120 results on '"De Gennaro Colonna V"'
Search Results
2. RESEARCH: Effects of Long-Term Disease-Modifying Antirheumatic Drugs on Endothelial Function in Patients with Early Rheumatoid Arthritis
- Author
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Turiel, M., Tomasoni, L., Sitia, S., Cicala, S., Gianturco, L., Ricci, C., Atzeni, F., De Gennaro Colonna, V., Longhi, M., and Sarzi-Puttini, P.
- Published
- 2010
- Full Text
- View/download PDF
3. Aspects of neurotransmitter control of GH secretion: basic and clinical studies
- Author
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Camanni, F., Ghigo, E., Mazza, E., Imperiale, E., Goffi, S., Martina, V., De Gennaro Colonna, V., Cella, S. G., Cocchi, D., Locatelli, V., Massara, F., Müller, E. E., MÜller, Eugenio E., editor, Cocchi, Daniela, editor, and Locatelli, Vittorio, editor
- Published
- 1989
- Full Text
- View/download PDF
4. Lipid-lowering therapy of everolimus-related severe hypertriglyceridaemia in a pancreatic neuroendocrine tumour (pNET)
- Author
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De Gennaro Colonna, V., primary, Pavanello, C., additional, Rusconi, F., additional, Sartore-Bianchi, A., additional, Siena, S., additional, Castelnuovo, S., additional, Sirtori, C. R., additional, and Mombelli, G., additional
- Published
- 2017
- Full Text
- View/download PDF
5. PP.13.06
- Author
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Rescaldani, M., primary, Gherbesi, E., additional, De Gennaro Colonna, V., additional, Bolla, G., additional, Sala, C., additional, and Lombardi, F., additional
- Published
- 2015
- Full Text
- View/download PDF
6. Endothelial dysfunction in early rheumatoid arthritis : 24 months follow-up study
- Author
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Sitia, S., Tomasoni, L., Cicala, S., Delfino, L., Bodini, B., Atzeni, F., Sarzi-Puttini, P., De Gennaro Colonna, V., and Turiel, M.
- Subjects
Settore MED/09 - Medicina Interna - Published
- 2008
7. Endothelial dysfunction in early rheumatoid arthritis
- Author
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Turiel, M., Tomasoni, L., Delfino, L., Bodini, B., Bacchiani, G., Atzeni, F., Sarzi-Puttini, P., and De Gennaro Colonna, V.
- Subjects
Settore MED/09 - Medicina Interna - Published
- 2008
8. Clinical implications of assessing coronary flow reserve and plasma asymmetric dimethylarginine in early rheumatoid arthritis
- Author
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Turiel, M., Tomasoni, L., Delfino, L., Bodini, B., Bacchiani, G., Atzeni, F., Sarzi Puttini, P., and De Gennaro Colonna, V.
- Subjects
Settore MED/09 - Medicina Interna - Published
- 2007
9. Leptin regulates GH secretion in the rat by acting on GHRH and somatostatin neurons
- Author
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Cocchi, Daniela, DE GENNARO COLONNA, V., Bagnasco, M., Bonacci, D., and Muller, E. E.
- Subjects
leptin ,obesity ,GHRH ,somatostatin - Published
- 1999
10. THU0320 New Parameters for Identifying Subclinical Atherosclerosis in Patients with Primary SjöGren’s Syndrome: A Pilot Study
- Author
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Atzeni, F., primary, Sarzi-Puttini, P., additional, Gianturco, L., additional, Signorello, M. C., additional, Boccassini, L., additional, Ricci, C., additional, De Gennaro Colonna, V., additional, and Turiel, M., additional
- Published
- 2013
- Full Text
- View/download PDF
11. AB0797 Impairment of coronary microcirculation in patients with diffuse systemic sclerosis
- Author
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Atzeni, F., primary, Gianturco, L., additional, Sarzi-Puttini, P., additional, Ricci, C., additional, Tommasoni, L., additional, De Gennaro Colonna, V., additional, Ferrario, P., additional, Epis, O., additional, and Turiel, M., additional
- Published
- 2013
- Full Text
- View/download PDF
12. Characterization of the hypothalamo-pituitary-IGF-1 axis in rats made obese by overfeeding
- Author
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Cattaneo, L., DE GENNARO COLONNA, V., Zoli, M., Muller, E. E., and Cocchi, Daniela
- Subjects
obesity ,somatotropic axis - Published
- 1996
13. SOMATOTROPIC DISREGULATION IN OLD MAMMALS
- Author
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Muller, Ee, Cella, Sg, Parenti, M, Deghenghi, R, Locatelli, V, DE GENNARO COLONNA, V, Torsello, A, and Cocchi, Daniela
- Subjects
rats ,dogs ,aging ,growth hormone - Published
- 1995
14. Cardiovascular involvement in psoriatic arthritis
- Author
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Atzeni, F., primary, Turiel, M., additional, Boccassini, L., additional, Sitia, S., additional, Tomasoni, L., additional, Battellino, M., additional, Marchesoni, A., additional, De Gennaro Colonna, V., additional, and Sarzi-Puttini, P., additional
- Published
- 2011
- Full Text
- View/download PDF
15. Cardiac involvement in rheumatoid arthritis
- Author
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Turiel, M., primary, Sitia, S., additional, Tomasoni, L., additional, Cicala, S., additional, Atzeni, F., additional, Gianturco, L., additional, Longhi, M., additional, De Gennaro Colonna, V., additional, and Sarzi-Puttini, P., additional
- Published
- 2011
- Full Text
- View/download PDF
16. Poster session V * Saturday 11 December 2010, 08:30-12:30
- Author
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Pham, Q. H., primary, Von Lueder, T. G., additional, Namtvedt, S. K., additional, Rosjo, H., additional, Omland, T., additional, Steine, K., additional, Timoteo, A. T., additional, Mota Carmo, M., additional, Simoes, M., additional, Branco, L. M., additional, Ferreira, R. C., additional, Kato, R., additional, Ito, J., additional, Tahara, T., additional, Yokoyama, Y., additional, Ashikaga, T., additional, Satoh, Y., additional, Na, J. O., additional, Hong, H. E., additional, Kim, M. N., additional, Shin, S. Y., additional, Choi, C. U., additional, Kim, E. J., additional, Rha, S. W., additional, Park, C. G., additional, Seo, H. S., additional, Oh, D. J., additional, Ticulescu, R., additional, Brigido, S., additional, Vriz, O., additional, Sparacino, L., additional, Popescu, B. A., additional, Ginghina, C., additional, Carerj, S., additional, Nicolosi, G. L., additional, Antonini-Canterin, F., additional, Onaindia Gandarias, J. J., additional, Romero, A., additional, Laraudogoitia, E., additional, Velasco, S., additional, Quintana, O., additional, Cacicedo, A., additional, Rodriguez, I., additional, Alarcon, J. A., additional, Gonzalez, J., additional, Lekuona, I., additional, Subinas, A., additional, Abdula, G., additional, Lund, L. H., additional, Winter, R., additional, Brodin, L., additional, Sahlen, A., additional, Masaki, M., additional, Cha, Y. M., additional, Yuasa, T., additional, Dong, K., additional, Dong, Y. X., additional, Mankad, S. V., additional, Oh, J. K., additional, Vallet, F., additional, Lequeux, B., additional, Diakov, C., additional, Sosner, P., additional, Christiaens, L., additional, Coisne, D., additional, Kihara, C., additional, Murata, K., additional, Wada, Y., additional, Uchida, K., additional, Ueyama, T., additional, Okuda, S., additional, Susa, T., additional, Matsuzaki, M., additional, Cho, E. J., additional, Choi, K. Y., additional, Kwon, B. J., additional, Kim, D. B., additional, Jang, S. W., additional, Cho, J. S., additional, Jung, H. O., additional, Jeon, H. K., additional, Youn, H. J., additional, Kim, J. H., additional, Cikes, M., additional, Bijnens, B., additional, Velagic, V., additional, Kopjar, T., additional, Milicic, D., additional, Biocina, B., additional, Gasparovic, H., additional, Almuntaser, I., additional, Brown, A., additional, Foley, B., additional, Mulvihill, N., additional, Crean, P., additional, King, G., additional, Murphy, R., additional, Takata, Y., additional, Taniguchi, M., additional, Nobusada, S., additional, Sugawara, M., additional, Toh, N., additional, Kusano, K., additional, Itoh, H., additional, Wellnhofer, E., additional, Kriatselis, C., additional, Nedios, S., additional, Gerds-Li, J. H., additional, Fleck, E., additional, Poulsen, M. K., additional, Henriksen, J. E., additional, Dahl, J., additional, Johansen, A., additional, Haghfelt, T., additional, Hoilund-Carlsen, P. F., additional, Beck-Nielsen, H., additional, Moller, J. E., additional, Dankowski, R., additional, Wierzchowiecki, M., additional, Michalski, M., additional, Nowicka, A., additional, Szymanowska, K., additional, Pajak, A., additional, Poprawski, K., additional, Szyszka, A., additional, Kasner, M., additional, Westermann, D., additional, Schultheiss, H. P., additional, Tschoepe, C., additional, Watanabe, T., additional, Iwai-Takano, M., additional, Kobayashi, A., additional, Machii, H., additional, Takeishi, Y., additional, Paelinck, B. P., additional, Van Herck, P. L., additional, Bosmans, J. M., additional, Vrints, C. J., additional, Lamb, H. J., additional, Doltra, A., additional, Vidal, B., additional, Silva, E., additional, Poyatos, S., additional, Mont, L., additional, Berruezo, A., additional, Castel, A., additional, Tolosana, J. M., additional, Brugada, J., additional, Sitges, M., additional, Dencker, M., additional, Bjorgell, O., additional, Hlebowicz, J., additional, Szelenyi, Z. S., additional, Szenasi, G., additional, Kiss, M., additional, Prohaszka, Z., additional, Patocs, A., additional, Karadi, I., additional, Vereckei, A., additional, Saha, S. K., additional, Anderson, P. L., additional, Govind, S., additional, Govindan, M., additional, Moggridge, J. C., additional, Kiotsekoglou, A., additional, Gopal, A. S., additional, Loegstrup, B. B., additional, Christophersen, T. B., additional, Hoefsten, D. E., additional, Moeller, J. E., additional, Boetker, H. E., additional, Egstrup, K., additional, Graefe, M., additional, Huang, F. Q., additional, Zhang, R. S., additional, Le, T. T., additional, Tan, R. S., additional, Sattarzadeh Badkoubeh, R., additional, Tavoosi, A., additional, Elahian, A. R., additional, Drapkina, O., additional, Ivashkin, V. I., additional, Fazakas, A., additional, Pepo, L., additional, Janosi, O., additional, Kopitovic, I., additional, Goncalves, A., additional, Marcos-Alberca, P., additional, Almeria, C., additional, Feltes, G., additional, Rodriguez, E., additional, Garcia, E., additional, Hernandez-Antolin, R., additional, Macaya, C., additional, Silva