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These results raise the possibility that chronic exposure to low, subanesthetic concentrations of ketamine, while not affecting cell survival, could still impair neuronal morphology and thus might lead to dysfunctions of neural networks.
Abnormalities in the constituent peptides of the NADPH oxidase enzyme system lead to dysfunctions characteristic of chronic granulomatous disease (CGD).
These highly sophisticated training and performance challenges may lead to dysfunctions or secondary injury pathologies emerging as a result, including inefficient compensatory movement patterns, joint hyper or hypo-mobility and nerve entrapments [ 6, 15, 16].
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However, elevated ROS and/or diminished antioxidant capacity leading to oxidative stress can lead to dysfunction.
One of the immediate consequences of sudden changes is that they lead to dysfunction.
Carriers of balanced translocations usually carry alterations in gene sequences, which lead to dysfunction during early and late embryogenesis.
Newer research has shown that this is not always the case, and that brain injury can lead to dysfunction of this barrier.
PD-1 expressed by T lymphocytes, particularly tumor-infiltrating lymphocytes (TILs), can lead to dysfunction of tumor-specific T cells to eliminate tumors (Tumeh et al., 2014).
This endogenous molecule has also bactericidal effect against a broad spectrum of bacteria, by nitrosation of cysteine and tyrosine residues, which lead to dysfunction of bacterial proteins.
In other diseases, defects in nuclear genes lead to dysfunction of mitochondrial proteins.
Abnormalities in TEC development lead to dysfunction of T cells which could cause chronic inflammatory disease.
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CEO of Professional Science Editing for Scientists @ prosciediting.com