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300 results on '"Gaia, E"'

1. Screening of Fabry Disease in Portuguese Patients With Idiopathic Cardiomyopathies (F-CHECK)

Author

Centro Hospitalar Universitário de São João, E.P.E., Hospital Pedro Hispano, Centro Hospitalar do Tâmega e Sousa, Hospital Padre Américo, Hospital Santa Maria Maior, Hospital da Luz, Lisboa, Hospital de Santa Luzia, Centro Hospitalar De Trás-Os-Montes E Alto Douro, E.P.E., Centro Hospitalar Universitário Lisboa Norte, EPE., Hospital de Santa Maria, Centro Hospitalar de Entre Douro e Vouga, E.P.E., Hospital São Sebastião, Centro Hospitalar de Leiria, Centro Hospitalar Universitário de Coimbra, Centro Hospitalar Lisboa Central, Hospital Santa Marta, Centro Hospitalar de Vila Nova de Gaia e Espinho, E.P.E., Centro Hospitalar Universitário de Santo António, Centro de Investigação em Tecnologias e Serviços de Saúde, and Rede de Investigação em Saúde

Published
2023

3. Correction to: ZIKA virus elicits P53 activation and genotoxic stress in human neural progenitors similar to mutations involved in severe forms of genetic microcephaly

Author

El Ghouzzi, Vincent, Bianchi, Federico T., Molineris, Ivan, Mounce, Bryan C., Berto, Gaia E., Rak, Malgorzata, Lebon, Sophie, Aubry, Laetitia, Tocco, Chiara, Gai, Marta, Chiotto, Alessandra M. A., Sgrò, Francesco, Pallavicini, Gianmarco, Simon-Loriere, Etienne, Passemard, Sandrine, Vignuzzi, Marco, Gressens, Pierre, and Di Cunto, Ferdinando

Published
2018
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4. Precision Revisited: Targeting Microcephaly Kinases in Brain Tumors

Author

Gianmarco Pallavicini, Gaia E. Berto, and Ferdinando Di Cunto

Subjects
microcephaly, kinase, brain tumor, glioblastoma multiforme, medulloblastoma, Biology (General), QH301-705.5, Chemistry, QD1-999
Abstract

Glioblastoma multiforme and medulloblastoma are the most frequent high-grade brain tumors in adults and children, respectively. Standard therapies for these cancers are mainly based on surgical resection, radiotherapy, and chemotherapy. However, intrinsic or acquired resistance to treatment occurs almost invariably in the first case, and side effects are unacceptable in the second. Therefore, the development of new, effective drugs is a very important unmet medical need. A critical requirement for developing such agents is to identify druggable targets required for the proliferation or survival of tumor cells, but not of other cell types. Under this perspective, genes mutated in congenital microcephaly represent interesting candidates. Congenital microcephaly comprises a heterogeneous group of disorders in which brain volume is reduced, in the absence or presence of variable syndromic features. Genetic studies have clarified that most microcephaly genes encode ubiquitous proteins involved in mitosis and in maintenance of genomic stability, but the effects of their inactivation are particularly strong in neural progenitors. It is therefore conceivable that the inhibition of the function of these genes may specifically affect the proliferation and survival of brain tumor cells. Microcephaly genes encode for a few kinases, including CITK, PLK4, AKT3, DYRK1A, and TRIO. In this review, we summarize the evidence indicating that the inhibition of these molecules could exert beneficial effects on different aspects of brain cancer treatment.

Published
2019
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5. Correction to: ZIKA virus elicits P53 activation and genotoxic stress in human neural progenitors similar to mutations involved in severe forms of genetic microcephaly

Author

Vincent El Ghouzzi, Federico T. Bianchi, Ivan Molineris, Bryan C. Mounce, Gaia E. Berto, Malgorzata Rak, Sophie Lebon, Laetitia Aubry, Chiara Tocco, Marta Gai, Alessandra M. A. Chiotto, Francesco Sgrò, Gianmarco Pallavicini, Etienne Simon-Loriere, Sandrine Passemard, Marco Vignuzzi, Pierre Gressens, Ferdinando Di Cunto, Neuroprotection du Cerveau en Développement / Promoting Research Oriented Towards Early Cns Therapies (PROTECT), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Robert Debré-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Molecular Biotechnology Centre [Turin], University of Turin, Populations virales et Pathogenèse, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Institut des cellules souches pour le traitement et l'étude des maladies monogéniques (I-STEM), Université d'Évry-Val-d'Essonne (UEVE)-Institut National de la Santé et de la Recherche Médicale (INSERM), Génétique fonctionnelle des Maladies infectieuses - Functional Genetics of Infectious Diseases, Département de génétique [Robert Debré], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-AP-HP Hôpital universitaire Robert-Debré [Paris], Center for Developing Brain [London], King‘s College London, and National Institute of Neuroscience [Turin, Italy]

Subjects
Cancer Research, Zika Virus Infection, Gene Expression Profiling, [SDV]Life Sciences [q-bio], [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Immunology, Correction, Apoptosis, Cell Biology, Zika Virus, Up-Regulation, Cellular and Molecular Neuroscience, Disease Models, Animal, Mice, Neural Stem Cells, [SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics, Mutation, [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], Microcephaly, Animals, Humans, Tumor Suppressor Protein p53, ComputingMilieux_MISCELLANEOUS, DNA Damage
Abstract

Epidemiological evidence from the current outbreak of Zika virus (ZIKV) and recent studies in animal models indicate a strong causal link between ZIKV and microcephaly. ZIKV infection induces cell-cycle arrest and apoptosis in proliferating neural progenitors. However, the mechanisms leading to these phenotypes are still largely obscure. In this report, we explored the possible similarities between transcriptional responses induced by ZIKV in human neural progenitors and those elicited by three different genetic mutations leading to severe forms of microcephaly in mice. We found that the strongest similarity between all these conditions is the activation of common P53 downstream genes. In agreement with these observations, we report that ZIKV infection increases total P53 levels and nuclear accumulation, as well as P53 Ser15 phosphorylation, correlated with genotoxic stress and apoptosis induction. Interestingly, increased P53 activation and apoptosis are induced not only in cells expressing high levels of viral antigens but also in cells showing low or undetectable levels of the same proteins. These results indicate that P53 activation is an early and specific event in ZIKV-infected cells, which could result from cell-autonomous and/or non-cell-autonomous mechanisms. Moreover, we highlight a small group of P53 effector proteins that could act as critical mediators, not only in ZIKV-induced microcephaly but also in many genetic microcephaly syndromes.

