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Outdoor pollution is a complex mix of more than 200 air contaminants. Among these pollutants, ozone, nitrogen dioxide and fine particles may generate bronchial inflammation and hyperreactivity. The hypothesis that pollution contributes to the development of asthma in children is based on epidemiological, clinical and experimental data. Many risk factors during the in utero and postnatal period have been identified in the aetiology of childhood asthma. During pregnancy, outdoor pollution was identified as a causal factor of respiratory disease in neonatal cohort studies. Several epidemiological studies also demonstrate that outdoor pollution is a trigger of asthma exacerbations. This review aims to highlight the current knowledge on outdoor pollution and asthma. [ABSTRACT FROM AUTHOR]

Abstract The interaction of NO and H 2 O 2 in the regulation of plant development is well documented. We have recently shown that the content of NO and H 2 O 2 changes in a characteristic way during the cell cycle of Chlamydomonas reinhardtii (Pokora et al., 2017), which implies participation of these molecules in the regulation of Chlamydomonas development. To verify this assumption, H 2 O 2 was supplied at a concentration about 1.5 times higher than that determined in the control cells. Cells were synchronized by alternating the light/dark (10/14 h) regimen. H 2 O 2 was added to zoospore suspensions, previously held in the dark, and cells growing for 3, 6, and 9 h in the light. The data indicate that, depending on the phase of the Chlamydomonas cell cycle, H 2 O 2 , via mild modification of redox homeostasis, may: a) accelerate or delay the duration of the cell cycle; b) increase the number of replication rounds occurring in one cell cycle; c) modify the biomass and cell volume of progeny cells and d) accelerate the liberation of daughter cells. This provides a tool to control the development of Chlamydomonas cell and thus offers the opportunity to obtain a population of cells with characteristics desired in biotechnology. [ABSTRACT FROM AUTHOR]

This study describes the successful synthesis of nitric oxide (NO)-releasing compounds with biodegradable and injectable properties and demonstrates that the kinetics of NO release vary according to the type of NO donor. The antimicrobial activity of NO-releasing compounds against three common periodontal pathogens, i.e., Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Actinomyces israelii, was investigated using a susceptibility assay. Human gingival fibroblasts were treated with NO-releasing compounds at the minimum concentrations required for bacterial growth and cytotoxicity was evaluated using the MTT cell proliferation assay. Our results suggest that NO-releasing compounds can be used topically to treat both gram-negative and gram-positive periodontal pathogens. Comparison of the antimicrobial activity and cytotoxicity assay results between the NO-releasing compounds revealed that an NO donor comprising a macromolecule without surface charge, a lower instantaneous NO concentration, and an adequate supply of NO were associated with a strong bactericidal effect and low cytotoxicity. NO-releasing compounds with these properties may be suitable for treatment of periodontitis. [ABSTRACT FROM AUTHOR]

Abstract This review aims to summarize the changes of the NOS/NO system which occur in the lungs, gills, kidney, heart, and myotomal muscle of air breathing fish of the genus Protopterus , i.e. P. dolloi and P. annectens , in relation to the switch from freshwater to aestivation, and vice-versa. The modifications of NOS and its partners Akt and Hsp-90, and HIF-1α, detected by immunohistochemical and molecular biology methods, are discussed together with the apoptosis rate, evaluated by TUNEL. We hypothesize that these molecular components are key elements of the stress-induced signal transduction/integration networks which allow the lungfish to overcome the dramatic environmental challenges experienced at the beginning, during, and at the end of the dry season. [ABSTRACT FROM AUTHOR]

Abstract: Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system. We investigated the effect of phytol in an animal model of MS, experimental autoimmune encephalomyelitis (EAE), as phytol, a plant-derived diterpene alcohol, exerts anti-inflammatory and redox-protective actions. We observed a significant amelioration of clinical symptoms in EAE C57BL/6N mice fed prophylactically with a phytol-enriched diet. Demyelination, DNA damage, and infiltration of immune cells, specifically TH1 cells, into the central nervous system were reduced in phytol-fed EAE mice. Furthermore, phytol reduced T-cell proliferation ex vivo. Phytanic acid — a metabolite of phytol — also reduced T-cell proliferation, specifically that of TH1 cells. Additionally, phytol-enriched diet increased the mRNA expression of nicotinamide adenine dinucleotide phosphate oxidase (NOX) 2 in white blood cells in the lymph nodes. Accordingly, phytol lost its anti-inflammatory effects in chimeric EAE C57BL/6N mice whose peripheral cells lack NOX2, indicating that phytol mediates its effects in peripheral cells via NOX2. Moreover, the effects of phytol on T-cell proliferation were also NOX2-dependent. In contrast, the T-cell subtype alterations and changes in proliferation induced by phytanic acid, the primary metabolite of phytol, were NOX2-independent. In conclusion, phytol supplementation of the diet leads to amelioration of EAE pathology in both a NOX2-dependent and a NOX2-independent manner via yet unknown mechanisms.Key messages: Phytol diet ameliorates EAE pathology.Phytol diet reduces demyelination, immune cell infiltration, and T-cell proliferation.Phytol diet increases NOX2 mRNA expression in white blood cells in the lymph nodes.Phytol mediates its effects in peripheral cells via NOX2.Effects of phytol on T-cell proliferation were NOX2-dependent. [ABSTRACT FROM AUTHOR]

Ferrochelatase (FECH) is an enzyme necessary for heme synthesis, which is essential for maintaining normal functions of endothelial nitric oxide synthase (eNOS) and soluble guanylyl cyclase (sGC). We tested the hypothesis that inhibition of vascular FECH to attenuate heme synthesis downregulates eNOS and sGC expression, resulting in impaired NO/cGMP-dependent relaxation. To this end, isolated bovine coronary arteries (BCAs) were in vitro incubated without (as controls) or with N-methyl protoporphyrin (NMPP; 10−5–10-7M; a selective FECH antagonist) for 24 and 72 hours respectively. Tissue FECH activity, heme, nitrite/NO and superoxide levels were sequentially measured. Protein expression of FECH, eNOS and sGC was detected by western blot analysis. Vascular responses to various vasoactive agents were evaluated via isometric tension studies. Treatment of BCAs with NMPP initiated a time- and dose-dependent attenuation of FECH activity without changes in its protein expression, followed by significant reduction in the heme level. Moreover, ACh-induced relaxation and ACh-stimulated release of NO were significant reduced, associated with suppression of eNOS protein expression in NMPP-treated groups. Decreased relaxation to NO donor spermine-NONOate reached the statistical significance in BCAs incubated with NMPP for 72 hours, concomitantly with downregulation of sGCβ1 expression that was independent of heat shock protein 90 (HSP90), nor did it significantly affect BCA relaxation caused by BAY 58–2667 that activates sGC in the heme-deficiency. Neither vascular responses to non-NO/sGC-mediators nor production of superoxide was affected by NMPP-treatment. In conclusion, deletion of vascular heme production via inhibiting FECH elicits downregulation of eNOS and sGC expression, leading to an impaired NO-mediated relaxation in an oxidative stress-independent manner. [ABSTRACT FROM AUTHOR]

