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Gilles Dietrich

Researcher at University of Toulouse

Publications -  77
Citations -  3188

Gilles Dietrich is an academic researcher from University of Toulouse. The author has contributed to research in topics: Autoantibody & Antibody. The author has an hindex of 30, co-authored 71 publications receiving 2798 citations. Previous affiliations of Gilles Dietrich include Centre national de la recherche scientifique & Université catholique de Louvain.

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Analgesic Effects of Topical Amitriptyline in Patients With Chemotherapy-Induced Peripheral Neuropathy: Mechanistic Insights From Studies in Mice.

TL;DR: Investigation of the mechanism of this analgesic action in mice revealed that this activity was mediated through local inhibition of nociceptor Nav channels, and suggested that topical amitriptyline could provide effective pain relief for chemotherapy-induced peripheral neuropathy patients without any systemic or local adverse events.
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Pain Management in a Model of Interstitial Cystitis/Bladder Pain Syndrome by a Vaccinal Strategy

TL;DR: In this article, a novel antinociceptive strategy exploiting the opioid-mediated analgesic properties of T lymphocytes to relieve from bladder pain was proposed for interstitial cystitis/bladder pain.
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Peripheral Opioid Receptor Blockade Enhances Epithelial Damage in Piroxicam-Accelerated Colitis in IL-10-Deficient Mice.

TL;DR: In this article, the consequences of a peripheral opioid receptor blockade by naloxone-methiodide, a general opioid receptor antagonist unable to cross the blood-brain barrier, on the development of piroxicam-accelerated colitis in IL-10-deficient mice were examined.
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Colitis Linked to Endoplasmic Reticulum Stress Induces Trypsin Activity Affecting Epithelial Functions.

TL;DR: In this article, the authors investigated the relationship between ER stress and serine protease activity in colitis-associated epithelial dysfunctions and its impact on intestinal functions. And they found that excessive ER stress in IECs caused an increased release of trypsin activity that, in turn, altered intestinal barrier function, then promoting the development of inflammatory process.