., Koepfli, P., Wyss, C., Kaufmann, P., Bartenstein, N., Hellermann, J., Pollack, C., Schurr, U., Zellweger, M., Burger, P., Mueller-Brand, J., Pfisterer, M., Gordon, L., Epps, A., Chiarameda, S., Navare, S., Ahlberg, A., Cyr, G., Katten, D., Ausef, A., Heller, G., Darrow, B., Thomas, G., Ip, T., Thompson, R., Kramer, D., Rice, D., Thomas, J., Miyamoto, M., Druz, R., Nichols, K., Akinboboye, O., Reichek, N., Podrasky, E., Tuttle, R., Shaw, L., Hanson, M., Borges-Neto, S., Lundbye, J., Werden, S., Kazi, F., Whalen, A., Noble, G., O'Sullivan, D., Boden, W., Danias, P., Papaioannou, G., Leka, I., Beretta, M., Viňas, S., Gonzalez, A., Vidal, I., and Rener, A.

30. Tirofiban induces VEGF production and stimulates migration and proliferation of endothelial cells

Author

Simona Romano, Paolo D'Arrigo, Michele Polimeno, Stefano Messina, Paolo Ferraro, Nicola Corcione, Anna D'Angelillo, Maria Fiammetta Romano, Rita Bisogni, Paolo Pepino, Arturo Giordano, Giordano, A, D'Angelillo, Anna, Romano, Simona, D'Arrigo, P, Corcione, N, Bisogni, Rita, Messina, S, Polimeno, M, Pepino, P, Ferraro, P, and Romano, MARIA FIAMMETTA

Subjects
Vascular Endothelial Growth Factor A, Endothelium, Physiology, Fibrinogen receptor, Proliferation, Umbilical vein, Endothelial, Fibrinolytic Agents, Cell Movement, Human Umbilical Vein Endothelial Cells, Humans, Medicine, Aorta, Cells, Cultured, Migration, Cell Proliferation, Pharmacology, business.industry, Cell growth, Endothelial Cells, Cell migration, Tirofiban, medicine.anatomical_structure, Gene Expression Regulation, Immunology, cardiovascular system, Cancer research, Tyrosine, Molecular Medicine, Endothelium, Vascular, GPIIb/IIIa, business, Wound healing, Ex vivo, medicine.drug
Abstract

Tirofiban is a fibrinogen receptor antagonist, generated using the tripeptide Arg-Gly-Asp (RGD) as a template. RGD activates integrin receptors and integrin-mediated signals are necessary for normal cells to promote survival and stimulate cell cycle progression. We investigated whether tirofiban activated growth-stimulatory signals in endothelium. For this study human umbilical vein endothelial cells (HUVEC) and human aortic endothelial cells (HAEC) were used. Analysis of cell proliferation, by cell counts, showed that the number of endothelial cells doubled after 72 h of culture in the absence of tirofiban, while they were tripled and even quadrupled, in the presence of increasing doses of the drug. Moreover, tirofiban-stimulated cells had a greater ability to migrate through the transwell filters of Boyden chamber, compared to unstimulated cells. The scratch assay, which mimics cell migration during wound healing, showed that tirofiban stimulated HUVECs to migrate into the leading hedge of the scratch. Western blot showed that tirofiban increased the expression levels of VEGF and the downstream effectors Erk and cyclin D. An inhibitor of VEGFR2 counteracted tirofiban-induced-proliferation, suggesting a role for VEGF in such effect. Our study shows that tirofiban stimulates the migration and proliferation of endothelial cells suggesting that it can promote endothelial repair. Ex vivo cultures of arterial rings confirmed the growth stimulatory effect of tirofiban on endothelium. Thus, the benefits of tirofiban in those with acute coronary syndromes undergoing PTCA may be due to rapid endothelization of damaged vessel, besides antiplatelet effects.

Published
2014

31. Differential effect of atorvastatin and tacrolimus on proliferation of vascular smooth muscle and endothelial cells

Author

Arturo Giordano, Nicola Corcione, Paolo Ferraro, Simona Romano, Antonio Sorrentino, Anna Laura Di Pace, Mario Monaco, Michele Polimeno, Maria Fiammetta Romano, Giovanna Nappo, Giordano, A, Romano, Simona, Monaco, M, Sorrentino, A, Corcione, N, Di Pace, Al, Ferraro, P, Nappo, G, Polimeno, M, and Romano, MARIA FIAMMETTA

Subjects
Male, Time Factors, Vascular smooth muscle, Physiology, medicine.medical_treatment, Atorvastatin, Pharmacology, Muscle, Smooth, Vascular, Myocyte, Phosphorylation, Receptor, Cells, Cultured, beta Catenin, Aged, 80 and over, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Endoglin, Drug-Eluting Stents, surgical procedures, operative, lipids (amino acids, peptides, and proteins), Signal transduction, Cardiology and Cardiovascular Medicine, medicine.drug, DNA Replication, proliferation, Myocytes, Smooth Muscle, Receptors, Cell Surface, chemical and pharmacologic phenomena, Cyclin B, Tacrolimus, Antigens, CD, Physiology (medical), Human Umbilical Vein Endothelial Cells, medicine, Humans, Pyrroles, cardiovascular diseases, Aged, Cell Proliferation, Dose-Response Relationship, Drug, vascular cell, business.industry, Growth factor, statin, nutritional and metabolic diseases, Cardiovascular Agents, Heptanoic Acids, Hydroxymethylglutaryl-CoA Reductase Inhibitors, business
Abstract