Published
2018

8. Abstract form for the Irish Journal of Medical Science v workshop on gastroduodenal pathology and Helicobacter pylori July 5th — 7th 1992 — Dublin, Ireland

Author

Logan, R. P. H., Gummett, P. A., Walker, M. M., Karim, Q. N., Baron, J. H., Misiewicz, J. J., Trieber, G., Walker, S., Klotz, U., Lozniewski, A., Weber, M., de Korwin, J. D., Floquet, J., Conroy, M. C., Burdin, J. C., Mannes, G. A., Bayerdörffer, E., Höchter, W., Weingart, J., Heldwein, W., Sommer, A., Müller-Lissner, S., Bomschein, W., Miehlke, S., Weinzierl, M., Ruckdeschel, G., von Wulffen, H., Köpcke, W., Stolte, M., Rune, S. J., Justesen, T., Hansen, J. M., Jensen, T. G., Eriksen, J., Thomsen, O. ø., Scheibel, J., Bonnevie, O., Bremmelgaard, A., Vilien, M., Knuhtsen, S., Elsborg, L., Hansen, J., Lauritsen, K., Wulff, H. R., Boixeda, D., Ballestero, S., Cantón, R., De Rafael, L., Martinm de Argila, C., Pozuelo, M. J., Sampedro, J., Baquero, F., Grigoriev, P. Ya., Isakov, V. A., Iakovenko, E. P., Hirschl, A. M., Brandstätter, G., Dragosics, B., Hentschel, E., Kundi, M., Rotter, M. L., Schütze, K., Taufer, M., Neri M, Susi D, Bovani I, Pindo R, Cuccurullo F., Coelho, L. G. V., Passos, M. C. F., Chausson, Y., Vieira, W. L. S., Castro, F. J., Franco, J. M. M., Fernandes, M. L. M., Castro, L. P., Jonas, C., De Koster, E., Van Gossum, M., Depierreux, M., Cheval, M., Deltenre, M., Schütz, E., Bethke, B., Lee, A., Hegedus, E., O’Rourke, J., Larsson, H., Sjöstedt, S., Veress, B., Nord, C. E., Sobala, G. M., George, R., Tompkins, D., Finlay, J., Manning, A., Sant, S., Xia, H. X., Daw, M., Gilvarry, J., Keane, C. T., O’Morain, C., Rubio, M. A., Hegarty, B., Blum, A. L., Sulser, E., Stadelmann, O., Munoz, N., Buiatti, E., Vivas, J., Oliver, W., Cano, E., Peraza, S., Castro, D., Sanchez, V., Andrade, O., Benz, M., Mendz, G. L., Hazell, S. L., Salmela, K. S., Roire, R. P., Hook-Nikanne, J., Kosunen, T. U., Salaspur, M., Luke, C. J., Reynolds, D. D. J., Penn, C. W., Bode, G., Mauch, F., Ditschuneit, H., Malfertheiner, P., Ferrero, Richard L., Agnes Labigne, Eaton, K. A., Krakowka, S., Mobley, H. L. T., Hu, Li-Tai, Foxall, P. A., Moran, A. P., Helander, I. M., Altman, C., Sobhani, I., Vissugaire, C., Migrant, M., Etienne, J. P., Sommi, P., Ricci, V., Fiocca, R., Cova, E., Figura, N., Romano, M., Ivey, K. J., Solcia, E., Ventura, U., Nilius, M., Schieffer, S., Hengels, K. J., Jablonowski, H., Strohmeyer, G., Cabrai, M. D., Barbosa, A. J. A., Lima Hr., G. F., Oliveira, C. A., Polak, J. M., Oderda, G., Villani, L., Altare, F., Morra, I., Miserendino, L., Ansaldi, N., Dixon, M. F., Wyatt, J. I., Axon, A. T. R., Beattie, S., Hamilton, H., Shabib, S., Cutz, E., Drumm, B., Sherman, P., Noach, L. A., Rolf, T., Bosma, N. B., Schwartz, M. P., Oosting, J., Rauws, E. A. J., Tytgat, G. N. J., Andrew, A., Nardone, G., d’Ormiento, F., Pontillo, M., Lobo, A. J., Uff, J. S., McNulty, C. N. M., Wilkinson, S. P., Suriani, R., Pallante, C., Ravizza, M., Galliano, D., Sallio, D., Malandrino, M., Oneglio, R., Colozza, M., Mazzucco, D., Gaia, E., Eidt, S., Vincent, P., Gottrand, F., Turck, D., Lecomte-Houcke, M., Leclerc, H., Bonvicini, F., Pretolani, S., Baraldini, M., Cilla, D., Baldinelli, S., Bazocchi, E., Acampora, P., Careddu, N., Brocchi, E., Gasbarrini, G., Joubert, M., Bazin, N., Thiaucourt, D., Protte, E., Gissler, C., Duprez, A., Merlin, P., Forestier, S., Labenz, J., Gyenes, E., Rühl, G. H., Börsch, G., Daskalopoulos, G., Carrick, J., Lian, R., Wagner, S., Bleck, J., Gebel, M., Bär, W., Manns, M., Lamouliatte, H., Bernard, P. H., Cayla, R., Vialette, G., Quinton, A., Mégraud, F., Lemaire, M., Quinten, A., De Mascarel, A., Webb, P., Forman, D., Knight, T., Wilson, A., Graves, S., Newell, D., Elder, J., Tonelli, E., Gatte, M. R. A., Ghironzi, G. C., Giulianelli, G., Bamford, K. B., Collins, J. S. A., Bickley, J., Johnston, B. T., Potts, S., Boston, V., Owen, R. J., Sloan, J., Basso, L., Lawlor, S., Clune, J., Szelényi, H., Stohmeyer, G., Macedo, G., Iglésias, I., Chaves, A. P., Loureiro, A., Katelaris, P. H., Seow, F., Lin, B., Napoli, J., Hones, D. B., Ngu, M. C., Akopyantz, Natalia S., Bukanov, Nikolay O., Westblom, T. Ulf, Berg, Douglas E., Nyst, J. F., Denis, P., Buset, M., De Reuck, M., Nielsen, H., Andersen, L. P., Birkholz, Sabine, Knipp, Ulrich, Nietzki, Claudia, Opferkuch, Wolfgang, Crabtree, J. E., Peichl, P., Lindly, I. J. D., Deusch, K., Seifirth, C., Funk, A., Dahie, I., Reut, K., Classen, M., Gionchetti, P., Vaira, D., Campieri, M., Bertinelli, E., Menegatti, M., Belluzzi, A., Briognola, C., Miglioli, M., Barbara, L., Tommaso, A. Di, Magistris, M. T. De, Bugnoli, M., Petracca, R., Covacci, A., Censini, S., Rappuoli, R., Abrignani, S., Territo, M. C., Smela, K. L., Reeve, J. R., Lee, T. D., Walsh, J. H., Armellini, D., Crabtree, J. E., Xiang, Z. Y., Mitchell, H. M., Hu, P. J., Li, Y. Y., Wang, Z. J., Zhao, S. M., Liu, Q., Chen, M., Du, G. G., Filipe, M. I., Reed, P. I., Craanen, M. E., Blok, P., Dekker, W., Colombo, E., Redaelli, D., Santangelo, M., Spinelli, M., Farinati, F., Valiante, F., Delia Libera, G., Germanà, B., Baffa, R., Rugge, M., Vianelo, F., Di Mario, F., Sipponen, Pentti, Rokkas, T., Popotheodorou, G., Kaldgeropoulos, N., Deprez, C., Galand, P., Fox, J. G., Wishnok, P., Murphy, J. C., Tannenbaum, S., Correa, P., Parsonnet, Julie, Macor, C., Da Broi, G. L., Avellinio, C., Reifen, R., Rasooly, I., Millson, M. E., Murphy, K., Thomas, J. E., Eastham, E. J., Malorgio, E., Dell’Olio, D., Kemmer, T. P., Dominguez-Munoz, J. E., Klingel, H., Gatto, M. R. A., Olivieri, R., Bayeli, R. F., Abate, L., De Gregorio, L., Aziz, J., Esposito, E., Basagni, C., Guilluy, R., Rousseau-Tsangaris, M., Brazier, J. L., Wadstiöm, Torkel, Tyszkiewicz, Tadeusz, Bergenzaun, Per, Olsson, Karin, Birac, C., Tall, F., Albenque, M., Labigne, A., Megraud, F., Feldman, R. A., Deeks, J., Glupczynski, Y., Burette, A., Goossens, H., Van den Boore, C., Butzler, J. P., Veldhuyzen van Zanten, S., Best, L., Benzanson, G., Haldane, D., Hazell, S., Mapstone, N. P., Lynch, D. A. F., Quirke, P., Taylor, D. E., Chang, N., Eaton, M., Stockdale, E., Salama, S. M., Thompson, L., Cockayne, A., Spiller, R. C., Leen, E., Sweeney, E., Klann, H., Hatz, R., Bornschein, W., Simon, T., Eimiller, A., Bolle, F., Schweikert, C., Köpeke, W., Moss, S. F., Bishop, A. E., Calam, J., Cahill, R. J., Xia, H., Solnick, J., and Tompkins, L.

