Search

The Farnsworth Unit in northern Texas is a field site for studying geologic carbon storage during enhanced oil recovery (EOR) using CO 2 . Microseismic monitoring is essential for risk assessment by detecting fluid leakage and fractures. We analyzed borehole microseismic data acquired during CO 2 injection and migration, including data denoising, event detection, event location, magnitude estimation, moment tensor inversion, and stress field inversion. We detected and located two shallow clusters, which occurred during increasing injection pressure. The two shallow clusters were also featured by large b values and tensile cracking moment tensors that are obtained based on a newly developed moment tensor inversion method using single-borehole data. The inverted stress fields at the two clusters showed large deviations from the regional stress field. The results provide evidence for microseismic responses to CO 2 /fluid injection and migration. [ABSTRACT FROM AUTHOR]

Hemagglutinin (HA) and neuraminidase (NA) are the two major envelope proteins of influenza viruses. The spatial organization of HA and NA on the virus surface needs to be optimized to promote viral fitness, host specificity, transmissibility, infectivity, and virulence. We previously demonstrated that the recombinant NA protein of the 2009 pandemic H1N1 (pH1N1) with the I365T/S366N mutation in the NA 370-loop elicited higher NA-inhibition antibody titers against the homologous pH1N1 virus and three heterologous H5N1, H3N2, and H7N9 viruses in mice. In this study, we used PR8-based reverse genetics (RG) by replacing the HA and NA genes of A/Texas/05/2009 pH1N1 virus to obtain the wild-type pH1N1 and three NA 370-loop mutant viruses of pH1N1 (I365T/S366N), RG pH1N1 (I365E/S366D), and RG pH1N1 (I365T/S366A). Our results revealed that the viral NA enzyme activity increased for the RG pH1N1(I365T/S366N) and RG pH1N1 (I365E/S366D) viruses but reduced for the RG pH1N1 (I365T/S366A) virus. The increased or decreased NA enzyme activity was found to correlate with the increase or decrease in HA titers of these NA 370-loop mutant viruses. All of these three NA 370-loop mutant RG pH1N1 viruses were less virulent than the wild-type RG pH1N1 virus in mice. Immunizations with the inactivated viruses carrying the three NA 370-loop mutations and the wild-type RG pH1N1 virus were found to elicit approximately the same titers of NA-inhibition antibodies against H1N1 and H5N1 viruses. These results may provide information for developing NA-based influenza virus vaccines. [ABSTRACT FROM AUTHOR]

Background: Traffic exhaust, refineries and industrial facilities are major sources of air toxics identified by the U.S. Environmental Protection Agency (U.S. EPA) for their potential risk to human health. In utero and early life exposures to air toxics such as benzene and 1,3-butadiene, which are known leukemogens in adults, may play an etiologic role in childhood leukemia that comprises the majority of pediatric cancers. We conducted a population based case-control study to examine individual effects of benzene, 1,3-butadiene and polycyclic organic matter (POM) in ambient residential air on acute lymphocytic leukemia (ALL) diagnosed in children under age 5 years in Texas from 1995-2011.Methods: Texas Cancer Registry cases were linked to birth records and then were frequency matched by birth month and year to 10 population-based controls. Maternal and infant characteristics from birth certificates were abstracted to obtain information about potential confounders. Modelled estimates of benzene, 1,3-butadiene and POM exposures at the census tract level were assigned by linking geocoded maternal addresses from birth certificates to U.S. EPA National-Scale Air Toxics Assessment data for single and co-pollutant statistical analyses. Mixed-effects logistic regression models were applied to evaluate associations between air toxics and childhood leukemia.Results: In adjusted single pollutant models, odds of childhood leukemia among mothers with the highest ambient air exposures compared to those in the lowest quartile were 1.11 (95 % CI: 0.94-1.32) for POM, 1.17 (95 % CI: 0.98-1.39) for benzene and 1.29 (95 % CI: 1.08-1.52) for 1,3-butadiene. In co-pollutant models, odds ratios for childhood leukemia remained elevated for 1,3-butadiene but were close to the null value for benzene and POM.Conclusions: We observed positive associations between 1,3-butadiene and childhood leukemia in single and co-pollutant models whereas effect estimates from single pollutant models were diminished for benzene and POM in co-pollutant models. Early life exposure to 1,3-butadiene rather than benzene or POM appears to increase early childhood risk of acute lymphocytic leukemia. [ABSTRACT FROM AUTHOR]

Epidemiology studies relying on one address to assign exposures over time share common methodological limitations in failing to account for mobility that may introduce potential exposure misclassification. Using Texas birth certificate and cancer registry data, we identified predictors of residential mobility among mothers of children diagnosed with early childhood leukemia in Texas from 1995 to 2011. We used U.S. Environmental Protection Agency (EPA) National Air Toxics Assessment data to estimate residential levels of benzene and 1,3-butadiene based on addresses at birth and diagnosis and applied mixed-effects ordinal logistic regression models to evaluate differences in exposure classification between the two time periods. In total, 55% of children moved from time of birth to diagnosis, although they generally did not move far (median distance moved was 8 km). Predictors of mobility, at delivery, included younger age, being unmarried and living in neighborhoods with high benzene levels, and, at diagnosis, increasing child's age and living in neighborhoods with low poverty rates. We observed that the odds of being assigned to a higher exposure quartile at diagnosis relative to the time of birth decreased by 31% for 1,3-butadiene (OR = 0.69, 95% CI 0.59-0.82) and by 12% for benzene (OR = 0.88, 95% CI 0.75, 1.05).