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The enhanced protein expression of p53 might be explained by reactive oxygen species-induced somatic mutations in p53 [ 45].
This phenomenon can most probably be explained by reactive oxygen species- mediated apotosis of neutrophils triggered by the engagement of innate receptors and not by abnormal myeloid differentiation [ 27].
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The majority of cases with synovitis in the early postoperative period resolved during the follow-up, which can be explained by its reactive nature [ 64].
Weathering rates in nature are commonly observed to be 1 3 orders of magnitude lower than in laboratory experiments (e.g., [20, 21, 34]), and this may in part be explained by differences in reactive and physical (total) surface area between experimental and natural systems.
Such behavior can be explained by retrieval of reactive thiol groups, which causing strong binding of cadmium ions.
The lower contact angle can be explained by the formation of reactive oxygen species and reactive nitrogen species as a result of plasma treatment and, consequently, their dispersion on the surface [8, 9, 15, 16].
The deviation from pseudo-first-order kinetics can be explained by interspecies competition for reactive sites between TCE and a dominant reaction product.
Basic concept of MNPs toxicity may be explained by the production of reactive oxygen species (ROS) which triggers oxidative stress.
However, this inhibition pattern can be explained by the substrate-like reactive loop of AAT with the scissile bond between P1 Met and P1′ Ser that should be preferred by chymotryptic proteases, albeit with a low reaction rate of KLK3 [175].
All these findings may be explained by hypothesizing that cross-reactive immunity is targeting the N1 NA antigen.
This might be explained by the present measurement of reactive aggression.
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