Published
1992
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9. Treatment

Author

Goodwin, C. S., Worsley, B., Pillai, E., Willems, V., Janisch, H. D., Langmaack, H., Sanchez, P., Alcalde, M., Lancho, A., Carpintero, P., Garcia, R., Pajares, J. M., Grigoriev, P. Ya., Isakov, V. A., Iakovenko, E. P., Iakovenko, A. V., Vogt, K., Hahn, H., Rehmann, I. H., Hedding-Eckerich, M., Blessing, J., Sobala, G. M., Lynch, D. A. F., Gallacher, B., Dixon, M. F., Axon, A. T. R., Bayerdörffer, E., Mannes, G., Sommer, A., Höchter, W., Weingart, J., Hatz, R., Miehlke, S., Lehn, N., Ruckdeschel, G., Dirschedl, P., Stolte, M., Adamek, R. J., Wegener, M., Birkholz, S., Opferkuch, W., Rühl, G. H., Wedmann, B., Labenz, J., Gyenes, E., R’hl, G. H., Börsch, G., Maieron, R., Rizzi, C., Zoratti, L., Andreoli, S., Da Broi, G. L., Beltrami, C. A., Chengyl, Zhuya, Yangiong, Mou, Jiesong, Hua, Zhenhua, Zhang, Bierti, L., Bolis, E. G., Di Battista, R., de Franchis, R., McAvinchey, D. J., Laurence, M., O’Riordan, J., Fantazi, M., Khawaja, M., Bologna, E, Stroppiana, M., Peyre, S., Pulitano’, R., Sategna-Guidetti, C., Martin, E., Alarcön, T., Sanz, J. C., Jimonez, M. I., López-Brea, M., Burette, A., Glupczynski, Y., Deprez, C., Di Mario, F., Ferrana, M., Battaglia, G., Dotto, P., Vianello, F., Grasso, G. A., Fiocca, R., Villiani, L., Luinetti, O., Gianatti, A., Boldorini, R., Lazzaroni, M., Bianchi Porro, G., Trespi, E., Perego, M., Alvisi, C., Cesana, B., Solcia, E., Logan, R. P. H., Greaves, R. R., Gummett, P. A., Walker, M. M., Karim, Q. N., Duggan, A. E., Baron, J. H., Misiewicz, J. J., Lohmarm, J., Porst, L. H. H., Schönlebe, J., Riedel, H., Catalano, F., Rizzo, G., Ayoubi Khajekini, M. T., Branciforte, G., Inserra, G., Liberti, A., Suriani, R., Pallante, C., Ravizza, M., Mazzucco, D., Galliano, D., Malandrino, M., Oneglio, R., Colozza, M., Gaia, E., Sallio, F., Colozza, D., Grandis, C., Forte, G. B., Bottiglieri, M. E., Durasco, R., Grimaldi, E., Rocco, P., Xia, H. X., Daw, M. A., Sant, S., Beattie, S., Keane, C. T., O’Morain, C. A., Larsson, H., Berglund, M. L., Tessaro, P., Schiavon, R., Contini, M. G., Ton, T., Norberto, L., Cassaro, M., Rugge, M., Guido, M., Baffa, R., Gloriosa, S., Turatello, F., Naccarato, R., Collins, R., O’Moram, C., Kemmer, T. P., Dominguez-Munoz, J. E., Klingel, H., Malfertheiner, P., McCarthy, C. J., McDermott, M., Hourihane, D., O’Morain, C., Droy-Lefiax, M. T., Forestier, B., Guillomain, D., Plique, O., Brugmann, D., Mégraud, F., Lamouliatte, H., Bernard, P. H., Cayla, R., Mégraud, M., de Mascarel, A., Quintonl, A., McLaren, A., McDowell, S. R., McColm, A. A., O’Malley, C., Bagshaw, J., Bouffant, F., Marelli, P., Cellini, L., Campa, M., Dainelli, B., Soldani, G., del Tacca, M., Ferrini, G., Larcinese, G., Semperlotti, N., Molnar, Gy., Fzentmihalyi, A., Takats, A., Gero, G., Penyige, J., Mark, Gy., Martínez-Gómez, J., García-Novo, D., Acuña-Quinõs, D., Gimeno, M., Vigneri, S., Termini, R., Scialabba, A., Pisciotta, G., Gusmaroli, R., Milesi, F., Mule, P., Menegatti, M., Reale, C., Holten, J., and Vaira, D.

