89 results on '"Romoli S"'
Search Results
2. A rare case of spine disappearing bone disease: Lesson learned and review of the literature
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Barbagli, G., Barni, I., and Romoli, S.
- Published
- 2019
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3. Treatment of unstable spinopelvic fractures: outcome of three surgical techniques—a retrospective single-center case series
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Romoli, S., primary, Petrella, L., additional, Becattini, Eleonora, additional, Pisano, A., additional, Wembagher, G. C., additional, and De Biase, P., additional
- Published
- 2022
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4. Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia
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La Starza, R, Aventin, A, Matteucci, C, Crescenzi, B, Romoli, S, Testoni, N, Pierini, V, Ciolli, S, Sambani, C, Locasciulli, A, Di Bona, E, Lafage-Pochitaloff, M, Martelli, M F, Marynen, P, and Mecucci, C
- Published
- 2006
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5. TPM3/PDGFRB fusion transcript and its reciprocal in chronic eosinophilic leukemia
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Rosati, R, La Starza, R, Luciano, L, Gorello, P, Matteucci, C, Pierini, V, Romoli, S, Crescenzi, B, Rotoli, B, Martelli, M F, Pane, F, and Mecucci, C
- Published
- 2006
6. Cervical Spondylotic Myelopathy: World Federation of Neurosurgical Societies (WFNS) to the Italian Neurosurgical Society (SINch) Recommendations
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Francesco Costa, Carla Daniela Anania, Umberto Agrillo, Assietti Roberto, Bernucci Claudio, Bistazzoni Simona, Bongetta Daniele, Brembilla Carlo, Cappelletto Barbara, Cocciaro Ardico, Costella Giovanni Battista, De Falco Raffaele, De Rosa Andrea, Del Vecchio Carlo, Dobran Mauro, Fiorenza Vito, Garbossa Diego, Guizzardi Giancarlo, Iaccarino Corrado, Irace Claudio, Incerti Michele, Gualtiero Innocenzi, Landi Alessandro, Lastrucci Giancarlo, Maida Giuseppe, Mastrantuoni Ciro, Maugeri Rosario, Meglio Vincenzo, Montemurro Nicola, Nina Pierpaolo, Parlangeli Andrea, Pinna Giovanni, Pretti Pier Federico, Rapanà Armando, Ricci Alessandro, Rispoli Rossella, Romoli Stefano, Per Filippo Sbaffi, Somma Teresa, Tessitore Enrico, Vitali Matteo, Alberto Zerbi, Zona Gianluigi, and Andrea Barbanera
- Subjects
cervical spondylotic myelopathy ,recommendations ,guidelines ,evidence-based medicine ,Neurology. Diseases of the nervous system ,RC346-429 - Abstract
Cervical spondylotic myelopathy (CSM) is a progressively growing pathology to afford by a spinal surgeon due to the aging of the population, associated with better treatment management and the best diagnosis and treatment solutions are greatly discussed. Nowadays that scientific literature is progressively increasing to identify the gold standard in diagnosis and treatment can be very challenging. This is particularly evident in spinal surgery with many different indications not only in different countries but also in the same local reality. In this scenario, many neurosurgical societies works to identify some guideline or recommendations to help spinal surgeons in daily practice. Furthermore, in an era in which legal issues are increasingly present in clinical practice to have some indications globally accepted can be very useful. World Federation of Neurosurgical Societies (WFNS) few years ago starts this process creating a list of recommendations originating from a worldwide steering committee to respect all the local reality. The spinal section of Italian Neurosurgical Society decides to adopt the WFNS recommendations with some revision basing on Italian scenario. The steering committee of the Spinal Section of Italian Neurosurgical Society identify 7 groups to review the literature of the last 10 years about different topics on CSM and to analyses the WFNS recommendations to adapt it to the Italian daily practice. The statements were discussed and voted in 2 sessions to obtain the final version. A list of recommendations on natural course and clinical presentation; diagnostic tests; conservative and surgical treatment; anterior, posterior and combined surgical treatment; role of neurophysiological monitoring and follow-up and outcome was created with only few new or revised statements respect the ones of WFNS. The Spine Section of Italian Neurosurgical Society create a list of recommendations that represent the more contemporary treatment concepts for CSM as presented in the highest quality clinical literature and best clinical practices available on this subject.
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- 2023
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7. 19. Intraoperative neurophysiological monitoring of spinal dural arteriovenous fistula
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Martinelli, C., primary, Grippo, A., additional, Ammannati, A., additional, Gabbanini, S., additional, Boccardi, C., additional, Caramelli, R., additional, Carrai, R., additional, de Scisciolo, G., additional, Romoli, S., additional, Mangiafico, S., additional, and Amantini, A., additional
- Published
- 2017
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8. Distinct genomic events in the myeloid and lymphoid lineages in simultaneous presentation of chronic myeloid leukemia and B-chronic lymphocytic leukemia
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Crescenzi, B, Sacchi, S, Marasca, R, Temperani, P, La Starza, R, Matteucci, C, Bonacorsi, G, Romoli, S, Martelli, MF, Mecucci, C, and Emilia, G
- Published
- 2002
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9. TPM3/PDGFRB fusion transcript and its reciprocal in chronic eosinophilic leukemia [4]
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Rosati, R, La Starza, R., Gorello, P., Matteucci, C., Pierini, V., Romoli, S., Crescenzi, B., Martelli, M. F., Mecucci, C., LUCIANO, LUIGIA, ROTOLI, BRUNO, PANE, FABRIZIO, Rosati, R, La Starza, R., Luciano, Luigia, Gorello, P., Matteucci, C., Pierini, V., Romoli, S., Crescenzi, B., Rotoli, Bruno, Martelli, M. F., Pane, Fabrizio, and Mecucci, C.
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Cancer Research ,DNA Primer ,Chromosomes, Human, Pair 10 ,Molecular Sequence Data ,Tropomyosin ,Hematology ,Receptor, Platelet-Derived Growth Factor beta ,Chromosomes, Human, Pair 1 ,Chronic Disease ,Hypereosinophilic Syndrome ,Chromosomes, Human, Pair 5 ,RNA, Messenger ,Gene Fusion ,In Situ Hybridization, Fluorescence ,Thyroid Neoplasm ,Human - Published
- 2006
10. Genexpressionsanalysen der Notch-AhR-IL 22-Achse bei Homöostase und als Reaktion auf Gewebeverletzung
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Weidenbusch, M., primary, Rodler, S., additional, Song, S., additional, Romoli, S., additional, Marschner, J., additional, Kraft, F., additional, Holderied, A., additional, Kumar, S., additional, Mulay, S.R., additional, Lech, M., additional, and Anders, H.-J., additional
- Published
- 2016
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11. Controller design for tracking paths in nonlinear biochemical processes
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Fernandez, C., primary, Pantano, N., additional, Romoli, S., additional, Patino, D., additional, Ortiz, O. A., additional, and Scaglia, G., additional
- Published
- 2016
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12. Von Podozyten stammendes CXCL12 spielt bei der glomerulären Schädigung und Regeneration eine Doppelrolle
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Romoli, S., primary, Kumar, S.V., additional, Mulay, S.R., additional, Desai, J., additional, Thomasova, D., additional, and Anders, H.-J., additional
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- 2015
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13. Controller design by monitoring desired concentration profiles for the penicillin production in a feed batch reactor
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Fernandez, M. C., primary, Romoli, S., additional, Pantano, M. N., additional, Patino, D., additional, Ortiz, O. A., additional, and Scaglia, G. J. E., additional
- Published
- 2015
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14. Tracking multivariable optimal profiles of induced foreign protein production by recombinant bacteria in a fed-batch reactor
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Pantano, M. N., primary, Serrano, M. E., additional, Fernandez, M. C., additional, Romoli, S., additional, Ortiz, O. A., additional, and Scaglia, G. J. E., additional
- Published
- 2015
- Full Text
- View/download PDF
15. COMBINED INTERPHASE FLUORESCENCE IN SITU HYBRIDIZATION (CI-FISH) DELINEATES THE GENOMIC PROFILE OF T-CELL ACUTE LYMPHOBLASTIC LEUKEMIA IN CHILDREN
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LA STARZA, R, Pierini, V, Crescenzi, B, Matteucci, C, Nofrini, V, Leszl, A, Cazzaniga, G, Gorello, P, Romoli, S, Lettieri, A, Aversa, F, Basso, Giuseppe, and Mecucci, C.
- Published
- 2010
16. ARTROPLASTICA CERVICALE CON PROTESI DISCOVER. NOSTRA ESPERIENZA
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Romoli, S and Parenti, GIULIANO FRANCESCO
- Published
- 2008
17. Unusual exophytic subependymoma in the bulbo-cerebellar angle. Case report
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Romoli, S, Abbruzzese, A, Castagna, Maura, Becherini, F, and Parenti, GIULIANO FRANCESCO
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Adult ,Male ,Fourth Ventricle ,Medulla Oblongata ,Muscle Weakness ,Cranial Nerves ,Nausea ,Cerebellopontine Angle ,Magnetic Resonance Imaging ,Neurosurgical Procedures ,Treatment Outcome ,Glioma, Subependymal ,Pons ,Humans ,Cerebral Ventricle Neoplasms ,Hydrocephalus - Abstract
Subependymoma was first described by Scheinker in 1945; it frequently occurs in the ventricles and rarely in the spinal canal representing 0.7% of all central nervous system tumours. Most of these intraventricular tumours are subclinical entities, remaining of small size and discovered at autopsy with 0.4%incidence. We report a case of subependymoma with a completely exophytic growth from the foramen of Luscka: only a similar one has been described in the literature but with a lesser cysternal involvement. Neuroradiological and anatomopathological features of subependymoma are discussed.