Although considered promising for use in drug-eluting stents (DES), tacrolimus failed clinically. Tacrolimus inhibits growth factor production but can also act as a growth factor on vascular smooth muscle cells (VSMC). This unexpected proliferative stimulus could reverse the beneficial effects of the drug on restenosis. We hypothesized that tacrolimus' association with statins, which lower cholesterol and impair cell proliferation, could restore tacrolimus' beneficial effect by abrogating the aberrant proliferative stimulus. Additionally, since maintenance of endothelial function represents a challenge for new-generation DES, we investigated the combined effect of tacrolimus and atorvastatin on endothelial cells. Human VSMC and umbilical vein endothelial cells (HUVEC) were incubated with 100 nM tacrolimus and increasing doses of atorvastatin (0–3.0 μM). Atorvastatin plus tacrolimus dose-dependently inhibited VSMC proliferation. The percentage of cells incorporating 5-bromo-2′-deoxyuridine (BrdU) in their DNA was 49 ± 14% under basal conditions, 62 ± 15% ( P = 0.01) with tacrolimus, 40 ± 22% with 3 μM atorvastatin, and 30 ± 7% ( P < 0.05) with 3 μM atorvastatin plus tacrolimus. Atorvastatin downregulated β-catenin, Erk1 and Erk2, and cyclin B in tacrolimus-stimulated VSMC. In contrast, atorvastatin plus tacrolimus did not affect proliferation of endothelial cells. The percentage of HUVEC incorporating BrdU in their DNA was 47 ± 8% under basal conditions, 58 ± 6% ( P = 0.01) with tacrolimus, 45 ± 4% with 3 μM atorvastatin, and 49 ± 1% with 3 μM atorvastatin plus tacrolimus. Both agents stimulated endoglin production by HUVEC. Taken together, these results suggest that, when combined with tacrolimus, atorvastatin exerts a dose-dependent antiproliferative effect on VSMC. In contrast, atorvastatin acts in concert with tacrolimus in HUVEC to stimulate production of endoglin, a factor that has an important role in endothelial repair. Our study supports the conclusion that prevention of postcoronary in-stent restenosis and late thrombosis may benefit of concomitant association of tacrolimus and high doses of atorvastatin.

Published
2012

32. Atorvastatin Sensitises Vascular Smooth Muscle Cells, but not Endothelial Cells, to TNF-alpha-induced Cell Death

Author

Maria Romano, Arturo Giordano, Simona Romano, Gaetano Calì, Giovanna Nappo, Nicola Corcione, Mario Monaco, Michele Polimeno, Nicola Zambrano, Stefano Messina, Paolo Ferraro, Giordano, A., Romano, Simona, Nappo, G., Messina, S., Polimeno, M., Corcione, N., Calì, G., Ferraro, P., Monaco, M., Zambrano, Nicola, and Romano, MARIA FIAMMETTA

Subjects
medicine.medical_specialty, Programmed cell death, Cell type, Vascular smooth muscle, Time Factors, Endothelium, Cell, Myocytes, Smooth Muscle, Enzyme Activators, Biology, Transfection, Muscle, Smooth, Vascular, Internal medicine, Drug Discovery, Protein Kinase C beta, medicine, Atorvastatin, Human Umbilical Vein Endothelial Cells, Humans, Pyrroles, Endothelial dysfunction, Protein Kinase Inhibitors, Cells, Cultured, Protein Kinase C, Pharmacology, Cell Death, Dose-Response Relationship, Drug, Tumor Necrosis Factor-alpha, Smooth muscle layer, JNK Mitogen-Activated Protein Kinases, NF-kappa B, medicine.disease, Endothelial stem cell, Enzyme Activation, medicine.anatomical_structure, Endocrinology, Heptanoic Acids, RNA Interference, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Signal Transduction
Abstract

Objective. Stimuli activating vascular smooth muscle cell death can constrain the neointimal response to arterial damage and prevent vascular thickening. Conversely, endothelial cell death increases endothelial dysfunction and thrombosis risk. We investigated the combined effect of atorvastatin and TNF-α on vascular cell death. Methods and Results. Cell death was investigated in cultures of human aortic smooth muscle cells (VSMCs) and human umbilical vein endothelial cells (HUVECs). Atorvastatin downregulated NF-κB and enhanced JNK activity and cell death in VSMC cultured with TNF- α. In the absence of TNF-α, percentages (mean and StDev) of annexin V positive cells were 17.4± 6.6%, 19.3± 5.9%, 22.9± 9.4% and 35.0± 20.0 % with 0, 1, 3 and 10 μM atorvastatin, respectively. The cytotoxic effect of statin was significant at the highest dose of 10 μM (p=0.001). In the presence of TNF-α, percentages of annexin V positive cells were 27.1±10.6%, 34.2±8.5%, 37.4±14.6, and 54.1±20.0% with 0, 1, 3 and 10 ±M atorvastatin, respectively. The cytotoxic effect of statin was significant at each dose used (p± 0.02), in the presence of TNF-α. The cell death sensitising effect of atorvastatin was apparently mediated by down modulation of PKCβ activity, because it was reproduced by the specific PKCβ inhibitor LY317615 and prevented by the PKC activator phorbol-12-myristate-13-acetate (PMA). This effect was cell context dependent because it was not observed in HUVECs. PKCβ was found to be constitutively active in VSMCs but not in HUVECs, thereby explaining the differential effect among the two cell types. Measurement of phosphoPKCβ protein levels in arterial specimens confirmed increased activation of this kinase in the smooth muscle layer, in comparison with endothelium. We show that PKCβ provides survival signals to vascular smooth muscle cells and not the endothelium. Conclusion. Our study suggests that atorvastatin enhances TNF-α-induced cell death in vascular smooth muscle- but not endothelial – cells; by a cell-context-dependent mechanism, involving PKCβ inhibition.

Published
2012

33. Synergy between direct coronary stenting technique and use of the novel thin strut cobalt chromium skylor™ stent: the mace in follow up patients treated with skylor stent [MILES Study]

Author

Luigi Di Lorenzo, Michele Polimeno, Paolo Ferraro, Giuseppe Biondi-Zoccai, Nicola Corcione, Luciano Fattore, Maria Fiammetta Romano, Arturo Giordano, Giordano, A., Polimeno, M., Corcione, N., Fattore, L., Di Lorenzo, L., Biondi Zoccai, G., Ferraro, P., and Romano, MARIA FIAMMETTA

Subjects
Male, "restenosis", medicine.medical_specialty, "angioplasty", medicine.medical_treatment, Myocardial Infarction, Kaplan-Meier Estimate, Prosthesis Design, Article, Coronary Restenosis, restenosis, Percutaneous Coronary Intervention, Restenosis, Internal medicine, Angioplasty, Humans, Medicine, cardiovascular diseases, Myocardial infarction, "stents", Aged, Retrospective Studies, business.industry, Hazard ratio, Percutaneous coronary intervention, Stent, General Medicine, Middle Aged, equipment and supplies, medicine.disease, angioplasty, stents, Surgery, Treatment Outcome, surgical procedures, operative, Conventional PCI, Cardiology, Female, Chromium Alloys, Cardiology and Cardiovascular Medicine, business, Mace
Abstract