The aim of this study was to explore the α 1 -adrenoceptor-independent mechanisms involved in the vasorelaxant properties of two non-quinazoline α 1 -adrenoceptors antagonists (MH-76 and MH-79). Endothelium intact and endothelium denuded rat aorta was contracted with 1 μM phenylephrine to plateau, and the vasodilatory effect of MH-76 and MH-79 was examined in the absence or presence of inhibitors of the different signal transduction pathways. cGMP concetration was measured in rat aorta (enzyme immunoassay kit). In human aortic endothelial cells (HAEC) NO production was examined using a DAF-FM DA fluorescent indicator, whereas in human aortic smooth muscle cells the influence of the title compounds on K + efflux was evaluated. The vasorelaxant effect of MH-76 and MH-79 was attenuated by endothelium removal, N ω -Nitro- l -arginine methyl ester (L-NAME) and 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) pretreatment to the level characteristic for α 1 -adrenoreceptor blocking activity. In addition, the MH-76 and MH-79 induced relaxation was reduced by K + channels blockers. In endothelium intact rat aorta, MH-76 and MH-79 caused an increase in cGMP level, whereas in HAEC they increased NO generation. In contrast, the reference, quinazoline based α 1 -antagonist prazosin, did not influence NO production. Our findings suggest that the mechanisms underlying the vasodilatory properties of non-quinazoline based α 1 -adrenoceptors antagonists MH-76 and MH-79 involve not only α 1 -adrenoceptor blocking activity but also the activation of the endothelial NO–cGMP signalling pathway and the subsequent opening of K + channels. Our studies show that such double mechanism of action is superior to pure α 1 -adrenoceptor blockade, and may be considered as a promising alternative for the prevention and treatment of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Background Triggers of multiple sclerosis (MS) relapses are essentially unknown. PM 10 exposure has recently been associated with an increased risk of relapses. Objectives We further explore the short-term associations between PM 10 , NO 2 , benzene (C 6 H 6 ), O 3 , and CO exposures, and the odds of MS relapses’ occurrence. Methods Using a case-crossover design, we studied 424 MS patients living in the Strasbourg area, France between 2000 and 2009 (1783 relapses in total). Control days were chosen to be ± 35 days relative to the case (relapse) day. Exposure was modeled through ADMS-Urban software at the census block scale. We consider single-pollutant and multi-pollutant conditional logistic regression models coupled with a distributed-lag linear structure, stratified by season ("hot" vs. "cold"), and adjusted for meteorological parameters, pollen count, influenza-like epidemics, and holidays. Results The single-pollutant analyses indicated: 1) significant associations between MS relapse incidence and exposures to NO 2 , PM 10 , and O 3 , and 2) seasonality in these associations. For instance, an interquartile range increase in NO 2 (lags 0–3) and PM 10 exposure were associated with MS relapse incidence (OR = 1.08; 95%CI: [1.03–1.14] and OR = 1.06; 95%CI: [1.01–1.11], respectively) during the "cold" season (i.e., October-March). We also observed an association with O 3 and MS relapse incidence during "hot" season (OR = 1.16; 95%CI: [1.07–1.25]). C 6 H 6 and CO were not significantly related to MS relapse incidence. However, using multi-pollutant models, only O 3 remained significantly associated with the odds of relapse triggering during "hot" season. Conclusion We observed significant single-pollution associations between the occurrence of MS relapses and exposures to NO 2 , O 3 and PM 10 , only O 3 remained significantly associated with occurrence of MS relapses in the multi-pollutant model. [ABSTRACT FROM AUTHOR]

Increasing demand of commercial markets for tea products is driving the conversion from rice paddies to tea plantations in subtropical China. So far, however, little is known on how this land-use change, along with the age of plantation establishment, will affect the fluxes of greenhouse gases (GHG) methane (CH 4 ) and nitrous oxide (N 2 O) and the air-pollutant nitric oxide (NO). Thus, we measured CH 4 , N 2 O and NO fluxes over an entire year from two tea plantations (one- and five-year-old plantations) and a native rice-fallow system under two system-specific nitrogen fertilizer options. On an annual scale, comparable or higher GHG emissions were measured for tea plantations as compared to the rice-fallow system. Besides the pollution swapping from CH 4 being the dominating GHG in rice paddies to N 2 O in tea plantations, annual NO emissions increased significantly. Annual direct emission factors of N 2 O and NO in tea plantations were 2.47–5.80% and 2.00–3.99%, respectively, significantly higher than in the rice-fallow system (N 2 O: 1.05–2.05%; NO: 0.033–0.051%). Differences in N fertilizer inputs and soil environmental conditions (e.g., soil water regime, pH and organic carbon) due to contrasting managements of these systems and their interactions are clearly driving the stimulation of N 2 O and NO emissions and contributing to the significant CH 4 reductions. Furthermore, we observed that increasing tea stand age, particularly under organic fertilization, further stimulated N 2 O and NO emissions that varied significantly intra-annually. Nevertheless, the higher N 2 O and NO emissions of tea plantations and the increasing emission strength with stand age deserve further research attention and consideration for future land-use conversions. [ABSTRACT FROM AUTHOR]

BACKGROUND:It has been well documented that ATP activates NOS enzymes and causes increased NO production in several cell types. Although RBC known to possesses eNOS enzyme activity, it has not been investigated whether RBC eNOS could be induced by extracellular ATP. OBJECTIVE:The aim of the present study is to evaluate extracellular ATP mediated eNOS activation and NO production in RBC. METHODS:RBC packed were isolated from healthy volunteers and re-suspended in Hepes solution at a hematocrit of 0.01 l/l. Intracellular NO and Ca+2 levels and eNOS activation measured by flow cytometry in response to P2X receptor agonist, Bz-ATP, in the absence and presence of NOS, P2 receptors and PI3K inhibitors. RESULTS:P2X receptor agonist Bz-ATP found to increase intracellular NO, Ca+2 and serine 1177 phosphorylated eNOS levels and these responses have shown to be suppressed by NOS enzyme, P2 receptors and PI3K inhibitors. CONCLUSIONS:The results of the study clearly demonstrated extracellular ATP induced NO generation in RBC through intracellular Ca+2 and PI3K/Akt pathways. The mechanism we described here might be important at basal conditions and also in conditions with increased ATP release. [ABSTRACT FROM AUTHOR]