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- 2007
18. Genetic profile of acute lymphoblastic leukemia in a patient with the noonan syndrome
- Author
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Roti, Giovanni, LA STARZA, Roberta, Crescenzi, B., Romoli, S., Ballanti1, S., Foà, R., Tartaglia, M., Martelli, M. F., and Mecucci, Cristina
- Published
- 2006
19. Molecular cytogenetic studies of myelodysplastic/ myloproliferative disease
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LA STARZA, Roberta, Roti, Giovanni, Crescenzi, B, Beacci, D, Perfetti, P, Romoli, S, Tartaglia, M, Fumagalli, M, Martelli, Mf, Gambacorti passerini, C, Pogliani, E, and Mecucci, Cristina
- Published
- 2005
20. Tumore teratoide rabdoide atipico. Considerazioni su un caso
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Romoli, S., Trivelli, I., Castagna, Maura, Salvatori, L., Favre, C., and Bellagamba, O.
- Published
- 2002
21. Correlazione fra edema-index, vascolarizzazione piale e grading istopatologico in una serie omogenea di 70 meningiomi. Risultati preliminari
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Romoli, S., Trivelli, I., Caniglia, M., Padolecchia, R., Castagna, Maura, and Parenti, G.
- Published
- 2002
22. Subependymoma esofitico ad estrinsecazione nell’angolo ponto-cerebellare: Case report
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Romoli, S., Foti, D., Grossi, G., and Castagna, Maura
- Published
- 2001
23. Experimental models of CKD
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Kanlaya, R., primary, Sintiprungrat, K., additional, Thongboonkerd, V., additional, Torremade, N., additional, Bindels, R., additional, Hoenderop, J., additional, Fernandez, E., additional, Dusso, A., additional, Valdivielso, J. M., additional, Krueger, T., additional, Boor, P., additional, Schafer, C., additional, Westenfeld, R., additional, Brandenburg, V., additional, Schlieper, G., additional, Jahnen-Dechent, W., additional, Ketteler, M., additional, Jee, W., additional, Li, X., additional, Richards, B., additional, Floege, J., additional, Goncalves, J. G., additional, Canale, D., additional, de Braganca, A. C., additional, Shimizu, M. H. M., additional, Moyses, R. M. A., additional, Andrade, L., additional, Seguro, A. C., additional, Volpini, R. A., additional, Romoli, S., additional, Migliorini, A., additional, Anders, H.-J., additional, Eskova, O., additional, Neprintseva, N., additional, Tchebotareva, N., additional, Bobkova, I., additional, Kozlovskaya, L., additional, Simic, I., additional, Tabatabaeifar, M., additional, Wlodkowski, T., additional, Denc, H., additional, Mollet, G., additional, Antignac, C., additional, Schaefer, F., additional, Ekaterina, I. A., additional, Giardino, L., additional, Rastaldi, M. P., additional, Van den Heuvel, L., additional, Levtchenko, E., additional, Okina, C., additional, Okamoto, T., additional, Kamata, M., additional, Murano, J., additional, Kobayashi, K., additional, Takeuchi, K., additional, Kamata, F., additional, Sakai, T., additional, Naito, S., additional, Aoyama, T., additional, Sano, T., additional, Takeuchi, Y., additional, Kamata, K., additional, Thomasova, D., additional, Bruns, H. A., additional, Liapis, H., additional, Iwashita, T., additional, Hasegawa, H., additional, Takayanagi, K., additional, Shimizu, T., additional, Asakura, J., additional, Okazaki, S., additional, Kogure, Y., additional, Hatano, M., additional, Hara, H., additional, Inamura, M., additional, Iwanaga, M., additional, Mitani, T., additional, Mitarai, T., additional, Savin, V. J., additional, Sharma, M., additional, Wei, C., additional, Reiser, J., additional, McCarthy, E. T., additional, Sharma, R., additional, Gauchat, J.-F., additional, Eneman, B., additional, Freson, K., additional, Van Geet, C., additional, Choi, D. E., additional, Jeong, J. Y., additional, Chang, Y. K., additional, Na, K.-R., additional, Lee, K. W., additional, Shin, Y. T., additional, Ni, H.-F., additional, Chen, J.-F., additional, Zhang, M.-H., additional, Pan, M.-M., additional, Liu, B.-C., additional, Kim, S. S., additional, Suzuki, T., additional, Iyoda, M., additional, Matsumoto, K., additional, Shindo-Hirai, Y., additional, Kuno, Y., additional, Wada, Y., additional, Yamamoto, Y., additional, Shibata, T., additional, Akizawa, T., additional, Munoz-Felix, J. M., additional, Lopez-Novoa, J. M., additional, Martinez-Salgado, C., additional, Ehling, J., additional, Babickova, J., additional, Gremse, F., additional, Kiessling, F., additional, Lammers, T., additional, Lech, M., additional, Gunthner, R., additional, Lorenz, G., additional, Ryu, M., additional, Grobmayr, R., additional, Susanti, H., additional, Kobayashi, K. S., additional, Flavell, R. A., additional, Rayego-Mateos, S., additional, Morgado, J., additional, Sanz, A. B., additional, Eguchi, S., additional, Pato, J., additional, Keri, G., additional, Egido, J., additional, Ortiz, A., additional, Ruiz-Ortega, M., additional, Leduc, M., additional, Geerts, L., additional, Grouix, B., additional, Sarra-Bournet, F., additional, Felton, A., additional, Gervais, L., additional, Abbott, S., additional, Duceppe, J.-S., additional, Zacharie, B., additional, Penney, C., additional, Laurin, P., additional, Gagnon, L., additional, Detsika, M. G., additional, Duann, P., additional, Lianos, E. A., additional, Leong, K. I., additional, Chiang, C.-K., additional, Yang, C.-C., additional, Wu, C.-T., additional, Chen, L.-P., additional, Hung, K.-Y., additional, Liu, S.-H., additional, Carvalho, F. F., additional, Teixeira, V. P., additional, Almeida, W. S., additional, Schor, N., additional, Small, D. M., additional, Bennett, N. C., additional, Coombes, J., additional, Johnson, D. W., additional, Gobe, G. C., additional, Montero, N., additional, Prada, A., additional, Riera, M., additional, Orfila, M., additional, Pascual, J., additional, Rodriguez, E., additional, Barrios, C., additional, Kokeny, G., additional, Fazekas, K., additional, Rosivall, L., additional, Mozes, M. M., additional, Hornigold, N., additional, Hughes, J., additional, Mooney, A., additional, Benardeau, A., additional, Riboulet, W., additional, Vandjour, A., additional, Jacobsen, B., additional, Apfel, C., additional, Conde-Knape, K., additional, Bienvenu, J.-F., additional, Tanaka, T., additional, Yamaguchi, J., additional, Nangaku, M., additional, Niwa, T., additional, Bolati, D., additional, Shimizu, H., additional, Yisireyili, M., additional, Nishijima, F., additional, Brocca, A., additional, Virzi, G., additional, de Cal, M., additional, Ronco, C., additional, Priante, G., additional, Musacchio, E., additional, Valvason, C., additional, Sartori, L., additional, Piccoli, A., additional, Baggio, B., additional, Perkuhn, M., additional, Weibrecht, M., additional, Zok, S., additional, Martin, I. V., additional, Schoth, F., additional, Ostendorf, T., additional, Kuhl, C., additional, Karabaeva, A., additional, Essaian, A., additional, Beresneva, O., additional, Parastaeva, M., additional, Kayukov, I., additional, Smirnov, A., additional, Audzeyenka, I., additional, Kasztan, M., additional, Piwkowska, A., additional, Rogacka, D., additional, Angielski, S., additional, Jankowski, M., additional, Bockmeyer, C. L., additional, Kokowicz, K., additional, Agustian, P. A., additional, Zell, S., additional, Wittig, J., additional, Becker, J. U., additional, Nishizono, R., additional, Venkatareddy, M. P., additional, Chowdhury, M. A., additional, Wang, S. Q., additional, Fukuda, A., additional, Wickman, L. T., additional, Yang, Y., additional, Wiggins, R. C., additional, Fazio, M. R., additional, Donato, V., additional, Lucisano, S., additional, Cernaro, V., additional, Lupica, R., additional, Trimboli, D., additional, Montalto, G., additional, Aloisi, C., additional, Mazzeo, A. T., additional, Buemi, M., additional, Gawrys, O., additional, Olszynski, K. H., additional, Kuczeriszka, M., additional, Gawarecka, K., additional, Swiezewska, E., additional, Chmielewski, M., additional, Masnyk, M., additional, Rafalowska, J., additional, Kompanowska-Jezierska, E., additional, Lee, W.-C., additional, Chau, Y.-Y., additional, Lee, L.-C., additional, Chiu, C.-H., additional, Lee, C.-T., additional, Chen, J.-B., additional, Kim, W.-K., additional, and Shin, S. J., additional
- Published
- 2013
- Full Text
- View/download PDF
24. Experimental pathology
