RESUMO
To understand factors contributing to the neonatal mortality rate (NMR), we studied trends in the NMR during 2000 to 2009 with respect to demographic factors and health care resources. Birth- and death-linked mortality data for 14,168 neonatal deaths that occurred between 2000 and 2009 were obtained from the Texas Department of Health and Human Services. Demographic factors and health care resource data were analyzed using analysis of variance, chi-square tests, and linear regression analysis. The average NMR increased from 3.37 in 2000 to 3.77 in 2009. The NMR in blacks ranged from 6.57 to 8.97 during the study period. Among the babies who died, the mean birthweight decreased from 1505 to 1275 g (P < 0.001) and the mean gestational age decreased from 28.4 to 27.8 weeks (P < 0.001). Cesarean section deliveries increased from 32.7% to 44.9% (P < 0.001). The percentage of mothers receiving prenatal care increased from 81.4% to 86.6% (P < 0.001). Mothers with a college education increased from 8.8% to 20.5% (P < 0.001). The median household income increased from $41,047 to $49,189 (P < 0.001). The number of neonatal intensive care unit beds increased from 33.4 to 56 per 10,000 births, and the number of neonatologists increased from 0.27 to 0.40 per 10,000 women of 15 to 44 years of age. In conclusion, the NMR didn't improve despite improvements in demographic factors and health care resources. Racial disparities persist, with a high NMR in the black population. We speculate a possible genetic predisposition related to ethnicity, and a potentially higher rate of extreme prematurity might have contributed to a high NMR in the study population.
RESUMO
OBJECTIVE: Microvascular hyperpermeability that occurs due to breakdown of the BBB is a major contributor of brain vasogenic edema, following IR injury. In microvascular endothelial cells, increased ROS formation leads to caspase-3 activation following IR injury. The specific mechanisms, by which ROS mediates microvascular hyperpermeability following IR, are not clearly known. We utilized an OGD-R in vitro model of IR injury to study this. METHODS: RBMEC were subjected to OGD-R in presence of a caspase-3 inhibitor Z-DEVD, caspase-3 siRNA or an ROS inhibitor L-AA. Cytochrome c levels were measured by ELISA and caspase-3 activity was measured fluorometrically. TJ integrity and cytoskeletal assembly were studied using ZO-1 immunofluorescence and rhodamine phalloidin staining for f-actin, respectively. RESULTS: OGD-R significantly increased monolayer permeability, ROS formation, cytochrome c levels, and caspase-3 activity (p < 0.05) and induced TJ disruption and actin stress fiber formation. Z-DEVD, L-AA and caspase-3 siRNA significantly attenuated OGD-R-induced hyperpermeability (p < 0.05) while only L-AA decreased cytochrome c levels. Z-DEVD and L-AA protected TJ integrity and actin cytoskeletal assembly. CONCLUSIONS: These results suggest that OGD-R-induced hyperpermeability is ROS and caspase-3 dependent and can be regulated by their inhibitors.