BACKGROUND: Despite significant improvements in stent platform, currently available bare-metal stents (BMS) are still associated with restenosis. Thin-strut design cobalt-chromium alloys hold the promise of improving results of BMS, especially when implanted with direct technique. We performed an observational study to appraise outcomes of the novel Skylor™ stent, stratifying outcomes according to stenting technique. METHODS and RESULTS: We included all consecutive patients undergoing coronary stenting with Skylor™ at 2 centers between 2006 and 2009. The primary end-point was the long-term rate of major adverse cardiac events (MACE, i.e. death, myocardial infarction (MI), coronary artery bypass grafting (CABG) or target vessel revascularization (TVR)). As pre-specified analysis, we compared patients undergoing direct stenting versus those stent implantation following predilation. A total of 1020 patients were included (1292 Skylor™ stents), with procedural success obtained in 99%. Comparing patients undergoing direct stenting (66%) versus pre-dilation (34%) at 16±7 months of follow-up, MACE had occurred in, respectively, 8% versus 14% (p=0.001), with death in 1% versus 2% (p=0.380), MI in 1% versus 2% (p=0.032), CABG in 0.2% versus 2% (p=0.012), and TVR in 6% versus 9% [p=0.071]. Even at multivariable analysis with propensity adjustment, direct stenting was associated with significantly fewer MACE [hazard ratio 0.60 [0.38-0.93], p=0.024]. CONCLUSIONS: This observational study suggests the presence of a beneficial synergy between direct coronary stenting technique and use of the novel thin-strut cobalt-chromium Skylor™ stent in real-world patients undergoing PCI.

Published
2012

34. Prognostic value of rest-redistribution 201-thallium imaging in patients with chronic coronary artery disease and left ventricular dysfunction

Author

A Zarrilli, Maria Assunta Cafiero, Michele Polimeno, Pasquale Perrone Filardi, Massimo Chiariello, Luigi Corrado, Roberta Camerino, Leonardo Pace, Antonio Maglione, Santo Dellegrottaglie, PERRONE FILARDI, Pasquale, Pace, L, Dellegrottaglie, S, Corrado, L, Cafiero, M, Polimeno, M, Camerino, R, Zarrilli, A, Maglione, A, and Chiariello, M.

Subjects
medicine.medical_specialty, business.industry, chemistry.chemical_element, medicine.disease, Coronary artery disease, chemistry, Internal medicine, Cardiology, medicine, Thallium, Radiology, Nuclear Medicine and imaging, In patient, Myocardial infarction, Cardiology and Cardiovascular Medicine, business
Published
2005

35. The identification of reversible dysfunctional myocardium is influenced by the severity of contractile dysfunction and by the length of follow-up

Author

Anna Maria Della Morte, Roberta Camerino, Maria Prastaro, Massimo Chiariello, A Zarrilli, Michele Polimeno, Leonardo Pace, Santo Dellegrottaglie, Pasquale Perrone-Filardi, Maria Assunta Cafiero, Luigi Corrado, Dellegrottaglie, S, PERRONE FILARDI, Pasquale, Pace, Leonardo, Prastaro, Maria, Corrado, L, Cafiero, M, DELLA MORTE, Am, Zarrilli, A, Camerino, R, Polimeno, M, and Chiariello, Massimo

Subjects
Adult, Male, medicine.medical_specialty, medicine.medical_treatment, chemistry.chemical_element, Coronary Artery Disease, Single-photon emission computed tomography, Revascularization, Sensitivity and Specificity, Severity of Illness Index, Coronary artery disease, Ventricular Dysfunction, Left, Dobutamine, Internal medicine, Severity of illness, medicine, Humans, Radiology, Nuclear Medicine and imaging, Wall motion, Thallium, Radionuclide Imaging, Aged, medicine.diagnostic_test, business.industry, Reproducibility of Results, Recovery of Function, General Medicine, Middle Aged, Prognosis, medicine.disease, Functional recovery, Myocardial Contraction, chemistry, Echocardiography, Cardiology, Female, Radiopharmaceuticals, business, Follow-Up Studies, medicine.drug
Abstract

To evaluate the influence of the severity of regional myocardial dysfunction and of the length of follow-up on the identification of myocardial viability with rest-redistribution Tl single photon emission computed tomography (SPECT) and low-dose dobutamine echocardiography (LDDE).Twenty-six patients with chronic coronary artery disease and wall motion abnormalities, candidates for revascularization, were included in this study. All patients underwent, in the same week, Tl SPECT and LDDE for pre-revascularization evaluation of myocardial viability. Reversibility of regional dysfunction was assessed by two-dimensional echocardiography, 40+/-20 days (early follow-up) and 12+/-5 months (late follow-up) after revascularization.In a/dyskinetic segments, Tl SPECT showed similar values of sensitivity (78% vs. 71%, P=NS) and slightly higher values of specificity (43% vs. 18%, P0.01) compared to hypokinetic segments, in predicting functional recovery at early follow-up. No significant changes were observed in the diagnostic accuracy of Tl SPECT at late follow-up. On the contrary, LDDE provided significantly lower values of sensitivity (56% vs. 94%, P0.05) and higher values of specificity (73% vs. 9%, P0.01) in a/dyskinetic compared to hypokinetic segments. Specificity of LDDE in a/dyskinetic segments significantly increased from early (73%) to late follow-up (95%; P0.05). Similarly, positive predictive value in a/dyskinetic segments significantly increased from early (69%) to late follow-up (96%; P0.05).The severity of regional dysfunction and the length of follow-up significantly influence the diagnostic accuracy of LDDE but not of rest-redistribution Tl SPECT in the identification of myocardial viability.

