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These contribute to the buildup of estrogenic compounds in the environment, which some scientists believe may explain falling sperm counts and premature maturation in girls.
These changes are believed to stem from the premature maturation of keratinocytes induced by an inflammatory cascade in the dermis involving dendritic cells, macrophages, and T cells (three subtypes of white blood cells).
Overall, we find that hypoxia induces premature maturation of OPCs.
We now report that hypoxia leads to surprising alterations in OPC maturation by inducing premature maturation.
Recently, we observed that hypoxia induces premature maturation of OPCs, leading to decreases in numbers of replicating OPCs, resulting in fewer myelinating OLs in the brain [12].
We postulate that premature maturation of OPCs will lead to decreases in numbers of replicating OLs, leading to fewer myelinating OLs in the brain.
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It has been suggested that, as premature ripening of fruit before seed maturation is not desirable for reproductive success, seed and fruit maturation are strictly synchronized and auxin may coordinate communication between seed and pericarp [ 9].
We showed previously that mice with skeletal thyrotoxicosis resulting from mutation of TRβ display short stature due to accelerated bone maturation in utero and premature growth plate quiescence in the post-weaning period [4,5,57].
As such, premature OPC maturation may contribute to hypomyelination in the developing hypoxic brain.
As such, premature OPC maturation may contribute to hypomyelination in the developing brain [12].
These results show that hypoxia interferes with the normal process of OL differentiation by inducing premature OPC maturation.
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