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Your search keyword '"Colombo, Emanuela"' showing total 313 results
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313 results on '"Colombo, Emanuela"'

5. Three different directions in which the European Union could replace Russian natural gas

Author

Nikas, Alexandros, Frilingou, Natasha, Heussaff, Conall, Fragkos, Panagiotis, Mittal, Shivika, Sampedro, Jon, Giarola, Sara, Sasse, Jan-Philipp, Rinaldi, Lorenzo, Doukas, Haris, Gambhir, Ajay, Giannousakis, Anastasis, Golinucci, Nicolò, Koasidis, Konstantinos, Rocco, Matteo Vincenzo, Trutnevyte, Evelina, Xexakis, Georgios, Zachmann, Georg, Zisarou, Eleftheria, Colombo, Emanuela, Hawkes, Adam, Yarlagadda, Brinda, Binsted, Matthew, Iyer, Gokul, Johannsen, Rasmus Magni, Thellufsen, Jakob Zinck, Lund, Henrik, and Van de Ven, Dirk-Jan

Published
2024
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7. Refinement of the diagnostic approach for the identification of children and adolescents affected by familial hypercholesterolemia: Evidence from the LIPIGEN study

Author

Anesi, Adriano, Arca, Marcello, Auricchio, Renata, Averna, Maurizio, Baldera, Davide, Banderali, Giuseppe, Beccuti, Guglielmo, Benso, Andrea, Berteotti, Martina, Bertolini, Stefano, Bianconi, Vanessa, Biasucci, Giacomo, Biolo, Gianni, Bonanni, Luca, Borghi, Claudio, Bossi, Antonio Carlo, Branchi, Adriana, Bruzzi, Patrizia, Bucci, Marco, Buonuomo, Paola Sabrina, Calabrò, Paolo, Calandra, Sebastiano, Carubbi, Francesca, Cavallaro, Raimondo, Cefalù, Angelo Baldassarre, Cesaro, Arturo, Cipollone, Francesco, Citroni, Nadia, Colombo, Emanuela, Coppola, Chiara, D'Addato, Sergio, Dal Pino, Beatrice, Dalla Nora, Edoardo, De Corrado, Giuseppe, Del Ben, Maria, Di Molfetta, Sergio, Di Taranto, Maria Donata, Fainelli, Giulia, Federici, Massimo, Ferri, Claudio, Fiorenza, Anna Maria, Formisano, Elena, Fortunato, Giuliana, Giaccari, Andrea, Giorgino, Francesco, Grigore, Liliana, Guardamagna, Ornella, Iannuzzi, Arcangelo, Iannuzzo, Gabriella, Iughetti, Lorenzo, Lia, Salvatore, Longo, Susanna, Lupi, Alessandro, Mandraffino, Giuseppe, Marcucci, Rossella, Maroni, Lorenzo, Massini, Giulia, Mazza, Elisa, Melchioda, Elena, Meregalli, Giancarla, Minicocci, Ilenia, Moffa, Simona, Mombelli, Giuliana, Muntoni, Sandro, Nascimbeni, Fabio, Negri, Emanuele Alberto, Notargiacomo, Serena, Panfili, Filippo Maria, Parati, Gianfranco, Passaro, Angelina, Pavanello, Chiara, Pecchioli, Valerio, Pecchioli, Lorenzo, Pellegatta, Fabio, Perla, Francesco Massimo, Pipolo, Antonio, Piro, Salvatore, Pirro, Matteo, Pisciotta, Livia, Pujia, Roberta, Putotto, Carolina, Repetti, Elena, Rinaldi, Elisabetta, Romandini, Alessandra, Sani, Elena, Sarnari, Silvia, Sarzani, Riccardo, Sbrana, Francesco, Scicali, Roberto, Scuruchi, Michele, Suppressa, Patrizia, Tarugi, Patrizia, Trenti, Chiara, Vinci, Pierandrea, Werba, José Pablo, Zambon, Sabina, Zambon, Alberto, Zenti, Maria Grazia, Casula, Manuela, Gazzotti, Marta, Capra, Maria Elena, Olmastroni, Elena, Galimberti, Federica, Catapano, Alberico L., and Pederiva, Cristina

Published
2023
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34. JAB1 deletion in oligodendrocytes causes senescence-induced inflammation and neurodegeneration in mice

Author

Rivellini, Cristina, Porrello, Emanuela, Dina, Giorgia, Mrakic-Sposta, Simona, Vezzoli, Alessandra, Bacigaluppi, Marco, Gullotta, Giorgia Serena, Chaabane, Linda, Leocani, Letizia, Marenna, Silvia, Colombo, Emanuela, Farina, Cinthia, Newcombe, Jia, Nave, Klaus-Armin, Pardi, Ruggero, Quattrini, Angelo, and Previtali, Stefano C.