Cardoso, J., additional, Zamorano, J. L., additional, Navarro, M. S., additional, Valentin, M., additional, Banes, C. M., additional, Rigo, F., additional, Grolla, E., additional, Tona, F., additional, Cuaia, V., additional, Moreo, A., additional, Badano, L., additional, Raviele, A., additional, Iliceto, S., additional, Tarzia, P., additional, Sestito, A., additional, Nerla, R., additional, Di Monaco, A., additional, Infusino, F., additional, Matera, D., additional, Greco, F., additional, Tacchino, R. M., additional, Lanza, G. A., additional, Crea, F., additional, Nemes, A., additional, Balazs, E., additional, Pinter, K. S., additional, Egyed, A., additional, Csanady, M., additional, Forster, T., additional, Holte, E., additional, Vegsundvag, J., additional, Hole, T., additional, Hegbom, K., additional, Wiseth, R., additional, Sharif, D., additional, Sharif-Rasslan, A., additional, Shahla, C., additional, Khalil, A., additional, Rosenschein, U., additional, Zagatina, A., additional, Zhuravskaya, N., additional, Tyurina, T. V., additional, Tagliamonte, E., additional, Cirillo, T., additional, Coppola, A., additional, Marinelli, U., additional, Romano, C., additional, Riccio, G., additional, Citro, R., additional, Astarita, C., additional, Capuano, N., additional, Quaranta, G., additional, Desiderio, A., additional, Frattini, S., additional, Faggiano, P., additional, Zilioli, V., additional, Locantore, E., additional, Longhi, S., additional, Bellandi, F., additional, Faden, G., additional, Triggiani, M., additional, Dei Cas, L., additional, Dalsgaard, M., additional, Kjaergaard, J., additional, Iversen, K., additional, Hassager, C., additional, Dinh, W., additional, Nickl, W. N., additional, Smettan, J. S., additional, Koehler, T. K., additional, Scheffold, T. D., additional, Coll Barroso, M. C. B., additional, Guelker, J. G., additional, Fueth, R. F., additional, Kamperidis, V., additional, Hadjimiltiades, S., additional, Sianos, G., additional, Efthimiadis, G., additional, Karvounis, H., additional, Parcharidis, G., additional, Styliadis, I. H., additional, Velasco Del Castillo, M. S., additional, Onaindia, J. J., additional, Telleria, M., additional, Carstensen, H. G., additional, Nordenberg, C., additional, Sogaard, P., additional, Fritz-Hansen, T., additional, Bech, J., additional, Galatius, S., additional, Jensen, J. S., additional, Mogelvang, R., additional, Bartko, P. E., additional, Graf, S., additional, Rosenhek, R., additional, Burwash, I. G., additional, Bergler-Klein, J., additional, Clavel, M.-A., additional, Baumgartner, H., additional, Pibarot, P., additional, Mundigler, G., additional, Kirilmaz, B., additional, Eser, I., additional, Tuzun, N., additional, Komur, B., additional, Dogan, H., additional, Taskiran Comez, A., additional, Ercan, E., additional, Cusma-Piccione, M., additional, Zito, C., additional, Oreto, G., additional, Piluso, S., additional, Tripepi, S., additional, Oreto, L., additional, Longordo, C., additional, Ciraci, L., additional, Di Bella, G., additional, Piatkowski, R., additional, Kochanowski, J., additional, Scislo, P., additional, Grabowski, M., additional, Marchel, M., additional, Roik, M., additional, Kosior, D., additional, Opolski, G., additional, Sknouril, L., additional, Dorda, M., additional, Holek, B., additional, Gajdusek, L., additional, Chovancik, J., additional, Branny, M., additional, Fiala, M., additional, Szymanski, P., additional, Lipczynska, M., additional, Klisiewicz, A., additional, Hoffman, P., additional, Jander, N., additional, Minners, J., additional, Martin, G., additional, Zeh, W., additional, Allgeier, M., additional, Gohlke-Baewolf, C., additional, Gohlke, H., additional, Nistri, S., additional, Porciani, M. C., additional, Attanasio, M., additional, Abbate, R., additional, Gensini, G. F., additional, Pepe, G., additional, Duncan, R. F., additional, Piantadosi, C., additional, Nelson, A. J., additional, Wittert, G., additional, Dundon, B., additional, Worthley, M. I., additional, Worthley, S. G., additional, Jung, P., additional, Berlinger, K., additional, Rieber, J., additional, Sohn, H. Z., additional, Schneider, P., additional, Leibig, M., additional, Koenig, A., additional, Klauss, V., additional, Tomkiewicz-Pajak, L., additional, Kolcz, J., additional, Olszowska, M., additional, Pieculewicz, M., additional, Podolec, P., additional, Przewlocki, T., additional, Suchon, E., additional, Sobien, B., additional, Wilkolek, P., additional, Ziembicka, A., additional, Hlawaty, M., additional, Van De Bruaene, A., additional, Hermans, H., additional, Buys, R., additional, Vanhees, L., additional, Delcroix, M., additional, Voigt, J.-U., additional, Budts, W., additional, De Cillis, E., additional, Acquaviva, T., additional, Basile, D., additional, Bortone, A. S., additional, Kalimanovska-Ostric, D., additional, Nastasovic, T., additional, Vujisic-Tesic, B., additional, Jovanovic, I., additional, Milakovic, B., additional, Dostanic, M., additional, Stosic, M., additional, Frogoudaki, A., additional, Andreou, K., additional, Parisis, J., additional, Triantafyllidi, E., additional, Gaitani, S., additional, Paraskevaidis, J., additional, Anastasiou-Nana, M., additional, De Pasquale, G., additional, Kuehn, A., additional, Petzuch, K., additional, Mueller, J., additional, Meierhofer, C., additional, Fratz, S., additional, Hager, A., additional, Hess, J., additional, Vogt, M., additional, Attenhofer Jost, C. H., additional, Dearani, J. A., additional, Scott, C. G., additional, Burkhart, H. M., additional, Connolly, H. M., additional, Vitarelli, A., additional, Battaglia, D., additional, Caranci, F., additional, Padella, V., additional, Continanza, G., additional, Dettori, O., additional, Capotosto, L., additional, Vitarelli, M., additional, De Cicco, V., additional, Cortez Morichetti, M., additional, Mohanan Nair, K. K., additional, Sasidaharan, B., additional, Thajudeen, A., additional, Tharakan, J. M., additional, Mertens, L., additional, Ahmad, N., additional, Kantor, P. K., additional, Grosse-Wortmann, L., additional, Friedberg, M. K., additional, Bernard, Y. F., additional, Morel, M. A., additional, Descotes-Genon, V., additional, Jehl, J., additional, Meneveau, N., additional, Schiele, F., additional, Kaldararova, M., additional, Simkova, I., additional, Tittel, P., additional, Masura, J., additional, Trojnarska, O., additional, Szczepaniak, L., additional, Mizia -Stec, K., additional, Cieplucha, A., additional, Bartczak, A., additional, Grajek, S., additional, Tykarski, A., additional, Gasior, Z., additional, Babovicvuksanovic, D., additional, Bonnichsen, C. R., additional, Morgan, G. J., additional, Slorach, C., additional, Hui, W., additional, Sarkola, T., additional, Lee, K. J., additional, Chaturvedi, R., additional, Benson, L., additional, Bradley, T., additional, Iancu, M. E., additional, Ghiorghiu, I., additional, Serban, M., additional, Craciunescu, I., additional, Hodo, A., additional, Morgan, J., additional, Roche, L., additional, Lee, K., additional, Milanesi, O., additional, Favero, V., additional, Padalino, M., additional, Biffanti, R., additional, Cerutti, A., additional, Maschietto, N., additional, Reffo, E., additional, Vida, V., additional, Stellin, G., additional, Irtyuga, O., additional, Gamazin, D., additional, Voronkina, I., additional, Tsoyi, N., additional, Gudkova, E., additional, Moiseeva, O., additional, Aggeli, C., additional, Kazazaki, C., additional, Felekos, I., additional, Lagoudakou, S., additional, Roussakis, G., additional, Skoumas, J., additional, Pitsavos, C., additional, Stefanadis, C., additional, Cueff, C., additional, Keenan, N., additional, Steg, P. G., additional, Cimadevilla, C., additional, Ducrocq, G., additional, Vahanian, A., additional, Messika-Zeitoun, D., additional, Petrella, L., additional, Mazzola, A. M., additional, Villani, C. V., additional, Giancola, R. G., additional, Ciocca, M. C., additional, Di Eusanio, D. E. M., additional, Nolan, S., additional, Ionescu, A., additional, Skaug, T. R., additional, Amundsen, B. H., additional, Hergum, T., additional, Torp, H., additional, Haugen, B. O., additional, Lopez Aguilera, J., additional, Mesa Rubio, D., additional, Ruiz Ortiz, M., additional, Delgado Ortega, M., additional, Villanueva Fernandez, E., additional, Cejudo Diaz Del Campo, L., additional, Toledano Delgado, F., additional, Leon Del Pino, M., additional, Romo Pena, E., additional, Suarez De Lezo Cruz-Conde, J., additional, De Marco, E., additional, Colucci, A., additional, Comerci, G., additional, Gabrielli, F. A., additional, Natali, R., additional, Garramone, B., additional, Savino, M., additional, Lotrionte, M., additional, Sonaglioni, A., additional, Loperfido, F., additional, Zdravkovic, M., additional, Perunicic, J., additional, Krotin, M., additional, Ristic, M., additional, Vukomanovic, V., additional, Zaja, M., additional, Radovanovic, S., additional, Saric, J., additional, Zdravkovic, D., additional, Cotrim, C., additional, Almeida, A. R., additional, Miranda, R., additional, Almeida, A. G., additional, Picano, E., additional, Carrageta, M., additional, D'andrea, A., additional, Cocchia, R., additional, Riegler, L., additional, Golia, E., additional, Scarafile, R., additional, Caso, P., additional, Russo, M. G., additional, Bossone, E., additional, Calabro', R., additional, Noman, H., additional, Adel, A., additional, Elfaramawy, A. M. R., additional, Abdelraouf, M., additional, Elnaggar, W. A. E. L., additional, Baligh, E., additional, Sargento, L., additional, Silva, D., additional, Goncalves, S., additional, Ribeiro, S., additional, Vinhas Sousa, G., additional, Almeida, A., additional, Lopes, M., additional, Rodriguez-Manero, M., additional, Aguado Gil, L., additional, Azcarate, P., additional, Lloret Luna, P., additional, Macias Gallego, A., additional, Castano, S. A. R. A., additional, Garcia, M., additional, Pujol Salvador, C., additional, Barba, J., additional, Redondo, P., additional, Tomasoni, L., additional, Sitia, S., additional, Atzeni, F., additional, Gianturco, L., additional, Ricci, C., additional, Sarzi-Puttini, P., additional, Turiel, M., additional, De Gennaro Colonna, V., additional, Uejima, T., additional, Jaroch, J., additional, Polombo, C., additional, Hughes, A., additional, Vinereanu, D., additional, Evanvelista, A., additional, Leftheriotis, G., additional, Fraser, A. G., additional, Lewczuk, A., additional, Sobkowicz, B., additional, Tomaszuk-Kazberuk, A., additional, Sawicki, R., additional, Hirnle, T., additional, Michalski, B. W., additional, Filipiak, D., additional, Kasprzak, J. D., additional, Lipiec, P., additional, Dalen, H., additional, Mjolstad, O. C., additional, Klykken, B. E., additional, Graven, T., additional, Martensson, M., additional, Olsson, M., additional, Brodin, L.