Published
2005

36. Inhibition of stromal CXCR4 impairs development of lung metastases

Author

Giosuè Scognamiglio, Crescenzo D'Alterio, Anna Maria Riccio, Antonio Barbieri, Caterina Ieranò, Domenica Rea, Renato Franco, Stefania Scala, Luigi Portella, Claudio Arra, Marianeve Polimeno, Giuseppe Palma, Jane Bryce, Antonio Luciano, D'Alterio, C, Barbieri, A, Portella, L, Palma, G, Polimeno, M, Riccio, A, Ierano, C, Franco, Renato, Scognamiglio, G, Bryce, J, Luciano, A, Rea, D, Arra, C, and Scala, S.

Subjects
Benzylamines, Receptors, CXCR4, Pathology, medicine.medical_specialty, Cancer Research, Lung Neoplasms, Stromal cell, Myeloid, Immunology, Melanoma, Experimental, Antineoplastic Agents, Cyclams, CXCR4, Metastasis, Mice, Antigen, Heterocyclic Compounds, medicine, Animals, Antigens, Ly, Immunology and Allergy, Lymphocyte homing receptor, Melanoma, Chemistry, Plerixafor, medicine.disease, Mice, Inbred C57BL, medicine.anatomical_structure, Oncology, Pulmonary metastases, Cancer research, Original Article, Female, Stromal Cells, Heterozygote mice, Granulocytes, medicine.drug
Abstract

Compelling evidence has emerged in recent years indicating that stromal cells play a critical role in disease progression. CXCR4 is a G-protein-coupled receptor with a major role in lymphocyte homing. Its ligand, CXCL12, is a highly efficient chemotactic factor for T cells, monocytes, pre-B cells, dendritic cells and myeloid bone marrow-derived cells (BMDCs). In addition, the CXCR4-CXCL12 axis plays a central role in tumor growth and metastasis. To evaluate the effect of genetic CXCR4 reduction on metastasis development, murine melanoma B16 cells were injected into the tail vein of C57BL/6 CXCR4(+/+) and CXCR4(+/-) mice in the presence of the CXCR4 inhibitor, Plerixafor (previously named AMD3100). Although lung metastases developed in wild-type CXCR4(+/+) and heterozygote CXCR4(+/-) mice, nodules were significantly smaller in the latter. CXCR4 pharmacological inhibition by Plerixafor further reduced lung metastases in CXCR4(+/-) mice, preserving the pulmonary architecture (4.18 ± 1.38 mm(2) vs. 1.11 ± 0.60 mm(2), p = 0.038). A reduction in LY6G-positive myeloid/granulocytic cells and in p38 MAPK activation was detected in lungs from CXCR4(+/-) mice compared to CXCR4(+/+) mice [LY6G-positive myeloid CXCR4(+/-) vs. CXCR4(+/+) (p = 0.0004); CXCR4(+/+) vs. CXCR4(+/+) Plerixafor-treated (p = 0.0031)] suggesting that CXCR4 reduction on myeloid-derived cells reduced their recruitment to the lung, consequently impairing lung metastases. Our findings argue in favor of a specific role of CXCR4 expressed in stromal cells that condition the pro-tumor microenvironment. In this scenario, CXCR4 antagonists will target neoplastic cells as well as the pro-tumor stromal microenvironment.

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37. Concomitant CXCR4 and CXCR7 expression predicts poor prognosis in renal cancer

Author

Luca Cindolo, Sisto Perdonà, Luigi Pucci, Renato Franco, Gaetano Facchini, Sandro Pignata, Stefania Scala, Luigi Marra, Alessandro Ottaiano, Susan Costantini, Giuseppe Castello, Michele Cioffi, Claudia Consales, L. Claudio, Giacomo Cartenì, Rosa Calemma, Marianeve Polimeno, Nicola Longo, Luigi Portella, Crescenzo D'Alterio, D'Alterio, C, Consales, C, Polimeno, M, Franco, Renato, Cindolo, L, Portella, L, Cioffi, M, Calemma, R, Marra, L, Claudio, L, Perdona, S, Pignata, S, Facchini, G, Carteni, G, Longo, N, Pucci, L, Ottaiano, A, Costantini, S, Castello, G, and Scala, S.

Subjects
Male, Aging, Receptors, CXCR4, Cancer Research, Pathology, medicine.medical_specialty, Biology, Kidney, CXCR4, Disease-Free Survival, Chemokine receptor, Renal cell carcinoma, Drug Discovery, medicine, Carcinoma, Humans, RNA, Messenger, Carcinoma, Renal Cell, Survival analysis, Aged, Neoplasm Staging, Receptors, CXCR, Pharmacology, Reverse Transcriptase Polymerase Chain Reaction, Cancer, Kidney metabolism, Prognosis, medicine.disease, Immunohistochemistry, Survival Analysis, Kidney Neoplasms, Oncology, Lymphatic Metastasis, Concomitant, Cancer research, Female, Neoplasm Recurrence, Local
Abstract

CXCR4 is a chemokine receptor implicated in the metastatic process. The CXCR4 ligand, CXCL12, was shown to bind also the CXCR7 receptor, a recently deorphanized chemokine receptor whose signalling pathway and function are still controversial. This study was conducted to determine patients clinic-pathological factors and outcome according to the expressions of CXCR4 and CXCR7 in renal cell carcinoma (RCC). CXCR4 and CXCR7 expression was evaluated in 223 RCC patients through immunohistochemistry; moreover CXCR4 and CXCR7 was detected in 49 others consecutive RCC patients trough RT- PCR. CXCR4 expression was low in 42/223 RCC (18.8%), intermediate in 71/223 (31.9%) and high in 110/223 (49.3%). CXCR7 expression was low in 44/223 RCC patients (19.8%), intermediate in 65/223 (29.1%) and high in 114/223 (51.1%). High CXCR4 and high CXCR7 expression predicted shorter disease free survival. In multivariate analysis, high CXCR4 expression (p= 0.0061), high CXCR7 (p= 0.0194) expression and the concomitant high expression of CXCR4 and CXCR7 (p= 0.0235) are independent prognosis factors. Through RT-PCR, CXCR4 was overexpressed in 36/49 and CXCR7 in 33/49 samples correlating with symptoms at diagnosis and lymph nodes status. So we can hypothesize that CXCR4 and CXCR7, singularly evaluated and in combination, are valuable prognostic factors in RCC patients.

