Sector-Based Top-Down Estimates of NO x , SO2, and CO Emissions in East Asia.

Top-down estimates using satellite data provide important information on the sources of air pollutants. We develop a sector-based 4D-Var framework based on the GEOS-Chem adjoint model to address the impacts of co-emissions and chemical interactions on top-down emission estimates. We apply OMI NO2, OMI SO2, and MOPITT CO observations to estimate NO x , SO2, and CO emissions in East Asia during 2005-2012. Posterior evaluations with surface measurements show reduced normalized mean bias (NMB) by 7% (NO2)-15% (SO2) and normalized mean square error (NMSE) by 8% (SO2)-9% (NO2) compared to a species-based inversion. This new inversion captures the peak years of Chinese SO2 (2007) and NO x (2011) emissions and attributes their drivers to industry and energy activities. The CO peak in 2007 in China is driven by residential and industry emissions. In India, the inversion attributes NO x and SO2 trends mostly to energy and CO trend to residential emissions.

Maternal calorie restriction modulates placental mitochondrial biogenesis and bioenergetic efficiency: putative involvement in fetoplacental growth defects in rats.

Low birth weight is associated with an increased risk for developing type 2 diabetes and metabolic diseases. The placental capacity to supply nutrients and oxygen to the fetus represents the main determiner of fetal growth. However, few studies have investigated the effects of maternal diet on the placenta. We explored placental adaptive proteomic processes implicated in response to maternal undernutrition. Rat term placentas from 70% food-restricted (FR30) mothers were used for a proteomic screen. Placental mitochondrial functions were evaluated using molecular and functional approaches, and ATP production was measured. FR30 drastically reduced placental and fetal weights. FR30 placentas displayed 14 proteins that were differentially expressed, including several mitochondrial proteins. FR30 induced a marked increase in placental mtDNA content and changes in mitochondrial functions, including modulation of the expression of genes implicated in biogenesis and bioenergetic pathways. FR30 mitochondria showed higher oxygen consumption but failed to maintain their ATP production. Maternal undernutrition induces placental mitochondrial abnormalities. Although an increase in biogenesis and bioenergetic efficiency was noted, placental ATP level was reduced. Our data suggest that placental mitochondrial defects may be implicated in fetoplacental pathologies.

Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat.

Mitochondrial dysfunction may be a long-term consequence of a poor nutritional environment during early life. Our aim was to investigate whether a maternal low-protein (LP) diet may program mitochondrial dysfunction in islets of adult progeny before glucose intolerance ensues. To address this, pregnant Wistar rats were fed isocaloric diets containing either 20% protein (control) or 8% protein (LP diet) throughout gestation. From birth, offspring received the control diet. The mitochondrial function was analyzed in islets of 3-mo-old offspring. Related to their basal insulin release, cultured islets from both male and female LP offspring presented a lower response to glucose challenge and a blunted ATP production compared with control offspring. The expression of malate dehydrogenase as well as the subunit 6 of the ATP synthase encoded by mitochondrial genome (mtDNA) was lower in these islets, reducing the capacity of ATP production through the Krebs cycle and oxidative phosphorylation. However, mtDNA content was unchanged in LP islets compared with control. Several consequences of protein restriction during fetal life were more marked in male offspring. Only LP males showed an increased reactive oxygen species production associated with a higher expression of mitochondrial subunits of the electron transport chain NADH-ubiquinone oxireductase subunit 4L, an overexpression of peroxisome proliferator-activated receptor-gamma and uncoupling protein-2, and a strongly reduced beta-cell mass. In conclusion, mitochondrial function is clearly altered in islets from LP adult offspring in a sex-specific manner. That may provide a cellular explanation for the earlier development of glucose intolerance in male than in female offspring of dams fed an LP diet.

Hybrid Mass Balance/4D-Var Joint Inversion of NO x and SO2 Emissions in East Asia.

