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Aim: To identify relationships between neonatal factors including conditions and treatments, nurturing environment, and psychosocial development of children born at very low birth weight (VLBW). Methods: In this longitudinal study, the medical records of 113 VLBW infants were examined, and the children were then followed up at 18 and 36 months of age. Their developmental quotient (DQ) was assessed using the Kyoto Scale of Psychological Development (KSPD), and their parents were asked about their own health, financial situation, education, and family support. Pearson's correlation and stepwise multiple regression analyses were used to explore relationships between DQ, potentially significant predictors on the KSPD, and nurturing environment. Results: DQ at 18 months was associated with the following neonatal factors: mechanical ventilation days (β = -.241, p = .020), Apgar score at 5 min (β = .278, p = .005), periventricular leukomalacia (β = -.218, p = .006), and treatment for retinopathy of prematurity (β = -.171, p = .048) (adjusted R² = .32). DQ at 36 months was associated with the following neonatal and parenting factors: mechanical ventilation days (β = -.354, p < .001), periventricular leukomalacia (β = -.207, p = .009), sex (β = -.199, p = .011), mother's educational background (β = -.304, p < .001), mother's health status (β = -.159, p = .042) (adjusted R² = .35). Conclusions: These findings suggest that in addition to neonatal clinical parameters including conditions and treatments, the nurturing environment after discharge from the neonatal intensive care unit influences the psychosocial development of VLBW infants. [ABSTRACT FROM AUTHOR]

The calciumion regulatesmany aspects of neuronal migration, which is an indispensable process in the development of the nervous system. Calmodulin (CaM) is a multifunctional calcium ion sensor that transduces much of the signal. To better understand the role of Ca2+-CaM in neuronal migration, we investigated mouse precerebellar neurons (PCNs), which undergo stereotyped, long-distance migration to reach their final position in the developing hindbrain. In mammals, CaMis encoded by three non-allelic CaM(Calm) genes (Calm1, Calm2 and Calm3), which produce an identical protein with no amino acid substitutions. We found that these CaM genes are expressed in migrating PCNs. When the expression of CaM from this multigene family was inhibited by RNAi-mediated acute knockdown, inhibition of Calm1 but not the other two genes caused defective PCN migration. Many PCNs treated with Calm1 shRNA failed to complete their circumferential tangential migration and thus failed to reach their prospective target position. Those that did reach the target position failed to invade the depth of the hindbrain through the required radial migration. Overall, our results suggest the participation of CaM in both the tangential and radial migration of PCNs. [ABSTRACT FROM AUTHOR]