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Giancarlo Solaini

Researcher at University of Bologna

Publications -  104
Citations -  6232

Giancarlo Solaini is an academic researcher from University of Bologna. The author has contributed to research in topics: Mitochondrion & ATPase. The author has an hindex of 33, co-authored 97 publications receiving 4953 citations. Previous affiliations of Giancarlo Solaini include Sant'Anna School of Advanced Studies & University of Southern California.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Hypoxia and mitochondrial oxidative metabolism.

Giancarlo Solaini, +3 more
- 01 Jun 2010 - 
TL;DR: Current knowledge of the mitochondrial role in hypoxia is reviewed, focusing mainly on their role in cellular energy and reactive oxygen species homeostasis in relation with HIF-1 stabilization.
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Rhodamine 123 as a probe of mitochondrial membrane potential: Evaluation of proton flux through F0 during ATP synthesis

Alessandra Baracca, +3 more
- 30 Sep 2003 - 
TL;DR: Findings indicate that RH-123 fluorescence quenching kinetics give reliable and sensitive evaluation of mitochondrial membrane potential, complementing steady-state fluorescence measurements, and provide a mean to study proton flow from the mitochondrial intermembrane space to the matrix through the F(0) channel.
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Cytochrome c oxidase and mitochondrial F1F0-ATPase (ATP synthase) activities in platelets and brain from patients with Alzheimer's disease.

Francesca Bosetti, +8 more
- 01 May 2002 - 
TL;DR: COX but not F(1)F(0)-ATPase is a mitochondrial target in AD, in both a brain association area and in platelets, which demonstrates that a reduced COX activity may make the tissue vulnerable to excitotoxicity or reduced oxygen availability.
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Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion.

Giancarlo Solaini, +1 more
- 01 Sep 2005 - 
TL;DR: This review considers ischaemic changes in the inner membrane complexes I-V, and how this might affect formation of ROS and high-energy phosphate production/degradation and the contribution of various mitochondrial cation channels to ionic imbalances.