Why do models overestimate surface ozone in the Southeast United States

Ozone pollution in the Southeast US involves complex chemistry driven by emissions of anthropogenic nitrogen oxide radicals (NOx  ≡  NO + NO2) and biogenic isoprene. Model estimates of surface ozone concentrations tend to be biased high in the region and this is of concern for designing effective emission control strategies to meet air quality standards. We use detailed chemical observations from the SEAC4RS aircraft campaign in August and September 2013, interpreted with the GEOS-Chem chemical transport model at 0.25°  ×  0.3125° horizontal resolution, to better understand the factors controlling surface ozone in the Southeast US. We find that the National Emission Inventory (NEI) for NOx from the US Environmental Protection Agency (EPA) is too high. This finding is based on SEAC4RS observations of NOx and its oxidation products, surface network observations of nitrate wet deposition fluxes, and OMI satellite observations of tropospheric NO2 columns. Our results indicate that NEI NOx emissions from mobile and industrial sources must be reduced by 30–60 %, dependent on the assumption of the contribution by soil NOx emissions. Upper-tropospheric NO2 from lightning makes a large contribution to satellite observations of tropospheric NO2 that must be accounted for when using these data to estimate surface NOx emissions. We find that only half of isoprene oxidation proceeds by the high-NOx pathway to produce ozone; this fraction is only moderately sensitive to changes in NOx emissions because isoprene and NOx emissions are spatially segregated. GEOS-Chem with reduced NOx emissions provides an unbiased simulation of ozone observations from the aircraft and reproduces the observed ozone production efficiency in the boundary layer as derived from a regression of ozone and NOx oxidation products. However, the model is still biased high by 6 ± 14 ppb relative to observed surface ozone in the Southeast US. Ozonesondes launched during midday hours show a 7 ppb ozone decrease from 1.5 km to the surface that GEOS-Chem does not capture. This bias may reflect a combination of excessive vertical mixing and net ozone production in the model boundary layer

Observed NO/NO2 Ratios in the Upper Troposphere Imply Errors in NO-NO2-O3 Cycling Kinetics or an Unaccounted NOx Reservoir

Observations from the SEAC4RS aircraft campaign over the southeast United States in August-September 2013 show NO/NO2 concentration ratios in the upper troposphere that are approximately half of photochemical equilibrium values computed from Jet Propulsion Laboratory (JPL) kinetic data. One possible explanation is the presence of labile NOx reservoir species, presumably organic, decomposing thermally to NO2 in the instrument. The NO2 instrument corrects for this artifact from known labile HNO4 and CH3O2NO2 NOx reservoirs. To bridge the gap between measured and simulated NO2, additional unaccounted labile NOx reservoir species would have to be present at a mean concentration of ~40 ppt for the SEAC4RS conditions (compared with 197 ppt for NOx). An alternative explanation is error in the low-temperature rate constant for the NO + O3 reaction (30% 1-σ uncertainty in JPL at 240 K) and/or in the spectroscopic data for NO2 photolysis (20% 1-σ uncertainty). Resolving this discrepancy is important for understanding global budgets of tropospheric oxidants and for interpreting satellite observations of tropospheric NO2 columns

Observed NO/NO_2 Ratios in the Upper Troposphere Imply Errors in NO-NO_2-O_3 Cycling Kinetics or an Unaccounted NO_x Reservoir

Observations from the SEAC^4RS aircraft campaign over the southeast United States in August–September 2013 show NO/NO_2 concentration ratios in the upper troposphere that are approximately half of photochemical equilibrium values computed from Jet Propulsion Laboratory (JPL) kinetic data. One possible explanation is the presence of labile NO_x reservoir species, presumably organic, decomposing thermally to NO_2 in the instrument. The NO_2 instrument corrects for this artifact from known labile HNO_4 and CH_3O_2NO_2 NO_x reservoirs. To bridge the gap between measured and simulated NO_2, additional unaccounted labile NO_x reservoir species would have to be present at a mean concentration of ~40 ppt for the SEAC^4RS conditions (compared with 197 ppt for NOx). An alternative explanation is error in the low‐temperature rate constant for the NO + O_3 reaction (30% 1‐σ uncertainty in JPL at 240 K) and/or in the spectroscopic data for NO_2 photolysis (20% 1‐σ uncertainty). Resolving this discrepancy is important for understanding global budgets of tropospheric oxidants and for interpreting satellite observations of tropospheric NO_2 columns

Cellular and developmental control of O2 homeostasis by hypoxia-inducible factor 1 alpha.