38. Differential role of CD133 and CXCR4 in renal cell carcinoma

Author

Crescenzo D'Alterio, Luca Cindolo, Claudia Consales, Giacomo Cartenì, L. Claudio, Anna Maria Riccio, Massimo Mascolo, Luigi Marra, Michele Cioffi, Vincenzo Mirone, Luigi Portella, Vincenzo Ficarra, Guido Martignoni, Paolo Chiodini, Stefania Staibano, Nicola Longo, Sisto Perdonà, Renato Franco, Mario Falsaperla, Stefania Scala, Giuseppe Castello, Marianeve Polimeno, M. Puglisi, D'Alterio, C, Cindolo, L, Portella, L, Polimeno, M, Consales, C, Riccio, A, Cioffi, M, Franco, Renato, Chiodini, Paolo, Cartenì, G, Mirone, V, Longo, N, Marra, L, Perdonà, S, Claudio, L, Mascolo, M, Staibano, S, Falsaperla, M, Puglisi, M, Martignoni, G, Ficarra, V, Castello, G, Scala, S., Franco, R, Chiodini, P, Mirone, Vincenzo, Longo, Nicola, and Staibano, Stefania

Subjects
Adult, Male, Oncology, Receptors, CXCR4, medicine.medical_specialty, renal cell carcinoma, Kaplan-Meier Estimate, Biology, Stem cell marker, CXCR4, Disease-Free Survival, Antigens, CD, Renal cell carcinoma, Cancer stem cell, Cell Line, Tumor, Internal medicine, medicine, Carcinoma, Humans, CD133, AC133 Antigen, Carcinoma, Renal Cell, neoplasms, Molecular Biology, Aged, Glycoproteins, Aged, 80 and over, Univariate analysis, Prognosis, Age Factors, Cancer, Cell Biology, Middle Aged, medicine.disease, Immunohistochemistry, Kidney Neoplasms, embryonic structures, Cancer cell, Cancer research, Female, Peptides, Developmental Biology
Abstract

The chemokine receptor CXCR4 and CD133, putative stem cell markers, were previously described in renal cancer (RCC). To evaluate the biological and prognostic role of CD133 and CXCR4 in RCC the expression was evaluated through qPCR and immunoblotting in human renal cancer cell lines (786-O, A498, ACHN, CAKI-1, SN12C, TK10, UO31) and patients biopsies. Renal cancer cells and surgical biopsies expressed functional CXCR4 while CD133 was not detectable. CXCR4 and CD133 expression was then evaluated in 240 renal cancer patients through immunohistochemistry. CXCR4 and CD133 were low in 19.1% and 59.6%; intermediate in 20% and 17.9%; high in 60.8% and 22.5% of the cases, respectively. CXCR4 was overexpressed in tumours (p= 0.02), while CD133 was over expressed in healthy tissues (p= 0.04). Disease free survival Kaplan Meier plots suggest that prognosis is unfavourable for patients whose primary tumours express CXCR4 (p= 0.0199) but nor CD133 (p= 0.151) neither the concomitant CXCR4-CD133 (p=0.848) high expression affected prognosis. Analysis of prognostic factors suggests that age, clinical presentation, AJCC stage and CXCR4 had a significant prognostic value at the univariate analysis. The CXCR4 predictive ability was confirmed at the multivariate analysis while no prognostic role was identified for CD133.Thus concomitant CD133 and CXCR4 evaluation is not worth in RCC patient while the CXCR4 prognostic role encourage CXCR4 antagonists as promising therapeutic option.

39. A 25-year-long journey into interventional cardiology: looking back, and rushing forward.

Author

Corcione N, Ferraro P, Morello A, Cimmino M, Albanese M, Avellino R, Turino S, Polimeno M, Messina S, Maresca G, Giordano S, Biondi-Zoccai G, Pepe M, and Giordano A

Subjects
Humans, History, 21st Century, History, 20th Century, Percutaneous Coronary Intervention, Drug-Eluting Stents, Cardiovascular Diseases therapy, Italy, Stents, Transcatheter Aortic Valve Replacement, Cardiology
Abstract

Cardiovascular disease remains decade after decade a leading cause of mortality, morbidity and resource use globally as well as locally. We have had the opportunity of being involved in several iterative breakthroughs in invasive cardiovascular procedures, ranging from the advent of coronary stents to transcatheter mitral valve repair. Building up such extensive clinical and research experience, we hereby present 25 years of cardiovascular interventions at Pineta Grande Hospital and Casa di Salute S. Lucia, respectively in Castel Volturno, and S. Giuseppe Vesuviano, both in the Italian Campania region, where the same team of interventional cardiologists has managed to adopt and master several cardiovascular innovations for the benefit of thousands of patients. Our experience showcases the evolution of invasive cardiology, especially in diagnostic and therapeutic practices. Key highlights include advancements in coronary procedures, with the introduction of bare-metal stents, drug-eluting stents and drug-coated balloons, despite the setback of bioresorbable vascular scaffolds, as well as transcatheter aortic valve implantation and innovative approaches to mitral regurgitation. Furthermore, this overview scrutinizes procedural challenges, patient outcomes, and quality of life improvements, providing a rich tapestry of clinical experiences and research insights. It serves as a testament to the dynamic nature of interventional cardiology, offering a forward-looking perspective on future trends and technologies. We hope that this overview will prove an informative and insightful read for those seeking to understand the intricate journey of invasive cardiovascular care over the past decades and its trajectory into the future.

Published
2024
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40. Validation of PLASMIC score in a cohort of patients with suspected thrombotic microangiopathy in an academic medical centre.