Background The South Durban (SD) area of Durban, South Africa, has a history of air pollution issues due to the juxtaposition of low-income communities with industrial areas. This study used measurements of oxides of nitrogen (NO x ) to develop a land use regression (LUR) model to explain the spatial variation of air pollution concentrations in this area. Methods Ambient NO x was measured over two two-week sampling periods at 32 sites using Ogawa badges. Following the ESCAPE approach, an annual adjusted average was calculated for these results and regressed against pre-selected geographic predictor variables in a multivariate regression model. The LUR model was then applied to predict the NO x exposure of a sample of pregnant women living in South Durban. Results Measured NO x levels ranged from 22.3–50.9 μg/m 3 with a median of 36 μg/m 3 . The model developed accounts for 73% of the variance in ambient NO x measurements using three input variables (length of minor roads within a 1000 m radius, length of major roads within a 300 m radius, and area of open space within a 1000 m radius). Model cross validation yielded a R 2 of 0.59. Subsequent participant exposure estimates indicated exposure to ambient NO x ranged from 19.9–53.2 μg/m 3 , with a mean of 39 μg/m 3 . Discussion and Conclusion This is the first study to develop a land use regression model that predicts ambient concentrations of NO x in a South African context. The findings of this study indicate that the participants in the South Durban are exposed to high levels of NO x that can be attributed mainly to traffic. [ABSTRACT FROM AUTHOR]

A copper-catalyzed aerobic oxidation of benzylpyridine N-oxides is reported. The N-oxide moiety acts as a built-in activator for the benzylic methylene oxidation, without requirement of additives. Reaction conditions were identified which suppress undesired benzoylpyridine formation via N-deoxygenation involving intermolecular oxygen transfer. The versatility of the N-oxide group of the benzoylpyridine N-oxide reaction products for post-functionalization of the pyridine ring is demonstrated through efficient C-C, C-N, C-O and C-Cl bond forming procedures, with both nucleophiles and electrophiles. Finally, the applicability of the new synthetic methodology is demonstrated in an alternative route towards the antihistaminic drug Acrivastine via three consecutive N-oxide activated C-H functionalization processes, starting from picoline N-oxide. [ABSTRACT FROM AUTHOR]

In present study, the effect of fuel premixing ratio, direct fuel injection timings and engine compression ratio on the soot particle emissions in nano-size range from a non-road compression ignition engine is investigated. Experiments are conducted on modified dual fuel single cylinder engine at 1500 rpm. To run the engine in dual fuel mode, port fuel injection (PFI) system is installed by modifying intake manifold of the engine and developing a PFI controller. Experiments are conducted for various fuel premixing ratio of gasoline/methanol-diesel at different engine load, diesel fuel injection timing and compression ratios. Differential mobility spectrometer based particle sizer is used for investigation of the soot particle number-size distribution, surface area-size distribution, particle mass-size distribution and total particle number concentration from the engine exhaust at various test conditions. Results revealed that total particle number concentration is higher at full engine load and increases with fuel premixing ratio (especially in case of methanol-diesel dual fuel operation). Additionally, the peak particle number and mass concentration reduces with an increase in compression ratio of the engine. [ABSTRACT FROM AUTHOR]

High-momentum jets, which are the key parameter to achieve moderate or intense low-oxygen dilution (MILD) combustion may lead to insufficient residence time and high CO emissions, especially for furnaces with a forward-flow configuration. A reflector for application in the furnace was proposed by two-dimensional numerical simulations to reduce the CO emissions and maintain low NOx emissions. The prediction showed a remarkable agreement with measurements. The effects of the reflector height H, the excess air factor λ (changes in the inlet methane-mass flow rate), and the hydrogen content in the blended gas were investigated. The numerical results indicate that the reflector blocks the reactant's flow, intensifies the combustion before it, and prolongs the residence time of flue gases both before and behind it. The added hydrogen in methane can intensify combustion, increase reaction temperature and NO emissions, and reduce CO emissions. The reaction rates of thermal, prompt, NNH, and N2O-intermediate routes increase with the decrease of λ. The addition of hydrogen decreases the rate of the prompt route, but the rates of NNH and thermal routes increase. MILD combustion is achieved under the reflector conditions, considering the nearly uniform temperature distribution and the low pollutants. [ABSTRACT FROM AUTHOR]

Temperature is an important factor governing the community traits of N 2 O-emission related functional guilds (mainly autotrophic ammonia oxidizers and heterotrophic denitrifiers) and their activities. However, there have been few attempts to explore the broad response patterns of these guilds to temperature changes across arable soils. For this, a temperature-controlled (15, 25 and 35 °C) microcosm experiment was conducted using three arable soils (Fujian, Gansu, and Jiangsu) in China under two different fertilizations (no fertilization control (CK) and inorganic fertilization (NPK)). In conjunction with the measurement of N 2 O emission, the community structure and abundance of ammonia oxidizing archaea (AOA) and bacteria (AOB), as well as nirS - and nirK -denitrifiers were assessed using T-RFLP and quantitative PCR, respectively. The analysis of community traits indicated a consistent response pattern of AOAs to temperature in terms of guild abundance, and a consistent effect of inorganic fertilization on the abundance of AOBs, but soil-dependent response patterns to fertilization and temperature were found for nirS - and nirK -denitrifiers in terms of abundance and community structure. The correlation analysis suggested that AOAs possibly assumed a role in N 2 O emission in all the tested soils, and nirS -denitrifiers probably participated in N 2 O emission in both the Fujian and Gansu soil, while a considerable amount of N 2 O emission in the Jiangsu soil might have been derived from heterotrophic nitrification. [ABSTRACT FROM AUTHOR]

Maximizing NO3− uptake during seedling development is important as it has a major influence on plant growth and yield. However, little is known about the processes leading to, and involved in, the initiation of root NO3− uptake capacity in developing seedlings. This study examines the physiological processes involved in root NO3− uptake and metabolism, to gain an understanding of how the NO3− uptake system responds to meet demand as maize seedlings transition from seed N use to external N capture. The concentrations of seed-derived free amino acids within root and shoot tissues are initially high, but decrease rapidly until stabilizing eight days after imbibition (DAI). Similarly, shoot N% decreases, but does not stabilize until 12-13 DAI. Following the decrease in free amino acid concentrations, root NO3− uptake capacity increases until shoot N% stabilizes. The increase in root NO3− uptake capacity corresponds with a rapid rise in transcript levels of putative NO3− transporters, ZmNRT2.1 and ZmNRT2.2. The processes underlying the increase in root NO3− uptake capacity to meet N demand provide an insight into the processes controlling N uptake. [ABSTRACT FROM AUTHOR]

It is challenging to reduce the nitrogen oxides (NO x ) in diesel engine exhaust due to the inhibiting effect of excess oxygen. In this study, a novel electrochemical deNO x system was developed, which eliminated the need for additional reducing materials or a sophisticated controlling system as used in current diesel after-treatment techniques. The electrochemical system consisted of an electrochemical cell modified with NO x adsorbents and a diesel oxidation catalyst placed upstream of the cell. The system offers highly selective NO x reduction and a strong resistance to oxygen interference with almost zero emission of secondary pollutants. [ABSTRACT FROM AUTHOR]