Published
1992
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13. Of rings and spines: The multiple facets of Citron proteins in neural development.

Author

Bianchi, Federico T., Gai, Marta, Berto, Gaia E., and Di Cunto, Ferdinando

Subjects
NERVE tissue proteins, NEURAL development, SPINE, MENTAL illness
Abstract

The Citron protein was originally identified for its capability to specifically bind the active form of RhoA small GTPase, leading to the simplistic hypothesis that it may work as a RhoA downstream effector in actin remodeling. More than two decades later, a much more complex picture has emerged. In particular, it has become clear that in animals, and especially in mammals, the functions of the Citron gene (CIT) are intimately linked to many aspects of central nervous system (CNS) development and function, although the gene is broadly expressed. More specifically, CIT encodes two main isoforms, Citron-kinase (CIT-K) and Citron-N (CIT-N), characterized by complementary expression pattern and different functions. Moreover, in many of their activities, CIT proteins act more as upstream regulators than as downstream effectors of RhoA. Finally it has been found that, besides working through actin, CIT proteins have many crucial functional interactions with the microtubule cytoskeleton and may directly affect genome stability. In this review, we will summarize these advances and illustrate their actual or potential relevance for CNS diseases, including microcephaly and psychiatric disorders. [ABSTRACT FROM AUTHOR]

Published
2020
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14. Italian consensus guidelines for chronic pancreatitis

Author

Frulloni, L, Falconi, M, Gabbrielli, A, Gaia, E, Graziani, R, Pezzilli, R, Uomo, G, Andriulli, A, Balzano, G, Benini, L, Calculli, L, Campra, D, Capurso, G, Cavestro, Gm, De Angelis, C, Ghezzo, L, Manfredi, R, Malesci, A, Mariani, A, Mutignani, M, Ventrucci, M, Zamboni, G, Amodio, A, Vantini, I, Bassi, C, Delle Fave, G, Capurso, Iv, Magarini, F, Albarello, L, Alfieri, S, Anti, M, Arcidiacono, P, Baiocchi, L, Berretti, D, Boraschi, P, Buscarini, E, Carroccio, A, Celebrano, Mr, Casadei, R, Chilovi, F, Conigliaro, R, Dall'Oglio, L, De Boni, M, De Pretis, G, Di Priolo, S, Di Sebastiano PL, Doglietto, Gb, Filauro, M, Frieri, G, Fuini, A, Loriga, P, Macarri, G, Manes, G, Massucco, P, Milani, S, Pasquali, Claudio, Pederzoli, P, Pietrangeli, M, Rocca, R, Russello, D, Siquini, W, Traina, M, Veneroni, L, Zilli, M, Italian Association for the Study of the Pancreas, Frulloni L, Falconi M, Gabbrielli A, Gaia E, Graziani R, Pezzilli R, Uomo G, Andriulli A, Balzano G, Benini L, Calculli L, Campra D, Capurso G, Cavestro GM, De Angelis C, Ghezzo L, Manfredi R, Malesci A, Mariani A, Mutignani M, Ventrucci M, Zamboni G, Amodio A, Vantini I, Italian Association for the Study of the Pancreas (AISP), Bassi C, Delle Fave G, Capurso IV, Magarini F, Albarello L, Alfieri S, Anti M, Arcidiacono P, Baiocchi L, Berretti D, Boraschi P, Buscarini E, Carroccio A, Celebrano MR, Casadei R, Chilovi F, Conigliaro R, Dall'Oglio L, De Boni M, De Pretis G, Di Priolo S, Di Sebastiano PL, Doglietto GB, Filauro M, Frieri G, Fuini A, Loriga P, Macarri G, Manes G, Massucco P, Milani S, Pasquali C, Pederzoli P, Pietrangeli M, Rocca R, Russello D, Siquini W, Traina M, Veneroni L, Zilli M, Zamboni G., Frulloni, L, Falconi, M, Gabbrielli, A, Gaia, E, Graziani, R, Pezzilli, R, Uomo, G, Andriulli, A, Balzano, G, Benini, L, Calculli, L, Campra, D, Capurso, G, Cavestro, Gm, De Angelis, C, Ghezzo, L, Manfredi, R, Malesci, A, Mariani, A, Mutignani, M, Ventrucci, M, Zamboni, G, Amodio, A, Vantini, I, Italian Association for the Study of the Pancreas, (AISP), Bassi, C, Delle Fave, G, Capurso, Iv, Magarini, F, Albarello, L, Alfieri, S, Anti, M, Arcidiacono, P, Baiocchi, L, Berretti, D, Boraschi, P, Carroccio, A, Celebrano, Mr, Casadei, R, Chilovi, F, Conigliaro, R, Dall'Oglio, L, De Boni, M, De Pretis, G, Di Priolo, S, Di Sebastiano, Pl, Doglietto, Gb, Filauro, M, Frieri, G, Fuini, A, Macarri, G, Manes, G, Massucco, P, Milani, S, Pasquali, C, Pederzoli, P, Pietrangeli, M, Rocca, R, Russello, D, Siquini, W, Traina, M, Veneroni, L, Zilli, M, and Zamboni, G.