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Yi Chun, D. X., primary, Alexandre, H., additional, Edith, B., additional, Nacera, O., additional, Julie, P., additional, Chantal, J., additional, Eric, R., additional, Zhang, X., additional, Jin, Y., additional, Miravete, M., additional, Dissard, R., additional, Klein, J., additional, Gonzalez, J., additional, Caubet, C., additional, Pecher, C., additional, Pipy, B., additional, Bascands, J.-L., additional, Mercier-Bonin, M., additional, Schanstra, J., additional, Buffin-Meyer, B., additional, Claire, R., additional, Rigothier, C., additional, Richard, D., additional, Sebastien, L., additional, Moin, S., additional, Chantal, B., additional, Christian, C., additional, Jean, R., additional, Migliori, M., additional, Cantaluppi, V., additional, Mannari, C., additional, Medica, D., additional, Giovannini, L., additional, Panichi, V., additional, Goldwich, A., additional, Alexander, S., additional, Andre, G., additional, Amann, K., additional, Migliorini, A., additional, Sagrinati, C., additional, Angelotti, M. L., additional, Mulay, S. R., additional, Ronconi, E., additional, Peired, A., additional, Romagnani, P., additional, Anders, H.-J., additional, Chiang, W. C., additional, Lai, C. F., additional, Peng, W.-H., additional, Wu, C. F., additional, Chang, F.-C., additional, Chen, Y.-T., additional, Lin, S.-L., additional, Chen, Y. M., additional, Wu, K. D., additional, Lu, K.-S., additional, Tsai, T. J., additional, Virgine, O., additional, Qing Feng, F., additional, Zhang, S.-Y., additional, Dominique, D., additional, Vincent, A., additional, Marina, C., additional, Philippe, L., additional, Georges, G., additional, Pawlak, A., additional, Sahali, D., additional, Matsumoto, S., additional, Kiyomoto, H., additional, Ichimura, A., additional, Dan, T., additional, Nakamichi, T., additional, Tsujita, T., additional, Akahori, K., additional, Ito, S., additional, Miyata, T., additional, Xie, S., additional, Zhang, B., additional, Shi, W., additional, Yang, Y., additional, Nagasu, H., additional, Satoh, M., additional, Kidokoro, K., additional, Nishi, Y., additional, Ihoriya, C., additional, Kadoya, H., additional, Sasaki, T., additional, Kashihara, N., additional, Wu, C.-F., additional, Chou, Y.-H., additional, Duffield, J., additional, Rocca, C., additional, Gregorini, M., additional, Corradetti, V., additional, Valsania, T., additional, Bedino, G., additional, Bosio, F., additional, Pattonieri, E. F., additional, Esposito, P., additional, Sepe, V., additional, Libetta, C., additional, Rampino, T., additional, Dal Canton, A., additional, Omori, H., additional, Kawada, N., additional, Inoue, K., additional, Ueda, Y., additional, Yamamoto, R., additional, Matsui, I., additional, Kaimori, J., additional, Takabatake, Y., additional, Moriyama, T., additional, Isaka, Y., additional, Rakugi, H., additional, Wasilewska, A., additional, Taranta-Janusz, K., additional, Deebek, W., additional, Kuroczycka-Saniutycz, E., additional, Lee, A. S., additional, Lee, J. E., additional, Jung, Y. J., additional, Kang, K. P., additional, Lee, S., additional, Kim, W., additional, Arfian, N., additional, Emoto, N., additional, Yagi, K., additional, Nakayama, K., additional, Hartopo, A. B., additional, Nugrahaningsih, D. A., additional, Yanagisawa, M., additional, Hirata, K.-I., additional, Munoz-Felix, J. M., additional, Lopez-Novoa, J. M., additional, Martinez-Salgado, C., additional, Oujo, B., additional, Arevalo, M., additional, Bernabeu, C., additional, Perez-Barriocanal, F., additional, Jesper, K., additional, Nathalie, V., additional, Pierre, G., additional, Yi Chun, D. X., additional, Iyoda, M., additional, Shibata, T., additional, Matsumoto, K., additional, Shindo-Hirai, Y., additional, Kuno, Y., additional, Wada, Y., additional, Akizawa, T., additional, Schwartz, I., additional, Schwartz, D., additional, Prot Bertoye, C., additional, Terryn, S., additional, Claver, J., additional, Beghdadi, W. B., additional, Monteiro, R., additional, Blank, U., additional, Devuyst, O., additional, Daugas, E., additional, Van Beneden, K., additional, Geers, C., additional, Pauwels, M., additional, Mannaerts, I., additional, Van den Branden, C., additional, Van Grunsven, L. A., additional, Seckin, I., additional, Pekpak, M., additional, Uzunalan, M., additional, Uruluer, B., additional, Kokturk, S., additional, Ozturk, Z., additional, Sonmez, H., additional, Yaprak, E., additional, Furuno, Y., additional, Tsutsui, M., additional, Morishita, T., additional, Shimokawa, H., additional, Otsuji, Y., additional, Yanagihara, N., additional, Kabashima, N., additional, Ryota, S., additional, Kanegae, K., additional, Miyamoto, T., additional, Nakamata, J., additional, Ishimatsu, N., additional, Tamura, M., additional, Nakagawa, T., additional, Ichikawa, K., additional, Miyamoto, M., additional, Takabayashi, D., additional, Yamazaki, H., additional, Kakeshita, K., additional, Koike, T., additional, Kagitani, S., additional, Tomoda, F., additional, Hamashima, T., additional, Ishii, Y., additional, Inoue, H., additional, Sasahara, M., additional, El Machhour, F., additional, Kerroch, M., additional, Mesnard, L., additional, Chatziantoniou, C., additional, Dussaule, J.-C., additional, Inui, K., additional, Sasai, F., additional, Maruta, Y., additional, Nishiwaki, H., additional, Kawashima, E., additional, Inoue, Y., additional, Yoshimura, A., additional, Musacchio, E., additional, Priante, G., additional, Valvason, C., additional, Sartori, L., additional, Baggio, B., additional, Kim, J. H., additional, Gross, O., additional, Diana, R., additional, Gry, D. H., additional, Asimal, B., additional, Johanna, T., additional, Imke, S.-E., additional, Lydia, W., additional, Gerhard-Anton, M., additional, Hassan, D., additional, Cano, J. L., additional, Griera, M., additional, Olmos, G., additional, Martin, P., additional, Cortes, M. A., additional, Lopez-Ongil, S., additional, Rodriguez-Puyol, D., additional, DE Frutos, S., additional, Gonzalez, M., additional, Luengo, A., additional, Rodriguez-Puyol, M., additional, Calleros, L., additional, Lupica, R., additional, Lacquaniti, A., additional, Donato, V., additional, Maggio, R., additional, Mastroeni, C., additional, Lucisano, S., additional, Cernaro, V., additional, Fazio, M. R., additional, Quartarone, A., additional, Buemi, M., additional, Kacik, M., additional, Goedicke, S., additional, Eggert, H., additional, Hoyer, J. D., additional, Wurm, S., additional, Steege, A., additional, Banas, M., additional, Kurtz, A., additional, Banas, B., additional, Lasagni, L., additional, Lazzeri, E., additional, Romoli, S., additional, Schaefer, I., additional, Teng, B., additional, Worthmann, K., additional, Haller, H., additional, Schiffer, M., additional, Prattichizzo, C., additional, Netti, G. S., additional, Rocchetti, M. T., additional, Cormio, L., additional, Carrieri, G., additional, Stallone, G., additional, Grandaliano, G., additional, Ranieri, E., additional, Gesualdo, L., additional, Kucher, A., additional, Smirnov, A., additional, Parastayeva, M., additional, Beresneva, O., additional, Kayukov, I., additional, Zubina, I., additional, Ivanova, G., additional, Abed, A., additional, Schlekenbach, L., additional, Foglia, B., additional, Kwak, B., additional, Chadjichristos, C., additional, Queisser, N., additional, Schupp, N., additional, Brand, S., additional, Himer, L., additional, Szebeni, B., additional, Sziksz, E., additional, Saijo, S., additional, Kis, E., additional, Prokai, A., additional, Banki, N. F., additional, Fekete, A., additional, Tulassay, T., additional, Vannay, A., additional, Hegner, B., additional, Schaub, T., additional, Lange, C., additional, Dragun, D., additional, Klinkhammer, B. M., additional, Rafael, K., additional, Monika, M., additional, Anna, M., additional, Van Roeyen, C., additional, Boor, P., additional, Eva Bettina, B., additional, Simon, O., additional, Esther, S., additional, Floege, J., additional, Kunter, U., additional, Janke, D., additional, Jankowski, J., additional, Hayashi, M., additional, Takamatsu, I., additional, Horimai, C., additional, Yoshida, T., additional, Seno DI Marco, G., additional, Koenig, M., additional, Stock, C., additional, Reiermann, S., additional, Amler, S., additional, Koehler, G., additional, Fobker, M., additional, Buck, F., additional, Pavenstaedt, H., additional, Lang, D., additional, Brand, M., additional, Plotnikov, E., additional, Morosanova, M., additional, Pevzner, I., additional, Zorova, L., additional, Pulkova, N., additional, Zorov, D., additional, Wornle, M., additional, Ribeiro, A., additional, Belling, F., additional, Merkle, M., additional, Nakazawa, D., additional, Nishio, S., additional, Shibasaki, S., additional, Tomaru, U., additional, Akihiro, I., additional, Kobayashi, I., additional, Imanishi, Y., additional, Kurajoh, M., additional, Nagata, Y., additional, Yamagata, M., additional, Emoto, M., additional, Michigami, T., additional, Ishimura, E., additional, Inaba, M., additional, Wu, C.-C., additional, Lu, K.-C., additional, Chen, J.-S., additional, Chu, P., additional, Lin, Y.