Background: Short-term exposure to air pollution is associated with morbidity and mortality. Metabolites are intermediaries in biochemical processes, and associations between air pollution and metabolites can yield unique mechanistic insights.Methods: We used independent cross-sectional samples with targeted metabolomics (138 metabolites across five metabolite classes) from three cohort studies, each a part of the Cooperative Health Research in the Region of Augsburg (KORA). The KORA cohorts are numbered (1 to 4) according to which survey they belong to, and lettered S or F according to whether the survey was a baseline or follow-up survey. KORA F4 (N = 3044) served as our discovery cohort, with KORA S4 (N = 485) serving as the primary replication cohort. KORA F4 and KORA S4 were primarily fasting cohorts. We used the non-fasting KORA F3 (N = 377) cohort to evaluate replicated associations in non-fasting individuals, and we performed a random effects meta-analysis of all three cohorts. Associations between the 0-4-day lags and the 5-day average of particulate matter (PM)2.5, NO2 and ozone were modelled via generalized additive models. All air pollution exposures were scaled to the interquartile range, and effect estimates presented as percent changes relative to the geometric mean of the metabolite concentration (ΔGM).Results: There were 10 discovery cohort associations, of which seven were lysophosphatidylcholines (LPCs); NO2 was the most ubiquitous exposure (5/10). The 5-day average NO2-LPC(28:0) association was associated at a Bonferroni corrected P-value threshold (P < 1.2x10-4) in KORA F4 [ΔGM = 11.5%; 95% confidence interval (CI) = 6.60, 16.3], and replicated (P < 0.05) in KORA S4 (ΔGM = 21.0%; CI = 4.56, 37.5). This association was not observed in the non-fasting KORA F3 cohort (ΔGM = -5.96%; CI = -26.3, 14.3), but remained in the random effects meta-analysis (ΔGM = 10.6%; CI = 0.16, 21).Conclusions: LPCs are associated with short-term exposure to air pollutants, in particular NO2 Further research is needed to understand the effect of nutritional/fasting status on these associations and the causal mechanisms linking air pollution exposure and metabolite profiles. [ABSTRACT FROM AUTHOR]

Cucumber is a chilling-sensitive vegetable, which is susceptible to chilling injury during storage and shipment at temperatures below 7–10 °C. MeJA and NO have been shown to be able to induce chilling tolerance, but how they are related and how H 2 O 2 is involved in the chilling responses they trigger remains unclear. Here postharvest application of 10 μM MeJA and 1 mM SNP, a NO donor, significantly reduced chilling injury of cucumbers stored at 5 °C. MeJA and SNP reduced H 2 O 2 in cucumber during storage, suggesting that H 2 O 2 may not function as a second messenger in chilling responses activated by MeJA or NO, and that, both MeJA and NO alleviated CI by inhibiting H 2 O 2 generation. This is confirmed by the evidence that diphenylene iodonium further strengthened the chilling tolerance induced by MeJA or SNP. The lower H 2 O 2 induced by MeJA and NO was coincident with enhanced catalase activity and gene expression, suggesting that CAT played an important role in control of H 2 O 2 accumulation. Two more independent experiments showed that, L-NAME and cPTIO, inhibitors of endogenous NO accumulation, significantly compromised MeJA-induced chilling tolerance, but IBU and SHAM, inhibitors of endogenous jasmonic acids biosynthesis, did not affect the chilling tolerance activated by SNP, suggesting MeJA may function upstream of and depend on NO in the signaling pathway that activates chilling tolerance in cucumber. [ABSTRACT FROM AUTHOR]

Conventional inhaled NO systems deliver NO by synchronized injection or continuous NO flow in the ventilator circuitry. Such methods can lead to variable concentrations during inspiration that may differ from desired dosing. NO concentrations in these systems are generally monitored through electrochemical methods that are too slow to capture this nuance and potential dosing error. A novel technology that reduces NO 2 into NO via low-resistance ascorbic-acid cartridges just prior to inhalation has recently been described. The gas volume of these cartridges may enhance gas mixing and reduce dosing inconsistency throughout inhalation. The impact of the ascorbic-acid cartridge technology on NO concentration during inspiration was characterized through rapid chemiluminescence detection during volume control ventilation, pressure control ventilation, synchronized intermittent mandatory ventilation and continuous positive airway pressure using an in vitro lung model configured to simulate the complete uptake of NO. Two ascorbic acid cartridges in series provided uniform and consistent dosing during inspiration during all modes of ventilation. The use of one cartridge showed variable inspiratory concentration of NO at the largest tidal volumes, whereas the use of no ascorbic acid cartridge led to highly inconsistent NO inspiratory waveforms. The use of ascorbic acid cartridges also decreased breath-to-breath variation in SIMV and CPAP ventilation. The ascorbic-acid cartridges, which are designed to convert NO 2 (either as substrate or resulting from NO oxidation during injection) into NO, also provide the benefit of minimizing the variation of inhaled NO concentration during inspiration. It is expected that the implementation of this method will lead to more consistent and predictable dosing. [ABSTRACT FROM AUTHOR]

This is the first study to show that polyamine spermine, a low-molecular-weight nitrogen-containing compound, can induce autophagy in plants. This process is accompanied by an increased generation of reactive oxygen species and nitric oxide, which play a signal role and are required for triggering autophagy. [ABSTRACT FROM AUTHOR]

2,6-Bis(benzimidazol-2-yl)pyridine was shown to exhibit potent anionophoric activity via a process of both Cl − /NO 3 − antiport and H + /Cl − symport. This is in sharp contrast to the finding that its corresponding N -methylated analog exhibited negligible activity and reveals the importance of the imidazolyl-N H fragments in the anion-transport process. [ABSTRACT FROM AUTHOR]

Tetrahydrobiopterin (BH 4 ) represents a potential strategy for the treatment of cardiac remodeling, fibrosis and/or diastolic dysfunction. The effects of oral treatment with BH 4 (Sapropterin™ or Kuvan™) are however dose-limiting with high dose negating functional improvements. Cardiomyocyte-specific overexpression of GTP cyclohydrolase I (mGCH) increases BH 4 several-fold in the heart. Using this model, we aimed to establish the cardiomyocyte-specific responses to high levels of BH 4 . Quantification of BH 4 and BH 2 in mGCH transgenic hearts showed age-based variations in BH 4 :BH 2 ratios. Hearts of mice (<6 months) have lower BH 4 :BH 2 ratios than hearts of older mice while both GTPCH activity and tissue ascorbate levels were higher in hearts of young than older mice. No evident changes in nitric oxide (NO) production assessed by nitrite and endogenous iron–nitrosyl complexes were detected in any of the age groups. Increased BH 4 production in cardiomyocytes resulted in a significant loss of mitochondrial function. Diminished oxygen consumption and reserve capacity was verified in mitochondria isolated from hearts of 12-month old compared to 3-month old mice, even though at 12 months an improved BH 4 :BH 2 ratio is established. Accumulation of 4-hydroxynonenal (4-HNE) and decreased glutathione levels were found in the mGCH hearts and isolated mitochondria. Taken together, our results indicate that the ratio of BH 4 :BH 2 does not predict changes in neither NO levels nor cellular redox state in the heart. The BH 4 oxidation essentially limits the capacity of cardiomyocytes to reduce oxidant stress. Cardiomyocyte with chronically high levels of BH 4 show a significant decline in redox state and mitochondrial function. [ABSTRACT FROM AUTHOR]

