988 resultados para NITROUS-OXIDE EMISSIONS


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This work describes the influence of a high annealing temperature of about 700C on the Si(substrate)/Si3N4/TiOx/Pt/LiCoO2 multilayer system for the fabrication of all-solid-state lithium ion thin film microbatteries. Such microbatteries typically utilize lithium cobalt oxide (LiCoO2) as cathode material with a platinum (Pt) current collector. Silicon nitride (Si3N4) is used to act as a barrier against Li diffusion into the substrate. For a good adherence between Si3N4 and Pt, commonly titanium (Ti) is used as intermediate layer. However, to achieve crystalline LiCoO2 the multilayer system has to be annealed at high temperature. This post-treatment initiates Ti diffusion into the Pt-collector and an oxidation to TiOx, leading to volume expansion and adhesion failures. To solve this adhesion problem, we introduce titanium oxide (TiOx) as an adhesion layer, avoiding the diffusion during the annealing process. LiCoO2, Pt and Si3N4 layers were deposited by magnetron sputtering and the TiOx layer by thermal oxidation of Ti layers deposited by e-beam technique. Asdeposited and annealed multilayer systems using various TiOx layer thicknesses were studied by scanning electron microscopy (SEM) and time-of-flight secondary ion mass spectrometry (ToF-SIMS) and x-ray photoelectron spectroscopy (XPS). The results revealed that an annealing process at temperature of 700C leads to different interactions of Ti atoms between the layers, for various TiOx layer thicknesses (25–45 nm).

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OBJECTIVE: To study the healing process of the myocardium in hypertensive rats undergoing inhibition of nitric oxide synthesis. METHODS: Two groups of animals were studied: one received L-NAME, 12mg/kg/day, and the other was a control group. The presence of type III collagen, fibronectin, and alpha-smooth muscle actin-positive cells was assessed by immunohistochemistry. RESULTS: Fibronectin was seen in both early and late lesions, while type III collagen was seen mainly in areas of incomplete healing, situated among myocytes and around the intramyocardial branches of the coronary arteries. Areas representing early and late lesions showed a population of spindle-shaped cells. Immunohistochemistry showed that these cells were positive for alpha-smooth muscle actin. CONCLUSION: In the myocardium of hypertensive rats, the alpha-smooth muscle actin-positive cells are related to the accumulation of type III collagen and fibronectin in the areas of myocardial damage.

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OBJECTIVE: To assess the effect of endogenous estrogens on the bioavailability of nitric oxide (·NO) and in the formation of lipid peroxidation products in pre- and postmenopausal women. METHODS: NOx and S-nitrosothiols were determined by gaseous phase chemiluminescence, nitrotyrosine was determined by ELISA, COx (cholesterol oxides) by gas chromatography, and cholesteryl linoleate hydroperoxides (CE18:2-OOH), trilinolein (TG18:2-OOH), and phospholipids (PC-OOH) by HPLC in samples of plasma. RESULTS: The concentrations of NOx, nitrotyrosine, COx, CE18:2-OOH, and PC-OOH were higher in the postmenopausal period (33.8±22.3 mM; 230±130 nM; 55±19 ng/mL; 17±8.7 nM; 2775±460 nM, respectively) as compared with those in the premenopausal period (21.1±7.3 mM; 114±41 nM; 31±13 ng/mL; 6±1.4 nM; 1635±373 nM). In contrast, the concentration of S-nitrosothiols was lower in the postmenopausal period (91±55 nM) as compared with that in the premenopausal p in the premenopausal period (237±197 nM). CONCLUSION: In the postmenopausal period, an increase in nitrotyrosine and a reduction of S-nitrosothiol formation, as well as an increase of COx, CE18:2-OOH and PC-OOH formation occurs. Therefore, •NO inactivation and the increase in lipid peroxidation may contribute to endothelial dysfunction and to the greater risk for atherosclerosis in postmenopausal women.

