Loss of the proliferative OPCs plays a major role in PWMI causation

Selective pressures and/or resistant bacteria seem to be more common at ground level; and GSK583 indicators of ATBR prevalence and mobility seem to increase the closer animals are to human settlements. GSK180736A However, other indicators, such as resistance to synthetic antibiotics, do not seem to follow this trend, as they were only found in isolates from arboreal animals far from human influence. The identification of non-antibioti pressures that select or maintain ATBR is one of the major gaps in our understanding of the emergence and evolution of these traits. It is also important to realize that human, animal and environmental health are not isolated realms, but a single continuum where factors apparently affecting only one of them, end up having wide repercussions. The need for information on the ecological drivers of ATBR in wildlife, its transmission dynamics, and the range of conditions under which gene/bacteria exchange occur is urgent, especially as major pharmaceutical companies have largely abandoned the antibiotic discovery field. PWMI is associated with significant morbidity, as affected individuals may have profound intellectual impairment and cerebral palsy. Highlighting the magnitude of PWMI, each year in the United States more than 400,000 infants are born prematurely. Of these infants, about 100,000 are born at risk for PWMI, and about 25,000 children per year will develop PWMI. Finding a treatment for PWMI is thus of major clinical importance. Oligodendrocytes are the myelinating cells of the central nervous system. OL development to mature myelin forming cells follows a complex series of events during which progenitor cells undergo dramatic morphological and biochemical changes. Four stages of OL differentiation are distinguished: oligodendrocyte precursor cells, late OL progenitors, immature OLs, and mature OLs. It is believed that loss of the proliferative OPCs plays a major role in PWMI causation. 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.

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