Panax notoginseng (Burk) F. H. Chen is a traditional medicinal herb in China. However, the high capacity of its roots to accumulate cadmium (Cd) poses a potential risk to human health. Although there is some evidence for the involvement of nitric oxide (NO) in mediating Cd toxicity, the origin of Cd-induced NO and its function in plant responses to Cd remain unknown. In this study, we examined NO synthesis and its role in Cd accumulation in P. notoginseng roots. Cd-induced NO production was significantly decreased by application of the nitrate reductase inhibitor tungstate but not the nitric oxide synthase inhibitor L-NAME (N G -methyl- l -arginine acetate), indicating that nitrate reductase is the major contributor to Cd-induced NO production in P. notoginseng roots. Under conditions of Cd stress, sodium nitroprusside (SNP, an NO donor) increased Cd accumulation in root cell walls but decreased Cd translocation to the shoot. In contrast, the NO scavenger cPTIO (2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide) and tungstate both significantly decreased NO-increased Cd retention in root cell walls. The amounts of hemicellulose 1 and pectin, together with pectin methylesterase activity, were increased with the addition of SNP but were decreased by cPTIO and tungstate. Furthermore, increases or decreases in hemicellulose 1 and pectin contents as well as pectin methylesterase activity fit well with the increased or decreased retention of Cd in the cell walls of P. notoginseng roots. The results suggest that nitrate reductase-mediated NO production enhances Cd retention in P. notoginseng roots by modulating the properties of the cell wall. [ABSTRACT FROM AUTHOR]

We revealed an immediate and hours-lasting particular NO-specific parallel miotic effect of L-NAME and L-arginine in rats and guinea pigs and a stable gastric pentadecapeptide BPC 157 157-particular effect vs. that of atropine-induced mydriasis while examining the NO system role in the normal pupils responses and pupils with atropine-induced mydriasis. We also assessed the responses to BPC 157 and its possible modulation of the changes caused by L-NAME/L-arginine and atropine. We administered locally (two drops/eye) or systemically (intraperitoneally/kg) [BPC 157 (0.4 µg/eye; 10 µg, 10 ng, 10 pg/kg), L-NAME (0.1 mg/eye; 5 mg/kg), and L-arginine (2 mg/eye; 100 mg/kg) alone and combined] at 3 min prior to assessment (normal pupils) or alternatively at maximal 1% atropine-induced mydriasis (30 min after two drops were administered to each eye). L-NAME/L-arginine. Normal pupil. L-NAME-miosis and L-arginine-miosis shortened and attenuated each other's responses when combined (L-NAME+L-arginine) (except with guinea pigs treated locally) and were thereby NO-specific. Atropine-pupil. Both L-NAME and L-arginine counteracted atropine-induced mydriasis. With few exceptions, the atropine+L-NAME+L-arginine-animals showed a consistent shift toward the left. BPC 157. Normal pupil. Always, BPC 157 alone (both species; locally; systemically; all regimens) did not affect normal pupils. Despite specific exceptions, BPC 157 distinctively affects L-arginine-miosis (prolongation) and L-NAME-miosis (shortening). When L-arginine and L-NAME were combined (L-NAME+L-arginine+BPC 157), the effect was less pronounced. Atropine-pupil. BPC 157 alone counteracted atropine-induced mydriasis. With few exceptions (when administered with L-NAME or L-arginine or L-NAME+L-arginine), BPC 157 augments their counteracting effects. Thus, along with its l-NAME/L-arginine effects, BPC 157 participates in ocular control, potentially via NO-mediated and cholinergic mechanisms. [ABSTRACT FROM AUTHOR]

During ischemia/reperfusion (IR), increased activation of angiotensin AT 1 receptors recruits NADPH oxidase 2 (NOX2) which contributes to oxidative stress. It is unknown whether this stimulus can induce oxidative activation of Ca 2+ /calmodulin-dependent protein kinase IIδ (CaMKIIδ) leading into the aggravation of cardiac function and whether these effects can be prevented by angiotensin AT 1 receptors blockade. Losartan, a selective AT 1 blocker, was used. Its effects were compared with effects of KN-93, an inhibitor of CaMKIIδ. Global IR was induced in Langendorff-perfused rat hearts. Protein expression was evaluated by immunoblotting and lipoperoxidation was measured by TBARS assay. Losartan improved LVDP recovery by 25%; however, it did not reduce reperfusion arrhythmias. Oxidized CaMKIIδ (oxCaMKIIδ) was downregulated at the end of reperfusion compared to before ischemia and losartan did not change these levels. Phosphorylation of CaMKIIδ mirrored the pattern of changes in oxCaMKIIδ levels. Losartan did not prevent the higher lipoperoxidation due to IR and did not influence NOX2 expression. Inhibition of CaMKII ameliorated cardiac IR injury; however, this was not accompanied with changes in the levels of either active form of CaMKIIδ in comparison to the angiotensin AT 1 receptor blockade. In spite of no changes of oxCaMKIIδ, increased cardiac recovery of either therapy was abolished when combined together. This study showed that oxidative activation of CaMKIIδ is not elevated at the end of R phase. NOX2-oxCAMKIIδ signaling is unlikely to be involved in cardioprotective action of angiotensin AT 1 receptor blockade which is partially abolished by concomitant CaMKII inhibition. [ABSTRACT FROM AUTHOR]