-A., additional, Enache, R., additional, Leiballi, E., additional, Penhall, A., additional, Perry, R., additional, Altman, M., additional, Sinhal, A., additional, Bennetts, J., additional, Chew, D. P., additional, Joseph, M. X., additional, Larsen, L. H., additional, Kristensen, T., additional, Kober, L. V., additional, Kofoed, K. F., additional, Moscoso Costa, F., additional, Ribeiras, R., additional, Brito, J., additional, Boshoff, S., additional, Neves, J., additional, Teles, R., additional, Canada, M., additional, Andrade, M. J., additional, Gouveia, R., additional, Silva, A., additional, Miskovic, A., additional, Poerner, T. P., additional, Stiller, C. S., additional, Goebel, B. G., additional, Moritz, A. M., additional, Stefani, L., additional, Galanti, G. G., additional, Moraldo, M., additional, Bergamini, C., additional, Pabari, P. A., additional, Dhutia, N. M., additional, Malaweera, A. S. N., additional, Willson, K., additional, Davies, J., additional, Hughes, A. D., additional, Xu, X. Y., additional, Francis, D. P., additional, Jasaityte, R., additional, Amundsen, B., additional, Barbosa, D., additional, Loeckx, D., additional, Kiss, G., additional, Orderud, F., additional, Robesyn, V., additional, Claus, P., additional, D'hooge, J., additional, Nao, T., additional, Miura, T., additional, Shams, K., additional, Samir, S., additional, Samir, R., additional, El-Sayed, M., additional, Anwar, A. M., additional, Nosir, Y., additional, Galal, A., additional, Chamsi-Pasha, H., additional, Ciobanu, A., additional, Dulgheru, R., additional, Bennett, S., additional, De Luca, A., additional, Toncelli, L., additional, Cappelli, F., additional, Cappelli, B., additional, Vono, M. C. R., additional, Galanti, G., additional, Zorman, Y., additional, Yilmazer, M. S., additional, Akyildiz, M., additional, Gurol, T., additional, Aydin, A., additional, Dagdeviren, B., additional, and Kalangos, A., additional
- Published
- 2010
- Full Text
- View/download PDF
17. Poster session II * Thursday 9 December 2010, 14:00-18:00
- Author
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Pabari, P. A., primary, Kyriacou, A., additional, Moraldo, M., additional, Unsworth, B., additional, Baruah, R., additional, Sutaria, N., additional, Hughes, A., additional, Mayet, J., additional, Francis, D. P., additional, Uejima, T., additional, Loboz, K., additional, Antonini-Canterin, F., additional, Polombo, C., additional, Carerj, S., additional, Vinereanu, D., additional, Evangelista, A., additional, Leftheriotis, G., additional, Fraser, A. G., additional, Kiotsekoglou, A., additional, Govindan, M., additional, Govind, S. C., additional, Saha, S. K., additional, Camm, A. J., additional, Azcarate, P. M., additional, Castano, S., additional, Rodriguez-Manero, M., additional, Arraiza, M., additional, Levy, B., additional, Barba, J., additional, Rabago, G., additional, Bastarrika, G., additional, Nemes, A., additional, Takacs, R., additional, Varkonyi, T., additional, Gavaller, H., additional, Baczko, I., additional, Forster, T., additional, Wittmann, T., additional, Papp, J. G., additional, Lengyel, C., additional, Varro, A., additional, Tumasyan, L. R., additional, Adamyan, K. G., additional, Savu, O., additional, Mieghem, T., additional, Dekoninck, P., additional, Gucciardo, L., additional, Jurcut, R., additional, Giusca, S., additional, Popescu, B. A., additional, Ginghina, C., additional, Deprest, J., additional, Voigt, J. U., additional, Versiero, M., additional, Galderisi, M., additional, Esposito, R., additional, Rapacciuolo, A., additional, Esposito, G., additional, Raia, R., additional, Morgillo, T., additional, Piscione, F., additional, De Simone, G., additional, Oraby, M. A., additional, Maklady, F. A., additional, Mohamed, E. M., additional, Eraki, A. 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T., additional, Shim, A., additional, Lipec, P., additional, Michalski, B., additional, Wozniakowski, B., additional, Stefanczyk, L., additional, Rotkiewicz, A., additional, Cameli, M., additional, Lisi, M., additional, Padeletti, M., additional, Bigio, E., additional, Bernazzali, S., additional, Tsoulpas, C., additional, Maccherini, M., additional, Henein, M., additional, Mondillo, S., additional, Garcia Lunar, I., additional, Mingo Santos, S., additional, Monivas Palomero, V., additional, Mitroi, C., additional, Beltran Correas, P., additional, Ruiz Bautista, L., additional, Muniz Lozano, A., additional, Gonzalez Gonzalez, M., additional, Pabari, P. A., additional, Stegemann, B., additional, Willson, K., additional, Zeppellini, R., additional, Iavernaro, A., additional, Zadro, M., additional, Carasi, M., additional, De Domenico, R., additional, Rigo, T., additional, Artuso, E., additional, Erente, G., additional, Ramondo, A., additional, Le, T. T., additional, Huang, F. Q., additional, Gu, Y., additional, and Tan, R. S., additional
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- 2010
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18. Poster session III * Friday 10 December 2010, 08:30-12:30
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Guldbrand, D., primary, Goetzsche, O., additional, Eika, B., additional, Watanabe, N., additional, Taniguchi, M., additional, Akagi, T., additional, Koide, N., additional, Sano, S., additional, Orbovic, B., additional, Obrenovic-Kircanski, B., additional, Ristic, S., additional, Soskic, L. J., additional, Alhabshan, F., additional, Jijeh, A., additional, Abo Remsh, H., additional, Alkhaldi, A., additional, Najm, H. K., additional, Gasior, Z., additional, Skowerski, M., additional, Kulach, A., additional, Szymanski, L., additional, Sosnowski, M., additional, Wang, M., additional, Siu, C. W., additional, Lee, K., additional, Yue, W. S., additional, Yan, G. H., additional, Lee, S., additional, Lau, C. P., additional, Tse, H. F., additional, O'connor, K., additional, Rosca, M., additional, Magne, J., additional, Romano, G., additional, Moonen, M., additional, Pierard, L. A., additional, Lancellotti, P., additional, Floria, M., additional, De Roy, L., additional, Blommaert, D., additional, Jamart, J., additional, Dormal, F., additional, Lacrosse, M., additional, Arsenescu Georgescu, C., additional, Mizariene, V., additional, Bucyte, S., additional, Bertasiute, A., additional, Pociute, E., additional, Zaliaduonyte-Peksiene, D., additional, Baronaite-Dudoniene, K., additional, Sileikiene, R., additional, Vaskelyte, J., additional, Jurkevicius, R., additional, Dencker, M., additional, Thorsson, O., additional, Karlsson, M. K., additional, Linden, C., additional, Wollmer, P., additional, Andersen, L. B., additional, Catalano, O., additional, Perotti, M. R., additional, Colombo, E., additional, De Giorgi, M., additional, Cattaneo, M., additional, Cobelli, F., additional, Priori, S. G., additional, Ober, C., additional, Iancu Adrian, I. A., additional, Andreea Parv, P. A., additional, Cadis Horatiu, C. H., additional, Ober Mihai, O. M., additional, Chmielecki, M., additional, Fijalkowski, M., additional, Galaska, R., additional, Dubaniewicz, W., additional, Lewicki, L., additional, Targonski, R., additional, Ciecwierz, D., additional, Puchalski, W., additional, Koprowski, A., additional, Rynkiewicz, A., additional, Hristova, K., additional, La Gerche, A., additional, Katova, T. Z., additional, Kostova, V., additional, Simova, Y., additional, Kempny, A., additional, Diller, G. P., additional, Orwat, S., additional, Kaleschke, G., additional, Kerckhoff, G., additional, Schmidt, R., additional, Radke, R. M., additional, Baumgartner, H., additional, Smarz, K., additional, Zaborska, B., additional, Jaxa-Chamiec, T., additional, Maciejewski, P., additional, Budaj, A., additional, Kiotsekoglou, A., additional, Govind, S. C., additional, Gadiyaram, V., additional, Moggridge, J. C., additional, Govindan, M., additional, Gopal, A. S., additional, Ramesh, S. S., additional, Brodin, L. A., additional, Saha, S. K., additional, Ramzy, I. S., additional, Lindqvist, P., additional, Lam, Y. Y., additional, Duncan, A. M., additional, Henein, M. Y., additional, Craciunescu, I. S., additional, Serban, M., additional, Iancu, M., additional, Revnic, C., additional, Popescu, B. A., additional, Alexandru, D., additional, Rogoz, D., additional, Uscatescu, V., additional, Ginghina, C., additional, Careri, G., additional, Di Monaco, A., additional, Nerla, R., additional, Tarzia, P., additional, Lamendola, P., additional, Sestito, A., additional, Lanza, G. A., additional, Crea, F., additional, Giannini, F., additional, Pinamonti, B., additional, Santangelo, S., additional, Perkan, A., additional, Vitrella, G., additional, Rakar, S., additional, Merlo, M., additional, Della Grazia, E., additional, Salvi, A., additional, Sinagra, G., additional, Scislo, P., additional, Kochanowski, J., additional, Piatkowski, R., additional, Roik, M., additional, Postula, M., additional, Opolski, G., additional, Castillo, J., additional, Herszkowicz, N., additional, Ferreira, C., additional, Lonnebakken, M. T., additional, Staal, E. M., additional, Nordrehaug, J. E., additional, Gerdts, E., additional, Przewlocka-Kosmala, M., additional, Orda, A., additional, Karolko, B., additional, Bajraktari, G., additional, Gustafsson, U., additional, Holmgren, A., additional, Frattini, S., additional, Faggiano, P., additional, Zilioli, V., additional, Locantore, E., additional, Longhi, S., additional, Bellandi, F., additional, Faden, G., additional, Triggiani, M., additional, Dei Cas, L., additional, Seo, S. M., additional, Jung, H. O., additional, An, S. H., additional, Jung, S. Y., additional, Park, C. S., additional, Jeon, H. K., additional, Youn, H. J., additional, Chung, W. B., additional, Kim, J. H., additional, Uhm, J. S., additional, Mampuya, W., additional, Brochu, M. C., additional, Do, D. H., additional, Essadiqi, B., additional, Farand, P., additional, Lepage, S., additional, Daly, M. 