Author

Tufano A, Polimeno M, Matani B, Cardillo G, Capasso F, Mormile R, Paladino F, and Di Minno G

Subjects
Humans, Retrospective Studies, Academic Medical Centers, Platelet Count, ADAMTS13 Protein, Purpura, Thrombotic Thrombocytopenic diagnosis, Purpura, Thrombotic Thrombocytopenic therapy, Thrombotic Microangiopathies diagnosis, Thrombotic Microangiopathies etiology, Thrombotic Microangiopathies therapy
Abstract

Background: The PLASMIC score is a rapid and inexpensive clinical assessment tool for predicting severe ADAMTS13 deficiency (<10% activity) in patients with suspected thrombotic thrombocytopenic purpura (TTP). The score includes 7 parameters: absence of active cancer, patient not having received stem cell transplant or organ transplant, platelet count <30×10 9 /L, hemolysis, mean corpuscular volume <90 fl, International Normalized Ratio <1.5, and serum creatinine <2 mg/dL., Materials and Methods: In this retrospective study, we evaluated a cohort of 59 consecutive patients with suspected thrombotic microangiopathy who had been referred to the Hemostasis and Thrombosis Center of the "Federico II" University of Naples, Italy, for measurement of ADAMTS13 activity. Relevant clinical and laboratory information were collected for all patients., Results: The PLASMIC score was calculated in 52 of the 59 patients included in the study. In the high-risk group (PLASMIC score 6 or 7), 12 out of 20 patients (60%) had ADAMTS13 <10%. Interestingly, all 6 patients (100%) with PLASMIC score 7 had ADAMTS13 <5%. In the intermediate risk group (score 5), only one case out of 17 (5.9%) had ADAMTS 13 <10%. In the low-risk group (score 0-4), none of the patients had severe ADAMTS13 deficiency. The collected data enabled the sensitivity and specificity of PLASMIC score in TTP to be calculated, achieving 92% (95% CI: 0.80-0.98) and 79% (95% CI: 0.66-0.89), respectively. The PLASMIC score was seen to be a very efficient tool in distinguishing between patients with severe ADAMTS13 deficiency from those without, with an AUC of 0.92 (95% CI: 0.82-1.0; p<0.001)., Discussion: In our cohort, a high-risk PLASMIC score successfully predicted patients with severe ADAMTS13 deficiency, allowing the clinician to quickly define the best therapeutic approach, especially useful for those clinicians not used to the diagnosis and treatment of thrombotic microangiopathies.

Published
2023
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41. Toward a Realistic Model of Diffusion-Limited Aggregation: Rotation, Size-Dependent Diffusivities, and Settling.

Author

Polimeno M, Kim C, and Blanchette F

Abstract

In this Brownian dynamics simulation study on the formation of aggregates made of spherical particles, we build on the well-established diffusion-limited cluster aggregation (DLCA) model. We include rotational effects, allow diffusivities to be size-dependent as is physically relevant, and incorporate settling under gravity. We numerically characterize the growth dynamics of aggregates and find that their radius of gyration, R g , grows approximately as R g ∼ t 1.02 for classical DLCA but slows to an approximate growth rate of R g ∼ t 0.71 when diffusivity is size-dependent. We also analyze the fractal structure of the resulting aggregates and find that their fractal dimension, d , decreases from d ≈ 1.8 for classical DLCA to d ≈ 1.7 when size-dependent rotational diffusion is included. The addition of settling effects further reduces the fractal dimension observed to d ≈ 1.6 and appears to result in aggregates with a vertical extent marginally smaller than their horizontal extent., Competing Interests: The authors declare no competing financial interest., (© 2022 The Authors. Published by American Chemical Society.)

Published
2022
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42. Paradigm shift for the treatment of hereditary haemophilia: Towards precision medicine.

Author

Spadarella G, Di Minno A, Milan G, Franco N, Polimeno M, Castaldo F, and Di Minno G

Subjects
Humans, Precision Medicine, Hemophilia A therapy, Hemophilia B therapy
Abstract

Patients with haemophilia A (HA) or B (HB) experience spontaneous limb- or life-threatening bleedings which are prevented by regular prophylactic intravenous infusions of the deficient coagulation factor (FVIII or FIX). Prophylaxis with subcutaneous long-acting non-factor products that improve in vivo thrombin generation is now under intensive investigation (concizumab, fitusiran) or successfully employed (emicizumab) in haemophilia patients. Both haemophilia patients with/without inhibitors take advantage of non-factor products employed alone. In those who also need bypassing agents (or FVIII concentrates) for breakthrough bleeds, thromboembolic events and/or thrombotic microangiopathy may occur. By enhancing thrombin generation, prothrombotic mutations co-segregating with FVIII/FIX gene mutations may trigger thrombotic episodes in HA patients carrying acquired thrombogenic factors (e.g. venous catheters). A thorough knowledge of individual needs increasingly contributed to improve comprehensive care and personalize treatments in haemophilia. Integrating genomics, lifestyle and environmental data is expected to be key to: 1) identify which haemophilia patients are less likely to benefit from a given intervention; 2) define optimal dosing and scheduling of bypassing agents (or FVIII) to employ in combination with non-factor products; 3) establish tests to monitor in vivo thrombin generation; 4) improve communication and deliver results to individuals. As individual outcomes will be improved and the risk of adverse events minimized, non-factor products will come into wider use within the haemophilia community, and patients will hopefully have no more risks of breakthrough bleeds. The risks of a normal life for a "former haemophilia patient" is likely to change the treatment landscape and the structure of haemophilia Centers., Competing Interests: Declaration of competing interest All the Authors assisted with the writing of this manuscript. None of the Authors received remuneration for preparation of this manuscript and no sponsors were involved with writing of the manuscript. The views expressed in the manuscript are those of the authors alone. The authors stated that they had no interests which might be perceived as posing a conflict or bias. PC, protein C; APC, activated protein C; AT, antithrombin; TF, tissue factor; TFPI, tissue factor pathway inhibitor; EPCR, endothelial protein C receptor; PAR1, protease activated receptor 1. Abbreviations: APC = activated protein C; TFPI = tissue factor pathway inhibitor; TF = tissue factor; EPCR = Endothelial protein C receptor (key for active transport and storage of FVIIa in extravascular tissue and for PAR1 activity [barrier protection]). See text for details. Natural anticoagulant mechanisms are indicated (red lines) and points of interventions of current non-factor products are reported (purple boxes). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.), (Copyright © 2019. Published by Elsevier Ltd.)

Published
2020
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43. Characterizing coherent structures in Bose-Einstein condensates through dynamic-mode decomposition.

