G
Giulia d'Amati
Researcher at Sapienza University of Rome
Publications - 197
Citations - 8429
Giulia d'Amati is an academic researcher from Sapienza University of Rome. The author has contributed to research in topics: Cardiomyopathy & Mitochondrial DNA. The author has an hindex of 48, co-authored 197 publications receiving 7019 citations. Previous affiliations of Giulia d'Amati include Columbia University & Women's College Hospital.
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Journal ArticleDOI
2011 Consensus statement on endomyocardial biopsy from the Association for European Cardiovascular Pathology and the Society for Cardiovascular Pathology
Ornella Leone,John P. Veinot,Annalisa Angelini,Ulrik Baandrup,Cristina Basso,Gerald J. Berry,Patrick Bruneval,Margaret Burke,Jagdish Butany,Fiorella Calabrese,Giulia d'Amati,William D. Edwards,John T. Fallon,Michael C. Fishbein,Patrick J. Gallagher,Marc K. Halushka,Bruce M. McManus,Angela Pucci,E. Rene Rodriguez,Jeffrey E. Saffitz,Mary N. Sheppard,Charles Steenbergen,James R. Stone,Carmela D. Tan,Gaetano Thiene,Allard C. van der Wal,Gayle L. Winters +26 more
TL;DR: Determining appropriate EMB use in the context of current diagnostic strategies for cardiac diseases and providing recommendations for its rational utilization and providing standard criteria and guidance for appropriate tissue triage and pathological analysis is suggested.
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Coronary microvascular dysfunction: mechanisms and functional assessment.
TL;DR: The coronary microvasculature (vessels <300 μm in diameter) cannot be directly imaged in vivo, but a number of invasive and non-invasive techniques, each with relative advantages and pitfalls, can be used to assess parameters that depend directly on coronary microvascular function as discussed by the authors.
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Leptin induces direct vasodilation through distinct endothelial mechanisms.
Giuseppe Lembo,Carmine Vecchione,Luigi Fratta,Gennaro Marino,Valentina Trimarco,Giulia d'Amati,Bruno Trimarco +6 more
TL;DR: Leptin-evoked vasorelaxation evoked by leptin is heterogeneous and related to the vascular bed, and the inhibition of nitric oxide synthase by NG-nitro-L-arginine-methyl ester does not modify blood pressure response to leptin, suggesting a predominant role of the EDHF mechanism in the hypotensive effect of leptin.
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Guidelines for autopsy investigation of sudden cardiac death: 2017 update from the Association for European Cardiovascular Pathology.
Cristina Basso,Beatriz Aguilera,Jytte Banner,Stephan Cohle,Giulia d'Amati,Rosa Gouveia,Cira Di Gioia,Aurelie Fabre,Patrick J. Gallagher,Ornella Leone,Joaquín Lucena,Lubov Mitrofanova,Pilar Molina,Sarah Parsons,Stefania Rizzo,Mary N. Sheppard,Maria Paz Suárez Mier,S. Kim Suvarna,Gaetano Thiene,Allard C. van der Wal,Aryan Vink,Katarzyna Michaud +21 more
TL;DR: These guidelines represent the minimum standard that is required in the routine autopsy practice for the adequate investigation of SCD and are believed to improve the standards of autopsy practice, allow meaningful comparisons between different communities and regions, and permit the identification of emerging patterns of diseases causing SCD.
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Efficient mitochondrial biogenesis drives incomplete penetrance in Leber's hereditary optic neuropathy.
Carla Giordano,Luisa Iommarini,Luca Giordano,Alessandra Maresca,Annalinda Pisano,Maria Lucia Valentino,Leonardo Caporali,Rocco Liguori,Stefania Deceglie,Marina Roberti,Francesca Fanelli,Flavio Fracasso,Fred N. Ross-Cisneros,Pio D'Adamo,Gavin Hudson,Angela Pyle,Patrick Yu-Wai-Man,Patrick F. Chinnery,Massimo Zeviani,Solange Rios Salomão,Adriana Berezovsky,Rubens Belfort,Dora Fix Ventura,Milton Rocha Moraes,Milton Moraes Filho,Piero Barboni,Federico Sadun,Annamaria De Negri,Alfredo A. Sadun,Andrea Tancredi,Massimiliano Mancini,Giulia d'Amati,Paola Loguercio Polosa,Palmiro Cantatore,Valerio Carelli +34 more
TL;DR: Giordano et al. show that mitochondrial DNA content and mitochondrial mass are both increased in tissues and cells from unaffected mutation carriers relative to affected relatives and control individuals, suggesting upregulation of mitochondrial biogenesis may represent a therapeutic target.