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R., additional, Slikkerveer, J., additional, Appelman, Y. E. A., additional, Veen, G., additional, Porter, T. R., additional, Kamp, O., additional, Colonna, P., additional, Ten Cate, F. J., additional, Bokor, D., additional, Daponte, A., additional, Cocciolo, M., additional, Bona, M., additional, Sacchi, S., additional, Becher, H., additional, Chai, S. C., additional, Tan, P. J., additional, Goh, Y. S., additional, Ong, S. H., additional, Chow, J., additional, Lee, L. L., additional, Goh, P. P., additional, Tong, K. L., additional, Kakihara, R., additional, Naruse, C., additional, Hironaka, H., additional, Tsuzuku, T., additional, Ozawa, K., additional, Tomaszuk-Kazberuk, A., additional, Sobkowicz, B., additional, Malyszko, J., additional, Malyszko, J. S., additional, Sawicki, R., additional, Hirnle, T., additional, Dobrzycki, S., additional, Mysliwiec, M., additional, Musial, W. J., additional, Mathias, W., additional, Kowatsch, I., additional, Saroute, A. L. R., additional, Osorio, A. F. F., additional, Sbano, J. C. N., additional, Ramires, J. A. F., additional, Tsutsui, J. M., additional, Sakata, K., additional, Ito, H., additional, Ishii, K., additional, Sakuma, T., additional, Iwakura, K., additional, Yoshino, H., additional, Yoshikawa, J., additional, Shahgaldi, K., additional, Lopez, A., additional, Fernstrom, B., additional, Sahlen, A., additional, Winter, R., additional, Kovalova, S., additional, Necas, J., additional, Amundsen, B. H., additional, Jasaityte, R., additional, Kiss, G., additional, Barbosa, D., additional, D'hooge, J., additional, Torp, H., additional, Szmigielski, C. A., additional, Newton, J. D., additional, Rajpoot, K., additional, Noble, J. A., additional, Kerber, R., additional, Koopman, L. P., additional, Slorach, C., additional, Chahal, N., additional, Hui, W., additional, Sarkola, T., additional, Bradley, T. J., additional, Jaeggi, E. T., additional, Mccrindle, B. W., additional, Staron, A., additional, Jasinski, M., additional, Wos, S., additional, Sengupta, P., additional, Hayat, D., additional, Kloeckner, M., additional, Nahum, J., additional, Dussault, C., additional, Dubois Rande, J. L., additional, Gueret, P., additional, Lim, P., additional, King, G. J., additional, Brown, A., additional, Ho, E., additional, Amuntaser, I., additional, Bennet, K., additional, Mc Elhome, N., additional, Murphy, R. T., additional, Cooper, R. M., additional, Somauroo, J. D., additional, Shave, R. E., additional, Williams, K. L., additional, Forster, J., additional, George, C., additional, Bett, T., additional, George, K. P., additional, D'andrea, A., additional, Riegler, L., additional, Cocchia, R., additional, Golia, E., additional, Gravino, R., additional, Salerno, G., additional, Citro, R., additional, Caso, P. I. O., additional, Bossone, E., additional, Calabro', R., additional, Crispi, F., additional, Figueras, F., additional, Bartrons, J., additional, Eixarch, E., additional, Le Noble, F., additional, Ahmed, A., additional, Gratacos, E., additional, Shang, Q., additional, Yip, W. K., additional, Tam, L. S., additional, Zhang, Q., additional, Li, C. M., additional, Wang, T., additional, Ma, C. Y., additional, Li, K. M., additional, Yu, C. M., additional, Dahlslett, T., additional, Helland, I., additional, Edvardsen, T., additional, Skulstad, H., additional, Magda, L. S., additional, Florescu, M., additional, Ciobanu, A., additional, Dulgheru, R., additional, Mincu, R., additional, Vinereanu, D., additional, Luckie, M., additional, Chacko, S., additional, Nair, S., additional, Mamas, M., additional, Khattar, R. 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U., additional, Zaidi, A., additional, Heatley, M., additional, Abildstrom, S. Z., additional, Hvelplund, A., additional, Berning, J., additional, Govind, S., additional, Brodin, L., additional, Gopal, A., additional, Castaldi, B., additional, Di Salvo, G., additional, Santoro, G., additional, Gaio, G., additional, Palladino, M. T., additional, Iacono, C., additional, Pacileo, G., additional, Russo, M. G., additional, Calabro, R., additional, Wang, Y. S., additional, Dong, L. L., additional, Shu, X. H., additional, Pan, C. Z., additional, Zhou, D. X., additional, Sen, T., additional, Tufekcioglu, O., additional, Ozdemir, M., additional, Tuncez, A., additional, Uygur, B., additional, Golbasi, Z., additional, Kisacik, H., additional, Delfino, L., additional, De Leo, F. D., additional, Chiappa, L. C., additional, Abdel Ghani, B., additional, Schiavina, R., additional, Salvade, P., additional, Morganti, A., additional, Bedogni, F., additional, Mahia, P., additional, Gutierrez, L., additional, Pineda, V., additional, Garcia, B., additional, Otaegui, I., additional, Rodriguez, J. F., additional, Gonzalez, M. T., additional, Descalzo, M., additional, Evangelista, A., additional, Garcia-Dorado, D., additional, Bruin De- Bon, H. A. C. M., additional, Van Den Brink, R. B. A., additional, Surie, S., additional, Bresser, P., additional, Vleugels, J., additional, Eckmann, H. M., additional, Samson, D. A., additional, Bouma, B. 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M., additional, Sieders, A., additional, Lamb, H., additional, Ajmone Marsan, N., additional, Westenberg, J., additional, De Roos, A., additional, Schuijf, J. D., additional, Bax, J. J., additional, Anwar, A. M., additional, Nosir, Y., additional, Chamsi-Pasha, H., additional, Tschernich, H. D., additional, Seeburger, J., additional, Borger, M., additional, Mukherjee, C., additional, Mohr, F. W., additional, Ender, J., additional, Obase, K., additional, Okura, H., additional, Yamada, R., additional, Miyamoto, Y., additional, Saito, K., additional, Imai, K., additional, Hayashida, A., additional, and Yoshida, K., additional
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- 2010
- Full Text
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19. Effects of treatment strategy on endothelial function
- Author
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Tomasoni, L., primary, Sitia, S., additional, Borghi, C., additional, Cicero, A.F.G., additional, Ceconi, C., additional, Cecaro, F., additional, Morganti, A., additional, De Gennaro Colonna, V., additional, Guazzi, M., additional, Morricone, L., additional, Malavazos, A.E., additional, Marino, P., additional, Cavallino, C., additional, Shoenfeld, Y., additional, and Turiel, M., additional
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- 2010
- Full Text
- View/download PDF
20. FEED BACK EFFECTS OF GROWTH HORMONE ON GROWTH HORMONE-RELEASING HORMONE AND SOMATOSTATIN ARE NOT EVIDENT IN AGED RATS
- Author
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DE GENNARO COLONNA, V, Fidone, F, Cocchi, Daniela, and Muller, Ee
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growth hormone ,aging ,growth hormone releasing hormone ,somatostatin - Published
- 1993
21. ASPECTS OF THE NEUROENDOCRINE CONTROL OF GROWTH HORMONE SECRETION IN AGEING MAMMALS
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Muller, Ee, Cella, Sg, DE GENNARO COLONNA, V, Cocchi, Daniela, and Locatelli, V.
- Subjects
aging ,growth hormone - Published
- 1993
22. Non-invasive assessment of coronary flow reserve and ADMA levels: a case-control study of early rheumatoid arthritis patients
- Author
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Turiel, M., primary, Atzeni, F., additional, Tomasoni, L., additional, de Portu, S., additional, Delfino, L., additional, Bodini, B. D., additional, Longhi, M., additional, Sitia, S., additional, Bianchi, M., additional, Ferrario, P., additional, Doria, A., additional, De Gennaro Colonna, V., additional, and Sarzi-Puttini, P., additional
- Published
- 2009
- Full Text
- View/download PDF
23. Hexarelin, but not growth hormone, protects heart from damage induced in vitro by calcium deprivation replenishment
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Torsello, A, Rossoni, G, Locatelli, V, De Gennaro Colonna, V, Bernareggi, M, Francolini, M, Müller, E, Berti, F, Torsello, A, Rossoni, G, Locatelli, V, De Gennaro Colonna, V, Bernareggi, M, Francolini, M, Müller, E, and Berti, F
- Abstract
The effects of hexarelin, a growth hormone (GH) secretagogue, and human GH on the mechanical and metabolic changes measured in isolated rat hearts submitted to 5 min of Ca2+ deprivation followed by reperfusion with Ca2+-containing medium, the so-called calcium paradox phenomenon, were studied. Hexarelin (80 microg/kg bid, subcutaneously) administered for 7 d to male rats effectively antagonized the sudden increase in resting tension measured in vitro on Ca2+ repletion. Moreover, during Ca2+ repletion the release of creatine kinase activity (an index of cell damage) in the perfusate of these hearts was reduced up to 40% compared with controls. By contrast, administration of hexarelin for 3 d or GH (400 microg/kg bid, subcutaneously) for 7 d did not affect the mechanical and metabolic alterations induced by the calcium paradox. To assess its direct and acute cardiac effects, hexarelin (8 microg/mL) was perfused in vitro in recirculating conditions for 60 min through the hearts of normal rats. In this case, hexarelin did not stimulate heart contractility and failed to prevent ventricular contracture upon Ca2+ readmission, whereas diltiazem, a Ca2+channel blocker, effectively antagonized the calcium paradox phenomenon. We conclude that short-term in vivo exposure to hexarelin, but not GH, enables cardiac myocyites to prevent cytoplasmatic electrolytic unbalance and to control intracellular Ca2+ gain, two functions largely impaired during the calcium paradox phenomenon. Moreover, because the effect of hexarelin is not acute but dependent on the length of in vivo treatment, we suggest that it requires modifications of myocardiocyte physiology.
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- 2001
24. CENTRAL MECHANISMS SUBSERVING THE IMPAIRED GROWTH HORMONE SECRETION INDUCED BY PERSISTENT BLOCKADE OF NMDA RECEPTORS IN IMMATURE RATS
- Author
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Cocilovo, L, DE GENNARO COLONNA, V, Zoli, M, Biagini, G, Muller, Ee, and Cocchi, Daniela
- Subjects
glutamate ,gonadotropins - Published
- 1992
25. Sildenafil reducesL-NAME-induced severe hypertension and worsening of myocardial ischaemia-reperfusion damage in the rat
- Author
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Rossoni, G, primary, Manfredi, B, additional, De Gennaro Colonna, V, additional, Berti, M, additional, Guazzi, M, additional, and Berti, F, additional
- Published
- 2007
- Full Text
- View/download PDF
26. Growth hormone-independent cardioprotective effects of hexarelin in the rat
- Author
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Locatelli, V, Rossoni, G, Schweiger, F, Torsello, A, De Gennaro Colonna, V, Bernareggi, M, Deghenghi, R, Müller, E, Berti, F, LOCATELLI, VITTORIO, TORSELLO, ANTONIO BIAGIO, Berti, F., Locatelli, V, Rossoni, G, Schweiger, F, Torsello, A, De Gennaro Colonna, V, Bernareggi, M, Deghenghi, R, Müller, E, Berti, F, LOCATELLI, VITTORIO, TORSELLO, ANTONIO BIAGIO, and Berti, F.