Author

Curtis CW, Carretero-González R, and Polimeno M

Abstract

We use the dynamic mode decomposition (DMD) methodology to study weakly turbulent flows in two-dimensional Bose-Einstein condensates modeled by a Gross-Pitaevskii equation subject to band-limited stochastic forcing. The forcing is balanced by the removal of energy at both ends of the energy spectrum through phenomenological hypoviscosity and hyperviscosity terms. Using different combinations of these parameters, we simulate three different regimes corresponding to weak-wave turbulence, and high- and low-frequency saturation. By extracting and ranking the primary DMD modes carrying the bulk of the energy, we are able to characterize the different regimes. In particular, the proposed DMD mode projection is able to seamlessly extract the vortices present in the condensate. This is achieved despite the fact that we do not use any phase information of the condensate as it is usually not directly available in realistic atomic BEC scenarios. Being model independent, this DMD methodology should be portable to other models and experiments involving complex flows. The DMD implementation could be used to elucidate different types of turbulent regimes as well as identifying and pinpointing the existence of delicate and hidden coherent structures within complex flows.

Published
2019
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44. CXCR4-CXCL12-CXCR7, TLR2-TLR4, and PD-1/PD-L1 in colorectal cancer liver metastases from neoadjuvant-treated patients.

Author

D'Alterio C, Nasti G, Polimeno M, Ottaiano A, Conson M, Circelli L, Botti G, Scognamiglio G, Santagata S, De Divitiis C, Nappi A, Napolitano M, Tatangelo F, Pacelli R, Izzo F, Vuttariello E, Botti G, and Scala S

Abstract

A neoadjuvant clinical trial was previously conducted in patients with resectable colorectal cancer liver metastases (CRLM). At a median follow up of 28 months, 20/33 patients were dead of disease, 8 were alive with disease and 5 were alive with no evidence of disease. To shed further insight into biological features accounting for different outcomes, the expression of CXCR4-CXCL12-CXCR7, TLR2-TLR4, and the programmed death receptor-1 (PD-1)/programmed death-1 ligand (PD-L1) was evaluated in excised liver metastases. Expression profiles were assessed through qPCR in metastatic and unaffected liver tissue of 33 CRLM neoadjuvant-treated patients. CXCR4 and CXCR7, TLR2/TLR4, and PD-1/PD-L1 mRNA were significantly overexpressed in metastatic compared to unaffected liver tissues. CXCR4 protein was negative/low in 10/31, and high in 21/31, CXCR7 was negative/low in 16/31 and high in 15/31, CXCL12 was negative/low in 14/31 and high in 17/31 CRLM. PD-1 was negative in 19/30 and positive in 11/30, PD-L1 was negative/low in 24/30 and high in 6/30 CRLM. Stromal PD-L1 expression, affected the progression-free survival (PFS) in the CRLM population. Patients overexpressing CXCR4 experienced a worse PFS and cancer specific survival (CSS) ( p = 0.001 and p = 0.0008); in these patients, KRAS mutation identified a subgroup with a significantly worse CSS ( p < 0.01). Thus, CXCR4 and PD-L1 expression discriminate patients with the worse PFS within the CRLM evaluated patients. Within the CXCR4 high expressing patients carrying Mut-KRAS in CRLM identifies the worst prognostic group. Thus, CXCR4 targeting plus anti-PD-1 therapy should be explored to improve the prognosis of Mut-KRAS-high CXCR4-CRLMs.

Published
2016
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45. CXCR4 expression affects overall survival of HCC patients whereas CXCR7 expression does not.

Author

Neve Polimeno M, Ierano C, D'Alterio C, Simona Losito N, Napolitano M, Portella L, Scognamiglio G, Tatangelo F, Maria Trotta A, Curley S, Costantini S, Liuzzi R, Izzo F, and Scala S

Subjects
Adult, Aged, Aged, 80 and over, Carcinoma, Hepatocellular metabolism, Disease-Free Survival, Female, Gene Expression Regulation, Neoplastic, Hep G2 Cells, Humans, Liver Neoplasms metabolism, Male, Middle Aged, Neoplasm Proteins biosynthesis, Receptors, CXCR biosynthesis, Receptors, CXCR4 biosynthesis, Survival Rate, Carcinoma, Hepatocellular immunology, Carcinoma, Hepatocellular mortality, Liver Neoplasms immunology, Liver Neoplasms mortality, Neoplasm Proteins immunology, Receptors, CXCR immunology, Receptors, CXCR4 immunology
Abstract

Hepatocellular carcinoma (HCC) is a heterogeneous disease with a poor prognosis and limited markers for predicting patient survival. Because chemokines and chemokine receptors play numerous and integral roles in HCC disease progression, the CXCR4-CXCL12-CXCR7 axis was studied in HCC patients. CXCR4 and CXCR7 expression was analyzed by immunohistochemistry in 86 HCC patients (training cohort) and validated in 42 unrelated HCC patients (validation cohort). CXCR4 levels were low in 22.1% of patients, intermediate in 30.2%, and high in 47.7%, whereas CXCR7 levels were low in 9.3% of patients, intermediate in 44.2% and high in 46.5% of the patients in the training cohort. When correlated to patient outcome, only CXCR4 affected overall survival (P=0.03). CXCR4-CXCL12-CXCR7 mRNA levels were examined in 33/86 patients. Interestingly, the common CXCR4-CXCR7 ligand CXCL12 was expressed at significantly lower levels in tumor tissues compared to adjacent normal liver (P=0.032). The expression and function of CXCR4 and CXCR7 was also analyzed in several human HCC cell lines. CXCR4 was expressed in Huh7, Hep3B, SNU398, SNU449 and SNU475 cells, whereas CXCR7 was expressed in HepG2, Huh7, SNU449 and SNU475 cells. Huh7, SNU449 and SNU475 cells migrated toward CXCL12, and this migration was inhibited by AMD3100/anti-CXCR4 and by CCX771/anti-CXCR7. Moreover, SNU449 and Huh7 cells exhibited matrix invasion in the presence of CXCL12 and CXCL11, a ligand exclusive to CXCR7. In conclusion, CXCR4 affects the prognosis of HCC patients but CXCR7 does not. Therefore, the CXCR4-CXCL12-CXCR7 axis plays a role in the interaction of HCC with the surrounding normal tissue and represents a suitable therapeutic target.

Published
2015
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46. A registry on distal popliteal and infrapopliteal revascularization with coronary drug-eluting stents.

