With the advance of modern neonatal management, the increase of survival of infants born with ELBW has resulted in collateral increase in incidence of infants with serious chronic lung disease, typically brnchopulmonary dysplasia (BPD). Long-term sensory, motor and cognitive impairments are common outcomes in survivals with moderate and severe BPD and may persist during school years and adolescence. Increasing evidence suggest that BPD exerts a significant effect on brain growth and development and may be associated with chronic sublethal hypoxia which compond the risk of extended brain injury and NS complications such as cerebral palsy. Animal studies have demonstrated progressive gliosis and cerebral ventriculomegaly, injured subcortical white matter and corpus callosum, dysynchrony synaptic development and disrupted neurotransmitssion in the hypoxia newborn brain. In this literature we built upon the review of neurogical and congnitive outcome in preterm infants with BPD and structural, functional and neurochemical alterations in ainimals following clinical and experimental hypoxia respectively, which may underlie the primary or potential mle for chronic sublethal hypoxia on premature brain development.

Melanogenesis is a biosynthetic pathway to produce melanin pigment in melanocyte, involving a series of intricate enzymatic and chemical catalyzed reactions. Melanogenesis involves five signaling pathways that converge on microphthalmia-associated transcription factor. In addition, many cytokines, involved in the regulation of melanogenesis, play an important role in the development, proliferation, differentiation and migration of melanocytes. Polyoxometalate can be used as a potential inhibitor of melanin production. Hence, this paper reviews the signaling pathways of melanogenesis and their regulatory mechanism, to apply polyoxometalates in the melanin production pathway, and briefly introduces the regulatory factors of related pathways.
Cell Differentiation ; Melanins ; Melanocytes ; Microphthalmia-Associated Transcription Factor ; Signal Transduction