- Abstract
We previously reported that induction of selective GH deficiency in the rat exacerbates cardiac dysfunction induced by experimental ischemia and reperfusion performed on the explanted heart. In the same model, short-term treatment with hexarelin, a GH-releasing peptide, reverted this effect, as did GH. To ascertain whether hexarelin had non-GH-mediated protective effects on the heart, we compared hexarelin and GH treatment in hypophysectomized rats. Hexarelin (80 microg/kg sc), given for 7 days, prevented exacerbation of the ischemia-reperfusion damage induced by hypophysectomy. We also demonstrate that hexarelin prevents increases in left ventricular end diastolic pressure, coronary perfusion pressure, reactivity of the coronary vasculature to angiotensin II, and release of creatine kinase in the heart perfusate. Moreover, hexarelin prevents the fall in prostacyclin release and enhances recovery of contractility. Treatment with GH (400 microg/kg sc) produced similar results, whereas administration of EP 51389 (80 microg/kg sc), another GH-releasing peptide that does not bind to the heart, was ineffective. In conclusion, we demonstrate that hexarelin prevents cardiac damage after ischemia-reperfusion, and that its action is not mediated by GH but likely occurs through activation of specific cardiac receptors
- Published
- 1999
27. Growth hormone and hexarelin prevent endothelial vasodilator dysfunction in aortic rings of the hypophysectomized rat
- Author
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Rossoni, G, Locatelli, V, De Gennaro Colonna, V, Torsello, A, Schweiger, F, Boghen, M, Nilsson, M, Bernareggi, M, Müller, E, Berti, F, LOCATELLI, VITTORIO, TORSELLO, ANTONIO BIAGIO, Berti, F., Rossoni, G, Locatelli, V, De Gennaro Colonna, V, Torsello, A, Schweiger, F, Boghen, M, Nilsson, M, Bernareggi, M, Müller, E, Berti, F, LOCATELLI, VITTORIO, TORSELLO, ANTONIO BIAGIO, and Berti, F.
- Abstract
The endothelial vasodilation mechanism(s) has been investigated in aortic rings of hypophysectomized male rats as well as hypophysectomized rats treated for 7 days with growth hormone (GH, 400 microg/kg, s.c.) or hexarelin (80 microg/kg, s.c.). Tissue preparations from intact animals were taken as controls. The results obtained indicate that the release of 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) from aortic rings of hypophysectomized rats was markedly reduced (51%; p<0.01) as compared with that of control preparations; the peak response to cumulative concentration of endothelin-1 (ET-1, from 10(-11) to 10(-5) M) was increased 2.4-fold (p<0.01) versus controls; the relaxant activity of acetylcholine (ACh, from 10(-10) to 10(-4) M) in norepinephrine-precontracted aortic rings was reduced by 39.5+/-4.4%. Pretreatment of hypophysectomized rats with GH or hexarelin markedly antagonized the hyperresponsiveness of the aortic tissue to ET-1 and allowed a consistent recovery of both the relaxant activity of ACh and the generation of 6-keto-PGF1alpha. Collectively these findings support the concept that dysfunction of vascular endothelial cells may be induced by a defective GH function. Because a replacement regimen of GH restored the somatotropic function and increased plasma insulin-like growth factor-I (IGF-I) concentrations in the hypophysectomized rats, it is suggested that IGF-I may have protected the vascular endothelium acting as a biologic mediator of GH action. In contrast to GH, hexarelin replacement neither increased body weight nor affected the plasma concentrations of IGF-I, indicating that its beneficial action on vascular endothelium was divorced from that on somatotropic function and was likely due to activation of specific endothelial receptors
- Published
- 1999
28. Somatotropic dysregulation in old mammals
- Author
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Müller, E, Cella, S, Parenti, M, Deghenghi, R, Locatelli, V, De Gennaro Colonna, V, Torsello, A, Cocchi, D, PARENTI, MARCO DOMENICO, LOCATELLI, VITTORIO, TORSELLO, ANTONIO BIAGIO, Cocchi, D., Müller, E, Cella, S, Parenti, M, Deghenghi, R, Locatelli, V, De Gennaro Colonna, V, Torsello, A, Cocchi, D, PARENTI, MARCO DOMENICO, LOCATELLI, VITTORIO, TORSELLO, ANTONIO BIAGIO, and Cocchi, D.
- Abstract
In old mammals, including humans, the spontaneous growth hormone (GH) secretory pattern is markedly reduced resulting in lower amounts of GH released over 24 h, and the GH response to administration of GH-releasing hormone (GHRH) is reduced. In agreement with these in vivo findings, an impaired responsiveness to GHRH is evident in the pituitary of old male and female rats in vitro, and this is linked with a diminished stimulation of adenylate cyclase by GHRH. The poor GH responsiveness to GHRH in old mammals, which in the rat is coupled to a defective number of GHRH receptors in the somatotrophs, is likely due to a primary deficiency of GHRH availability, as implied by the diminished GHRH immunoreactivity and gene expression in and GHRH release from the hypothalamus of old rats. Attempts have been made to stimulate the sluggish somatotrophic function in elderly humans and dogs using GHRH; in either species positive results were obtained though, overall, it would seem that the GHRH hypofunction does not entirely account for the GH hyposecretory state during ageing. Concerning somatostatin, although the expression of this peptide decreases with age in the rat hypothalamus, secretion and activity of this hormone is increased, resulting in an altered relationship between GHRH and somatostatin gene expression and secretion. It is likely that defects, especially in catecholaminergic and cholinergic neurons, are instrumental in altering specific peptidergic neurons. Reportedly, catecholamines induce GH release by stimulating GHRH neurons and inhibiting somatostatin-releasing neurons; acetylcholine stimulates GH release via muscarinic receptors, in this way inhibiting the action of somatostatin neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
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- 1995
29. Endocrine, metabolic and cardioprotective effects of hexarelin in obese Zucker rats
- Author
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De Gennaro-Colonna, V, primary, Rossoni, G, additional, Cocchi, D, additional, Rigamonti, AE, additional, Berti, F, additional, and Muller, EE, additional
- Published
- 2000
- Full Text
- View/download PDF
30. Somatotropic dysfunction in growth hormone-releasing hormone-deprived neonatal rats: effect of growth hormone replacement therapy
- Author
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Cella, S, De Gennaro Colonna, V, Locatelli, V, Bestetti, G, Rossi, G, Torsello, A, Wehrenberg, W, Müller, E, Müller, E., LOCATELLI, VITTORIO, TORSELLO, ANTONIO BIAGIO, Cella, S, De Gennaro Colonna, V, Locatelli, V, Bestetti, G, Rossi, G, Torsello, A, Wehrenberg, W, Müller, E, Müller, E., LOCATELLI, VITTORIO, and TORSELLO, ANTONIO BIAGIO
- Abstract
In a previous work, we reported that passive immunization with anti-growth hormone-releasing hormone (GHRH) antibodies (GHRH-Ab) in neonatal rats caused disruption of somatotropic function that was still present 60 d posttreatment. We studied the reversibility of this condition by growth hormone (GH) replacement therapy. Neonatal rats received GHRH-Ab (50 microL/rat, s.c.) or normal rabbit serum every second day from birth up to postnatal d 10 and received hGH (0.4 microgram/g body weight, s.c., b.i.d.) or vehicle in a 2 x 2 factorial design. Animals were studied on d 11 of age. In GHRH-Ab-treated rats, GH therapy 1) counteracted the reduced body weight and low plasma IGF-I levels; 2) failed to modify the reduced pituitary weight and GH content; 3) further reduced the low plasma GH levels; 4) partially restored the defective GH responsiveness to GHRH; 5) failed to modify the reduced hypothalamic somatostatin and increased GHRH gene expression in the hypothalamus; and 6) reverted the decreased pituitary somatostatin binding. Morphologic and morphometric evaluation of the pituitary gland from GHRH-AB+GH pups showed that the number of GH-labeled structures was lower than in normal rat serum-GH-treated pups, whereas the total GH immunoreactivity per unit surface, an index of intracellular hormone concentration, was slightly higher than in vehicle-GH or GHRH-Ab pups. As determined by electron microscopy, somatotropes from GHRH-Ab+GH pups had morphologic features of high cellular activity. It appears that in GHRH-deprived pups GH replacement therapy can normalize most but not all altered indices of the somatotropic function.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1994
31. Long-term changes of somatotrophic function induced by deprivation of growth hormone-releasing hormone during the fetal life of the rat
- Author
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Cella, S, Locatelli, V, Broccia, M, Menegola, E, Giavini, E, De Gennaro Colonna, V, Torsello, A, Wehrenberg, W, Müller, E, LOCATELLI, VITTORIO, TORSELLO, ANTONIO BIAGIO, Müller, E., Cella, S, Locatelli, V, Broccia, M, Menegola, E, Giavini, E, De Gennaro Colonna, V, Torsello, A, Wehrenberg, W, Müller, E, LOCATELLI, VITTORIO, TORSELLO, ANTONIO BIAGIO, and Müller, E.
