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For various neoplasias, it has been shown that an increasing number of chromosomal alterations is accompanied by a worse prognosis.
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These structural alterations are accompanied by characteristic inflammatory changes and extensive remodeling of the extracellular matrix (ECM) together with increased smooth muscle mass in small pulmonary arteries and airways [4].
These metabolic alterations are accompanied by the involvement of mitochondria in biosynthetic pathways to support continuous growth, while reducing the deleterious effects of high-rate production of ROS, a characteristic feature of cancer cells.
We have previously reported that exposure to cadmium (Cd) induces pulmonary γ-GCS-HS mRNA and protein, and that these alterations are accompanied by increases in GSH synthesis and its steady-state level.
These alterations were accompanied by an increase in the levels of GAD and the α1 subunit of the GABAA receptor, and a reduction in the GluK1 (previously known as GluR5) subunit, as determined by Western blots.
These structural alterations were accompanied by decreased expressions of proteins specific of podocyte (nephrin, podocin), or tubular epithelial cell (E-cadherin and megalin) integrity.
These alterations are accompanied by functional abnormalities, such as renal hyperperfusion, increased filtration and albuminuria.
These hippocampal alterations were accompanied by a significant impairment in short-term novelty recognition memory.
Furthermore, these immunological alterations were accompanied by a significant increase of sepsis-induced mortality.
We set out to determine whether the phenotypic alterations were accompanied by a detectable cellular phenotype.
These alterations were accompanied by increases in hepatic total ROS, oxidized glutathione, and thiobarbituric acid-reactive substance levels.
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