Identifying the rates of nitrate absorption by almond plants under water stress is important for improving nitrogen use efficiency in almond orchards. This study aimed to determine the rates of nitrate absorption by almond plants subjected to short-term water stress and no water stress, and the kinetic NO 3 − absorption parameters in well-watered three-year-old almond plants. Two assays were performed. In the first, fourteen plants arranged in completely randomized design received nutrient solutions with water potentials (Ψ w ) of 0.0, −0.2, −0.4 and −0.7 MPa and containing 1.2 mmol l −1 KNO 3 . We accessed the NO 3 − depletion in these solutions over an 8-h interval and estimated regression curves of the quantity of nitrate in the nutrient solution ( Q ) as a function of time ( t ). Subsequently nitrate uptake rates were calculated. Water loss; nitrate reductase activity; nitrate and total N of the sap; nitrate concentration of leaf dry matter; and nitrate and nitrite concentration of root dry matter were, either, evaluated. The second assay was performed the same way of the first one, with four well-watered plants submitted to 0.3 mmol l −1 KNO 3 as initial concentration, and allowed estimating NO 3 − absorption parameters V max , K m and C min . We observed a linear decrease in the nitrate content of the containers receiving 1.2 mmol l −1 of NO 3 − over a period of 8 h. In this concentration, the rates of NO 3 − uptake ranged from 1.11 to 3.43 μmol g −1 h −1 and decreased in low water potentials at the root medium. Root nitrate reductase activity followed the same trend of nitrate absorption. In the low NO 3 − concentration range, the absorption showed a Michaelis–Menten pattern, being the kinetic parameters of NO 3 − absorption 1.15 ± 0.27 μmol g −1 h −1 , 28.81 ± 4.12 μmol l −1 and 17.93 ± 1.1 μmol l −1 for V max , K m , and C min , respectively. We concluded that NO 3 − uptake of almonds is affected by short periods of water stress, with harmful effects occurring at Ψ w below −0.18 MPa. [ABSTRACT FROM AUTHOR]

Encephalomyocarditis virus (EMCV) infection of macrophages results in the expression of a number of inflammatory and antiviral genes, including inducible NO synthase (iNOS) and cyclooxygenase (COX)-2. EMCV-induced macrophage activation has been shown to require the presence of CCR5 and the activation of PI3K-dependent signaling cascades. The purpose of this study was to determine the role of PI3K in regulating the macrophage responses to EMCV. We show that PI3K regulates EMCV-stimulated iNOS and COX-2 expression by two independent mechanisms. In response to EMCV infection, Akt is activated and regulates the translation of iNOS and COX-2 through the mammalian target of rapamycin complex (mTORC)1. The activation of mTORC1 during EMCV infection is CCR5-dependent and appears to function in a manner that promotes the translation of iNOS and COX-2. CCR5-dependent mTORC1 activation functions as an antiviral response, as mTORC1 inhibition increases the expression of EMCV polymerase. PI3K also regulates the transcriptional induction of iNOS and COX-2 in response to EMCV infection by a mechanism that is independent of Akt and mTORC1 regulation. These findings indicate that macrophage expression of the inflammatory genes iNOS and COX-2 occurs via PI3K- and Akt-dependent translational control of mTORC1 and PI3K-dependent, Akt-independent transcriptional control. [ABSTRACT FROM AUTHOR]

A laboratory and field experiment compared fluxes of CO 2 , CH 4 and N 2 O measured with cavity ring-down spectroscopy (CRDS) and gas chromatography (GC). The comparison between CRDS and GC showed that average CO 2 fluxes were significantly higher for CRDS in both the laboratory and field, but the same experimental treatments effects were detected for both techniques. Compared to CRDS, the GC technique was severely limited in detecting CH 4 fluxes in both the laboratory and field. Thus, only 16% of measured GC fluxes were detectable in the laboratory and none in the field whereas CRDS could detect 65% and 97% of the CH 4 fluxes in the laboratory and field. In contrast, N 2 O fluxes measured with CRDS and GC were not different for both the laboratory and field. It was observed that a lower proportion of N 2 O fluxes could be detected with CRDS (73%) than GC (92%) in the laboratory and similar recovery (65% and 68%) for the field. Thus, the same treatment effects were observed for both CRDS and GC. Furthermore, the comparison between CRDS and GC showed that enclosure times as short as 600 s for our field study site are suitable to estimate the same treatment effects, but not necessarily flux magnitude. We conclude that CRDS and GC can provide the same level of information regarding treatment effects in both laboratory and field experiments for CO 2 and N 2 O, but not for CH 4 and it is possible to reduce enclosure time without comprising comparability between the two techniques. [ABSTRACT FROM AUTHOR]

Thrombosis is the main outcome of many cardiovascular diseases. Current treatments to prevent thrombotic events involve the long-term use of antiplatelet drugs. However, this therapy has several limitations, thereby justifying the development of new drugs. A series of N-oxide derivatives (furoxan and benzofuroxan) were synthesized and characterized as potential antiplatelet/antithrombotic compounds. All compounds (3a,b, 4a,b, 8a,b, 9a,b, 13a,b and 14a,b) inhibited platelet aggregation induced by adenosine-5-diphosphate, collagen, and arachidonic acid. All compounds protected mice from pulmonary thromboembolism induced by a mixture of collagen and epinephrine; however, benzofuroxan derivatives (13a,b and 14a,b) were the most active compounds, reducing thromboembolic events by up to 80%. N-oxide derivative 14a did not induce genotoxicity in vivo. In conclusion, 14a has emerged as a new antiplatelet/antithrombotic prototype useful for the prevention of atherothrombotic events. [ABSTRACT FROM AUTHOR]

Exposure to road traffic noise, fine particulate matter (aerodynamic diameter ≤2.5 μm; PM 2.5 ) and nitrogen oxides (NO x ) has been associated with transient changes in blood pressure, but whether an interaction exists remains unclear. This panel study investigated whether noise, PM 2.5 and NO x exposure were independently associated with changes in 24-h ambulatory blood pressure. We recruited 33 males and 33 females aged 18–32 years as study subjects. Personal noise exposure and ambulatory blood pressure were monitored simultaneously in 2007. During the data collection periods, 24-h data on PM 2.5 and NO x from five air-quality monitors within 6 km of participants' home addresses were used to estimate their individual exposures. Linear mixed-effects regression models were used to estimate single and combined effects on ambulatory blood pressure. Exposure to both noise and PM 2.5 was significantly associated with increased systolic blood pressure (SBP) and diastolic blood pressure (DBP) over 24 h; NO x exposure was only significantly related to elevated DBP. Twenty-four-hour ambulatory blood pressure increased with the current noise exposure of 5 A-weighted decibels (dBA) (SBP 1.44 [95% confidence interval: 1.16, 1.71] mmHg and DBP 1.40 [1.18, 1.61] mmHg) and PM 2.5 exposure of 10-µg/m 3 (SBP 0.81 [0.19, 1.43] mmHg and DBP 0.63 [0.17, 1.10] mmHg), as well as the current NO x exposure of 10-ppb (DBP 0.54 [0.12, 0.97] mmHg) after simultaneous adjustment. These findings suggest that exposure to noise and air pollutants may independently increase ambulatory blood pressure and the risk of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Fall armyworm, Spodoptera frugiperda (J.E. Smith) is a polyphagous insect with natural resistance to insecticide; various strategies have been used for its control. Novel compounds derived from N-oxide have low toxicity to humans but are biologically activity against bacteria, fungi, parasites, and even insects. Five Noxide derivatives (QX1, QX2, QX3, QX4, and QX5) were evaluated through diet and spray assays to determine toxic activity and most-effective administration route in three Mexican populations of S. frugiperda. Larvae were collected from fields of maize, Zea mays L., in three regions of Mexico: Mante, Tamaulipas (Northeast); Durango, Durango (Northwest); and Tapachula, Chiapas (Southern). The three Mexican populations were sensitive to QX5 (benzofuroxan N-oxide derivative) that when ingested killed 100% of larvae, and had variable sensitivity to quinoxaline 1,4- di-N-oxide derivatives that negatively affected growth of larvae. Ingested QX2, QX3, and QX4 most inhibited growth (54-64%) of the Mante population. QX3 most inhibited growth (almost 90%) of the Tapachula population, and QX1 inhibited growth of 91% of the larvae in the Durango population. With topical application, all compounds killed less than 10% of the larvae, and only QX2 and QX3 inhibited growth of 31% of fall armyworm larvae from the Durango population. Benzofuroxane killed most and quinoxalines caused variation in growth inhibition of fall armyworm larvae; in both cases, ingestion was most effective in killing larvae. The benzofuroxan N-oxide derivative might have good potential for development of safer and more effective insecticides against this pest. [ABSTRACT FROM AUTHOR]

