20 research outputs found
High-Resolution Mapping of Sources Contributing to Urban Air Pollution Using Adjoint Sensitivity Analysis: Benzene and Diesel Black Carbon
The adjoint of the Community Multiscale
Air Quality (CMAQ) model
at 1 km horizontal resolution is used to map emissions that contribute
to ambient concentrations of benzene and diesel black carbon (BC)
in the San Francisco Bay area. Model responses of interest include
population-weighted average concentrations for three highly polluted
receptor areas and the entire air basin. We consider both summer (July)
and winter (December) conditions. We introduce a novel approach to
evaluate adjoint sensitivity calculations that complements existing
methods. Adjoint sensitivities to emissions are found to be accurate
to within a few percent, except at some locations associated with
large sensitivities to emissions. Sensitivity of model responses to
emissions is larger in winter, reflecting weaker atmospheric transport
and mixing. The contribution of sources located within each receptor
area to the same receptor’s air pollution burden increases
from 38–74% in summer to 56–85% in winter. The contribution
of local sources is higher for diesel BC (62–85%) than for
benzene (38–71%), reflecting the difference in these pollutants’
atmospheric lifetimes. Morning (6–9am) and afternoon (4–7
pm) commuting-related emissions dominate region-wide benzene levels
in winter (14 and 25% of the total response, respectively). In contrast,
afternoon rush hour emissions do not contribute significantly in summer.
Similar morning and afternoon peaks in sensitivity to emissions are
observed for the BC response; these peaks are shifted toward midday
because most diesel truck traffic occurs during off-peak hours
Baseline characteristics of whites from the discovery cohort stratified by perioperative baseline eGFR.
<p>Baseline characteristics of whites from the discovery cohort stratified by perioperative baseline eGFR.</p
Multivariable logistic regression model for acute kidney injury (AKI) in whites with baseline eGFR > 60 mL/min/1.73m<sup>2</sup> in the replication cohort adjusted for age, sex, body mass index, baseline estimated glomerular filtration rate, history of diabetes, and cardiopulmonary bypass graft use.
<p>Multivariable logistic regression model for acute kidney injury (AKI) in whites with baseline eGFR > 60 mL/min/1.73m<sup>2</sup> in the replication cohort adjusted for age, sex, body mass index, baseline estimated glomerular filtration rate, history of diabetes, and cardiopulmonary bypass graft use.</p
Multivariable logistic regression model for acute kidney injury (AKI) in the discovery cohort adjusted for age, sex, race, body mass index, baseline estimated glomerular filtration rate, history of diabetes, and cardiopulmonary bypass graft use.
<p>Multivariable logistic regression model for acute kidney injury (AKI) in the discovery cohort adjusted for age, sex, race, body mass index, baseline estimated glomerular filtration rate, history of diabetes, and cardiopulmonary bypass graft use.</p
Association of gain-of-function <i>EPHX2</i> polymorphism Lys55Arg with acute kidney injury following cardiac surgery
<div><p>Twenty to thirty percent of patients undergoing cardiac surgery develop acute kidney injury (AKI). In mice, inhibition of soluble epoxide hydrolase (sEH) attenuates renal injury following ischemia-reperfusion. We tested the hypothesis that functional variants of <i>EPHX2</i>, encoding sEH, are associated with AKI after cardiac surgery. We genotyped patients in two independent cardiac surgery cohorts for functional <i>EPHX2</i> polymorphisms, Lys55Arg and Arg287Gln, and determined AKI using Acute Kidney Injury Network criteria. The 287Gln variant was not associated with AKI. In the discovery cohort, the gain-of-function 55Arg variant was associated with an increased incidence of AKI in univariate (p = 0.03) and multivariable (p = 0.04) analyses. In white patients without chronic kidney disease (CKD), the 55Arg variant was independently associated with AKI with an OR of 2.04 (95% CI 0.95–4.42) for 55Arg heterozygotes and 31.53 (1.57–633.19) for homozygotes (p = 0.02), after controlling for age, sex, body mass index, baseline estimated glomerular filtration rate, and use of cardiopulmonary bypass. These findings were replicated in the second cardiac surgery cohort. 12,13- and total- dihydroxyoctadecanoic acids (DiHOME): epoxyoctadecanoic acids (EpOME) ratios were increased in <i>EPHX2</i> 55Arg variant carriers, consistent with increased hydrolase activity. The <i>EPHX2</i> Lys55Arg polymorphism is associated with AKI following cardiac surgery in patients without preexisting CKD. Pharmacological strategies to decrease sEH activity might decrease postoperative AKI.</p></div
Dihydroxy-12Z-octadecenoic acids:epoxy-12Z-octadecenoic acids (DiHOME:EpOME) ratios in plasma from 33 patients collected before surgery, following surgery and on post-operative day one according to Lys55Arg genotype.
<p>By analysis of repeated measures, carriers of the 55Arg variant G allele had higher sEH activity over time than homozygous AA. *p<0.05 for post hoc comparison.</p
Baseline characteristics of whites from the replication cohort with a baseline eGFR ≥ 60 mL/min/1.73m<sup>2</sup>.
<p>Baseline characteristics of whites from the replication cohort with a baseline eGFR ≥ 60 mL/min/1.73m<sup>2</sup>.</p
Multivariable logistic regression model for acute kidney injury (AKI) in whites with baseline eGFR ≥ 60 mL/min/1.73m<sup>2</sup> in the discovery cohort adjusted for age, sex, body mass index, baseline estimated glomerular filtration rate, history of diabetes, and cardiopulmonary bypass graft use.
<p>Multivariable logistic regression model for acute kidney injury (AKI) in whites with baseline eGFR ≥ 60 mL/min/1.73m<sup>2</sup> in the discovery cohort adjusted for age, sex, body mass index, baseline estimated glomerular filtration rate, history of diabetes, and cardiopulmonary bypass graft use.</p
A comparison of previously identified significant SNPs from literature to African Americans from Vanderbilt AF cohort.
<p>The case/control sample size for the previously published studies are: Ellinor et. al n = 14,179 (11); Kaab et. al. n = 36,196 (9); Benjamin et. al. n = 46,736 (10); and Gudbjartsson et al. n = 39,014 (50). AA =  Subjects with self-reported African American race.</p