- Abstract
We have studied the effects of intra-amniotic administration of an anti-GH-releasing hormone serum (GHRH-Ab) on day 16 of fetal life in the rat, when the ontogenetic development of the GHRH neuronal system occurs. Control animals received normal rabbit serum. Following delivery, body weight was monitored for the next 30 days as an index of somatic growth, and the following indices of somatotrophic function were determined: plasma and pituitary GH, pituitary GH mRNA, hypothalamic GHRH and somatostatin mRNA, and the in vivo GH responsiveness to GHRH. At birth, GHRH-Ab-treated rats had a body weight that was equivalent to that of control rats but, starting from postnatal day 6 up to day 30, they had a significantly reduced body weight. Pituitary weight, the absolute pituitary GH content and GH mRNA levels were lower in experimental compared with control rats, while pituitary GH concentrations were similar in the two groups, thus implying that there was a defect, not only in GH synthesis, but also in GH release. In agreement with this theory, basal GH levels and GHRH-stimulated GH secretion were reduced in GHRH-Ab-treated rats but, in contrast, hypothalamic regulation of GH secretion appeared to be working in these rats as they were still able to respond to the low plasma GH by increasing GHRH and decreasing somatostatin mRNA levels. These findings indicate that deprivation of GHRH during fetal life induces long-lasting changes of growth rate and somatotrophic function.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1994
32. Leptin regulates GH secretion in the rat by acting on GHRH and somatostatinergic functions
- Author
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Cocchi, D, primary, De Gennaro Colonna, V, additional, Bagnasco, M, additional, Bonacci, D, additional, and Muller, EE, additional
- Published
- 1999
- Full Text
- View/download PDF
33. Hexarelin exhibits protective activity against cardiac ischaemia in hearts from growth hormone-deficient rats
- Author
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Berti, F., primary, Mler, E., additional, De Gennaro Colonna, V., additional, and Rossoni, G., additional
- Published
- 1998
- Full Text
- View/download PDF
34. Characterization of the hypothalamo–pituitary–IGF-I axis in rats made obese by overfeeding
- Author
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Cattaneo, L, primary, De Gennaro Colonna, V, additional, Zoli, M, additional, Müller, E E, additional, and Cocchi, D, additional
- Published
- 1996
- Full Text
- View/download PDF
35. Long-term changes of somatotrophic function induced by deprivation of growth hormone-releasing hormone during the fetal life of the rat
- Author
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Cella, S G, primary, Locatelli, V, additional, Broccia, M L, additional, Menegola, E, additional, Giavini, E, additional, De Gennaro Colonna, V, additional, Torsello, A, additional, Wehrenberg, W B, additional, and Müller, E E, additional
- Published
- 1994
- Full Text
- View/download PDF
36. Growth Hormone Secretion Is Differently Affected in Genetically Obese Male and Female Rats
- Author
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Cocchi, Daniela, primary, Parenti, Marco, additional, Cattaneo, Lorena, additional, De Gennaro Colonna, V., additional, Zocchetti, Andrea, additional, and Müller, Eugenio E., additional
- Published
- 1993
- Full Text
- View/download PDF
37. Effects of Long-Term Disease-Modifying Antirheumatic Drugs on Endothelial Function in Patients with Early Rheumatoid Arthritis.
- Author
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Turiel, M., Tomasoni, L., Sitia, S., Cicala, S., Gianturco, L., Ricci, C., Atzeni, F., De Gennaro Colonna, V., Longhi, M., and Sarzi-Puttini, P.
- Subjects
RHEUMATOID arthritis treatment ,IMMUNOSUPPRESSIVE agents ,BLOOD hyperviscosity syndrome ,RHEUMATISM ,ARTHRITIS - Abstract
Rheumatoid arthritis (RA) is associated with enhanced atherosclerosis and impaired endothelial function early after the onset of the disease and cardiovascular (CV) disease represents one of the leading causes of morbidity and mortality. It is well known that disease modifying antirheumatic drugs (DMARDs) are able to improve the course of the disease and the quality of life of these patients, but little is known about the effects of DMARDs on CV risk and endothelial dysfunction. Our goal was to examine the effects of long-term therapy with DMARDs on endothelial function and disease activity in early RA (ERA). Twenty-five ERA patients (mean age 52 ± 14.6 years, disease duration 6.24 ± 4.10 months) without evidence of CV involvement were evaluated for disease activity score (DAS-28), 2D-echo derived coronary flow reserve (CFR), common carotid intima-media thickness (IMT) and plasma asymmetric dimethylarginine (ADMA) levels at baseline and after 18 months of treatment with DMARDs (10 patients with methotrexate and 10 with adalimumab). DMARDs significantly reduced DAS-28 (6.0 ± 0.8 vs. 2.0 ± 0.7; P < 0.0001) and improved CFR (2.4 ± 0.2 vs. 2.7 ± 0.5; P < 0.01). Common carotid IMT and plasma ADMA levels did not show significant changes. The present study shows that DMARDs, beyond the well known antiphlogistic effects, are able to improve coronary microcirculation without a direct effect on IMT and ADMA, clinical markers of atherosclerosis. Treatment strategies in ERA patients with high inflammatory activity must be monitored to identify beneficial effects on preclinical markers of vascular function. [ABSTRACT FROM AUTHOR]
- Published
- 2010
- Full Text
- View/download PDF
38. Sildenafil reduces L-NAME-induced severe hypertension and worsening of myocardial ischaemia–reperfusion damage in the rat.
- Author
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Rossoni, G., Manfredi, B., de Gennaro Colonna, V., Berti, M., Guazzi, M., and Berti, F.
- Subjects
SILDENAFIL ,PULMONARY hypertension ,CONGESTIVE heart failure ,CORONARY disease ,ISCHEMIA ,REPERFUSION injury - Abstract
Background and purpose:Phosphodiesterase-5 inhibitors are beneficial in pulmonary hypertension and congestive heart failure, the two conditions associated with coronary heart disease and ischaemia. We investigated whether sildenafil counteracts the cardiovascular alterations induced by N
ω -nitro-L-arginine methyl ester (L-NAME) in the rat.Experimental approach:Sildenafil was given orally to rats at doses of 0.37, 0.75 or 1.5 mg kg−1 day−1 for four weeks, either alone or with L-NAME (35-40 mg kg−1 day−1 in the drinking water). Systolic blood pressure and urinary parameters (6-keto-prostaglandin F1α , thromboxane B2 , 8-isoprostane-prostaglandin F2α and nitrite/nitrate) were measured in conscious rats. Isolated hearts were subjected to low flow ischaemia–reperfusion, and myocardial levels of guanosine 3’, 5’cyclic monophosphate (cGMP) were determined. Endothelial vascular dysfunction was examined in aortic rings.Key results:Sildenafil dose-dependently prevented the rise in systolic blood pressure in L-NAME-treated rats. This activity was associated with a normalization of urinary 8-isoprostane-prostaglandin F2α and other biochemical parameters. In perfused hearts, the post-ischaemic ventricular dysfunction was worse in preparations from L-NAME-treated rats than in controls. Sildenafil dose-dependently reduced this effect, and creatine kinase and lactate dehydrogenase release were lower too. cGMP levels, which were low in myocardial tissue from L-NAME-treated rats, were restored by sildenafil. In noradrenaline-precontracted aortic rings from L-NAME-treated rats acetylcholine lost its vasorelaxant effect, and sildenafil restored it.Conclusion and implications:In a rat model of chronic nitric oxide deprivation, where hypertension and aggravation of post-ischaemic ventricular dysfunction are associated with loss of vascular endothelium-relaxant function, sildenafil provided significant cardiovascular protection, primarily by maintaining tissue cGMP levels.British Journal of Pharmacology (2007) 150, 567–576. doi:10.1038/sj.bjp.0707131; published online 22 January 2007 [ABSTRACT FROM AUTHOR]- Published
- 2007
- Full Text
- View/download PDF
39. Growth hormone (GH) autofeedback action in the neonatal rat: involvement of GH-releasing hormone and somatostatin
- Author
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Cella, S. G., primary, De Gennaro Colonna, V., additional, Locatelli, V., additional, Moiraghi, V., additional, Loche, S., additional, Wehrenberg, W. B., additional, and Müller, E. E., additional
- Published
- 1990
- Full Text
- View/download PDF
40. Effects of single and short-term administration of clonidine on hypothalamic-pituitary somatotropic function of the adult male rat: an in situ hybridization study.
- Author
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De Gennaro Colonna, V, Zoli, M, Settembrini, B P, Ciceri, S, De Marco, A, Cella, S G, Agnati, L F, and Muller, E E
- Abstract
The effects of the alpha-2 adrenoceptor agonist clonidine (CLO) on the growth hormone (GH) regulatory neuronal systems, growth hormone-releasing hormone (GHRH) and somatostatin (SS), were studied in adult male rats given a single or a short-term administration (1, 3 and 6 days) of the drug. Acute administration of CLO significantly decreased hypothalamic GHRH content [leaving unaltered GHRH messenger RNA (mRNA) levels] and increased plasma GH levels; hypothalamic SS content/mRNA levels and pituitary GH content/mRNA levels remained unchanged. In 1- and 3-day CLO-treated rats, by contrast, decreased hypothalamic GHRH content was coupled with a significant reduction in GHRH mRNA levels. In these rats, pituitary GH content and mRNA levels were also significantly increased, whereas hypothalamic SS content and mRNA levels remained unaltered. In 6-day CLO-treated rats, hypothalamic GHRH content and mRNA levels were still significantly reduced, plasma GH levels were increased, but to a lesser extent than in 1- and 3-day CLO-treated rats, and pituitary GH content and mRNA reverted to control levels. Hypothalamic SS content and mRNA levels remained unaltered. These results indicate that 1) functional activation of alpha-2 adrenergic receptors by CLO increases GHRH release from the hypothalamus, 2) CLO, via GHRH, increases GH secretion and biosynthesis, which in turn feeds back in the hypothalamus to reduce GHRH biosynthesis, and 3) reduction of hypothalamic GH-stimulatory activity tones down the initial pituitary somatotropic hyperfunction. Unaltered hypothalamic SS content and mRNA levels in all CLO-treated rats suggests that the somatostatinergic system is less sensitive than the GHRH system to changes in circulating GH levels.