Subjects
Binding proteins -- Physiological aspects -- Health aspects, Oligodendroglia -- Genetic aspects -- Health aspects, Demyelinating diseases -- Development and progression -- Genetic aspects, Health care industry
Abstract

Oligodendrocytes are the primary target of demyelinating disorders, and progressive neurodegenerative changes may evolve in the CNS. DNA damage and oxidative stress are considered key pathogenic events, but the underlying molecular mechanisms remain unclear. Moreover, animal models do not fully recapitulate human diseases, complicating the path to effective treatments. Here we report that mice with cell-autonomous deletion of the nuclear COP9 signalosome component CSN5 (JAB1) in oligodendrocytes develop DNA damage and defective DNA repair in myelinating glial cells. Interestingly, oligodendrocytes lacking JAB1 expression underwent a senescence-like phenotype that fostered chronic inflammation and oxidative stress. These mutants developed progressive CNS demyelination, microglia inflammation, and neurodegeneration, with severe motor deficits and premature death. Notably, blocking microglia inflammation did not prevent neurodegeneration, whereas the deletion of [p21.sup.CIP1] but not [p.sup.6 INK4a] pathway ameliorated the disease. We suggest that senescence is key to sustaining neurodegeneration in demyelinating disorders and may be considered a potential therapeutic target., Introduction Myelin is a highly specialized protein- and lipid-rich membrane that wraps around axons in the central and peripheral nervous systems (CNS and PNS). It is made by oligodendrocytes in [...]

Published
2022
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36. Evaluation of the performance of Dutch Lipid Clinic Network score in an Italian FH population: The LIPIGEN study

Author

Arca, Marcello, Averna, Maurizio, Bertolini, Stefano, Calandra, Sebastiano, Catapano, Alberico Luigi, Tarugi, Patrizia, Pellegatta, Fabio, Angelico, Francesco, Bartuli, Andrea, Biasucci, Giacomo, Biolo, Gianni, Bonanni, Luca, Bonomo, Katia, Borghi, Claudio, Bossi, Antonio Carlo, Branchi, Adriana, Carubbi, Francesca, Cipollone, Francesco, Citroni, Nadia, Federici, Massimo, Ferri, Claudio, Fiorenza, Anna Maria, Giaccari, Andrea, Giorgino, Francesco, Guardamagna, Ornella, Iannuzzi, Arcangelo, Iughetti, Lorenzo, Lupattelli, Graziana, Lupi, Alessandro, Mandraffino, Giuseppe, Marcucci, Rossella, Maroni, Lorenzo, Miccoli, Roberto, Mombelli, Giuliana, Muntoni, Sandro, Pecchioli, Valerio, Pederiva, Cristina, Pipolo, Antonio, Pisciotta, Livia, Pujia, Arturo, Purrello, Francesco, Repetti, Elena, Rubba, Paolo, Sabbà, Carlo, Sampietro, Tiziana, Sarzani, Riccardo, Tagliabue, Milena Paola, Trenti, Chiara, Vigna, Giovanni Battista, Werba, Josè Pablo, Zambon, Sabina, Zenti, Maria Grazia, Minicocci, Ilenia, Noto, Davide, Fortunato, Giuliana, Banderali, Giuseppe, Benso, Andrea, Bigolin, Paola, Bonora, Enzo, Bruzzi, Patrizia, Bucci, Marco, Buonuomo, Paola Sabrina, Capra, Maria Elena, Cardolini, Iris, Cefalù, Baldassarre, Cervelli, Nazzareno, Chiariello, Giuseppe, Cocci, Guido, Colombo, Emanuela, Cremonini, Anna Laura, D'Addato, Sergio, D'Erasmo, Laura, Dal Pino, Beatrice, De Sanctis, Luisa, De Vita, Emanuele, Del Ben, Maria, Di Costanzo, Alessia, Di Taranto, Maria Donata, Fasano, Tommaso, Gentile, Luigi, Gentile, Marco, Ghirardello, Omar, Grigore, Liliana, Lussu, Milena, Meregalli, Giancarla, Moffa, Simona, Montalcini, Tiziana, Morgia, Valeria, Nascimbeni, Fabio, Pasta, Andrea, Pavanello, Chiara, Saitta, Antonino, Scicali, Roberto, Siepi, Donatella, Spagnolli, Walter, Spina, Rossella, Sticchi, Elena, Suppressa, Patrizia, Vigo, Lorenzo, Vinci, Pierandrea, Casula, Manuela, Manzato, Enzo, Olmastroni, Elena, Tragni, Elena, Zampoleri, Veronica, and Pirillo, Angela

Published
2018
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38. Caloric restriction leads to druggable LSD1-dependent cancer stem cells expansion.