Subjects
medicine.medical_specialty, complications, pancreatic supplements, diagnostic imaging, pancreatitis, MEDLINE, cholangiopancreatography, chronic, endoscopic retrograde, pain, quality of life, radiography, sphincterotomy, steatorrhea, surgery, therapy, ultrasonography, Appropriate use, guidelines, chronica pancreatitis, Pancreatitis, Chronic, Pancreatitis, chronic, Complications, Surgery, Medical imaging, Medicine, Humans, Pancreatic stones, Intensive care medicine, Surgical treatment, Hepatology, medicine.diagnostic_test, business.industry, Pancreatitis, Radiography, Therapy, Ultrasonography, Cholangiopancreatography, Sphincterotomy, Diagnostic imaging, Pain, Quality of life, Steatorrhea, Pancreatic supplements, Gastroenterology, medicine.disease, Endoscopy, Pancreatic pain, Italy, CHRONIC PANCREATITIS, Radiology, business
Abstract

This paper gives practical guidelines for diagnosis and treatment of chronic pancreatitis. Statements have been elaborated by working teams of experts, by searching for and analysing the literature, and submitted to a consensus process by using a Delphi modified procedure. The statements report recommendations on clinical and nutritional approach, assessment of pancreatic function, treatment of exocrine pancreatic failure and of secondary diabetes, treatment of pain and prevention of painful relapses. Moreover, the role of endoscopy in approaching pancreatic pain, pancreatic stones, duct narrowing and dilation, and complications was considered. Recommendations for most appropriate use of various imaging techniques and of ultrasound endoscopy are reported. Finally, a group of recommendations are addressed to the surgical treatment, with definition of right indications, timing, most appropriate procedures and techniques in different clinical conditions and targets, and clinical and functional outcomes following surgery. © 2010 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved. Keywords: Pancreatitis, chronic; Complications; Surgery; Radiography; Therapy; Ultrasonography; Cholangiopancreatography

Published
2010

15. Democritos: preparing demonstrators for high power nuclear electric space propulsion

Author

Masson, F., Ruault, J. -M, Worms, J. -C, Emmanuel Detsis, Beaurain, A., Lassouiere, F., Gaia, E., Tosi, M. C., Jansen, F., Bauer, W., Semenkm, A., Tinsley, T., and Hodgson, M. Z.

Subjects
Controlling, Logistik, DEMOCRITOS, nukleare elektrische Antriebe, MEGAHIT
Abstract

The Democritos project aims at preparing demonstrators for a megawatt class nuclearelectric space propulsion. It is funded by Horizon 2020, the R&T program of the European Community. It is a new European and Russian project, including as partners: Nuclear National Laboratory (U.K.), DLR (Germany), The Keldysh Research Center (Russia), Thales Alenia Space Italia (Italy), Snecma (France), ESF (France) and CNES (France). IEAV (Brazil) will join as an observer. Democritos is the follow-up of the Megahit project (www.megahit-eu.org). During Megahit project, a reference architecture was established for 1MWe nuclear electric propulsion INPPS (International Nuclear Propulsion and Power System) , and a roadmap was proposed to have a spacecraft available by the early 30's. The main aim of Democritos is to start implementing the Megahit roadmaps by preparing demonstrators for some of the necessary technologies. Democritos features a technical part, with preliminary design of the demonstrators and their test benches. It features also a programmatic part, which will deal with financial and organizational aspects of such an endeavour: the ambition of the project is to initiate or join international cooperations, as broad as possible, which will lead to the implementation of the demonstrators.

Published
2015

16. Italian consensus guidelines for chronic pancreatitis

Author

Frulloni, L., Falconi, M., Gabbrielli, A., Gaia, E., Graziani, R., Pezzilli, R., Uomo, G., Andriulli, A., Balzano, G., Benini, L., Calculli, L., Campra, D., Capurso, G., Cavestro, G., De Angelis, C., Ghezzo, L., Manfredi, R., Malesci, A., Mariani, A., Mutignani, M., Ventrucci, M., Zamboni, G., Amodio, A., Vantini, I., Italian Association for the Study of the Pancreas, Bassi, C., Delle Fave, G., Capurso, I., Magarini, F., Albarello, L., Alfieri, S., Anti, M., Arcidiacono, P., Baiocchi, L., Berretti, D., Boraschi, P., Buscarini, E., Carroccio, A., Frulloni, L., Falconi, M., Gabbrielli, A., Gaia, E., Graziani, R., Pezzilli, R., Uomo, G., Andriulli, A., Balzano, G., Benini, L., Calculli, L., Campra, D., Capurso, G., Cavestro, G., De Angelis, C., Ghezzo, L., Manfredi, R., Malesci, A., Mariani, A., Mutignani, M., Ventrucci, M., Zamboni, G., Amodio, A., Vantini, I., Italian Association for the Study of the Pancreas, Bassi, C., Delle Fave, G., Capurso, I., Magarini, F., Albarello, L., Alfieri, S., Anti, M., Arcidiacono, P., Baiocchi, L., Berretti, D., Boraschi, P., Buscarini, E., and Carroccio, A.