-F., additional, Eller, K., additional, Schroll, A., additional, Kirsch, A., additional, Huber, J., additional, Weiss, G., additional, Theurl, I., additional, Rosenkranz, A. R., additional, Zawada, A., additional, Rogacev, K., additional, Achenbach, M., additional, Fliser, D., additional, Held, G., additional, Heine, G. H., additional, Miyamoto, Y., additional, Iwao, Y., additional, Watanabe, H., additional, Kadowaki, D., additional, Ishima, Y., additional, Chuang, V. T. G., additional, Sato, K., additional, Otagiri, M., additional, Maruyama, T., additional, Iwatani, H., additional, Honda, D., additional, Noguchi, T., additional, Tanaka, M., additional, Tanaka, H., additional, Fukagawa, M., additional, Pircher, J., additional, Koppel, S., additional, Mannell, H., additional, Krotz, F., additional, Virzi, G. M., additional, Bolin, C., additional, Cruz, D., additional, Scalzotto, E., additional, De Cal, M., additional, Vescovo, G., additional, Ronco, C., additional, Grobmayr, R., additional, Lech, M., additional, Ryu, M., additional, Aoshima, Y., additional, Mizobuchi, M., additional, Ogata, H., additional, Kumata, C., additional, Nakazawa, A., additional, Kondo, F., additional, Ono, N., additional, Koiwa, F., additional, Kinugasa, E., additional, Freisinger, W., additional, Lale, N., additional, Lampert, A., additional, Ditting, T., additional, Heinlein, S., additional, Schmieder, R. E., additional, Veelken, R., additional, Nave, H., additional, Perthel, R., additional, Suntharalingam, M., additional, Bode-Boger, S., additional, Beutel, G., additional, Kielstein, J., additional, Rodrigues-Diez, R., additional, Rayego-Mateos, S., additional, Lavoz, C., additional, Stark Aroeira, L. G., additional, Orejudo, M., additional, Alique, M., additional, Ortiz, A., additional, Egido, J., additional, Ruiz-Ortega, M., additional, Oskar, W., additional, Rusan, C., additional, Padberg, J.-S., additional, Wiesinger, A., additional, Reuter, S., additional, Grabner, A., additional, Kentrup, D., additional, Lukasz, A., additional, Oberleithner, H., additional, Pavenstadt, H., additional, Kumpers, P., additional, Eberhardt, H. U., additional, Skerka, C., additional, Chen, Q., additional, Hallstroem, T., additional, Hartmann, A., additional, Kemper, M. J., additional, Zipfel, P. F., additional, N'gome-Sendeyo, K., additional, Fan, Q.-F., additional, Toblli, J., additional, Cao, G., additional, Giani, J. F., additional, Dominici, F. P., additional, Kim, J. S., additional, Yang, J. W., additional, Kim, M. K., additional, Han, B. G., additional, and Choi, S. O., additional
- Published
- 2012
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25. 253 Insights on centromeric breakpoints of 5q deletions
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Nofrini, V., primary, La Starza, R., additional, Crescenzi, B., additional, Pierini, V., additional, Beacci, D., additional, Matteucci, C., additional, Arcioni, F., additional, Berchicci, L., additional, Romoli, S., additional, Musto, P., additional, Sambani, C., additional, Aventin, A., additional, and Mecucci, C., additional
- Published
- 2011
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26. Cryptic chromosome 9q34 deletion generates TAF-I /CAN and TAF-I /CAN fusion transcripts in acute myeloid leukemia
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Rosati, R., primary, La Starza, R., additional, Barba, G., additional, Gorello, P., additional, Pierini, V., additional, Matteucci, C., additional, Roti, G., additional, Crescenzi, B., additional, Romoli, S., additional, Aloisi, T., additional, Aversa, F., additional, Martelli, M. F., additional, and Mecucci, C., additional
- Published
- 2007
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27. Il seno cavernoso
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Buric, J., primary, Conti, P., additional, Mangiafico, S., additional, and Romoli, S., additional
- Published
- 2000
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28. Il seno cavernoso: Aspetti embriologici, anatomici e neuroradiologici
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Buric, J., Conti, P., Mangiafico, S., and Romoli, S.
- Abstract
Il lavoro comprende la descrizione dettagliata dell'anatomia microchirurgica del seno cavernoso e della regione parasellare con particolare attenzione posta allo sviluppo embrionale della regione come spiegazione di molteplici variazioni anatomiche che si osservano durante lo studio neuroradiologico e durante l'approccio chirurgico alle lesioni che prendono sviluppo in questa regione. La descrizione dell'anatomia è suddivisa per diversi sistemi organici presenti in questa regione cosi da offrire un'adeguata rappresentazione di ognuna di esse come pure i loro rapporti tridimensionali. Infine vengono messe in risalto quelle particolarità delle strutture anatomiche importanti per l'interpretazione neuroradiologica e per l'impostazione del trattamento chirurgico ed endovascolare.
- Published
- 2000
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29. Synthesis of taurine analogues. Part 1: 2-Aminosulfonic acids from alkene-sulfur monochloride adducts
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Machetti, F., Cacciarini, M., Catrambone, F., Franca M. Cordero, Romoli, S., and Sarlo, F.
- Subjects
polycyclic compounds - Abstract
(+/-) Trans-2-aminocyclohexanesulfonic acid and (+/-) trans-2-aminocyclopentanesulfonic acid were prepared respectively from cyclohexene and cyclopentene by sulfur monochloride addition, followed by oxidation to 2-chlorosulfonic acid and substitution of chlorine
30. L'autotutela contenziosa
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M. Bellavista, G. Buia, B. Giliberti, L. Maccari, M. Monteduro, L. R. Perfetti, F. Romoli, S. Sticchi Damiani, F. Tuccari, S. Valaguzza, S. Villamena, M. Bellavista, G. Buia, B. Giliberti, L. Maccari, M. Monteduro, L.R. Perfetti, F. Romoli, S. Sticchi Damiani, F. Tuccari, S. Valaguzza, S. Villamena, Bellavista, M., Buia, G., Giliberti, B., Maccari, L., Monteduro, M., Perfetti, L. R., Romoli, F., Sticchi Damiani, S., Tuccari, F., Valaguzza, S., and Villamena, S.
- Subjects
Autotutela contenziosa, funzione giustiziale, ricorsi amministrativi, ricorso in opposizione, ricorso gerarchico, ricorso straordinario al Presidente della Repubblica, giurisdizionalizzazione - Abstract
Il contributo ha ad oggetto lo studio del sistema dei ricorsi amministrativi, di cui vengono analizzati criticamente profili, problemi e novità, con particolare riferimento al ricorso straordinario al Presidente della Repubblica e alla dibattuta questione della relativa natura giuridica
- Published
- 2017
31. Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia
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Silvia Romoli, Anna Aventin, Barbara Crescenzi, Peter Marynen, Nicoletta Testoni, Caterina Matteucci, E. Di Bona, M F Martelli, R La Starza, Marina Lafage-Pochitaloff, Anna Locasciulli, Stefania Ciolli, Christina Mecucci, Valentina Pierini, Constantina Sambani, La Starza R, Aventin A, Matteucci C, Crescenzi B, Romoli S, Testoni N, Pierini V, Ciolli S, Sambani C, Locasciulli A, Di Bona E, Lafage-Pochitaloff M, Martelli MF, Marynen P, and Mecucci C.
- Subjects
Adult ,Male ,Cancer Research ,Biology ,Sensitivity and Specificity ,Translocation, Genetic ,Fanconi anemia ,hemic and lymphatic diseases ,medicine ,Secondary Acute Myeloid Leukemia ,Humans ,In Situ Hybridization, Fluorescence ,Aged ,Genetics ,Aged, 80 and over ,medicine.diagnostic_test ,Myelodysplastic syndromes ,Secondary Myelodysplastic Syndrome ,Myeloid leukemia ,Neoplasms, Second Primary ,Hematology ,Gene rearrangement ,Middle Aged ,medicine.disease ,Oncology ,Leukemia, Myeloid ,Myelodysplastic Syndromes ,Acute Disease ,Cytogenetic Analysis ,Chromosomes, Human, Pair 6 ,Female ,Fluorescence in situ hybridization ,Comparative genomic hybridization - Abstract
Fluorescence in situ hybridization and comparative genomic hybridization characterized 6p rearrangements in eight primary and in 10 secondary myeloid disorders (including one patient with Fanconi anemia) and found different molecular lesions in each group. In primary disorders, 6p abnormalities, isolated in six patients, were highly heterogeneous with different breakpoints along the 6p arm. Reciprocal translocations were found in seven. In the 10 patients with secondary acute myeloid leukemia/myelodysplastic syndrome (AML/MDS), the short arm of chromosome 6 was involved in unbalanced translocations in 7. The other three patients showed full or partial trisomy of the 6p arm, that is, i(6)(p10) (one patient) and dup(6)(p) (two patients). In 5/7 patients with unbalanced translocations, DNA sequences were overrepresented at band 6p21 as either cryptic duplications (three patients) or cryptic low-copy gains (two patients). In the eight patients with cytogenetic or cryptic 6p gains, we identified a common overrepresented region extending for 5-6 megabases from the TNF gene to the ETV-7 gene. 6p abnormalities were isolated karyotype changes in four patients. Consequently, in secondary AML/MDS, we hypothesize that 6p gains are major pathogenetic events arising from acquired and/or congenital genomic instability.