Author

Pallavi, Rani, Gatti, Elena, Durfort, Tiphanie, Stendardo, Massimo, Ravasio, Roberto, Leonardi, Tommaso, Falvo, Paolo, Duso, Bruno Achutti, Punzi, Simona, Xieraili, Aobuli, Polazzi, Andrea, Verrelli, Doriana, Trastulli, Deborah, Ronzoni, Simona, Frascolla, Simone, Perticari, Giulia, Elgendy, Mohamed, Varasi, Mario, Colombo, Emanuela, and Giorgio, Marco

Subjects
CANCER stem cells, LOW-calorie diet, ACUTE promyelocytic leukemia, ACUTE myeloid leukemia, TRIPLE-negative breast cancer, INSULIN receptors
Abstract

Caloric Restriction (CR) has established anti-cancer effects, but its clinical relevance and molecular mechanism remain largely undefined. Here, we investigate CR's impact on several mouse models of Acute Myeloid Leukemias, including Acute Promyelocytic Leukemia, a subtype strongly affected by obesity. After an initial marked anti-tumor effect, lethal disease invariably re-emerges. Initially, CR leads to cell-cycle restriction, apoptosis, and inhibition of TOR and insulin/IGF1 signaling. The relapse, instead, is associated with the non-genetic selection of Leukemia Initiating Cells and the downregulation of double-stranded RNA (dsRNA) sensing and Interferon (IFN) signaling genes. The CR-induced adaptive phenotype is highly sensitive to pharmacological or genetic ablation of LSD1, a lysine demethylase regulating both stem cells and dsRNA/ IFN signaling. CR + LSD1 inhibition leads to the re-activation of dsRNA/IFN signaling, massive RNASEL-dependent apoptosis, and complete leukemia eradication in ~90% of mice. Importantly, CR-LSD1 interaction can be modeled in vivo and in vitro by combining LSD1 ablation with pharmacological inhibitors of insulin/IGF1 or dual PI3K/MEK blockade. Mechanistically, insulin/IGF1 inhibition sensitizes blasts to LSD1-induced death by inhibiting the anti-apoptotic factor CFLAR. CR and LSD1 inhibition also synergize in patient-derived AML and triple-negative breast cancer xenografts. Our data provide a rationale for epi-metabolic pharmacologic combinations across multiple tumors. Caloric restriction (CR) has been demonstrated to have a role in tumour growth and therapy response but its effects on cancer stem cells are less known. Here, in Acute Promyelocytic Leukemia, the authors show that despite initial anti-tumour effect, CR drives the selection of leukaemia-initiating cells resulting in relapse which could be prevented by ablation of LSD1. [ABSTRACT FROM AUTHOR]

Published
2024
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39. High-sensitivity analysis of clonal hematopoiesis reveals increased clonal complexity of potential-driver mutations in severe COVID-19 patients.

Author

Ronchini, Chiara, Caprioli, Chiara, Tunzi, Gianleo, D'Amico, Francesco Furio, Colombo, Emanuela, Giani, Marco, Foti, Giuseppe, Conconi, Donatella, Lavitrano, Marialuisa, Passerini, Rita, Pase, Luca, Capizzi, Silvio, Mastrilli, Fabrizio, Alcalay, Myriam, Orecchia, Roberto, Natoli, Gioacchino, and Pelicci, Pier Giuseppe

Subjects
HEMATOPOIESIS, COVID-19, GENETIC mutation, OVERALL survival, GENE frequency, LONG-Term Evolution (Telecommunications)
Abstract

Whether Clonal Hematopoiesis (CH) represents a risk factor for severity of the COVID-19 disease remains a controversial issue. We report the first high- sensitivity analysis of CH in COVID-19 patients (threshold of detection at 0.5% vs 1 or 2% in previous studies). We analyzed 24 patients admitted to ICU for COVID-19 (COV-ICU) and 19 controls, including healthy subjects and asymptomatic SARS-CoV2-positive individuals. Despite the significantly higher numbers of CH mutations identified (80% mutations with <2% variant allele frequency, VAF), we did not find significant differences between COV-ICU patients and controls in the prevalence of CH or in the numbers, VAF or functional categories of the mutated genes, suggesting that CH is not overrepresented in patients with COVID-19. However, when considering potential drivers CH mutations (CH-PD), COV-ICU patients showed higher clonal complexity, in terms of both mutation numbers and VAF, and enrichment of variants reported in myeloid neoplasms. However, we did not score an impact of increased CH-PD on patient survival or clinical parameters associated with inflammation. These data suggest that COVID-19 influence the clonal composition of the peripheral blood and call for further investigations addressing the potential long-term clinical impact of CH on people experiencing severe COVID-19. We acknowledge that it will indispensable to perform further studies on larger patient cohorts in order to validate and generalize our conclusions. Moreover, we performed CH analysis at a single time point. It will be necessary to consider longitudinal approaches with long periods of follow-up in order to assess if the COVID-19 disease could have an impact on the evolution of CH and long-term consequences in patients that experienced severe COVID-19. [ABSTRACT FROM AUTHOR]

Published
2024
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