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OBJECTIVE: To determine whether arginine vasopressin releases endothelium-derived nitric oxide (EDNO) from the epicardial coronary artery. METHODS: We studied segments of canine left circumflex coronary arteries suspended in organ chambers to measure isometric force. The coronary artery segments were contracted with prostaglandin F2alpha (2 x 10-6M) and exposed to a unique, strong arginine vasopressin concentration (10-6M) or titrated concentrations (10-9 a 10-5 M). RESULTS: The unique dose of arginine vasopressin concentration (10-6M) induced transient, but significant (p<0.05), relaxation in arterial segments with endothelium, and an increase, not significant, in tension in arteries without endothelium. Endothelium-dependent relaxation to arginine vasopressin was inhibited by Ng-monomethyl-L-arginine (L-NMMA, 10-5M) or N G-nitro-L-arginine (L-NOARG) (10-4M), 2 inhibitors of nitric oxide synthesis from L-arginine. Exogenous L-arginine (10-4M), but not D-arginine (10-4M), reversed the inhibitory effect of L-NMMA on vasopressin-mediated vasorelaxation. Endothelium dependent relaxation to vasopressin was also reversibly inhibited by the vasopressin V1-receptor blocker d(CH2)5Try(Me) arginine vasopressin (10-6M) (n=6, P<0.05). CONCLUSION: Vasopressin acts through V1 endothelial receptors to stimulate nitric oxide release from L-arginine.

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Background: Ischemic postconditioning (IPost) is a method of protecting the heart against ischemia-reperfusion (IR) injury. However, the effectiveness of IPost in cases of ischemic heart disease accompanied by co-morbidities such as hypothyroidism remains unclear. Objective: The aim of this study was to determine the effect of IPost on myocardial IR injury in hypothyroid male rats. Methods: Propylthiouracil in drinking water (500 mg/L) was administered to male rats for 21 days to induce hypothyroidism. The hearts from control and hypothyroid rats were perfused in a Langendorff apparatus and exposed to 30 min of global ischemia, followed by 120 min of reperfusion. IPost was induced immediately following ischemia. Results: Hypothyroidism and IPost significantly improved the left ventricular developed pressure (LVDP) and peak rates of positive and negative changes in left ventricular pressure (±dp/dt) during reperfusion in control rats (p < 0.05). However, IPost had no add-on effect on the recovery of LVDP and ±dp/dt in hypothyroid rats. Furthermore, hypothyroidism significantly decreased the basal NO metabolite (NOx) levels of the serum (72.5 ± 4.2 vs. 102.8 ± 3.7 μmol/L; p < 0.05) and heart (7.9 ± 1.6 vs. 18.8 ± 3.2 μmol/L; p < 0.05). Heart NOx concentration in the hypothyroid groups did not change after IR and IPost, whereas these were significantly (p < 0.05) higher and lower after IR and IPost, respectively, in the control groups. Conclusion: Hypothyroidism protects the heart from IR injury, which may be due to a decrease in basal nitric oxide (NO) levels in the serum and heart and a decrease in NO after IR. IPost did not decrease the NO level and did not provide further cardioprotection in the hypothyroid group.

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Background: Nitric oxide (NO) has been largely associated with cardiovascular protection through improvement of endothelial function. Recently, new evidence about modulation of NO release by microRNAs (miRs) has been reported, which could be involved with statin-dependent pleiotropic effects, including anti-inflammatory properties related to vascular endothelium function. Objective: To evaluate the effects of cholesterol-lowering drugs including the inhibitors of cholesterol synthesis, atorvastatin and simvastatin, and the inhibitor of cholesterol absorption ezetimibe on NO release, NOS3 mRNA expression and miRs potentially involved in NO bioavailability. Methods: Human umbilical vein endothelial cells (HUVEC) were exposed to atorvastatin, simvastatin or ezetimibe (0 to 5.0 μM). Cells were submitted to total RNA extraction and relative quantification of NOS3 mRNA and miRs -221, -222 and -1303 by qPCR. NO release was measured in supernatants by ozone-chemiluminescence. Results: Both statins increased NO levels and NOS3 mRNA expression but no influence was observed for ezetimibe treatment. Atorvastatin, simvastatin and ezetimibe down-regulated the expression of miR-221, whereas miR-222 was reduced only after the atorvastatin treatment. The magnitude of the reduction of miR-221 and miR-222 after treatment with statins correlated with the increment in NOS3 mRNA levels. No influence was observed on the miR-1303 expression after treatments. Conclusion: NO release in endothelial cells is increased by statins but not by the inhibitor of cholesterol absorption, ezetimibe. Our results provide new evidence about the participation of regulatory miRs 221/222 on NO release induction mediated by statins. Although ezetimibe did not modulate NO levels, the down-regulation of miR-221 could involve potential effects on endothelial function.