Accurate estimates of NO x and SO2 emissions are important for air quality modeling and management. To incorporate chemical interactions of the two species in emission estimates, we develop a joint hybrid inversion framework to estimate their emissions in China and India (2005-2012). Pseudo observation tests and posterior evaluation with surface measurements demonstrate that joint assimilation of SO2 and NO2 can provide more accurate constraints on emissions than single-species inversions. This occurs through synergistic change of O3 and OH concentrations, particularly in conditions where satellite retrievals of the species being optimized have large uncertainties. The percentage changes of joint posterior emissions from the single-species posterior emissions go up to 242% at grid scales, although the national average of monthly emissions, seasonality, and interannual variations are similar. In China and India, the annual budget of joint posterior SO2 emissions is lower, but joint NO x posterior emissions are higher, because NO x emissions increase to increase SO2 concentration and better match Ozone Monitoring Instrument SO2 observations in high-NO x regions. Joint SO2 posterior emissions decrease by 16.5% from 2008 to 2012, while NO x posterior emissions increase by 24.9% from 2005 to 2011 in China-trends which are consistent with the MEIC inventory. Joint NO x and SO2 posterior emissions in India increase by 15.9% and 19.2% from 2005 to 2012, smaller than the 59.9% and 76.2% growth rate using anthropogenic emissions from EDGARv4.3.2. This work shows the benefit and limitation of joint assimilation in emission estimates and provides an efficient framework to perform the inversion.

TROPOMI enables high resolution SO2 flux observations from Mt. Etna, Italy, and beyond.

The newly launched imaging spectrometer TROPOMI onboard the Sentinel-5 Precursor satellite provides atmospheric column measurements of sulfur dioxide (SO2) and other gases with a pixel resolution of 3.5 × 7 km2. This permits mapping emission plumes from a vast number of natural and anthropogenic emitters with unprecedented sensitivity, revealing sources which were previously undetectable from space. Novel analysis using back-trajectory modelling of satellite-based SO2 columns allows calculation of SO2 flux time series, which would be of great utility and scientific interest if applied globally. Volcanic SO2 emission time series reflect magma dynamics and are used for risk assessment and calculation of the global volcanic CO2 gas flux. TROPOMI data make this flux time series reconstruction approach possible with unprecedented spatiotemporal resolution, but these new data must be tested and validated against ground-based observations. Mt. Etna (Italy) emits SO2 with fluxes ranging typically between 500 and 5000 t/day, measured automatically by the largest network of scanning UV spectrometers in the world, providing the ideal test-bed for this validation. A comparison of three SO2 flux datasets, TROPOMI (one month), ground-network (one month), and ground-traverse (two days) shows acceptable to excellent agreement for most days. The result demonstrates that reliable, nearly real-time, high temporal resolution SO2 flux time series from TROPOMI measurements are possible for Etna and, by extension, other volcanic and anthropogenic sources globally. This suggests that global automated real-time measurements of large numbers of degassing volcanoes world-wide are now possible, revolutionizing the quantity and quality of magmatic degassing data available and insights into volcanic processes to the volcanological community.

SO2 Emission Estimates Using OMI SO2 Retrievals for 2005-2017.

SO2 column densities from Ozone Monitoring Instrument provide important information on emission trends and missing sources, but there are discrepancies between different retrieval products. We employ three Ozone Monitoring Instrument SO2 retrieval products (National Aeronautics and Space Administration (NASA) standard (SP), NASA prototype, and BIRA) to study the magnitude and trend of SO2 emissions. SO2 column densities from these retrievals are most consistent when viewing angles and solar zenith angles are small, suggesting more robust emission estimates in summer and at low latitudes. We then apply a hybrid 4D-Var/mass balance emission inversion to derive monthly SO2 emissions from the NASA SP and BIRA products. Compared to HTAPv2 emissions in 2010, both posterior emission estimates are lower in United States, India, and Southeast China, but show different changes of emissions in North China Plain. The discrepancies between monthly NASA and BIRA posterior emissions in 2010 are less than or equal to 17% in China and 34% in India. SO2 emissions increase from 2005 to 2016 by 35% (NASA)-48% (BIRA) in India, but decrease in China by 23% (NASA)-33% (BIRA) since 2008. Compared to in situ measurements, the posterior GEOS-Chem surface SO2 concentrations have reduced NMB in China, the United States, and India but not in South Korea in 2010. BIRA posteriors have better consistency with the annual growth rate of surface SO2 measurement in China and spatial variability of SO2 concentration in China, South Korea, and India, whereas NASA SP posteriors have better seasonality. These evaluations demonstrate the capability to recover SO2 emissions using Ozone Monitoring Instrument observations.