Author

Giordano A, Messina S, Polimeno M, Corcione N, Ferraro P, Biondi-Zoccai G, and Giordano G

Subjects
Aged, Aged, 80 and over, Feasibility Studies, Female, Humans, Leg blood supply, Limb Salvage methods, Male, Middle Aged, Registries, Retrospective Studies, Treatment Outcome, Drug-Eluting Stents, Ischemia therapy, Peripheral Arterial Disease therapy, Popliteal Artery
Abstract

Aims: Endovascular therapy for popliteal and infrapopliteal artery disease in patients with critical limb ischemia (CLI) remains challenging, given the high risk of adverse events. Favorable results for coronary balloon-expandable drug-eluting stents (DESs) in this arterial district have been reported in selected studies, but uncertainty persists on their risk-benefit balance in real-world patients. We, thus, sought to appraise our outcomes with DES implantation for distal popliteal or infrapopliteal lesions., Methods: Our institutional databases were retrospectively queried to identify patients undergoing DES implantation for distal popliteal or infrapopliteal artery disease. Baseline, lesion, procedural, and outcome data were systematically collected., Results: A total of 25 patients were treated with coronary DES, 12 (48.0%) for distal popliteal and 13 (52.0%) for infrapopliteal lesions. Four (16.0%) patients received two stents, whereas the others only one. Breakdown of DES was as follows: biolimus-eluting, everolimus-eluting, paclitaxel-eluting, and sirolimus-eluting stents in, respectively, two (8.0%), one (4.0%), one (4.0%), and 21 (84.0%), with an average stent length of 33.6 ± 13.1 mm. Improvement in Fontaine stage was achieved in 23 (92.0%) patients at 1 month and in 22 (88.0%) patients at long-term (28.8 ± 20.6 months). In this highly selected case series, no repeat revascularizations or unplanned amputations were recorded, whereas two (8.0%) patients died, the first 15.5 months and the second 19.5 months after the procedure., Conclusion: Implantation of coronary balloon-expandable DES appears feasible, safe, and effective in selected patients with focal lesions in the distal popliteal and infrapopliteal arteries.

Published
2014
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47. The renal artery conundrum: solving the puzzle of concomitant resistant hypertension and angiographic stenosis.

Author

Giordano A, Polimeno M, Messina S, Corcione N, Ferraro P, Biondi-Zoccai G, and Giordano G

Subjects
Humans, Hypertension surgery, Radiography, Renal Artery diagnostic imaging, Renal Artery surgery, Renal Artery Obstruction surgery, Hypertension complications, Hypertension diagnostic imaging, Renal Artery Obstruction complications, Renal Artery Obstruction diagnostic imaging, Sympathectomy methods
Published
2014
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48. Tirofiban induces VEGF production and stimulates migration and proliferation of endothelial cells.

Author

Giordano A, D'Angelillo A, Romano S, D'Arrigo P, Corcione N, Bisogni R, Messina S, Polimeno M, Pepino P, Ferraro P, and Romano MF

Subjects
Aorta cytology, Aorta drug effects, Cell Movement drug effects, Cells, Cultured, Endothelial Cells metabolism, Endothelium, Vascular cytology, Endothelium, Vascular drug effects, Fibrinolytic Agents pharmacology, Gene Expression Regulation drug effects, Human Umbilical Vein Endothelial Cells drug effects, Human Umbilical Vein Endothelial Cells metabolism, Humans, Tirofiban, Tyrosine pharmacology, Vascular Endothelial Growth Factor A genetics, Vascular Endothelial Growth Factor A metabolism, Cell Proliferation drug effects, Endothelial Cells drug effects, Tyrosine analogs & derivatives, Vascular Endothelial Growth Factor A drug effects
Abstract

Tirofiban is a fibrinogen receptor antagonist, generated using the tripeptide Arg-Gly-Asp (RGD) as a template. RGD activates integrin receptors and integrin-mediated signals are necessary for normal cells to promote survival and stimulate cell cycle progression. We investigated whether tirofiban activated growth-stimulatory signals in endothelium. For this study human umbilical vein endothelial cells (HUVEC) and human aortic endothelial cells (HAEC) were used. Analysis of cell proliferation, by cell counts, showed that the number of endothelial cells doubled after 72 h of culture in the absence of tirofiban, while they were tripled and even quadrupled, in the presence of increasing doses of the drug. Moreover, tirofiban-stimulated cells had a greater ability to migrate through the transwell filters of Boyden chamber, compared to unstimulated cells. The scratch assay, which mimics cell migration during wound healing, showed that tirofiban stimulated HUVECs to migrate into the leading hedge of the scratch. Western blot showed that tirofiban increased the expression levels of VEGF and the downstream effectors Erk and cyclin D. An inhibitor of VEGFR2 counteracted tirofiban-induced-proliferation, suggesting a role for VEGF in such effect. Our study shows that tirofiban stimulates the migration and proliferation of endothelial cells suggesting that it can promote endothelial repair. Ex vivo cultures of arterial rings confirmed the growth stimulatory effect of tirofiban on endothelium. Thus, the benefits of tirofiban in those with acute coronary syndromes undergoing PTCA may be due to rapid endothelization of damaged vessel, besides antiplatelet effects., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Published
2014
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49. Transcatheter renal sympathetic denervation despite angiographically significant proximal stenosis: proof of concept from a case report.

Author

Giordano A, Polimeno M, Messina S, Corcione N, Ferraro P, Marullo L, Biondi-Zoccai G, and Giordano G

Subjects
Aged, Angiography, Humans, Hypertension, Renal diagnostic imaging, Male, Renal Artery diagnostic imaging, Renal Artery Obstruction diagnostic imaging, Hypertension, Renal surgery, Renal Artery innervation, Renal Artery Obstruction surgery, Sympathectomy methods
Published
2014
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50. No surprising forward jump when deploying a self-expandable stent: two cases exploiting the combination of Emboshield Nav6 BareWire and Stentys devices.

Author

Giordano A, Corcione N, Polimeno M, Messina S, Biondi-Zoccai G, and Ferraro P

Subjects
Aged, Female, Humans, Intraoperative Complications prevention & control, Male, Middle Aged, Prosthesis Design, Coronary Disease surgery, Prosthesis Implantation instrumentation, Prosthesis Implantation methods, Stents
Published
2013
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