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It has been reported that reactive oxygen species (ROS) and the enzymatic systems that govern their metabolism, for example superoxide dismutase (SOD), catalase (CAT) and peroxidases may play a role in pathogenesis (Baker and Orlandi [1995]).
It has also been reported that reactive chemicals which are covalently bonded to an engineered cysteine (H287C) at the peripheral site of mammalian AChEs (Figure 2)—are able to interfere with the substrate binding and subsequently inhibit the enzymes [20], [21].
It has been reported that reactive oxygen species (ROS) may play an important role in the pathogenesis of RA [ 4, 5].
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It is reported that reactive oxygen species (ROS) can regulate MAPK and NFKB signaling pathways, thus generation of ROS in MSCs was examined.
It was reported that reactive oxygen species (ROS), a component of oxidative stress, contributed to transactivation of TonEBP, and the activation of TonEBP was associated with suppression of ROS formation.
In addition, it has been reported that ROS (reactive oxygen species) homeostasis is the central regulatory mechanism for cotton fibre initiation and differentiation [ 8].
Moreover, it has been reported that the increased reactive oxygen species (ROS) in the kidney may contribute to the development of hypertension.
It has been reported that CD-1 reactive NKT cells are required for the development of systemic tolerance and defects of NKT cells affect autoimmunity [ 42, 43].
It has also been reported that production of reactive oxygen species (ROS) is selectively increased in the adipose tissue of obese mice and that increased oxidative stress in fat is a key mechanism underlying the occurrence of insulin resistance related to obesity [ 50].
It has been reported that pre-membrane (prM -reactive antibodies do not efficiently neutralize DENV infection but instead prM -reactiveote antibodiesion.
It has been reported that the nucleocapsid domain contains reactive cysteine residues which, when oxidized, reversibly affect polyprotein processing [24].
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