- Published
- 2006
32. Multi-omics and imaging mass cytometry characterization of human kidneys to identify pathways and phenotypes associated with impaired kidney function.
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Asowata EO, Romoli S, Sargeant R, Tan JY, Hoffmann S, Huang MM, Mahbubani KT, Krause FN, Jachimowicz D, Agren R, Koulman A, Jenkins B, Musial B, Griffin JL, Soderberg M, Ling S, Hansen PBL, Saeb-Parsy K, and Woollard KJ
- Subjects
- Humans, Male, Middle Aged, Metabolomics methods, Female, Kidney Transplantation adverse effects, Adult, Image Cytometry methods, Kidney pathology, Kidney metabolism, Phospholipases A2 metabolism, Arachidonic Acid metabolism, Kidney Tubules, Proximal metabolism, Kidney Tubules, Proximal pathology, Transcriptome, Dinoprostone metabolism, Dinoprostone analysis, Fibroblasts metabolism, Gene Expression Profiling, Epithelial Cells metabolism, Epithelial Cells pathology, Biopsy, Multiomics, Phenotype, Acute Kidney Injury metabolism, Acute Kidney Injury pathology, Acute Kidney Injury etiology
- Abstract
Despite the recent advances in our understanding of the role of lipids, metabolites, and related enzymes in mediating kidney injury, there is limited integrated multi-omics data identifying potential metabolic pathways driving impaired kidney function. The limited availability of kidney biopsies from living donors with acute kidney injury has remained a major constraint. Here, we validated the use of deceased transplant donor kidneys as a good model to study acute kidney injury in humans and characterized these kidneys using imaging and multi-omics approaches. We noted consistent changes in kidney injury and inflammatory markers in donors with reduced kidney function. Neighborhood and correlation analyses of imaging mass cytometry data showed that subsets of kidney cells (proximal tubular cells and fibroblasts) are associated with the expression profile of kidney immune cells, potentially linking these cells to kidney inflammation. Integrated transcriptomic and metabolomic analysis of human kidneys showed that kidney arachidonic acid metabolism and seven other metabolic pathways were upregulated following diminished kidney function. To validate the arachidonic acid pathway in impaired kidney function we demonstrated increased levels of cytosolic phospholipase A2 protein and related lipid mediators (prostaglandin E2) in the injured kidneys. Further, inhibition of cytosolic phospholipase A2 reduced injury and inflammation in human kidney proximal tubular epithelial cells in vitro. Thus, our study identified cell types and metabolic pathways that may be critical for controlling inflammation associated with impaired kidney function in humans., (Copyright © 2024 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)
- Published
- 2024
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33. Chromothripsis is a frequent event and underlies typical genetic changes in early T-cell precursor lymphoblastic leukemia in adults.
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Arniani S, Pierini V, Pellanera F, Matteucci C, Di Giacomo D, Bardelli V, Quintini M, Mavridou E, Lema Fernandez AG, Nardelli C, Moretti M, Gorello P, Crescenzi B, Romoli S, Beacci D, Cerrano M, Fracchiolla N, Sica S, Forghieri F, Giglio F, Dargenio M, Elia L, La Starza R, and Mecucci C
- Subjects
- Humans, Gene Rearrangement, Mutation, Adult, Chromothripsis, Precursor Cells, T-Lymphoid, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma genetics
- Abstract
Chromothripsis is a mitotic catastrophe that arises from multiple double strand breaks and incorrect re-joining of one or a few chromosomes. We report on incidence, distribution, and features of chromothriptic events in T-cell acute lymphoblastic leukemias (T-ALL). SNP array was performed in 103 T-ALL (39 ETP/near ETP, 59 non-ETP, and 5 with unknown stage of differentiation), including 38 children and 65 adults. Chromothripsis was detected in 11.6% of all T-ALL and occurred only in adult cases with an immature phenotype (12/39 cases; 30%). It affected 1 to 4 chromosomes, and recurrently involved chromosomes 1, 6, 7, and 17. Abnormalities of genes typically associated with T-ALL were found at breakpoints of chromothripsis. In addition, it gave rise to new/rare alterations, such as, the SFPQ::ZFP36L2 fusion, reported in pediatric T-ALL, deletions of putative suppressors, such as IKZF2 and CSMD1, and amplification of the BCL2 gene. Compared to negative cases, chromothripsis positive T-ALL had a significantly higher level of MYCN expression, and a significant downregulation of RGCC, which is typically induced by TP53 in response to DNA damage. Furthermore we identified mutations and/or deletions of DNA repair/genome stability genes in all cases, and an association with NUP214 rearrangements in 33% of cases., (© 2022. The Author(s).)
- Published
- 2022
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34. High grade B-cell lymphoma with MYC , BCL2 and/or BCL6 rearrangements: unraveling the genetic landscape of a rare aggressive subtype of non-Hodgkin lymphoma.
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Ferrari A, Arniani S, Crescenzi B, Ascani S, Flenghi L, Pierini V, Moretti M, Beacci D, Romoli S, Bardelli V, Calistri D, Martinelli G, Mecucci C, and La Starza R
- Subjects
- Gene Rearrangement, Humans, Pilot Projects, Lymphoma, Large B-Cell, Diffuse genetics, Lymphoma, Large B-Cell, Diffuse pathology, Proto-Oncogene Proteins c-bcl-2 genetics, Proto-Oncogene Proteins c-bcl-6 genetics, Proto-Oncogene Proteins c-myc genetics
- Abstract
High-grade B-cell lymphoma with MYC and BCL2 and/or BCL6 rearrangements (DH/TH-HGBL) still miss an in-depth genomic characterization. To identify accompanying genetic events, we performed a pilot study on 7 cases by applying DNA microarray and targeted NGS sequencing. Interestingly, the genetic background of DH/TH-HGBL is largely overlapping with that of other high-grade/poor prognosis lymphomas. Namely, copy number abnormalities were trisomy of chromosome 7 and chromosome 8q gain, encompassing MYC . Among gene variants, those affecting transcription factors ( MYC, FOXO1 ), epigenetic modulators ( KMT2D , EZH2 and CREEBP ), and anti-apoptotic gene ( BCL2 ), were recurrent. MYC and BCL2 were mutated in 3 and 5 cases, respectively. In addition, mutations of FOXO1, previously reported in Diffuse Large B-Cell Lymphomas, were also detected. Clarifying the genomic background of this subset of high-risk lymphomas will pave the way for the clinical use of new biomarkers to: (1) monitor treatment response and; (2) consider alternative targeted therapies.
- Published
- 2022
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35. Progressive and atypical neurological symptoms in refractory systemic AL amyloidosis.
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Perfetto F, Casagrande S, Barilaro A, Di Gioia M, Santi R, Allinovi M, Romoli S, Boschi A, Desideri I, Taborchi G, Ungar A, and Cappelli F
- Subjects
- Aged, Clinical Reasoning, Humans, Immunoglobulin Light-chain Amyloidosis blood, Italy, Male, Outcome Assessment, Health Care, Shoulder physiopathology, Treatment Failure, Amyloidosis drug therapy, Amyloidosis physiopathology
- Published
- 2021
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36. Calcifying Pseudoneoplasms of the Neuraxis: Not Only Surgical Treatment.
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Boschi A, Pisano A, and Romoli S
- Abstract
Competing Interests: There are no conflicts of interest.
- Published
- 2020
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37. Minimally invasive posterior extraforaminal approach for presacral schwannoma of L5.
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Cipolleschi E, Wembagher GC, Barni I, and Romoli S
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- Female, Humans, Middle Aged, Minimally Invasive Surgical Procedures methods, Neurilemmoma diagnosis, Positron Emission Tomography Computed Tomography methods, Sacrum diagnostic imaging, Treatment Outcome, Lumbar Vertebrae surgery, Neurilemmoma surgery, Sacrum surgery
- Published
- 2019
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38. CXCL12 blockade preferentially regenerates lost podocytes in cortical nephrons by targeting an intrinsic podocyte-progenitor feedback mechanism.