- Published
- 1996
41. Reduced growth hormone releasing factor (GHRF)-like immunoreactivity and GHRF gene expression in the hypothalamus of aged rats
- Author
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De Gennaro Colonna, V., primary, Zoli, M., additional, Cocchi, D., additional, Maggi, A., additional, Marrama, P., additional, Agnati, L.F., additional, and Müller, E.E., additional
- Published
- 1989
- Full Text
- View/download PDF
42. Growth Hormone and Hexarelin Prevent Endothelial Vasodilator Dysfunction in Aortic Rings of the Hypophysectomized Rat
- Author
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Antonio Torsello, M Bernareggi, Boghen M, Locatelli, Nilsson M, Eugenio E. Müller, Ferruccio Berti, Giuseppe Rossoni, Schweiger F, De Gennaro Colonna, Rossoni, G, Locatelli, V, De Gennaro Colonna, V, Torsello, A, Schweiger, F, Boghen, M, Nilsson, M, Bernareggi, M, Müller, E, and Berti, F
- Subjects
Male ,medicine.medical_specialty ,Hypophysectomy ,Endothelium ,medicine.medical_treatment ,Vasodilation ,6-Ketoprostaglandin F1 alpha ,Biology ,Protective Agents ,Rats, Sprague-Dawley ,Internal medicine ,medicine.artery ,Homeostasi ,medicine ,Animals ,Homeostasis ,Humans ,Enzyme Inhibitor ,Enzyme Inhibitors ,BIO/14 - FARMACOLOGIA ,Aorta ,Protective Agent ,Pharmacology ,omega-N-Methylarginine ,Endothelin-1 ,Animal ,Human Growth Hormone ,Body Weight ,Biological activity ,Endothelin 1 ,Acetylcholine ,Rats ,Endocrinology ,medicine.anatomical_structure ,Circulatory system ,Rat ,Oligopeptide ,Endothelium, Vascular ,Cardiology and Cardiovascular Medicine ,Oligopeptides ,Human ,Blood vessel - Abstract
The endothelial vasodilation mechanism(s) has been investigated in aortic rings of hypophysectomized male rats as well as hypophysectomized rats treated for 7 days with growth hormone (GH, 400 microg/kg, s.c.) or hexarelin (80 microg/kg, s.c.). Tissue preparations from intact animals were taken as controls. The results obtained indicate that the release of 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) from aortic rings of hypophysectomized rats was markedly reduced (51%; p
- Published
- 1999
43. Somatotropic Dysfunction in Growth Hormone-Releasing Hormone-Deprived Neonatal Rats: Effect of Growth Hormone Replacement Therapy
- Author
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Gilberto E. Bestetti, De Gennaro Colonna, William B. Wehrenberg, Silvano G. Cella, Giovanni L. Rossi, Eugenio E. Müller, Antonio Torsello, Locatelli, Cella, S, De Gennaro Colonna, V, Locatelli, V, Bestetti, G, Rossi, G, Torsello, A, Wehrenberg, W, and Müller, E
- Subjects
endocrine system ,medicine.medical_specialty ,Pituitary gland ,Somatotropic cell ,Gene Expression ,Peptide hormone ,Biology ,Growth Hormone-Releasing Hormone ,Rats, Sprague-Dawley ,Random Allocation ,Growth Disorder ,Internal medicine ,medicine ,Animals ,Somatostatin binding ,BIO/14 - FARMACOLOGIA ,Growth Disorders ,Animal ,Organ Size ,Growth hormone–releasing hormone ,Immunohistochemistry ,Rats ,Microscopy, Electron ,Endocrinology ,Somatostatin ,medicine.anatomical_structure ,Animals, Newborn ,Evaluation Studies as Topic ,Hypothalamus ,Pituitary Gland ,Growth Hormone ,Pediatrics, Perinatology and Child Health ,Rat ,hormones, hormone substitutes, and hormone antagonists ,Densitometry ,Hormone - Abstract
In a previous work, we reported that passive immunization with anti-growth hormone-releasing hormone (GHRH) anti-bodies (GHRH-Ab) in neonatal rats caused disruption of somatotropic function that was still present 60 d posttreatment. We studied the reversibility of this condition by growth hormone (GH) replacement therapy. Neonatal rats received GHRH-Ab (50 μ L/rat, s.c.) or normal rabbit serum every second day from birth up to postnatal d 10 and received hGH (0.4 μg/g body weight, s.c, b.i.d.) or vehicle in a 2 χ 2 factorial design. Animals were studied on d 11 of age. In GHRH-Ab-treated rats, GH therapy l) counteracted the reduced body weight and low plasma IGF-I levels; 2) failed to modify the reduced pituitary weight and GH content; 3) further reduced the low plasma GH levels; 4) partially restored the defective GH responsiveness to GHRH; 5) failed to modify the reduced hypothalamic somatostatin and increased GHRH gene expression in the hypothalamus; and 6) reverted the decreased pituitary somatostatin binding. Morphologic and morphometric evaluation of the pituitary gland from GHRH-Ab+GH pups showed that the number of GH-labeled structures was lower than in normal rat serum-GH-treated pups, whereas the total GH immunorcactrvify per unit surface, an index of intracellular hormone concentration, was slightly higher than in vehicle-GH or GHRH-Ab pups. As determined by electron microscopy, somatotropcs from GHRH-Ab+GH pups had morphologic features of high cellular activity. It appears that in GHRH-deprived pups GH replacement therapy can normalize most but not all altered indices of the somatotropic function. The effects of GH are mainly directed at the pituitary, whereas the sensitivity of the hypothalamus to GH replacement is lower.
- Published
- 1994
44. Effects of treatment strategy on endothelial function
- Author
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V. De Gennaro Colonna, Claudio Borghi, C. Cavallino, Y. Shoenfeld, Maurizio Turiel, Claudio Ceconi, Fabrizio Cecaro, Livio Tomasoni, Alberto Morganti, P. Marino, Simona Sitia, Alexis Elias Malavazos, Marco Guazzi, Lelio Morricone, Arrigo F G Cicero, Tomasoni L, Sitia S, Borghi C, Cicero AF, Ceconi C, Cecaro F, Morganti A, De Gennaro Colonna V, Guazzi M, Morricone L, Malavazos AE, Marino P, Cavallino C, Shoenfeld Y, and Turiel M.
- Subjects
medicine.medical_specialty ,Endothelium ,Adrenergic beta-Antagonists ,Immunology ,Anti-Inflammatory Agents ,Angiotensin-Converting Enzyme Inhibitors ,Vasodilation ,Inflammation ,Pharmacology ,Renin-Angiotensin System ,Internal medicine ,Renin–angiotensin system ,medicine ,Humans ,Immunology and Allergy ,Endothelial dysfunction ,Antihypertensive Agents ,Endothelium-Dependent Relaxing Factors ,biology ,business.industry ,Angiotensin-converting enzyme ,Atherosclerosis ,medicine.disease ,Endocrinology ,medicine.anatomical_structure ,Blood pressure ,Pathophysiology of hypertension ,Hypertension ,biology.protein ,Endothelium, Vascular ,Hydroxymethylglutaryl-CoA Reductase Inhibitors ,medicine.symptom ,business - Abstract
A large body of evidence indicates that endothelial dysfunction is a characteristic of patients with arterial hypertension. As functional abnormalities lead to impaired endothelium-dependent vasodilation, this early step of atherogenesis is potentially reversible. In addition to reducing blood pressure, the major families of anti-hypertensive drugs have a number of pleiotropic effects that could improve endothelial function. In particular, the renin–angiotensin system plays an important role in the pathogenesis of both arterial hypertension and endothelial dysfunction, and so drugs capable of limiting the dangerous effects of this hormonal axis, such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers and renin inhibitors, could help prevent/delay/reverse the atherosclerotic process. New third-generation β-blockers and 5-phosphodiesterase inhibitors may affect endothelial function. Furthermore, the HMGCoA-reductase inhibitors currently used to reduce cholesterol levels have major pleiotropic anti-inflammatory and anti-hypertensive effects. The preservation or recovery of endothelial function in hypertensive patients is crucial to inhibit the development of atherosclerosis and the onset of cardiovascular events. This review focuses on the ancillary effects of hypertensive drugs and HMGCoA-reductase inhibitors that go beyond lowering blood pressure and cholesterol levels.
- Published
- 2010
45. Cardiovascular involvement in systemic autoimmune diseases
- Author
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Salvatore La Carrubba, Fabiola Atzeni, Vitantonio Di Bello, Simona Sitia, L. Delfino, Maurizio Turiel, Vito De Gennaro Colonna, Giovanni Di Salvo, Livio Tomasoni, Piercarlo Sarzi-Puttini, Francesco Antonini-Canterin, Scipione Carerj, Sitia, S, Atzeni, F, SARZI PUTTINI, P, DI BELLO, V, Tomasoni, L, Delfino, L, ANTONINI CANTERIN, F, DI SALVO, Giovanni, DE GENNARO COLONNA, V, LA CARRUBBA, S, Carerj, S, and Turiel, M.
- Subjects
Coronary angiography ,Immunology ,Population ,Systemic autoimmune diseases ,Microcirculation abnormalities ,Non invasive diagnostic tools ,CORONARY FLOW RESERVE ,PRIMARY ANTIPHOSPHOLIPID SYNDROME ,VENTRICULAR DIASTOLIC FUNCTIONS ,DIMETHYL L ARGININE ,RHEUMATOID ARTHRITIS ,ASYMMETRIC DIMETHYLARGININE ,DOPPLER ECHOCARDIOGRAPHY ,ENDOTHELIAL DYSFUNCTION ,COMPUTED TOMOGRAPHY ,LUPUS ERYTHEMATOSUS ,Arthritis ,Disease ,Asymptomatic ,Risk Assessment ,Autoimmune Diseases ,Arthritis, Rheumatoid ,Rheumatoid ,Non-invasive diagnostic tools ,Antirheumatic Agents ,Coronary Angiography ,Echocardiography ,Humans ,Cardiovascular Diseases ,medicine ,Immunology and Allergy ,education ,Subclinical infection ,Autoimmune disease ,education.field_of_study ,business.industry ,medicine.disease ,Rheumatoid arthritis ,medicine.symptom ,business ,Systemic vasculitis - Abstract
Autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), primary antiphospholipid syndrome (APS), systemic sclerosis and systemic vasculitis, affect a large number of people in whom one of the leading causes of morbidity and mortality is cardiovascular disease. Cardiovascular disease is associated with the development of accelerated atherosclerosis. It seems to occur at a younger age than in the general population, is often asymptomatic and, in addition to traditional risk factors, also involves specific risk factors as chronic inflammation, the duration and activity of the autoimmune disease, and immunosuppressive therapy. The early phases of cardiovascular involvement in patients with autoimmune diseases may be clinically silent, with only a microcirculation disorder present. There are various means of detecting morphological cardiac damage: coronary angiography remains the gold standard for diagnosing coronary stenosis, but new, non invasive and more reliable methods have been introduced into clinical practice in order to detect subclinical microcirculation abnormalities.
- Published
- 2009
46. Hexarelin, but not growth hormone, protects heart from damage induced in vitro by calcium deprivation replenishment
- Author
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Antonio Torsello, M Bernareggi, Maura Francolini, Vito De Gennaro Colonna, Ferruccio Berti, Giuseppe Rossoni, Eugenio E. Müller, Vittorio Locatelli, Torsello, A, Rossoni, G, Locatelli, V, De Gennaro Colonna, V, Bernareggi, M, Francolini, M, Müller, E, and Berti, F
- Subjects
Male ,medicine.medical_specialty ,Endocrinology, Diabetes and Metabolism ,chemistry.chemical_element ,In Vitro Techniques ,Calcium ,Rats, Sprague-Dawley ,Endocrinology ,Growth hormone secretagogue ,In vivo ,Internal medicine ,medicine ,Animals ,Channel blocker ,Diltiazem ,Insulin-Like Growth Factor I ,Cell damage ,Creatine Kinase ,BIO/14 - FARMACOLOGIA ,Chemistry ,Animal ,Myocardium ,Body Weight ,Heart ,Organ Size ,medicine.disease ,Hormone ,Myocardial Contraction ,Hormones ,Rats ,Perfusion ,Growth Hormone ,Rat ,Oligopeptide ,Secretagogue ,Oligopeptides ,Intracellular ,medicine.drug - Abstract
The effects of hexarelin, a growth hormone (GH) secretagogue, and human GH on the mechanical and metabolic changes measured in isolated rat hearts submitted to 5 min of Ca2+ deprivation followed by reperfusion with Ca2+-containing medium, the so-called calcium paradox phenomenon, were studied. Hexarelin (80 microg/kg bid, subcutaneously) administered for 7 d to male rats effectively antagonized the sudden increase in resting tension measured in vitro on Ca2+ repletion. Moreover, during Ca2+ repletion the release of creatine kinase activity (an index of cell damage) in the perfusate of these hearts was reduced up to 40% compared with controls. By contrast, administration of hexarelin for 3 d or GH (400 microg/kg bid, subcutaneously) for 7 d did not affect the mechanical and metabolic alterations induced by the calcium paradox. To assess its direct and acute cardiac effects, hexarelin (8 microg/mL) was perfused in vitro in recirculating conditions for 60 min through the hearts of normal rats. In this case, hexarelin did not stimulate heart contractility and failed to prevent ventricular contracture upon Ca2+ readmission, whereas diltiazem, a Ca2+channel blocker, effectively antagonized the calcium paradox phenomenon. We conclude that short-term in vivo exposure to hexarelin, but not GH, enables cardiac myocyites to prevent cytoplasmatic electrolytic unbalance and to control intracellular Ca2+ gain, two functions largely impaired during the calcium paradox phenomenon. Moreover, because the effect of hexarelin is not acute but dependent on the length of in vivo treatment, we suggest that it requires modifications of myocardiocyte physiology.