Hypoxia is an essential developmental and physiological stimulus that plays a key role in the pathophysiology of cancer, heart attack, stroke, and other major causes of mortality. Hypoxia-inducible factor 1 (HIF-1) is the only known mammalian transcription factor expressed uniquely in response to physiologically relevant levels of hypoxia. We now report that in Hif1a-/- embryonic stem cells that did not express the O2-regulated HIF-1alpha subunit, levels of mRNAs encoding glucose transporters and glycolytic enzymes were reduced, and cellular proliferation was impaired. Vascular endothelial growth factor mRNA expression was also markedly decreased in hypoxic Hif1a-/- embryonic stem cells and cystic embryoid bodies. Complete deficiency of HIF-1alpha resulted in developmental arrest and lethality by E11 of Hif1a-/- embryos that manifested neural tube defects, cardiovascular malformations, and marked cell death within the cephalic mesenchyme. In Hif1a+/+ embryos, HIF-1alpha expression increased between E8.5 and E9.5, coincident with the onset of developmental defects and cell death in Hif1a-/- embryos. These results demonstrate that HIF-1alpha is a master regulator of cellular and developmental O2 homeostasis

Expression of the RNA helicase DDX3 and the hypoxia response in breast cancer

<p>Aims: DDX3 is an RNA helicase that has antiapoptotic properties, and promotes proliferation and transformation. In addition, DDX3 was shown to be a direct downstream target of HIF-1α (the master regulatory of the hypoxia response) in breast cancer cell lines. However, the relation between DDX3 and hypoxia has not been addressed in human tumors. In this paper, we studied the relation between DDX3 and the hypoxic responsive proteins in human breast cancer.</p> <p>Methods and Results: DDX3 expression was investigated by immunohistochemistry in breast cancer in comparison with hypoxia related proteins HIF-1α, GLUT1, CAIX, EGFR, HER2, Akt1, FOXO4, p53, ERα, COMMD1, FER kinase, PIN1, E-cadherin, p21, p27, Transferrin receptor, FOXO3A, c-Met and Notch1. DDX3 was overexpressed in 127 of 366 breast cancer patients, and was correlated with overexpression of HIF-1α and its downstream genes CAIX and GLUT1. Moreover, DDX3 expression correlated with hypoxia-related proteins EGFR, HER2, FOXO4, ERα and c-Met in a HIF-1α dependent fashion, and with COMMD1, FER kinase, Akt1, E-cadherin, TfR and FOXO3A independent of HIF-1α.</p> <p>Conclusions: In invasive breast cancer, expression of DDX3 was correlated with overexpression of HIF-1α and many other hypoxia related proteins, pointing to a distinct role for DDX3 under hypoxic conditions and supporting the oncogenic role of DDX3 which could have clinical implication for current development of DDX3 inhibitors.</p&gt

Observed NO/NO_2 Ratios in the Upper Troposphere Imply Errors in NO-NO_2-O_3 Cycling Kinetics or an Unaccounted NO_x Reservoir

Observations from the SEAC^4RS aircraft campaign over the southeast United States in August–September 2013 show NO/NO_2 concentration ratios in the upper troposphere that are approximately half of photochemical equilibrium values computed from Jet Propulsion Laboratory (JPL) kinetic data. One possible explanation is the presence of labile NO_x reservoir species, presumably organic, decomposing thermally to NO_2 in the instrument. The NO_2 instrument corrects for this artifact from known labile HNO_4 and CH_3O_2NO_2 NO_x reservoirs. To bridge the gap between measured and simulated NO_2, additional unaccounted labile NO_x reservoir species would have to be present at a mean concentration of ~40 ppt for the SEAC^4RS conditions (compared with 197 ppt for NOx). An alternative explanation is error in the low‐temperature rate constant for the NO + O_3 reaction (30% 1‐σ uncertainty in JPL at 240 K) and/or in the spectroscopic data for NO_2 photolysis (20% 1‐σ uncertainty). Resolving this discrepancy is important for understanding global budgets of tropospheric oxidants and for interpreting satellite observations of tropospheric NO_2 columns