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Romoli S, Angelotti ML, Antonelli G, Kumar Vr S, Mulay SR, Desai J, Anguiano Gomez L, Thomasova D, Eulberg D, Klussmann S, Melica ME, Conte C, Lombardi D, Lasagni L, Anders HJ, and Romagnani P
- Subjects
- Animals, Aptamers, Nucleotide therapeutic use, Cell Differentiation drug effects, Cells, Cultured, Chemokine CXCL12 metabolism, Disease Models, Animal, Doxorubicin toxicity, Feedback, Physiological drug effects, Glomerulosclerosis, Focal Segmental chemically induced, Glomerulosclerosis, Focal Segmental complications, Humans, Imaging, Three-Dimensional, Male, Mice, Mice, Transgenic, Microscopy, Confocal methods, Podocytes drug effects, Podocytes pathology, Proteinuria drug therapy, Proteinuria etiology, Stem Cells physiology, Treatment Outcome, Aptamers, Nucleotide pharmacology, Chemokine CXCL12 antagonists & inhibitors, Glomerulosclerosis, Focal Segmental drug therapy, Regeneration drug effects, Stem Cells drug effects
- Abstract
Insufficient podocyte regeneration after injury is a central pathomechanism of glomerulosclerosis and chronic kidney disease. Podocytes constitutively secrete the chemokine CXCL12, which is known to regulate homing and activation of stem cells; hence we hypothesized a similar effect of CXCL12 on podocyte progenitors. CXCL12 blockade increased podocyte numbers and attenuated proteinuria in mice with Adriamycin-induced nephropathy. Similar studies in lineage-tracing mice revealed enhanced de novo podocyte formation from parietal epithelial cells in the setting of CXCL12 blockade. Super-resolution microscopy documented full integration of these progenitor-derived podocytes into the glomerular filtration barrier, interdigitating with tertiary foot processes of neighboring podocytes. Quantitative 3D analysis revealed that conventional 2D analysis underestimated the numbers of progenitor-derived podocytes. The 3D analysis also demonstrated differences between juxtamedullary and cortical nephrons in both progenitor endowment and Adriamycin-induced podocyte loss, with more robust podocyte regeneration in cortical nephrons with CXCL12 blockade. Finally, we found that delayed CXCL12 inhibition still had protective effects. In vitro studies found that CXCL12 inhibition uncoupled Notch signaling in podocyte progenitors. These data suggest that CXCL12-driven podocyte-progenitor feedback maintains progenitor quiescence during homeostasis, but also limits their intrinsic capacity to regenerate lost podocytes, especially in cortical nephrons. CXCL12 inhibition could be an innovative therapeutic strategy in glomerular disorders., (Copyright © 2018 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)
- Published
- 2018
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39. Gene expression profiling of the Notch-AhR-IL22 axis at homeostasis and in response to tissue injury.
- Author
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Weidenbusch M, Rodler S, Song S, Romoli S, Marschner JA, Kraft F, Holderied A, Kumar S, Mulay SR, Honarpisheh M, Kumar Devarapu S, Lech M, and Anders HJ
- Subjects
- Acute Kidney Injury pathology, Animals, Basic Helix-Loop-Helix Transcription Factors economics, Basic Helix-Loop-Helix Transcription Factors genetics, Cytochrome P-450 CYP1A1 genetics, Gene Expression Profiling methods, Gene Expression Regulation, Humans, Inflammation physiopathology, Mice, Receptors, Notch genetics, Repressor Proteins economics, Signal Transduction genetics, Interleukin-22, Acute Kidney Injury genetics, Inflammation genetics, Interleukins genetics, Receptors, Aryl Hydrocarbon genetics
- Abstract
Notch and interleukin-22 (IL-22) signaling are known to regulate tissue homeostasis and respond to injury in humans and mice, and the induction of endogenous aryl hydrocarbon receptor (Ahr) ligands through Notch links the two pathways in a hierarchical fashion. However in adults, the species-, organ- and injury-specific gene expression of the Notch-AhR-IL22 axis components is unknown. We therefore performed gene expression profiling of DLL1, DLL3, DLL4, DLK1, DLK2, JAG1, JAG2, Notch1, Notch2, Notch3, Notch4, ADAM17/TNF-α ADAM metalloprotease converting enzyme (TACE), PSEN1, basigin (BSG)/CD147, RBP-J, HES1, HES5, HEY1, HEYL, AHR, ARNT, ARNT2, CYP1A1, CYP24A1, IL-22, IL22RA1, IL22RA2, IL10RB, and STAT3 under homeostatic conditions in ten mature murine and human organs. Additionally, the expression of these genes was assessed in murine models of acute sterile inflammation and progressive fibrosis. We show that there are organ-specific gene expression profiles of the Notch-AhR-IL22 axis in humans and mice. Although there is an overall interspecies congruency, specific differences between human and murine expression signatures do exist. In murine tissues with AHR/ARNT expression CYP1A1 and IL-22 were correlated with HES5 and HEYL expression, while in human tissues no such correlation was found. Notch and AhR signaling are involved in renal inflammation and fibrosis with specific gene expression changes in each model. Despite the presence of all Notch pathway molecules in the kidney and a model-specific induction of Notch ligands, IL-22 was only up-regulated in acute inflammation, but rapidly down-regulated during regeneration. This implies that for targeting injury responses, e.g. via IL-22, species-specific differences, injury type and time points have to be considered., (© 2017 The Author(s).)
- Published
- 2017
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- View/download PDF
40. Immunomodulatory Molecule IRAK-M Balances Macrophage Polarization and Determines Macrophage Responses during Renal Fibrosis.
- Author
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Steiger S, Kumar SV, Honarpisheh M, Lorenz G, Günthner R, Romoli S, Gröbmayr R, Susanti HE, Potempa J, Koziel J, and Lech M
- Subjects
- Animals, Cytokines immunology, Disease Models, Animal, Disease Progression, Fibrosis pathology, Humans, Immunomodulation, Inflammation pathology, Interleukin-1 Receptor-Associated Kinases deficiency, Interleukin-1 Receptor-Associated Kinases genetics, Kidney immunology, Mice, Mice, Inbred C57BL, Signal Transduction, Tumor Necrosis Factor-alpha immunology, Ureteral Obstruction pathology, Fibrosis immunology, Interleukin-1 Receptor-Associated Kinases immunology, Kidney pathology, Macrophage Activation, Macrophages cytology, Macrophages immunology, Renal Insufficiency, Chronic immunology
- Abstract
Activation of various innate immune receptors results in IL-1 receptor-associated kinase (IRAK)-1/IRAK-4-mediated signaling and secretion of proinflammatory cytokines such as IL-12, IL-6, or TNF-α, all of which are implicated in tissue injury and elevated during tissue remodeling processes. IRAK-M, also known as IRAK-3, is an inhibitor of proinflammatory cytokine and chemokine expression in intrarenal macrophages. Innate immune activation contributes to both acute kidney injury and tissue remodeling that is associated with chronic kidney disease (CKD). Our study assessed the contribution of macrophages in CKD and the role of IRAK-M in modulating disease progression. To evaluate the effect of IRAK-M in chronic renal injury in vivo, a mouse model of unilateral ureteral obstruction (UUO) was employed. The expression of IRAK-M increased within 2 d after UUO in obstructed compared with unobstructed kidneys. Mice deficient in IRAK-M were protected from fibrosis and displayed a diminished number of alternatively activated macrophages. Compared to wild-type mice, IRAK-M-deficient mice showed reduced tubular injury, leukocyte infiltration, and inflammation following renal injury as determined by light microscopy, immunohistochemistry, and intrarenal mRNA expression of proinflammatory and profibrotic mediators. Taken together, these results strongly support a role for IRAK-M in renal injury and identify IRAK-M as a possible modulator in driving an alternatively activated profibrotic macrophage phenotype in UUO-induced CKD., (Copyright © 2017 by The American Association of Immunologists, Inc.)
- Published
- 2017
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- View/download PDF
41. Intestinal Dysbiosis, Barrier Dysfunction, and Bacterial Translocation Account for CKD-Related Systemic Inflammation.
- Author
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Andersen K, Kesper MS, Marschner JA, Konrad L, Ryu M, Kumar Vr S, Kulkarni OP, Mulay SR, Romoli S, Demleitner J, Schiller P, Dietrich A, Müller S, Gross O, Ruscheweyh HJ, Huson DH, Stecher B, and Anders HJ
- Subjects
- Animals, Mice, Bacterial Translocation, Dysbiosis, Inflammation etiology, Inflammation microbiology, Intestines microbiology, Renal Insufficiency, Chronic complications
- Abstract
CKD associates with systemic inflammation, but the underlying cause is unknown. Here, we investigated the involvement of intestinal microbiota. We report that collagen type 4 α3-deficient mice with Alport syndrome-related progressive CKD displayed systemic inflammation, including increased plasma levels of pentraxin-2 and activated antigen-presenting cells, CD4 and CD8 T cells, and Th17- or IFNγ-producing T cells in the spleen as well as regulatory T cell suppression. CKD-related systemic inflammation in these mice associated with intestinal dysbiosis of proteobacterial blooms, translocation of living bacteria across the intestinal barrier into the liver, and increased serum levels of bacterial endotoxin. Uremia did not affect secretory IgA release into the ileum lumen or mucosal leukocyte subsets. To test for causation between dysbiosis and systemic inflammation in CKD, we eradicated facultative anaerobic microbiota with antibiotics. This eradication prevented bacterial translocation, significantly reduced serum endotoxin levels, and fully reversed all markers of systemic inflammation to the level of nonuremic controls. Therefore, we conclude that uremia associates with intestinal dysbiosis, intestinal barrier dysfunction, and bacterial translocation, which trigger the state of persistent systemic inflammation in CKD. Uremic dysbiosis and intestinal barrier dysfunction may be novel therapeutic targets for intervention to suppress CKD-related systemic inflammation and its consequences., (Copyright © 2016 by the American Society of Nephrology.)
