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Julio Cesar B. Fernandes

Researcher at Université de Montréal

Publications -  169
Citations -  8830

Julio Cesar B. Fernandes is an academic researcher from Université de Montréal. The author has contributed to research in topics: Osteoarthritis & Gene delivery. The author has an hindex of 45, co-authored 163 publications receiving 8203 citations. Previous affiliations of Julio Cesar B. Fernandes include Universidade Municipal de São Caetano do Sul & Federal University of Ceará.

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Journal Article

The role of cytokines in osteoarthritis pathophysiology.

TL;DR: The neutralization of IL-1 and/or TNF-alpha up-regulation of MMP gene expression appears to be a logical development in the potential medical therapy of OA, and experimental evidence showing that neutralizing T NF-alpha suppressed cartilage degradation in arthritis also support such strategy.
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Chitosan-DNA nanoparticles as non-viral vectors in gene therapy: strategies to improve transfection efficacy

TL;DR: The objective of this paper was to summarize the state of the art in gene therapy and particularly the use of chitosan to improve the transfection efficiency in vivo and in vitro.
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Chondroprotective effect of intraarticular injections of interleukin‐1 receptor antagonist in experimental osteoarthritis. Suppression of collagenase‐1 expression

TL;DR: Recombinant human IL-1Ra exerted a dose-dependent protective effect on the development of osteophytes and cartilage lesions in vivo and could result, at least in part, from a reduction of collagenase-1 expression in OA cartilage.
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Characterization of folate-chitosan-DNA nanoparticles for gene therapy

TL;DR: FA-nanoparticles have lower cytoxicity, good DNA condensation, positive zeta potential and particle size around 118 nm, which makes them a promising candidate as a non-viral gene vector.
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In vivo suppression of early experimental osteoarthritis by interleukin-1 receptor antagonist using gene therapy

TL;DR: It is shown that a local increase in IL-1Ra production in OA knee joints by intraarticular injection of transduced synovial cells can reduce the progression of experimentally induced lesions.