Subjects
chronic pancreatitis, Settore MED/09 - Medicina Interna, Italian, consensus guideline, consensus guidelines
Published
2010

17. Pratical guidelines for acute pancreatitis

Author

PEZZILLI, RAFFAELE, CASADEI, RICCARDO, FANTINI, MARIA PIA, DALLOLIO, LAURA, FABBRI, GIULIANA, MORSELLI LABATE, ANTONIO MARIA, CALCULLI, LUCIA, A. Zerbi, V. Di Carlo, C. Bassi, G. F. Delle Fave, Bassi, C, Castoldi, L, Rabitti, P, Balzano, G, Gaia, E, Mutignani, M, Uomo, G, Brazzi, L, D'Alessandro, A, Frulloni, L, Scarpellini, P, Gabbrielli, A, Del Chiaro, M, Mariani, A, De Rai, P, Billi, P, Casadei, R, Nicoletti, R, R. Pezzilli, A. Zerbi, V. Di Carlo, C. Bassi, G.F. Delle Fave, Working Group of the Italian Association for the Study of the Pancreas on Acute Pancreatitis […, Fantini, M P, Dallolio, L, Fabbri, G, Morselli-Labate, A M, Bassi, C, Calculli, L, Castoldi, L, Rabitti, P, Balzano, G, Gaia, E, Mutignani, M, Uomo, G, Brazzi, L, D'Alessandro, A, Frulloni, L, Scarpellini, P, Gabbrielli, A, Del Chiaro, M, Mariani, A, De Rai, P, Billi, P, Casadei, R, Nicoletti, R, and …]

Subjects
medicine.medical_specialty, acute pancreatitis, diagnosis, diagnostic imaging, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, pancreatitis, Gastroenterology, Basal (phylogenetics), Severity assessment, Enteral Nutrition, Internal medicine, medicine, therapeutics, Humans, In patient, Cholecystectomy, guidelines, pancreas, APACHE, acute pancreatiti, therapy, Analgesics, Hepatology, business.industry, Pancreatitis, Acute Necrotizing, disease management, pancreatic necrosis, prognosis, Alanine Transaminase, Lipase, medicine.disease, Surgery, Buprenorphine, Parenteral nutrition, Acute Disease, Etiology, Pancreatitis, Acute pancreatitis, business, Tomography, X-Ray Computed, guideline, management
Abstract

INTRODUCTION: The following is a summary of the official guidelines of the Italian Association for the Study of the Pancreas regarding the medical, endoscopic and surgical management of acute pancreatitis. STATEMENTS: Clinical features together with elevation of the plasma concentrations of pancreatic enzymes are the cornerstones of diagnosis (recommendation A). Contrast-enhanced computed tomography (CT) provides good evidence for the presence of pancreatiti (recommendation C) and it should be carried out 48-72 h after the onset of symptoms in patients with predicted severe pancreatitis. Severity assessment is essential for the selection of the proper initial treatment in the management of acute pancreatitis (recommendation A) and should be done using the APACHE II score, serum C-reactive protein and CT assessment (recommendation C). The etiology of acute pancreatitis should be able to be determined in at least 80% of cases (recommendation B). An adequate volume of intravenous fluid should be administered promptly to correct the volume deficit and maintain basal fluid requirements (recommendation A); analgesia is crucial for the correct treatment of the disease (recommendation A). Enteral feeding is indicated in severe necrotizing pancreatitis and it is better than total parenteral nutrition (recommendation A). The use of prophylactic broad-spectrum antibiotics reduces infection rates in CT-proven necrotizing pancreatitis (recommendation A). Infected pancreatic necrosis in patients with clinical signs and symptoms of sepsis is an indication for intervention, including surgery and radiological drainage (recommendation B). CONCLUSIONS: The participants agreed to revise the guidelines every 3 years in order to re-evaluate each question on the management of acute pancreatitis patients according to the most recent literature.

Published
2010

19. Citron kinase-dependent F-actin maintenance at midbody secondary ingression sites mediates abscission.

Author

Dema, Alessandro, Macaluso, Francesca, Sgrò, Francesco, Berto, Gaia E., Bianchi, Federico T., Chiotto, Alessandra A., Pallavicini, Gianmarco, Di Cunto, Ferdinando, and Gai, Marta

Subjects
F-actin, ABSCISSION (Botany), CITRON
Abstract

Abscission is the final step of cytokinesis whereby the intercellular bridge (ICB) linking the two daughter cells is cut. The ICB contains a structure called the midbody, required for the recruitment and organization of the abscission machinery. Final midbody severing is mediated by formation of secondary midbody ingression sites, where the ESCRT III component CHMP4B is recruited tomediate membrane fusion. It is presently unknown how cytoskeletal elements cooperate with CHMP4B to mediate abscission. Here, we show that F-actin is associated with midbody secondary sites and is necessary for abscission. F-actin localization at secondary sites depends on the activity of RhoA and on the abscission regulator citron kinase (CITK). CITK depletion accelerates loss of F-actin proteins at the midbody and subsequent cytokinesis defects are reversed by restoring actin polymerization. Conversely, midbody hyperstabilization produced by overexpression of CITK and ANLN is reversed by actin depolymerization. CITK is required for localization of F-actin and ANLN at the abscission sites, as well as for CHMP4B recruitment. These results indicate that control of actin dynamics downstream of CITK prepares the abscission site for the final cut. [ABSTRACT FROM AUTHOR]

Published
2018
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21. Colonoscopy practice in Italy: a prospective survey on behalf of the Italian Association of Hospital Gastroenterologists

