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Caroline Maria Oliveira Volpe

Researcher at Santa Casa Hospital

Publications -  26
Citations -  1102

Caroline Maria Oliveira Volpe is an academic researcher from Santa Casa Hospital. The author has contributed to research in topics: Oxidative stress & Inflammation. The author has an hindex of 10, co-authored 24 publications receiving 764 citations. Previous affiliations of Caroline Maria Oliveira Volpe include Oswaldo Cruz Foundation & National Council for Scientific and Technological Development.

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Cellular death, reactive oxygen species (ROS) and diabetic complications.

TL;DR: This review will emphasize the therapeutical targets for controlling the signaling pathways, when aimed at the downregulation of ROS generation, oxidative stress, and, consequently, cellular death—with all of these conditions being a problem in diabetes.
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HMGB1, TLR and RAGE: a functional tripod that leads to diabetic inflammation

TL;DR: Considering the involvement of the innate immune system, in association with the role of HMGB1 as an activator of TLR and RAGE, diabetes should be considered and treated as a metabolic and immunological disease, triggered by hyperglycemia.
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The production of nitric oxide, IL-6, and TNF-alpha in palmitate-stimulated PBMNCs is enhanced through hyperglycemia in diabetes.

TL;DR: The results suggest that hyperglycemia primes PBMNCs for NO, IL-6, and TNF-alpha secretion under in vitro FFA stimulation are associated with the secretion of inflammatory biomarkers in diabetes.
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Differential gene expression in Trypanosoma cruzi populations susceptible and resistant to benznidazole.

TL;DR: Differential gene expression in three pairs of Trypanosoma cruzi populations or clones susceptible or resistant to benznidazole was investigated, and results suggest that TcHSP70 is not directly associated with the T. cruzi drug resistance phenotype.
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The dual role of free fatty acid signaling in inflammation and therapeutics.

TL;DR: It is suggested that FFA may act as either pro- or anti-inflammatory agents depending on the chemical structure and Toll Like Receptor-4 (TLR4) and G protein-coupled receptors (GPCR) activating signaling pathways that promote production and release of inflammatory cytokines (IL-6 and TFN-α).