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Irrespectively of the trigger, impairment of mitochondrial function, often associated with a drop of the mitochondrial membrane potential, is followed by a release of proapoptotic factors, such as cytochrome c from the intermembrane space with subsequent activation of caspases [91, 92].
Irrespectively of the trigger, impairment of mitochondrial function, often associated with a drop of the mitochondrial membrane potential, is followed by a release of proapoptotic factors, such as cytochrome c from the intermembrane space with subsequent activation of caspases [ 91, 92].
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Together, these results suggest the possibility that oxidative stress could trigger impairments of mt dynamics and function in the glaucomatous retina.
In contrast, mice lacking Tfam triggered impairment of mtDNA transcription and loss of mtDNA.
The imbalance of prooxidants/antioxidant ratio favouring the former causes an alteration in the normal redox signaling of the cell triggering impairment in several pathways of the cell's metabolism, a critical feature in diabetes [ 13].
Alternatively, e-GST hyper-expression could be due to an unknown factor that triggers impairments of specific organs but it is not caused by them.
These results suggest that the coexistence of a high insulin level and an established diabetic state may lead to an excessive generation of peroxynitrite, and that this may in turn trigger an impairment of endothelium-dependent relaxation via a decrease in SERCA function.
Thus, OS induced by HFD might be the initial factor that triggers cognitive impairment.
Although any content with moving diagonal edges may be used, interlacing problems are more easily seen on strong contrast edges, which may trigger additional impairments.
It may also exist from early childhood onwards, without a known incidence that triggered the impairment.
We conclude that increased brain HA triggers memory impairment and that this condition deteriorates with amyloid and leads to subsequent neurodegeneration in mouse models of AD.
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