Author

Radaelli, F, Meucci, G, Minoli, G, Italian Association of Hospital Gastroenterologists Alluminio, P, Amuso, M, Angelini, G, Anti, M, Baldi, F, Balzana, M, Barberani, F, Bargiggia, S, Barresi, G, Bedosti, M, Belmonte, A, Benedetti, A, Benedetti, E, Benini, M, Beretta, L, Beretta, P, Fontana, A, Mauro, B, Bianco, R, Bierti, L, Bigazzi, U, Boccia, S, Bonello, F, Boscarino, S, Bottini, E, Bresci, G, Briglia, U, Brunelli, E, Buggiani, D, Calandra, A, Candidi, A, Caneschi, F, Cannizzaro, R, Cappuccino, V, Caputi, O, Cardelli, A, Caronia, V, Cattuto, C, Cestari, E, Chilovi, F, Cifatte, D, Ciliberto, E, Cimino, F, Cipolletta, V, Cirillo, M, Cocozza, U, Colantuoni, E, Coli, A, Colombo, E, Comin, U, Conti, W, Cortini, C, Criscione, S, Crotta, S, Cutela, P, D'Imperio, N, Dalia, G, Dall'Oglio, L, Dal Pane, M, Dante, P, Dato, D, Dattola, L, De Bernardin, M, De Boni, M, De Conca, V, Dell'Amico, I, Dell'Anna, A, Della Spoletina, A, Delogu, G, Del Piano, M, Di Cicco, M, Di Filippo, G, Di Giorgio, P, Di Mitri, R, Di Piero, A, Di Piramo, D, Di Todaro, E, Dicillo, M, Dodero, C, Doldo, P, Drago, D, Dubla, G, Dughera, L, Dusio, P, Ederle, A, Evola, M, Fachinetti, F, Faraldo, G, Farroni, F, Fasoli, R, Ferrara, A, Ferrari, A, Ferrari, C, Ferraris, L, Ferraris, R, Ferrini, G, Ferrini, L, Foco, A, Forte, G, Francavilla, A, Franzè, A, Fregoni, D, Frieri, Giuseppe, Gaia, E, Galasso, F, Galgani, P, Gamberucci, G, Gatti, L, Gatti, M, Gemme, C, Ghione, S, Ghisotti, E, Giaccari, S, Giannelli, C, Giorcelli, V, Giuri, G, Giurissa, A, Grassini, M, Grasso, G, Graziani, Mg, Gualtiero, J, Gullini, S, Gullotta, R, Iaquinto, G, Jacoponi, S, Laganà, S, Lamanda, R, Lattanzio, R, Lauri, A, Lecis, Pe, Ledda, P, Leone, S, Ligas, E, Liuzzi, N, Lochis, D, Longaroni, M, Lorenzini, I, Loriga, P, Lussu, B, Luzza, F, Madia, D, Malfitana, G, Mallozzi, Ef, Mancini, S, Mangiarotti, R, Manildo, M, Manneschi, L, Marcon, V, Marino, M, Marrucci, A, Martines, H, Maruelli, A, Massari, M, Massidda, C, Mauri, R, Mazzarello, Pl, Mazzolla, E, Mellone, C, Meloni, M, Merighi, A, Mescia, P, Michetti, P, Milan, L, Milandri, G, Miori, G, Monastra, S, Moncelli, G, Monica, F, Montanaro, F, Moretti, M, Morini, S, Mosca, F, Mosca, D, Moschetta, R, Mura, G, Naim, G, Nardella, G, Natale, A, Negrini, F, Niccoli, G, Nova, A, Occhipinti, P, Ocera, S, Orlandi, Pg, Orsini, O, Pagani, E, Paliani, O, Pardocchi, D, Parodi, Cm, Pasini, D, Pasquale, L, Pasquali, L, Paterlini, A, Pellecchia, A, Pera, A, Perego, M, Perugini, B, Petracca, F, Peyre, S, Piccoli, F, Pilati, S, Pierucci, E, Pizzetti, P, Pizzolato, S, Polimeni, F, Politano, S, Polo, S, Portaluri, F, Prada, A, Privitera, U, Quaranta, S, Raguzzi, I, Ravelli, P, Recchia, S, Revetria, P, Ripoli, D, Rocca, F, Roda, E, Rogheto, M, Rosati, S, Rosina, F, Rossi, A, Rotolo, A, Sabadini, Gr, Saffiotti, O, Salerno, D, Sanesi, A, Sanna, S, Saracco, G, Savarino, V, Scaccianoce, G, Scarpulla, G, Schiffino, L, Schippa, P, Sebastiani, P, Servillo, F, Sgarbi, D, Sigillito, D, Snider, L, Sorrentini, I, Spadaccini, A, Sticchi, V, Sturniolo, Gc, Suriani, R, Tammaro, L, Tarchi, F, Tasini, E, Tebaldi, M, Terruzzi, V, Testoni, Pa, Tonelli, F, Trapè, R, Triossi, O, Usai, P, Usula, E, Vecchi, M, Vecchi, E, Ventrucci, M, Viero, K, Virgilio, C, Viviani, G, Zampaletta, U, and Zilli, M.

Subjects
Colonoscopy, Endoscopy
Published
2008

22. c-Jun N-terminal kinase upregulation as a key event in the proapoptotic interaction between transforming growth factor-β 1 and 4-hydroxynonenal in colon mucosa

Author

Biasi, F., Vizio, B., Mascia, C., Gaia, E., Žarković, Neven, Chiarpotto, E., Leonarduzzi, G., and Poli, G.

Subjects
4-hydroxynonenal, apoptosis, colon cancer, HNE, JNK, JNK inhibitors, Smads, TGF-beta1
Abstract

Cells of colonic mucosa are sensitive to the Smad-mediated growth-inhibitory effect of transforming growth factor-β 1 (TGF-β 1). Another important cell growth inhibitor is the polyunsaturated lipid peroxidation end product, 4-hydroxynonenal (HNE), which triggers apoptosis through c-Jun N-terminal kinase (JNK) activation. Interestingly, a close association between TGF-β 1 and HNE was found in the progression of human colon cancer, with concentration of both molecules inversely related to the malignancy. We investigated the cross talk between Smads and JNK signal transduction pathways in inducing apoptosis. To this purpose TGF-β 1 and HNE were added singly or in combination to CaCo-2 human colon adenocarcinoma cells. The cotreatment induced a marked enhancement of apoptosis and of JNK and Smad4 activities much more than either individual molecule. Cell preincubation with the JNK inhibitor SP600125 significantly prevented JNK and Smad4 enhancement and, subsequently, the cooperative proapoptotic effect was abolished. The primary role of JNK activity in TGF-β 1/HNE cooperative signaling was fully confirmed in a second set of experiments by using JNKi I, a more selective kinase inhibitor. Hence, in tumor cells becoming resistant to TGF-β 1-mediated growth inhibition, increased induction of the remaining TGF-β 1 pathways by interaction with other antiproliferative molecules, such as HNE, could help in inhibiting tumor growth.