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Neural nitric oxide synthase, neuroendocrine stress response, forced swimming, nNOS KO mice, hypothalamus, adrenal gland

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Heavy duty Diesel engine, alternative fuels, EGR, exhaust emissions, HC, NOx, FSN

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Extending the traditional input-output model to account for the environmental impacts of production processes reveals the channels by which environmental burdens are transmitted throughout the economy. In particular, the environmental input-output approach is a useful technique for quantifying the changes in the levels of greenhouse emissions caused by changes in the final demand for production activities. The inputoutput model can also be used to determine the changes in the relative composition of greenhouse gas emissions due to exogenous inflows. In this paper we describe a method for evaluating how the exogenous changes in sectorial demand, such as changes in private consumption, public consumption, investment and exports, affect the relative contribution of the six major greenhouse gases regulated by the Kyoto Protocol to total greenhouse emissions. The empirical application is for Spain, and the economic and environmental data are for the year 2000. Our results show that there are significant differences in the effects of different sectors on the composition of greenhouse emissions. Therefore, the final impact on the relative contribution of pollutants will basically depend on the activity that receives the exogenous shock in final demand, because there are considerable differences in the way, and the extent to which, individual activities affect the relative composition of greenhouse gas emissions. Keywords: Greenhouse emissions, composition of emissions, sectorial demand, exogenous shock.

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In a market where firms with different characteristics decide upon both the level of emissions and their reports, we study the optimal audit policy for an enforcement agency whose objective is to minimize the level of emissions. We show that it is optimal to devote the resources primarily to the easiest-to-monitor firms and to those firms that value pollution the less. Moreover, unless the budget for monitoring is very large, there are always firms that do not comply with the environmental objective and others that do comply; but all of them evade the environmental taxes.

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The purpose of this paper is to study the possible differences among countries as CO2 emitters and to examine the underlying causes of these differences. The starting point of the analysis is the Kaya identity, which allows us to break down per capita emissions in four components: an index of carbon intensity, transformation efficiency, energy intensity and social wealth. Through a cluster analysis we have identified five groups of countries with different behavior according to these four factors. One significant finding is that these groups are stable for the period analyzed. This suggests that a study based on these components can characterize quite accurately the polluting behavior of individual countries, that is to say, the classification found in the analysis could be used in other studies which look to study the behavior of countries in terms of CO2 emissions in homogeneous groups. In this sense, it supposes an advance over the traditional regional or rich-poor countries classifications .

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This paper analyses the inequality in CO2 emissions across countries (and groups of countries) and the relationship of this inequality with income inequality across countries for the period (1971-1999). The research employs the tools that are usually applied in income distribution analysis. The methodology used here gives qualitative and quantitative information on some of the features of the inequalities across countries that are considered most relevant for the design and discussion of policies aimed at mitigating climate change. The paper studies the relationship between CO2 emissions and GDP and shows that income inequality across countries has been followed by an important inequality in the distribution of emissions. This inequality has diminished mildly, although the inequality in emissions across countries ordered in the increasing value of income (inequality between rich and poor countries) has diminished less than the “simple” inequality in emissions. Lastly, the paper shows that the inequality in CO2 emissions is mostly explained by the inequality between groups with different per capita income level. The importance of the inequality within groups of similar per capita income is much lower and has diminished during the period, especially in the low-middle income group.

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Here we present an approach that allows the identification of the "key" productive sectors responsible for CO2 emission. For this purpose, we develop an input–output methodology from a supply perspective. We focus on the impact of an increase in the value-added of the different productive sectors on total CO2 emissions and we identify the productive sectors responsible for the increase in CO2 emissions when there is an increase in the income of the economy. The approach shows the contribution of the various sectors to CO2 emission from a production perspective and allows us to identify the sectors that deserve more consideration for mitigation policies. This analysis is complementary to the input–output analysis from a demand perspective. The methodology is applied to the Spanish economy.

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Emissions distribution is a focus variable for the design of future international agreements to tackle global warming. This paper specifically analyses the future path of emissions distribution and its determinants in different scenarios. Whereas our analysis is driven by tools which are typically applied in the income distribution literature and which have recently been applied to the analysis of CO2 emissions distribution, a new methodological approach is that our study is driven by simulations run with a popular regionalised optimal growth climate change model over the 1995-2105 period. We find that the architecture of environmental policies, the implementation of flexible mechanisms and income concentration are key determinants of emissions distribution over time. In particular we find a robust positive relationship between measures of inequalities.