- Published
- 2017
- Full Text
- View/download PDF
42. Systems biology analysis reveals role of MDM2 in diabetic nephropathy.
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Saito R, Rocanin-Arjo A, You YH, Darshi M, Van Espen B, Miyamoto S, Pham J, Pu M, Romoli S, Natarajan L, Ju W, Kretzler M, Nelson R, Ono K, Thomasova D, Mulay SR, Ideker T, D'Agati V, Beyret E, Belmonte JCI, Anders HJ, and Sharma K
- Subjects
- Albuminuria, Animals, Computational Biology, Diabetes Mellitus, Experimental metabolism, Humans, Kidney Glomerulus physiopathology, Kidney Tubules physiopathology, Mice, Mice, Inbred C57BL, Mice, Knockout, Podocytes, Diabetic Nephropathies metabolism, Proto-Oncogene Proteins c-mdm2 metabolism, Systems Biology
- Abstract
To derive new insights in diabetic complications, we integrated publicly available human protein-protein interaction (PPI) networks with global metabolic networks using metabolomic data from patients with diabetic nephropathy. We focused on the participating proteins in the network that were computationally predicted to connect the urine metabolites. MDM2 had the highest significant number of PPI connections. As validation, significant downregulation of MDM2 gene expression was found in both glomerular and tubulointerstitial compartments of kidney biopsy tissue from 2 independent cohorts of patients with diabetic nephropathy. In diabetic mice, chemical inhibition of MDM2 with Nutlin-3a led to reduction in the number of podocytes, increased blood urea nitrogen, and increased mortality. Addition of Nutlin-3a decreased WT1
+ cells in embryonic kidneys. Both podocyte- and tubule-specific MDM2 -knockout mice exhibited severe glomerular and tubular dysfunction, respectively. Interestingly, the only 2 metabolites that were reduced in both podocyte and tubule-specific MDM2 -knockout mice were 3-methylcrotonylglycine and uracil, both of which were also reduced in human diabetic kidney disease. Thus, our bioinformatics tool combined with multi-omics studies identified an important functional role for MDM2 in glomeruli and tubules of the diabetic nephropathic kidney and links MDM2 to a reduction in 2 key metabolite biomarkers.- Published
- 2016
- Full Text
- View/download PDF
43. Next generation sequencing and functional analysis of patient urine renal progenitor-derived podocytes to unravel the diagnosis underlying refractory lupus nephritis.
- Author
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Romagnani P, Giglio S, Angelotti ML, Provenzano A, Becherucci F, Mazzinghi B, Müller S, Amann K, Weidenbusch M, Romoli S, Lazzeri E, and Anders HJ
- Subjects
- Adolescent, Female, Humans, Lupus Nephritis etiology, Podocytes pathology, Recurrence, Stem Cells pathology, High-Throughput Nucleotide Sequencing methods, Kidney physiopathology, Lupus Nephritis diagnosis, Lupus Nephritis urine, Podocytes metabolism, Stem Cells metabolism
- Abstract
Often the cause of refractory lupus nephritis (RLN) remains unclear. We performed next-generation sequencing for podocyte genes in an RLN patient and identified compound heterozygosity for APOL1 risk alleles G1 and G2 and a novel homozygous c.[1049C>T]+[1049C>T] NPHS1 gene variant of unknown significance. To test for causality renal progenitor cells isolated from urine of this patient were differentiated into podocytes in vitro. Podocytes revealed aberrant nephrin trafficking, cytoskeletal structure and lysosomal leakage, and increased detachment as compared with podocytes isolated from controls. Thus, lupus podocytopathy can be confirmed as a cause of RLN by functional genetics on patient-derived podocytes., (© The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
44. Murine Double Minute-2 Inhibition Ameliorates Established Crescentic Glomerulonephritis.
- Author
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Mulay SR, Romoli S, Desai J, Honarpisheh MM, Kumar SV, Anders HJ, and Thomasova D
- Subjects
- Animals, Blotting, Western, Disease Models, Animal, Glomerulonephritis metabolism, Immunohistochemistry, Mice, Mice, Inbred C57BL, Microscopy, Confocal, Real-Time Polymerase Chain Reaction, Signal Transduction physiology, Tumor Suppressor Protein p53 metabolism, Glomerulonephritis pathology, Imidazoles pharmacology, Piperazines pharmacology, Proto-Oncogene Proteins c-mdm2 antagonists & inhibitors
- Abstract
Rapidly progressive glomerulonephritis is characterized by glomerular necroinflammation and crescent formation. Its treatment includes unspecific and toxic agents; therefore, the identification of novel therapeutic targets is required. The E3-ubiquitin ligase murine double minute (MDM)-2 is a nonredundant element of NF-κB signaling and the negative regulator of tumor suppressor gene TP53-mediated cell cycle arrest and cell death. We hypothesized that the MDM2 would drive crescentic glomerulonephritis by NF-κB-dependent glomerular inflammation and by p53-dependent parietal epithelial cell hyperproliferation. Indeed, the pre-emptive MDM2 blockade by nutlin-3a ameliorated all aspects of crescentic glomerulonephritis. MDM2 inhibition had identical protective effects in Trp53-deficient mice, with the exception of crescent formation, which was not influenced by nutlin-3a treatment. In vitro experiments confirmed the contribution of MDM2 for induction of NF-κB-dependent cytokines in murine glomerular endothelial cells and for p53-dependent parietal epithelial cell proliferation. To evaluate MDM2 blockade as a potential therapeutic intervention in rapidly progressive glomerulonephritis, we treated mice with established glomerulonephritis with nutlin-3a. Delayed onset of nutlin-3a treatment was equally protective as the pre-emptive treatment in abrogating crescentic glomerulonephritis. Together, the pathogenic effects of MDM2 are twofold, that is, p53-independent NF-κB activation increasing intraglomerular inflammation and p53-dependent parietal epithelial cell hyperplasia and crescent formation. We therefore propose MDM2 blockade as a potential novel therapeutic strategy in rapidly progressive glomerulonephritis., (Copyright © 2016 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
45. Oxalate-induced chronic kidney disease with its uremic and cardiovascular complications in C57BL/6 mice.
- Author
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Mulay SR, Eberhard JN, Pfann V, Marschner JA, Darisipudi MN, Daniel C, Romoli S, Desai J, Grigorescu M, Kumar SV, Rathkolb B, Wolf E, Hrabě de Angelis M, Bäuerle T, Dietel B, Wagner CA, Amann K, Eckardt KU, Aronson PS, Anders HJ, and Knauf F
- Subjects
- Animals, Fibroblast Growth Factor-23, Fibrosis, Hypertension pathology, Mice, Mice, Inbred C57BL, Myocardium pathology, Renal Insufficiency, Chronic chemically induced, Renal Insufficiency, Chronic pathology, Uremia pathology, Disease Models, Animal, Hypertension etiology, Oxalic Acid, Renal Insufficiency, Chronic complications, Uremia etiology
- Abstract
Chronic kidney disease (CKD) research is limited by the lack of convenient inducible models mimicking human CKD and its complications in experimental animals. We demonstrate that a soluble oxalate-rich diet induces stable stages of CKD in male and female C57BL/6 mice. Renal histology is characterized by tubular damage, remnant atubular glomeruli, interstitial inflammation, and fibrosis, with the extent of tissue involvement depending on the duration of oxalate feeding. Expression profiling of markers and magnetic resonance imaging findings established to reflect inflammation and fibrosis parallel the histological changes. Within 3 wk, the mice reproducibly develop normochromic anemia, metabolic acidosis, hyperkalemia, FGF23 activation, hyperphosphatemia, and hyperparathyroidism. In addition, the model is characterized by profound arterial hypertension as well as cardiac fibrosis that persist following the switch to a control diet. Together, this new model of inducible CKD overcomes a number of previous experimental limitations and should serve useful in research related to CKD and its complications., (Copyright © 2016 the American Physiological Society.)
- Published
- 2016
- Full Text
- View/download PDF
46. Cytotoxicity of crystals involves RIPK3-MLKL-mediated necroptosis.
- Author
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Mulay SR, Desai J, Kumar SV, Eberhard JN, Thomasova D, Romoli S, Grigorescu M, Kulkarni OP, Popper B, Vielhauer V, Zuchtriegel G, Reichel C, Bräsen JH, Romagnani P, Bilyy R, Munoz LE, Herrmann M, Liapis H, Krautwald S, Linkermann A, and Anders HJ
- Subjects
- Animals, Calcium Oxalate chemistry, Calcium Oxalate metabolism, Calcium Pyrophosphate chemistry, Calcium Pyrophosphate metabolism, Humans, Kidney Diseases genetics, Kidney Diseases metabolism, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Necrosis, Phosphorylation, Protein Kinases genetics, Receptor-Interacting Protein Serine-Threonine Kinases genetics, Tumor Necrosis Factor-alpha genetics, Tumor Necrosis Factor-alpha metabolism, Uric Acid chemistry, Uric Acid metabolism, Apoptosis, Calcium Oxalate toxicity, Calcium Pyrophosphate toxicity, Kidney Diseases physiopathology, Protein Kinases metabolism, Receptor-Interacting Protein Serine-Threonine Kinases metabolism, Uric Acid toxicity
- Abstract
Crystals cause injury in numerous disorders, and induce inflammation via the NLRP3 inflammasome, however, it remains unclear how crystals induce cell death. Here we report that crystals of calcium oxalate, monosodium urate, calcium pyrophosphate dihydrate and cystine trigger caspase-independent cell death in five different cell types, which is blocked by necrostatin-1. RNA interference for receptor-interacting protein kinase 3 (RIPK3) or mixed lineage kinase domain like (MLKL), two core proteins of the necroptosis pathway, blocks crystal cytotoxicity. Consistent with this, deficiency of RIPK3 or MLKL prevents oxalate crystal-induced acute kidney injury. The related tissue inflammation drives TNF-α-related necroptosis. Also in human oxalate crystal-related acute kidney injury, dying tubular cells stain positive for phosphorylated MLKL. Furthermore, necrostatin-1 and necrosulfonamide, an inhibitor for human MLKL suppress crystal-induced cell death in human renal progenitor cells. Together, TNF-α/TNFR1, RIPK1, RIPK3 and MLKL are molecular targets to limit crystal-induced cytotoxicity, tissue injury and organ failure.