Published
2006

26. ASPM and CITK regulate spindle orientation by affecting the dynamics of astral microtubules.

Author

Gai, Marta, Bianchi, Federico T, Vagnoni, Cristiana, Vernì, Fiammetta, Bonaccorsi, Silvia, Pasquero, Selina, Berto, Gaia E, Sgrò, Francesco, Chiotto, Alessandra MA, Annaratone, Laura, Sapino, Anna, Bergo, Anna, Landsberger, Nicoletta, Bond, Jacqueline, Huttner, Wieland B, and Di Cunto, Ferdinando

Abstract

Correct orientation of cell division is considered an important factor for the achievement of normal brain size, as mutations in genes that affect this process are among the leading causes of microcephaly. Abnormal spindle orientation is associated with reduction of the neuronal progenitor symmetric divisions, premature cell cycle exit, and reduced neurogenesis. This mechanism has been involved in microcephaly resulting from mutation of ASPM, the most frequently affected gene in autosomal recessive human primary microcephaly ( MCPH), but it is presently unknown how ASPM regulates spindle orientation. In this report, we show that ASPM may control spindle positioning by interacting with citron kinase ( CITK), a protein whose loss is also responsible for severe microcephaly in mammals. We show that the absence of CITK leads to abnormal spindle orientation in mammals and insects. In mouse cortical development, this phenotype correlates with increased production of basal progenitors. ASPM is required to recruit CITK at the spindle, and CITK overexpression rescues ASPM phenotype. ASPM and CITK affect the organization of astral microtubules ( MT), and low doses of MT-stabilizing drug revert the spindle orientation phenotype produced by their knockdown. Finally, CITK regulates both astral- MT nucleation and stability. Our results provide a functional link between two established microcephaly proteins. [ABSTRACT FROM AUTHOR]

Published
2016
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28. Chronic pancreatitis: Report from a multicenter Italian survey (PanCroInfAISP) on 893 patients.

Author

Frulloni, L., Gabbrielli, A., Pezzilli, R., Zerbi, A., Cavestro, G.M., Marotta, F., Falconi, M., Gaia, E., Uomo, G., Maringhini, A., Mutignani, M., Maisonneuve, P., Di Carlo, V., and Cavallini, G.

Subjects
PANCREATITIS, ENDOSCOPIC surgery, DYSTROPHY, DISEASE risk factors
Abstract

Abstract: Background: No data on chronic pancreatitis in Italy are available yet. Aim: To evaluate demographic, clinical, diagnostic and therapeutic aspects in patients suffering from chronic pancreatitis. Patients and methods: Eligible patients were prospectively enrolled from 2000 to 2005. Information concerning demographic data, lifestyle risk factors, family and clinical history, associated factors (alcohol, autoimmunity, cystic dystrophy of the duodenal wall, obstruction, genetic mutations) concomitant diseases, diagnostic findings, and pharmacological, endoscopic and surgical therapy were gathered. Results: 893 patients (74% males, mean age 53.7±15.2 years) were evaluated. 519/859 patients (60%) were drinkers and 555/840 (66%) were smokers. A strong positive correlation between drinking and cigarette consumption (R =0.53; p <0.0001) was found. Heavy alcohol consumption (>80g of alcohol/day for more than 5 years) was considered the most important risk factor in 300 patients (34%), obstruction in 238 (27%), alcohol and obstruction in 82 (9%), autoimmunity in 34 (4%), cystic dystrophy of the duodenal wall/groove pancreatitis in 55 (6%), gene mutations in 36 (4%), and none (idiopathic) in 148 (17%). Bile stones were diagnosed in 287 patients (33%) and cholecystectomy was performed in 329 patients (38%). Pancreatic calcifications were diagnosed in 547/879 patients (62%). Pancreatic surgery was performed in 273 patients (31%). Endoscopic sphincterotomy was performed in 371 patients (42%). Exocrine and endocrine insufficiency were found, respectively, in 373/834 (45%) and 275/885 patients (31%). Conclusions: An unexpected low frequency of alcohol abuse and new emerging associated risk factors for chronic pancreatitis were observed in Italy. [Copyright &y& Elsevier]

Published
2009
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39. Precision Revisited: Targeting Microcephaly Kinases in Brain Tumors.

Author

Pallavicini, Gianmarco, Berto, Gaia E., and Di Cunto, Ferdinando

Subjects
*GLIOBLASTOMA multiforme, *MEDULLOBLASTOMA, *MICROCEPHALY, *BRAIN tumors, *CELL proliferation, *CANCER chemotherapy
Abstract

Glioblastoma multiforme and medulloblastoma are the most frequent high-grade brain tumors in adults and children, respectively. Standard therapies for these cancers are mainly based on surgical resection, radiotherapy, and chemotherapy. However, intrinsic or acquired resistance to treatment occurs almost invariably in the first case, and side effects are unacceptable in the second. Therefore, the development of new, effective drugs is a very important unmet medical need. A critical requirement for developing such agents is to identify druggable targets required for the proliferation or survival of tumor cells, but not of other cell types. Under this perspective, genes mutated in congenital microcephaly represent interesting candidates. Congenital microcephaly comprises a heterogeneous group of disorders in which brain volume is reduced, in the absence or presence of variable syndromic features. Genetic studies have clarified that most microcephaly genes encode ubiquitous proteins involved in mitosis and in maintenance of genomic stability, but the effects of their inactivation are particularly strong in neural progenitors. It is therefore conceivable that the inhibition of the function of these genes may specifically affect the proliferation and survival of brain tumor cells. Microcephaly genes encode for a few kinases, including CITK, PLK4, AKT3, DYRK1A, and TRIO. In this review, we summarize the evidence indicating that the inhibition of these molecules could exert beneficial effects on different aspects of brain cancer treatment. [ABSTRACT FROM AUTHOR]

Published
2019
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48. ZIKA virus elicits P53 activation and genotoxic stress in human neural progenitors similar to mutations involved in severe forms of genetic microcephaly and p53.

Author

Ghouzzi, Vincent El, Bianchi, Federico T, Molineris, Ivan, Mounce, Bryan C, Berto, Gaia E, Rak, Malgorzata, Lebon, Sophie, Aubry, Laetitia, Tocco, Chiara, Gai, Marta, Chiotto, Alessandra MA, Sgrò, Francesco, Pallavicini, Gianmarco, Simon-Loriere, Etienne, Passemard, Sandrine, Vignuzzi, Marco, Gressens, Pierre, and Di Cunto, Ferdinando

Published
2017
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