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Bioinformatics approaches led to the identification of three main drug-responsive genomic networks and indicated neurobiological pathways that mediate the alterations in transcription.
To better understand the mechanisms in the bone material that mediate the alterations in gross fracture risk and deformability in metabolic bone disease, we have investigated mice with X-linked hypophosphatemic rickets, a disease that is associated with progressive weakness and wasting of skeletal muscle [45] as well as a reduction in lowered bone mineral content.
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We next assessed whether or not IRAK-M mediated the alterations in selected histone PTMs during sepsis.
The few recent neuroimaging studies that investigated the neural correlates mediating the alterations in cognitive processing in anxiety reported an under recruitment of dorsal cognitive/executive brain regions including the lateral PFC and dorsal anterior cingulate cortex (ACC) [3], [11], [14].
Increased axoplasmic Ca2+ mediated the alterations in mitochondrial length and transport.
The potential role of tumour-derived Dkk-1 in mediating the alterations of osteoblastic and/or osteolytic activity associated with breast cancer however remains to be investigated.
A role for the kidney in mediating the alterations in lifespans was suggested by the differences found in renal telomere lengths (unlike telomere lengths from the brains and livers), where relatively longer telomeres were found in kidneys from 13-month-old animals exposed to maternal protein restriction in the first few weeks of life [ 2].
Furthermore, PRMT5 and PRMT4s co-regulated the expression and splicing of key regulatory genes associated with transcription, RNA processing, responses to light, flowering, and abiotic stress tolerance, being candidates to mediate the physiological alterations observed in the mutants.
Mitochondria play an essential role in metabolism, bioenergetics and cell death regulation and consequently oncogenic modifications characteristic of many cancer types mediate the array of metabolic alterations of cancer cells by impairing key mitochondrial functions.
Recent clinical and animal studies identified candidate mechanisms that may mediate the development of cardiovascular alterations in the setting of IUGR consistent with the hypothesis of perinatal programming [11, 12].
We have focused on the hypotheses that epigenetic alterations mediate the association between maternal tobacco smoking and adverse birth outcomes.
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