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Franco Folli

Researcher at University of Milan

Publications -  227
Citations -  16975

Franco Folli is an academic researcher from University of Milan. The author has contributed to research in topics: Insulin & Insulin resistance. The author has an hindex of 64, co-authored 214 publications receiving 15482 citations. Previous affiliations of Franco Folli include Yale University & Brigham and Women's Hospital.

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Identification of the 64K autoantigen in insulin-dependent diabetes as the GABA-synthesizing enzyme glutamic acid decarboxylase.

TL;DR: The pancreatic islet β-cell autoantigen of relative molecular mass 64,000 (64K), which is a major target of autoantibodies associated with the development of insulin-dependent diabetes mel-litus (IDDM), has been identified as glutamic acid decarboxylase, the biosynthesizing enzyme of the inhibitory neurotransmitter GABA.
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Autoantibodies to GABA-ergic neurons and pancreatic beta cells in stiff-man syndrome.

TL;DR: The hypothesis that stiff-man syndrome is an autoimmune disease is supported and GAD is suggested to be the primary autoantigen involved in stiff- man syndrome and the associated insulin-dependent diabetes mellitus is suggested.
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Hyperglycemia-induced oxidative stress and its role in diabetes mellitus related cardiovascular diseases

TL;DR: In this article, the benefits of antioxidant therapies in the prevention/treatment of diabetic cardiovascular complications are discussed, where the authors show that appropriate glycemic control, in which both hypoglycemic and hyperglycemic episodes are reduced, in association to the treatment of dyslipidemia, hypertension, kidney dysfunction and obesity, conditions which are also associated to reactive oxygen species (ROS) overproduction, can counteract oxidative stress and, therefore, both microvascular and macrovascular complications of diabetes mellitus.
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Autoantibodies to Glutamic Acid Decarboxylase in a Patient with Stiff-Man Syndrome, Epilepsy, and Type I Diabetes Mellitus

TL;DR: The findings support the idea that an impairment of neuronal pathways that operate through gamma-aminobutyric acid is involved in the pathogenesis of stiff-man syndrome, and they raise the possibility of an autoimmune pathogenesis.