- Published
- 2016
- Full Text
- View/download PDF
47. PMA and crystal-induced neutrophil extracellular trap formation involves RIPK1-RIPK3-MLKL signaling.
- Author
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Desai J, Kumar SV, Mulay SR, Konrad L, Romoli S, Schauer C, Herrmann M, Bilyy R, Müller S, Popper B, Nakazawa D, Weidenbusch M, Thomasova D, Krautwald S, Linkermann A, and Anders HJ
- Subjects
- Animals, Blotting, Western, Extracellular Traps immunology, Female, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, Microscopy, Confocal, Neutrophils immunology, Neutrophils metabolism, Phosphorylcholine analogs & derivatives, Phosphorylcholine toxicity, Polymethacrylic Acids toxicity, Protein Kinases immunology, Receptor-Interacting Protein Serine-Threonine Kinases immunology, Uric Acid toxicity, Extracellular Traps metabolism, Protein Kinases metabolism, Receptor-Interacting Protein Serine-Threonine Kinases metabolism, Signal Transduction immunology
- Abstract
Neutrophil extracellular trap (NET) formation contributes to gout, autoimmune vasculitis, thrombosis, and atherosclerosis. The outside-in signaling pathway triggering NET formation is unknown. Here, we show that the receptor-interacting protein kinase (RIPK)-1-stabilizers necrostatin-1 or necrostatin-1s and the mixed lineage kinase domain-like (MLKL)-inhibitor necrosulfonamide prevent monosodium urate (MSU) crystal- or PMA-induced NET formation in human and mouse neutrophils. These compounds do not affect PMA- or urate crystal-induced production of ROS. Moreover, neutrophils of chronic granulomatous disease patients are shown to lack PMA-induced MLKL phosphorylation. Genetic deficiency of RIPK3 in mice prevents MSU crystal-induced NET formation in vitro and in vivo. Thus, neutrophil death and NET formation may involve the signaling pathway defining necroptosis downstream of ROS production. These data imply that RIPK1, RIPK3, and MLKL could represent molecular targets in gout or other crystallopathies., (© 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)
- Published
- 2016
- Full Text
- View/download PDF
48. Neutrophil Extracellular Trap-Related Extracellular Histones Cause Vascular Necrosis in Severe GN.
- Author
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Kumar SV, Kulkarni OP, Mulay SR, Darisipudi MN, Romoli S, Thomasova D, Scherbaum CR, Hohenstein B, Hugo C, Müller S, Liapis H, and Anders HJ
- Subjects
- Animals, Cattle, Extracellular Traps drug effects, Glomerulonephritis drug therapy, Glomerulonephritis etiology, Histones drug effects, Mice, Necrosis etiology, Severity of Illness Index, Blood Vessels pathology, Extracellular Traps physiology, Glomerulonephritis complications, Histones physiology
- Abstract
Severe GN involves local neutrophil extracellular trap (NET) formation. We hypothesized a local cytotoxic effect of NET-related histone release in necrotizing GN. In vitro, histones from calf thymus or histones released by neutrophils undergoing NETosis killed glomerular endothelial cells, podocytes, and parietal epithelial cells in a dose-dependent manner. Histone-neutralizing agents such as antihistone IgG, activated protein C, or heparin prevented this effect. Histone toxicity on glomeruli ex vivo was Toll-like receptor 2/4 dependent, and lack of TLR2/4 attenuated histone-induced renal thrombotic microangiopathy and glomerular necrosis in mice. Anti-glomerular basement membrane GN involved NET formation and vascular necrosis, whereas blocking NET formation by peptidylarginine inhibition or preemptive anti-histone IgG injection significantly reduced all aspects of GN (i.e., vascular necrosis, podocyte loss, albuminuria, cytokine induction, recruitment or activation of glomerular leukocytes, and glomerular crescent formation). To evaluate histones as a therapeutic target, mice with established GN were treated with three different histone-neutralizing agents. Anti-histone IgG, recombinant activated protein C, and heparin were equally effective in abrogating severe GN, whereas combination therapy had no additive effects. Together, these results indicate that NET-related histone release during GN elicits cytotoxic and immunostimulatory effects. Furthermore, neutralizing extracellular histones is still therapeutic when initiated in established GN., (Copyright © 2015 by the American Society of Nephrology.)
- Published
- 2015
- Full Text
- View/download PDF
49. Podocyte Regeneration Driven by Renal Progenitors Determines Glomerular Disease Remission and Can Be Pharmacologically Enhanced.
- Author
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Lasagni L, Angelotti ML, Ronconi E, Lombardi D, Nardi S, Peired A, Becherucci F, Mazzinghi B, Sisti A, Romoli S, Burger A, Schaefer B, Buccoliero A, Lazzeri E, and Romagnani P
- Subjects
- Animals, Cells, Cultured, Glycogen Synthase Kinase 3 antagonists & inhibitors, Indoles pharmacology, Indoles therapeutic use, Mice, Mice, Inbred C57BL, Oximes pharmacology, Oximes therapeutic use, Podocytes drug effects, Podocytes metabolism, Renal Insufficiency, Chronic drug therapy, Stem Cells drug effects, Stem Cells metabolism, Cell Differentiation, Podocytes cytology, Regeneration, Renal Insufficiency, Chronic pathology, Stem Cells cytology
- Abstract
Podocyte loss is a general mechanism of glomerular dysfunction that initiates and drives the progression of chronic kidney disease, which affects 10% of the world population. Here, we evaluate whether the regenerative response to podocyte injury influences chronic kidney disease outcome. In models of focal segmental glomerulosclerosis performed in inducible transgenic mice where podocytes are tagged, remission or progression of disease was determined by the amount of regenerated podocytes. When the same model was established in inducible transgenic mice where renal progenitors are tagged, the disease remitted if renal progenitors successfully differentiated into podocytes, while it persisted if differentiation was ineffective, resulting in glomerulosclerosis. Treatment with BIO, a GSK3s inhibitor, significantly increased disease remission by enhancing renal progenitor sensitivity to the differentiation effect of endogenous retinoic acid. These results establish renal progenitors as critical determinants of glomerular disease outcome and a pharmacological enhancement of their differentiation as a possible therapeutic strategy., (Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2015
- Full Text
- View/download PDF
50. Murine Double Minute-2 Prevents p53-Overactivation-Related Cell Death (Podoptosis) of Podocytes.
- Author
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Thomasova D, Bruns HA, Kretschmer V, Ebrahim M, Romoli S, Liapis H, Kotb AM, Endlich N, and Anders HJ
- Subjects
- Analysis of Variance, Animals, Blotting, Western, Cell Survival genetics, Cells, Cultured, Disease Models, Animal, Genes, p53 genetics, Glomerulosclerosis, Focal Segmental pathology, Glomerulosclerosis, Focal Segmental physiopathology, Homeostasis genetics, Immunohistochemistry, Kidney Function Tests, Mice, Mice, Knockout, Microscopy, Confocal, Podocytes cytology, Podocytes physiology, Real-Time Polymerase Chain Reaction methods, Sensitivity and Specificity, Transcriptional Activation physiology, Zebrafish, Autophagy genetics, Cell Death genetics, Genes, p53 physiology, Glomerulosclerosis, Focal Segmental genetics, Proto-Oncogene Proteins c-mdm2 genetics, Transcriptional Activation genetics
- Abstract
Murine double minute-2 (MDM2), an E3 ligase that regulates the cell cycle and inflammation, is highly expressed in podocytes. In podocyte injury, MDM2 drives podocyte loss by mitotic catastrophe, but the function of MDM2 in resting podocytes has not been explored. Here, we investigated the effects of podocyte MDM2 deletion in vitro and in vivo. In vitro, MDM2 knockdown by siRNA caused increased expression of p53 and podocyte death, which was completely rescued by coknockdown of p53. Apoptosis, pyroptosis, pyronecrosis, necroptosis, ferroptosis, and parthanatos were excluded as modes of occurrence for this p53-overactivation-related cell death (here referred to as podoptosis). Podoptosis was associated with cytoplasmic vacuolization, endoplasmic reticulum stress, and dysregulated autophagy (previously described as paraptosis). MDM2 knockdown caused podocyte loss and proteinuria in a zebrafish model, which was consistent with the phenotype of podocyte-specific MDM2-knockout mice that also showed the aforementioned ultrastructual podocyte abnormalities before and during progressive glomerulosclerosis. The phenotype of both animal models was entirely rescued by codeletion of p53. We conclude that MDM2 maintains homeostasis and long-term survival in podocytes by preventing podoptosis, a p53-regulated form of cell death with unspecific features previously classified as paraptosis., (Copyright © 2015 by the American Society of Nephrology.)
- Published
- 2015
- Full Text
- View/download PDF
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