Important contributions of sea-salt aerosols to atmospheric bromine cycle in the Antarctic coasts.

Polar sunrise activates reactive bromine (BrOx) cycle on the Antarctic coasts. BrOx chemistry relates to depletion of O3 and Hg in polar regions. Earlier studies have indicated "blowing snow" as a source of atmospheric BrOx. However, surface O3 depletion and BrO enhancement occurs rarely under blowing snow conditions at Syowa Station, Antarctica. Therefore, trigger processes for BrOx activation other than the heterogeneous reactions on blowing snow particles must be considered. Results of this study show that enhancement of sea-salt aerosols (SSA) and heterogeneous reactions on SSA are the main key processes for atmospheric BrOx cycle activation. Blowing snow had Br- enrichment, in contrast to strong Br- depletion in SSA. In-situ aerosol measurements and satellite BrO measurements demonstrated clearly that a BrO plume appeared simultaneously in SSA enhancement near the surface. Results show that surface O3 depletion at Syowa Station occurred in aerosol enhancement because of SSA dispersion during the polar sunrise. Amounts of depleted Br- from SSA were matched well to the tropospheric vertical column density of BrO and BrOx concentrations found in earlier work. Our results indicate that SSA enhancement by strong winds engenders activation of atmospheric BrOx cycles via heterogeneous reactions on SSA.

Systematic expression analysis of Hox genes at adulthood reveals novel patterns in the central nervous system.

Hox proteins are key regulators of animal development, providing positional identity and patterning information to cells along the rostrocaudal axis of the embryo. Although their embryonic expression and function are well characterized, their presence and biological importance in adulthood remains poorly investigated. We provide here the first detailed quantitative and neuroanatomical characterization of the expression of the 39 Hox genes in the adult mouse brain. Using RT-qPCR we determined the expression of 24 Hox genes mainly in the brainstem of the adult brain, with low expression of a few genes in the cerebellum and the forebrain. Using in situ hybridization (ISH) we have demonstrated that expression of Hox genes is maintained in territories derived from the early segmental Hox expression domains in the hindbrain. Indeed, we show that expression of genes belonging to paralogy groups PG2-8 is maintained in the hindbrain derivatives at adulthood. The spatial colinearity, which characterizes the early embryonic expression of Hox genes, is still observed in sequential antero-posterior boundaries of expression. Moreover, the main mossy and climbing fibres precerebellar nuclei express PG2-8 Hox genes according to their migration origins. Second, ISH confirms the presence of Hox gene transcripts in territories where they are not detected during development, suggesting neo-expression in these territories in adulthood. Within the forebrain, we have mapped Hoxb1, Hoxb3, Hoxb4, Hoxd3 and Hoxa5 expression in restricted areas of the sensory cerebral cortices as well as in specific thalamic relay nuclei. Our data thus suggest a requirement of Hox genes beyond their role of patterning genes, providing a new dimension to their functional relevance in the central nervous system.

Alteration of mitochondrial function in adult rat offspring of malnourished dams.

Under-nutrition as well as over-nutrition during pregnancy has been associated with the development of adult diseases such as diabetes and obesity. Both epigenetic modifications and programming of the mitochondrial function have been recently proposed to explain how altered intrauterine metabolic environment may produce such a phenotype. This review aims to report data reported in several animal models of fetal malnutrition due to maternal low protein or low calorie diet, high fat diet as well as reduction in placental blood flow. We focus our overview on the ß cell. We highlight that, notwithstanding early nutritional events, mitochondrial dysfunctions resulting from different alteration by diet or gender are programmed. This may explain the higher propensity to develop obesity and diabetes in later life.

Maternal malnutrition programs pancreatic islet mitochondrial dysfunction in the adult offspring.