Background: Air quality degraded by black smoke (particulate matter, PM10), sulphur dioxide (SO2) and nitrogen oxide (NOx) affects human health. Improvements following national legislation have lowered death rates. Whether background air pollution levels continue to affect human health remains unclear.Aim: To determine impact of air pollutant concentrations (PM10, SO2 and NOx) on in-hospital mortality for acute medical admissions to St James’s Hospital over a decade (2002–11).Design: All emergency admissions (55 596 episodes in n = 32 581 patients) were tracked prospectively and mortality assessed. Daily levels of PM10, SO2 and NOx were obtained from monitoring stations in our catchment area.Methods: Univariate and multivariate logistic regression was employed to examine relationships between pollutant concentration and odds ratio (OR) for death following adjustment for other mortality predictors.Results: Mortality related to each pollutant variable assessed (as quintiles of increasing atmospheric concentration) was significantly predictive. For PM10 and SO2, mortality in the highest three quintile concentrations (compared with base quintile) was significantly increased (P < 0.001) with univariate ORs of 1.24, 1.36 and 1.25 for PM10 and 1.43, 1.54 and 1.58 for SO2, respectively. Mortality in all quintile concentrations (compared with base quintile) was significantly increased (P < 0.05) for NOx with univariate ORs of 1.14, 1.18, 1.28 and 1.35, respectively. Following adjustment for other mortality predictors such as acute illness severity, all three air pollutants were independently predictive of mortality.Conclusion: Despite improvement to air quality in Dublin, the prevailing background pollutant concentrations continue to affect human health at levels considered safe and below that previously recognized. [ABSTRACT FROM PUBLISHER]

Thedetailed mechanism of CO-induced N–N bond cleavage ofN2O mediated by molybdenum complexes leading to the nitrosylisocyanate complex has been investigated via density functional theory(DFT) calculations at the B3LYP level. On the basis of the calculations,we proposed a new reaction mechanism of CO-induced N–N bondcleavage of N2O with an overall free energy barrier of23.6 kcal/mol, significantly lower than that of the reaction mechanism(42.2 kcal/mol) proposed by Sita et al. The calculations also indicatedthat CO-induced N–N bond cleavage of N2O is competitivewith oxygen atom transfer (OAT) to carbon monoxide due to the comparablefree energy barriers. The metal-bound carbonyl complex obtained fromOAT can be recycled to give more nitrosyl isocyanate complexes. Inaddition, we demonstrated why the analogous tungsten complex cannotgive the nitrosyl isocyanate complex via CO-induced N–N bondcleavage of N2O. The calculations are consistent with experimentalobservations. [ABSTRACT FROM AUTHOR]

Abstract: Little is known about whether trans-isoferulic acid (TIA) regulates the production of lipopolysaccharide (LPS)-induced proinflammatory mediators. Therefore, we examined the effect of TIA isolated from Clematis mandshurica on LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in BV2 microglial cells. We found that TIA inhibited the production of LPS-induced NO and PGE2 without accompanying cytotoxicity in BV2 microglial cells. TIA also downregulated the expression levels of specific regulatory genes such as inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) by suppressing LPS-induced NF-κB activity via dephosphorylation of PI3K/Akt. In addition, we demonstrated that a specific NF-κB inhibitor PDTC and a selective PI3K/Akt inhibitor, LY294002 effectively attenuated the expression of LPS-stimulated iNOS and COX-2 mRNA, while LY294002 suppressed LPS-induced NF-κB activity, suggesting that TIA attenuates the expression of these proinflammatory genes by suppressing PI3K/Akt-mediated NF-κB activity. Our results showed that TIA suppressed NO and PGE2 production through the induction of nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent heme oxygenase-1 (HO-1). Taken together, our data indicate that TIA suppresses the production of proinflammatory mediators such as NO and PGE2, as well as their regulatory genes, in LPS-stimulated BV2 microglial cells, by inhibiting PI3K/Akt-dependent NF-κB activity and enhancing Nrf2-mediated HO-1 expression. [Copyright &y& Elsevier]

We have explored species-specific preferences for nitrate (NO) and ammonium (NH) as an alternative niche separation in ecosystems where nitrogen (N) is present mostly in inorganic forms. The Patagonian steppe is dominated by shrubs and grasses. Shrubs absorb water and nutrients from deep soil layers, which are poor in N, while grasses have the opposite pattern, absorbing most of their water and nutrients from the upper layers of the soil. We hypothesized that the preferences of shrub and grass for inorganic N forms are different and that the rate of potential N uptake is greater in shrubs than in grasses. To test this hypothesis, we grew individuals of six dominant species in solutions of different NH:NO concentration ratios. Nitrate uptake was found to be higher in shrubs, while ammonium uptake was similar between plant functional types. The NH:NO uptake ratio was significantly lower for shrubs than grasses. Shrubs, which under field conditions have deeper rooting systems than grasses, showed a higher N absorption capacity than grasses and a preference for the more mobile N form, nitrate. Grasses, which had lower N uptake rates than shrubs, preferred ammonium over nitrate. These complementary patterns between grasses and shrubs suggest a more thorough exploitation of resources by diverse ecosystems than those dominated by just one functional type. The loss of one plant functional group or a significant change in its abundance would therefore represent a reduction in resource use efficiency and ecosystem functioning. [ABSTRACT FROM AUTHOR]