- Published
- 2001
47. Growth hormone-independent cardioprotective effects of hexarelin in the rat
- Author
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V, Locatelli, G, Rossoni, F, Schweiger, A, Torsello, V, De Gennaro Colonna, M, Bernareggi, R, Deghenghi, E E, Müller, F, Berti, Locatelli, V, Rossoni, G, Schweiger, F, Torsello, A, De Gennaro Colonna, V, Bernareggi, M, Deghenghi, R, Müller, E, and Berti, F
- Subjects
Male ,Animal ,Angiotensin II ,Myocardium ,Myocardial Ischemia ,Heart ,Myocardial Reperfusion Injury ,6-Ketoprostaglandin F1 alpha ,In Vitro Techniques ,Rats ,Rats, Sprague-Dawley ,Growth Hormone ,Animals ,Rat ,Oligopeptide ,Insulin-Like Growth Factor I ,Oligopeptides ,Creatine Kinase ,BIO/14 - FARMACOLOGIA - Abstract
We previously reported that induction of selective GH deficiency in the rat exacerbates cardiac dysfunction induced by experimental ischemia and reperfusion performed on the explanted heart. In the same model, short-term treatment with hexarelin, a GH-releasing peptide, reverted this effect, as did GH. To ascertain whether hexarelin had non-GH-mediated protective effects on the heart, we compared hexarelin and GH treatment in hypophysectomized rats. Hexarelin (80 microg/kg sc), given for 7 days, prevented exacerbation of the ischemia-reperfusion damage induced by hypophysectomy. We also demonstrate that hexarelin prevents increases in left ventricular end diastolic pressure, coronary perfusion pressure, reactivity of the coronary vasculature to angiotensin II, and release of creatine kinase in the heart perfusate. Moreover, hexarelin prevents the fall in prostacyclin release and enhances recovery of contractility. Treatment with GH (400 microg/kg sc) produced similar results, whereas administration of EP 51389 (80 microg/kg sc), another GH-releasing peptide that does not bind to the heart, was ineffective. In conclusion, we demonstrate that hexarelin prevents cardiac damage after ischemia-reperfusion, and that its action is not mediated by GH but likely occurs through activation of specific cardiac receptors.
- Published
- 1999
48. Somatotropic dysregulation in old mammals
- Author
-
Romano Deghenghi, Eugenio E. Müller, V. De Gennaro Colonna, Daniela Cocchi, Marco Parenti, Antonio Torsello, Silvano G. Cella, Vittorio Locatelli, Müller, E, Cella, S, Parenti, M, Deghenghi, R, Locatelli, V, De Gennaro Colonna, V, Torsello, A, and Cocchi, D
- Subjects
Male ,Cholinergic Agent ,medicine.medical_specialty ,Aging ,Somatotropic cell ,Growth-hormone-releasing hormone receptor ,Endocrinology, Diabetes and Metabolism ,Cholinergic Agents ,Hypothalamus ,Biology ,Growth Hormone-Releasing Hormone ,Synaptic Transmission ,Mammal ,Endocrinology ,Catecholamines ,Thyrotropin-releasing hormone receptor ,Parasympathetic Nervous System ,Internal medicine ,Hypothalamu ,medicine ,Animals ,Humans ,BIO/14 - FARMACOLOGIA ,Mammals ,Animal ,Growth hormone–releasing hormone ,Rats ,Somatostatin ,Hormone receptor ,Ageing ,Growth Hormone ,Catecholamine ,Rat ,Female ,Acetylcholine ,Human ,medicine.drug - Abstract
In old mammals, including humans, the spontaneous growth hormone (GH) secretory pattern is markedly reduced resulting in lower amounts of GH released over 24 h, and the GH response to administration of GH-releasing hormone (GHRH) is reduced. In agreement with these in vivo findings, an impaired responsiveness to GHRH is evident in the pituitary of old male and female rats in vitro, and this is linked with a diminished stimulation of adenylate cyclase by GHRH. The poor GH responsiveness to GHRH in old mammals, which in the rat is coupled to a defective number of GHRH receptors in the somatotrophs, is likely due to a primary deficiency of GHRH availability, as implied by the diminished GHRH immunoreactivity and gene expression in and GHRH release from the hypothalamus of old rats. Attempts have been made to stimulate the sluggish somatotrophic function in elderly humans and dogs using GHRH; in either species positive results were obtained though, overall, it would seem that the GHRH hypofunction does not entirely account for the GH hyposecretory state during ageing. Concerning somatostatin, although the expression of this peptide decreases with age in the rat hypothalamus, secretion and activity of this hormone is increased, resulting in an altered relationship between GHRH and somatostatin gene expression and secretion. It is likely that defects, especially in catecholaminergic and cholinergic neurons, are instrumental in altering specific peptidergic neurons. Reportedly, catecholamines induce GH release by stimulating GHRH neurons and inhibiting somatostatin-releasing neurons; acetylcholine stimulates GH release via muscarinic receptors, in this way inhibiting the action of somatostatin neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1995
49. Long-term changes of somatotrophic function induced by deprivation of growth hormone-releasing hormone during the fetal life of the rat
- Author
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William B. Wehrenberg, Vittorio Locatelli, M. L. Broccia, V. De Gennaro Colonna, Antonio Torsello, Eugenio E. Müller, Erminio Giavini, Silvano G. Cella, Elena Menegola, Cella, S, Locatelli, V, Broccia, M, Menegola, E, Giavini, E, De Gennaro Colonna, V, Torsello, A, Wehrenberg, W, and Müller, E
- Subjects
endocrine system ,medicine.medical_specialty ,Somatotropic cell ,Endocrinology, Diabetes and Metabolism ,Hypothalamus ,Gene Expression ,Biology ,Growth Hormone-Releasing Hormone ,Rats, Sprague-Dawley ,Basal (phylogenetics) ,Embryonic and Fetal Development ,Endocrinology ,In vivo ,Internal medicine ,Hypothalamu ,medicine ,Animals ,RNA, Messenger ,BIO/14 - FARMACOLOGIA ,Fetus ,Animal ,Immune Sera ,Growth hormone–releasing hormone ,Growth hormone secretion ,Rats ,Somatostatin ,Animals, Newborn ,Growth Hormone ,Pituitary Gland ,Rat ,Female ,hormones, hormone substitutes, and hormone antagonists ,Hormone - Abstract
We have studied the effects of intra-amniotic administration of an anti-GH-releasing hormone serum (GHRH-Ab) on day 16 of fetal life in the rat, when the ontogenetic development of the GHRH neuronal system occurs. Control animals received normal rabbit serum. Following delivery, body weight was monitored for the next 30 days as an index of somatic growth, and the following indices of somatotrophic function were determined: plasma and pituitary GH, pituitary GH mRNA, hypothalamic GHRH and somatostatin mRNA, and the in vivo GH responsiveness to GHRH. At birth, GHRH-Ab-treated rats had a body weight that was equivalent to that of control rats but, starting from postnatal day 6 up to day 30, they had a significantly reduced body weight. Pituitary weight, the absolute pituitary GH content and GH mRNA levels were lower in experimental compared with control rats, while pituitary GH concentrations were similar in the two groups, thus implying that there was a defect, not only in GH synthesis, but also in GH release. In agreement with this theory, basal GH levels and GHRH-stimulated GH secretion were reduced in GHRH-Ab-treated rats but, in contrast, hypothalamic regulation of GH secretion appeared to be working in these rats as they were still able to respond to the low plasma GH by increasing GHRH and decreasing somatostatin mRNA levels. These findings indicate that deprivation of GHRH during fetal life induces long-lasting changes of growth rate and somatotrophic function. In addition, when comparing these changes with those in rats given GHRH-Ab postnatally, it would appear that deprivation of GHRH affects different regulatory levels of the hypothalamo-pituitary-somatotroph axis depending on when the deprivation occurs. Journal of Endocrinology (1994) 140, 111–117
- Published
- 1994
50. Curcumin and Gut Microbiota: A Narrative Overview with Focus on Glycemic Control.
- Author
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Servida S, Piontini A, Gori F, Tomaino L, Moroncini G, De Gennaro Colonna V, La Vecchia C, and Vigna L
- Subjects
- Humans, Animals, Dysbiosis microbiology, Hypoglycemic Agents therapeutic use, Hypoglycemic Agents pharmacology, Gastrointestinal Microbiome drug effects, Curcumin therapeutic use, Curcumin pharmacology, Glycemic Control methods, Diabetes Mellitus, Type 2 drug therapy, Diabetes Mellitus, Type 2 metabolism, Diabetes Mellitus, Type 2 microbiology
- Abstract
Turmeric is a spice widely used in China, Southeast Asia, and in traditional Ayurvedic medicine. Its safety profile and efficacy as an antioxidant, anti-inflammatory, antimicrobial, antitumor, antidiabetic, and anti-obesity agent have led to extensive research into its potential role in preventing and treating metabolic diseases. The active compound in turmeric is curcumin, which exhibits low systemic bioavailability after oral administration. However, it is detectable in the gut, where it bidirectionally interacts with the gut microbiota (GM), which plays a crucial role in maintaining host health. The favorable effects of curcumin, particularly its hypoglycemic properties, are linked to alteration in intestinal dysbiosis observed in type 2 diabetes mellitus and metabolic syndrome patients. Restoration of the eubiotic GM may contribute to glycemic homeostasis. Preclinical and clinical studies have demonstrated the involvement of the GM in the regulation of glucose and lipid metabolism. Although the underlying mechanism remains incompletely understood, intestinal dysbiosis is associated with insulin resistance, hyperglycemia, and low-grade inflammation. In the present overview, we summarize the biological properties of curcumin, focusing on its link with GM and, therefore, on its potential role in metabolic diseases.
- Published
- 2024
- Full Text
- View/download PDF
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