Exact(7)
One notable feature of tachycardia in sepsis is that the observed myocardial dysfunction may arise from a perturbation in the force frequency and frequency-dependent acceleration of relaxation (FDAR) mechanisms, whereby tachycardia my worsen contractility due to decreased reuptake of calcium in the sarcoplasmic reticulum [59].
Potential underlying mechanisms through which cardiac hypertrophy and cardiac dysfunction may arise have been suggested by previous molecular studies.
Usually, a low level of heteroplasmy does not impair mitochondrial function, but once the level of mutant mtDNA exceeds a certain threshold, OXPHOS dysfunction may arise [ 1, 2].
In the electroretinogram (ERG), this complicates interpretation of inner retinal changes as dysfunction may arise from "upstream" neurons or may indicate a direct loss to that neural generator.
In HD, mitochondrial dysfunction may arise from intrinsic abnormalities of transcription, including of PGC-1α (peroxisome-proliferator-activated receptor γ co-activator-1α), Ca2+ overload, NMDAR dysfunction and/or abnormal dopaminergic activity.
Myocardial dysfunction may arise from a number of distinct processes, including micro- and macrovascular coronary ischemia, myocardial inflammation (myocarditis), and/or myocardial fibrosis [ 8], any of which may be active in RA.
Similar(53)
Centrosomal amplification may be a direct effect of midbody protein dysfunction or may arise due to the accumulation of centrosomes from failed mitoses.
Bone dysfunction may also arise following the production of RANKL by activated T cells, by directly triggering osteoclastogenesis [ 12].
The elevated occurrence of apoptosis within a tissue upon mitochondrial dysfunction may additionally arise from an increased susceptibility of cells toward environmental cues such as oxidative stress.
Pulmonary dysfunction in the parturient may arise from thoracic or extra-thoracic pathologies but both may be defined as acute lung injury.
Furthermore, our findings raise the intriguing possibility that the neurological dysfunction in MLIV patients may arise from amino acid deprivation in neurons.
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