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The development of septic multiple organ failure is linked to the impairment of the microcirculation of vital and nonvital organs.
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Our finding that Aβ oligomers decrease neuronal ATP levels indicates that they are linked to the impairment of energy metabolism in neurons.
In both animal [ 17] and human studies [ 18- 20], RV formation has been linked to the impairment of autophagy, a catabolic process that targets cytoplasmic organelles and protein aggregates for lysosomal degradation [ 21].
Cognition impairment is linked to the effects of medication and the length of the euthymic phase at time of patient evaluation [ 23, 25].
We propose that impairment of DHODH activity is linked to the Miller syndrome phenotype.
It is not known whether these defects are linked to the biological impairments described above.
Furthermore, similar molecular mechanisms that underlie NMDA receptor-dependent homosynaptic LTD in the rat visual cortex have been linked to the characteristic visual impairment resulting from hours of monocular deprivation during early postnatal life [ 97, 98].
Furthermore, the severity of psoriasis symptoms, and pruritus in particular, has been linked to the degree of HRQOL impairment [ 3, 4].
In fact, the vast majority of genes associated with type 2 diabetes have been linked to the β-cell, and impairments in β-cell mass and in insulin secretion have been reported in numerous studies in patients with type 2 diabetes.
Long-term exposure is linked to impairment of the immune system, the developing nervous system, the endocrine system and reproductive functions.
In particular, while IL-2 inhibition is linked to an impairment of the transcription factor nuclear factor of activated T cells (NF-AT) complex formation, VDR ligand-induced IFN γ negative regulation has been explained by a direct interaction of the ligand-bound VDR complex with vitamin D responsive element (VDRE) within IFN γ promoter [ 78– 80].
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