Accumulating evidence has shown that maternal malnutrition increases the risk of metabolic disease in the progeny. We previously reported that prenatal exposure to a low-protein diet (LP) leads to mitochondrial dysfunction in pancreatic islets from adult rodent offspring that could relate physiological and cellular alterations due to early diet. We aim to determine whether mitochondrial dysfunction could be a common consequence of prenatal nutritional unbalances. Pregnant Wistar rats received either a global food restriction (GFR), consisting in the reduction by 50% of the normal daily food intake, or a high-fat diet (HF) throughout gestation. GFR or HF diet during pregnancy leads to a lack of increase in insulin release and ATP content in response to glucose stimulation in islets from 3-month-old male and female offspring. These similar consequences originated from impairment in either glucose sensing or glucose metabolism, depending on the type of early malnutrition and on the sex of the progeny. Indeed, the glucose transport across ß-cell membrane seemed compromised in female HF offspring, since GLUT-2 gene was markedly underexpressed. Additionally, for each progeny, consequences downstream the entry of glucose were also apparent. Expression of genes involved in glycolysis, TCA cycle and oxidative phosphorylations was altered in GFR and HF rats in a sex- and diet-dependent manner. Moreover, prenatal malnutrition affected the regulators of mitochondrial biogenesis, namely, PPAR coactivator 1 alpha (PGC-1α), since its expression was higher in islets from GFR rats. In conclusion, programming of mitochondrial dysfunction is a consequence of maternal malnutrition, which may predispose to glucose intolerance in the adult offspring.

Impairment of rat fetal beta-cell development by maternal exposure to dexamethasone during different time-windows.

AIM: Glucocorticoids (GCs) take part in the direct control of cell lineage during the late phase of pancreas development when endocrine and exocrine cell differentiation occurs. However, other tissues such as the vasculature exert a critical role before that phase. This study aims to investigate the consequences of overexposure to exogenous glucocorticoids during different time-windows of gestation for the development of the fetal endocrine pancreas. METHODS: Pregnant Wistar rats received dexamethasone acetate in their drinking water (1 µg/ml) during the last week or throughout gestation. Fetuses and their pancreases were analyzed at day 15 and 21 of gestation. Morphometrical analysis was performed on pancreatic sections after immunohistochemistry techniques and insulin secretion was evaluated on fetal islets collected in vitro. RESULTS: Dexamethasone given the last week or throughout gestation reduced the beta-cell mass in 21-day-old fetuses by respectively 18% or 62%. This was accompanied by a defect in insulin secretion. The alpha-cell mass was reduced similarly. Neither islet vascularization nor beta-cell proliferation was affected when dexamethasone was administered during the last week, which was however the case when given throughout gestation. When given from the beginning of gestation, dexamethasone reduced the number of cells expressing the early marker of endocrine lineage neurogenin-3 when analyzed at 15 days of fetal age. CONCLUSIONS: GCs reduce the beta- and alpha-cell mass by different mechanisms according to the stage of development during which the treatment was applied. In fetuses exposed to glucocorticoids the last week of gestation only, beta-cell mass is reduced due to impairment of beta-cell commitment, whereas in fetuses exposed throughout gestation, islet vascularization and lower beta-cell proliferation are involved as well, amplifying the reduction of the endocrine mass.

Maternal malnutrition programs the endocrine pancreas in progeny.

Type 2 diabetes arises when the endocrine pancreas fails to secrete sufficient insulin to cope with metabolic demands resulting from ß cell secretory dysfunction, decreased ß cell mass, or both. Epidemiologic studies have shown strong relations between poor fetal and early postnatal nutrition and susceptibility to diabetes later in life. Animal models have been established, and studies have shown that a reduction in the availability of nutrients during fetal development programs the endocrine pancreas and insulin-sensitive tissues. We investigated several modes of early malnutrition in rats. Regardless of the type of diet investigated, whether there was a deficit in calories or protein in food or even in the presence of a high-fat diet, malnourished pups were born with a defect in their ß cell population, with fewer ß cells that did not secrete enough insulin and that were more vulnerable to oxidative stress; such populations of ß cells will never completely recover. Despite the similar endpoint, the cellular and physiologic mechanisms that contribute to alterations in ß cell mass differ depending on the nature of the nutritional insult. Hormones that are operative during fetal life, such as insulin, insulin-like growth factors, and glucocorticoids; specific molecules, such as taurine; and islet vascularization have been implicated as possible factors in amplifying this defect. The molecular mechanisms responsible for intrauterine programming of ß cells are still elusive, but among them the programming of mitochondria may be a strong central candidate.