Abstract: Endothelial dysfunction causes an imbalance in endothelial NO and O2 − production rates and increased peroxynitrite formation. Peroxynitrite and its decomposition products cause multiple deleterious effects including tyrosine nitration of proteins, superoxide dismutase (SOD) inactivation, and tissue damage. Studies have shown that peroxynitrite formation during endothelial dysfunction is strongly dependent on the NO and O2 − production rates. Previous experimental and modeling studies examining the role of NO and O2 − production imbalance on peroxynitrite formation showed different results in biological and synthetic systems. However, there is a lack of quantitative information about the formation and biological relevance of peroxynitrite under oxidative, nitroxidative, and nitrosative stress conditions in the microcirculation. We developed a computational biotransport model to examine the role of endothelial NO and O2 − production on the complex biochemical NO and O2 − interactions in the microcirculation. We also modeled the effect of variability in SOD expression and activity during oxidative stress. The results showed that peroxynitrite concentration increased with increase in either O2 − to NO or NO to O2 − production rate ratio (Q O2 −/Q NO or Q NO/Q O2 −, respectively). The peroxynitrite concentrations were similar for both production rate ratios, indicating that peroxynitrite-related nitroxidative and nitrosative stresses may be similar in endothelial dysfunction or inducible NO synthase (iNOS)-induced NO production. The endothelial peroxynitrite concentration increased with increase in both Q O2 −/Q NO and Q NO/Q O2 − ratios at SOD concentrations of 0.1–100μM. The absence of SOD may not mitigate the extent of peroxynitrite-mediated toxicity, as we predicted an insignificant increase in peroxynitrite levels beyond Q O2 −/Q NO and Q NO/Q O2 − ratios of 1. The results support the experimental observations of biological systems and show that peroxynitrite formation increases with increase in either NO or O2 − production, and excess NO production from iNOS or from NO donors during oxidative stress conditions does not reduce the extent of peroxynitrite mediated toxicity. [Copyright &y& Elsevier]

Introduction: Air pollution occurs when the concentration of certain substances (pollutants) reaches a size which causes its toxicity, or in other words, begins to cause harm to human health, flora and wildlife. Methods: Measurements were performed in the period from 2005 to 2010, at the measuring point Bjelave-Sarajevo by the method of Griess-Saltzmann. It encompasses the following parameters: NO, NO2, NOx, measured concentrations of pollutants in the atmosphere reduced to normal atmospheric conditions of 293 K (Kelvin) and pressure of 101.3 kPa (kilopascal). Results: NO concentration in the period from 2005 to 2008 was above the permitted value, but the results of research in the period between 2009 and 2010, have shown that there was a decrease in NO concentration in the atmosphere. Measurements show that the concentration of this pollutant is currently declining, which is a positive result compared to the pollution of the atmosphere by nitrogen monoxide. Furthermore, the results of the research showed that the concentration of NO2 for the period of 2005 to 2010, is in the limited values, and that has a decreasing trend, which is also a positive result compared to the pollution of the atmosphere by nitrogen dioxide. Related to the total concentration of NOx in the atmosphere, the results of the research show that their representation corresponds to the limit values existing in the Rulebook on limit values for air quality. Conclusion: The results of the research for the pollution of the atmosphere by nitrogen oxides in the investigated area show that the amount of nitrogen oxides in the atmosphere is in constant decline. [ABSTRACT FROM AUTHOR]

Abstract: This study investigated the in vitro effects of nitrite on reactive oxygen species (ROS) production, NO production, esterase activity and cell apoptosis of Penaeus monodon haemocytes. Haemocytes were in vitro exposed to different dose of nitrite (0, 0.1, 0.5, 1, 5 and 10μM). Cellular responses of nitrite-treated haemocytes were determined by flow cytometry. The results revealed that haemocytes treated by nitrite in vitro showed conspicuous time- and dose-dependent decreases in ROS and NO production as well as esterase activity. Additionally, 0.1 and 0.5μM nitrite did not affect the apoptotic cell ratio during the 3h experimental time, while significant increases in apoptotic cells were observed after haemocyte exposure to nitrite at 1μM for 3h, and at 5 or 10μM for 1h. These results indicated that nitrite suppresses cellular functions, including production of ROS and NO, and activity of esterase. Cell apoptosis of haemocytes would be induced by extracellular nitrite as doses exceed 1μM. [Copyright &y& Elsevier]

Background Short-term exposure to air pollution can trigger hospital admissions for asthma in children, but it is not known which components of air pollution are most important. There are no available studies on the particular effect of ultrafine particles (UFPs) on paediatric admissions for asthma. Aim To study whether short-term exposure to air pollution is associated with hospital admissions for asthma in children. It is hypothesised that (1) the association between asthma admissions and air pollution is stronger with UFPs than with coarse (PM10) and fine (PM2.5) particles, nitrogen oxides (NOx) or nitrogen dioxide (NO2); and (2) infants are more susceptible to the effects of exposure to air pollution than older children. Method Daily counts of admissions for asthma in children aged 0-18 years to hospitals located within a 15 km radius of the central fixed background urban air pollution measurement station in Copenhagen between 2001 and 2008 were extracted from the Danish National Patient Registry. A time-stratified case crossover design was applied and data were analysed using conditional logistic regression to estimate the effect of air pollution on asthma admissions. Results A significant association was found between hospital admissions for asthma in children aged 0-18 years and NOx (OR 1.11; 95% CI 1.05 to 1.17), NO2 (1.10; 95% Cl 1.04 to 1.16), PM10 (1.07; 95% CI 1.03 to 1.12) and PM2.5 (1.09; 95% CI 1.04 to 1.13); there was no association with UFPs. The association was stronger in infants than in older children for all pollutants, but no statistically significant interaction was detected. Conclusion Short-term exposure to air pollution can trigger hospital admission for asthma in children, with infants possibly being most susceptible. These effects seemed to be mediated by larger particles and trafficrelated gases, whereas UFPs showed no effect. INSET: Key messages. [ABSTRACT FROM AUTHOR]

Background: Lack of research on the effects of gaseous pollutants (nitrogen oxides [NOx], sulfur dioxide [SO2], carbon monoxide [CO] and ozone [O3]) in the ambient environment on health outcomes from within low and middle income countries (LMICs) is leading to reliance on results from studies performed within high income countries (HICs). This systematic review and meta-analysis examines the cardiorespiratory health effects of gaseous pollutants in LMICs exclusively.Methods: Systematic searching was carried out and estimates pooled by pollutant, lag and outcome, and presented as excess relative risk per 10 μg/m3 (NOx, SO2, O3) or 1 ppm (CO) increase pollutant. Sub-group analysis was performed examining estimates by specific outcomes, city and co-pollutant adjustment.Results: Sixty studies met the inclusion criteria, most (44) from the East Asia and Pacific region. A 10 μg/m3 increase in same day NOx was associated with 0.92% (95% CI: 0.44, 1.39), and 0.70% (0.01, 1.40) increases in cardiovascular and respiratory mortality respectively, same day NOx was not associated with morbidity. Same day sulfur dioxide was associated with 0.73% (0.04, 1.42) and 0.50% (0.01, 1.00) increases in respiratory morbidity and in cardiovascular mortality respectively.Conclusions: Acute exposure to gaseous ambient air pollution (AAP) is associated with increases in morbidity and mortality in LMICs, with greatest associations observed for cardiorespiratory mortality. [ABSTRACT FROM AUTHOR]