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Chiara Dalla Man

Researcher at University of Padua

Publications -  210
Citations -  12307

Chiara Dalla Man is an academic researcher from University of Padua. The author has contributed to research in topics: Insulin & Postprandial. The author has an hindex of 52, co-authored 177 publications receiving 10805 citations. Previous affiliations of Chiara Dalla Man include University of Rochester & University of Pittsburgh.

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Meal Simulation Model of the Glucose-Insulin System

TL;DR: A new simulation model in normal humans that describes the physiological events that occur after a meal, by employing the quantitative knowledge that has become available in recent years, is presented.
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In Silico Preclinical Trials: A Proof of Concept in Closed-Loop Control of Type 1 Diabetes

TL;DR: A system for in silico testing of control algorithms that has been shown to represent adequate glucose fluctuations in T1DM observed during meal challenges, and has been accepted by the Food and Drug Administration as a substitute to animal trials in the preclinical testing of closed-loop control strategies.
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The UVA/PADOVA Type 1 Diabetes Simulator New Features

TL;DR: A new version of the UVA/PADOVA Type 1 Diabetes Simulator, which was submitted to FDA in 2013, provides a more reliable framework for in silico trials, for testing glucose sensors and insulin augmented pump prediction methods, and for closed-loop single/dual hormone controller design, testing, and validation.
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DHEA in Elderly Women and DHEA or Testosterone in Elderly Men

TL;DR: Neither DHEA nor low-dose testosterone replacement in elderly people has physiologically relevant beneficial effects on body composition, physical performance, insulin sensitivity, or quality of life.
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Mechanisms of the Age-Associated Deterioration in Glucose Tolerance: Contribution of Alterations in Insulin Secretion, Action, and Clearance

TL;DR: It is concluded that the deterioration in glucose tolerance that occurs in healthy elderly subjects is due to a decrease in both insulin secretion and action with the severity of the defect in insulin action being explained by the degree of fatness rather than age per se.