Early low protein diet aggravates unbalance between antioxidant enzymes leading to islet dysfunction.

BACKGROUND: Islets from adult rat possess weak antioxidant defense leading to unbalance between superoxide dismutase (SOD) and hydrogen peroxide-inactivating enzymatic activities, catalase (CAT) and glutathione peroxidase (GPX) rending them susceptible to oxidative stress. We have shown that this vulnerability is influenced by maternal diet during gestation and lactation. METHODOLOGY/PRINCIPAL FINDINGS: The present study investigated if low antioxidant activity in islets is already observed at birth and if maternal protein restriction influences the development of islet antioxidant defenses. Rats were fed a control diet (C group) or a low protein diet during gestation (LP) or until weaning (LPT), after which offspring received the control diet. We found that antioxidant enzymatic activities varied with age. At birth and after weaning, normal islets possessed an efficient GPX activity. However, the antioxidant capacity decreased thereafter increasing the potential vulnerability to oxidative stress. Maternal protein malnutrition changed the antioxidant enzymatic activities in islets of the progeny. At 3 months, SOD activity was increased in LP and LPT islets with no concomitant activation of CAT and GPX. This unbalance could lead to higher hydrogen peroxide production, which may concur to oxidative stress causing defective insulin gene expression due to modification of critical factors that modulate the insulin promoter. We found indeed that insulin mRNA level was reduced in both groups of malnourished offspring compared to controls. Analyzing the expression of such critical factors, we found that c-Myc expression was strongly increased in islets from both protein-restricted groups compared to controls. CONCLUSION AND SIGNIFICANCE: Modification in antioxidant activity by maternal low protein diet could predispose to pancreatic islet dysfunction later in life and provide new insights to define a molecular mechanism responsible for intrauterine programming of endocrine pancreas.

Modeling dynamic exchange of gaseous elemental mercury at polar sunrise.

At polar sunrise, gaseous elemental mercury (GEM) undergoes an exceptional dynamic exchange in the air and at the snow surface during which GEM can be rapidly removed from the atmosphere (the so-called atmospheric mercury depletion events (AMDEs)) as well as re-emitted from the snow within a few hours to days in the Polar Regions. Although high concentrations of total mercury in snow following AMDEs is well documented, there is very little data available on the redox transformation processes of mercury in the snow and the fluxes of mercury at the air/snow interface. Therefore, the net gain of mercury in the Polar Regions as a result of AMDEs is still an open question. We developed a new version of the global mercury model, GRAHM, which includes for the first time bidirectional surface exchange of GEM in Polar Regions in spring and summer by developing schemes for mercury halogen oxidation, deposition, and re-emission. Also for the first time, GOME satellite data-derived boundary layer concentrations of BrO have been used in a global mercury model for representation of halogen mercury chemistry. Comparison of model simulated and measured atmospheric concentrations of GEM at Alert, Canada, for 3 years (2002-2004) shows the model's capability in simulating the rapid cycling of mercury during and after AMDEs. Brooks et al. (1) measured mercury deposition, reemission, and net surface gain fluxes of mercury at Barrow, AK, during an intensive measurement campaign for a 2 week period in spring (March 25 to April 7, 2003). They reported 1.7, 1.0 +/- 0.2, and 0.7 +/- 0.2 microg m(-2) deposition, re-emission, and net surface gain, respectively. Using the optimal configuration of the model, we estimated 1.8 microg m(-2) deposition, 1.0 microg m(-2) re-emission, and 0.8 microg m(-2) net surface gain of mercury for the same time period at Barrow. The estimated net annual accumulation of mercury within the Arctic Circle north of 66.5 degrees is approximately 174 t with +/-7 t of interannual variability for 2002-2004 using the optimal configuration. We estimated the uncertainty of the model results to the Hg/Br reaction rate coefficient to be approximately 6%. Springtime is clearly demonstrated as the most active period of mercury exchanges and net surface gain (approximately 46% of annual accumulation) in the Arctic.