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Nicola Di Daniele

Researcher at University of Rome Tor Vergata

Publications -  195
Citations -  13542

Nicola Di Daniele is an academic researcher from University of Rome Tor Vergata. The author has contributed to research in topics: Internal medicine & Kidney disease. The author has an hindex of 29, co-authored 173 publications receiving 9553 citations. Previous affiliations of Nicola Di Daniele include University of Miami & Boston Children's Hospital.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
Journal Article

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Lorenzo Galluzzi, +168 more
- 01 Jan 2018 - 
TL;DR: An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed.
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Impact of Mediterranean diet on metabolic syndrome, cancer and longevity

TL;DR: The Mediterranean Diet represents a possible therapy for metabolic syndrome, preventing adiposopathy or “sick fat” formation and exerts protective effects in elderly subjects with and without baseline of chronic diseases.
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Obesity-related metabolic syndrome: Mechanisms of sympathetic overactivity

TL;DR: Current understanding of some mechanisms through which sympathetic overactivity may be interlaced to the metabolic syndrome is focused on, with particular regard to the role of insulin resistance and of some adipokines.