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However, the mechanism(s) by which corticosteroids accelerate the pathogenesis of AD remain to be fully elucidated [22].
Finally, because HA is formed from homocysteine and methionine [13], it may accelerate the pathogenesis of AD.
Periostin may accelerate the pathogenesis of OA.
In the case of macrophage foam cells, elevated free cholesterol induces TLR-mediated as well as TLR-independent proinflammatory pathways that accelerate the pathogenesis of CHD [ 54].
Periostin deficiency may influence the propensity for fatigue fractures [ 34], and may accelerate the pathogenesis of OA in cooperation with an imbalance in bone repair mechanisms.
However, in the light of findings in TgM83 mice [ 56, 62, 92] it appears conceivable that exogenous α-synuclein seeds may accelerate the pathogenesis of genetically predisposed α-synuclein aggregation diseases.
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In the roots a similar interaction was observed, where P. aphanidermatum reduced root galling compared to M. incognita alone and M. incognita accelerated the pathogenesis of P. aphanidermatum.
In animal models, 12 weeks of high-fat feeding increased NADPH oxidase, an important marker in the generation of oxidative stress, and accelerated the pathogenesis of endothelial dysfunction [86].
Our hypothesis that HA accelerated the pathogenesis of AD was confirmed by the immunohistochemical observations.
Physical inactivity accelerates the pathogenesis of type 2 diabetes and subsequently leads to excess morbidity and mortality [ 5].
These data imply that the markedly increased number of IL-17+ F4/80 macrophages in local joint tissue accelerated the pathogenesis of RA.
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