OCO-3 early mission operations and initial (vEarly) XCO₂ and SIF retrievals

NASA's Orbiting Carbon Observatory-3 (OCO-3) was installed on the International Space Station (ISS) on 10 May 2019. OCO-3 combines the flight spare spectrometer from the Orbiting Carbon Observatory-2 (OCO-2) mission, which has been in operation since 2014, with a new Pointing Mirror Assembly (PMA) that facilitates observations of non-nadir targets from the nadir-oriented ISS platform. The PMA is a new feature of OCO-3, which is being used to collect data in all science modes, including nadir (ND), sun-glint (GL), target (TG), and the new snapshot area mapping (SAM) mode. This work provides an initial assessment of the OCO-3 instrument and algorithm performance, highlighting results from the first 8 months of operations spanning August 2019 through March 2020. During the In-Orbit Checkout (IOC) phase, critical systems such as power and cooling were verified, after which the OCO-3 spectrometer and PMA were subjected to a series of rigorous tests. First light of the OCO-3 spectrometer was on 26 June 2019, with full science operations beginning on 6 August 2019. The OCO-3 spectrometer on-orbit performance is consistent with that seen during preflight testing. Signal to noise ratios are in the expected range needed for high quality retrievals of the column-averaged carbon dioxide (CO₂) dry-air mole fraction (XCO₂) and solar-induced chlorophyll fluorescence (SIF), which will be used to help quantify and constrain the global carbon cycle. The first public release of OCO-3 Level 2 (L2) data products, called “vEarly”, is being distributed by NASA's Goddard Earth Sciences Data and Information Services Center (GES DISC). The intent of the vEarly product is to evaluate early mission performance, facilitate comparisons with OCO-2 products, and identify key areas to improve for the next data release. The vEarly XCO2 exhibits a root-mean-squared-error (RMSE) of ≃ 1, 1, 2 ppm versus a truth proxy for nadir-land, TG&SAM, and glint-water observations, respectively. The vEarly SIF shows a correlation with OCO-2 measurements of >0.9 for highly coincident soundings. Overall, the Level 2 SIF and XCO₂ products look very promising, with performance comparable to OCO-2. A follow-on version of the OCO-3 L2 product containing a number of refinements, e.g., instrument calibration, pointing accuracy, and retrieval algorithm tuning, is anticipated by early in 2021

Expression of hypoxia-inducible factor-1α and cell cycle proteins in invasive breast cancer are estrogen receptor related

BACKGROUND: The transcription factor hypoxia-inducible factor-1 (HIF-1) is a key regulator of the cellular response to hypoxia. Previous studies showed that concentrations of its subunit HIF-1α, as a surrogate for HIF-1 activity, are increased during breast carcinogenesis and can independently predict prognosis in breast cancer. During carcinogenesis, the cell cycle is progressively deregulated, and proliferation rate is a strong prognostic factor in breast cancer. In this study we undertook a detailed evaluation of the relationships between HIF-1α and cell cycle-associated proteins. METHODS: In a representative estrogen receptor (ER) group of 150 breast cancers, the expression of HIF-1α, vascular endothelial growth factor, the ER, HER-2/neu, Ki-67, cyclin A, cyclin D(1), p21, p53, and Bcl-2 was investigated by immunohistochemistry. RESULTS: High concentrations (5% or more) of HIF-1α were associated with increased proliferation as shown by positive correlations with Ki-67 (P < 0.001) and the late S–G2-phase protein cyclin A (P < 0.001), but not with the G1-phase protein cyclin D(1). High HIF-1α concentrations were also strongly associated with p53 positivity (P < 0.001) and loss of Bcl-2 expression (P = 0.013). No association was found between p21 and HIF-1α (P = 0.105) in the whole group of patients. However, the subgroup of ER-positive cancers was characterized by a strong positive association between HIF-1α and p21 (P = 0.023), and HIF-1α lacked any relation with proliferation. CONCLUSION: HIF-1α overexpression is associated with increased proliferation, which might explain the adverse prognostic impact of increased concentrations of HIF-1α in invasive breast cancer. In ER-positive tumors, HIF-1α is associated with p21 but not against proliferation. This shows the importance of further functional analysis to unravel the role of HIF-1 in late cell cycle progression, and the link between HIF-1, p21, and ER