低热值高炉煤气燃气轮机NOx生成研究分析

根据NOx生成原理及影响因素,对比多个同类型机组NOx排放量,可知影响燃机NOx生成的关键因素为燃料型NOx的生成量.依据氮元素守恒,测量FBN含量可计算出燃料型NOx的生成量,与机组排放实际数据基本吻合,并提出了降低此类型机组NOx排放的建议.     

基于带式焙烧机的NOx生成规律研究

带式焙烧机工艺的NOx排放量较高,高值达到400 mg/m3以上,环保排放压力较大.目前对带式焙烧机的NOx排放规律并无系统研究,普遍按锅炉等的排放规律,认为带式焙烧机的NOx排放量由温度决定.通过对数据的分析,揭示煤气流量与NOx排放量的关系,归纳了带式焙烧机NOx,的排放规律,对带式焙烧机NOx排放的控制具有指导意...     

轧钢加热炉采用低氮燃烧法降低NOx排放的改造与实践

新中型轧线建设项目热试发现两座加热炉排放烟气NOx浓度超标,为保证NOx达标排放,研究出低氮燃烧法,通过燃烧器控制燃烧初期NOx的生成.采用空气分级来减少燃料氮转化为NOx,同时通过快速响应自动调节空燃比的控制措施,进一步减少热力型NOx生成.实践表明,改造方案解决了 NOx浓度超标这一问题,满足了国家和地方相关环保标...     

蓄热式辐射管中低NOx燃烧过程的数值模拟

通过数值模拟的方法,建立蓄热式辐射管内低NOx燃烧过程的数学模型,在验证模型正确的基础上,分析了不同低NOx燃烧技术对NOx抑制效果的影响.研究结果为低NOx燃烧器的优化设计提供了理论依据.     

DBS吸附剂治理高浓度NOx的实践

介绍DBS吸附剂净化器治理高浓度NOx的原理和特点,通过对用硝酸溶解银粉制备电解液产生的NOx废气的治理实践表明,采用本工艺治理间断的、阵发性排放的高浓度NOx废气,净化率可以达到98%以上,净化后的废气NOx浓度低于排放标准,工艺设备简单,易操作,对高浓度NOx的治理具有很好的推广及应用价值。     

不同煤种燃烧过程中NOx形成规律的数值模拟与分析

燃煤过程对大气造成的污染正日益引起人们的关注,控制NOx的排放是煤燃烧利用研究中亟需解决的课题.采用数值模拟方法,研究不同煤种在不同燃烧温度下NOx的生成规律,并对燃烧过程中的NOx生成的影响因素及抑制方法进行分析和归纳.结果表明:中挥发分煤(mv)燃烧生成的NOx最多,低挥发分煤(lv)燃烧生成的NOx最少;热力型NOx的生成与温度有直接的关系.因此,缩短燃烧产物在高温区的滞留时间有助于减少NOx的生成,减少反应中氧气的质量浓度能够抑制NOx的生成,其计算结果可为今后的工业性实验提供理论依据.     

顶燃式热风炉高温低氧燃烧技术

 NOx是制约热风炉实现高风温长寿的主要技术障碍。为有效抑制和降低热风炉燃烧过程生成的NOx,研究分析了NOx的生成机制,运用热力型NOx生成模型计算了热风炉燃烧过程NOx生成速率和生成量,开发设计了基于高温低氧燃烧技术（HTAC）的新型顶燃式热风炉,采用CFD仿真模型对比研究了常规热风炉和高温低氧热风炉的燃烧过程和特性。计算得出2种热风炉的温度场分布和火焰形状、浓度场分布以及NOx的浓度分布。研究结果表明,高温低氧热风炉的温度场分布均匀,在相同拱顶温度下,NOx生成量仅为80×10-6,比常规热风炉降低约76%。高温低氧热风炉可以获得更高的风温并可以有效减少NOx排放,实现热风炉高效长寿和节能减排。     

我国工业炉窑NOx治理的思考

我国工业炉窑NOx排放量已达到世界第一位,NOx主要来自燃料的燃烧.介绍了影响工业炉窑NOx生成的因素;工业炉窑与工业锅炉、电站锅炉脱硝方式的区别;并介绍了几种工业炉窑NOx的治理方法.     

烧结原燃料中N的转化及影响因素研究

针对烧结工序NOx排放的现状,从源头治理的角度对烧结原燃料中N元素含量以及烧结过程中NOx浓度分布进行了检测分析,对不同铁精矿和燃料的NOx排放受温度、气氛、粒度以及熔剂等因素的影响进行了研究,初步摸清了烧结原燃料中NOx的排放规律,并通过烧结杯试验探索了烧结过程中NOx浓度随工艺参数的变化规律,指出燃烧温度和烟气负压是烧结过程中影响烟气NOx浓度的主要因素。     

新钢烧结生产NO_x排放规律及减排措施

钢铁厂烧结工序是有害气体NOx的主要来源之一,减少烧结烟气中NOx的排放,对环境保护具有重要意义。本文针对目前新钢烧结过程NOx排放浓度高的问题,结合新钢实际烧结过程中原燃料条件参数、工艺条件参数对烟气中NOx排放浓度的影响规律,提出了一些有效的烧结过程NOx减排控制方法,并在生产过程中采取从源头降低原燃料带入N、降低固体燃料配比、强化制粒改善料层透气性、提高料层厚度等措施抑制烧结过程中NOx的产生。结果表明,文中采取的措施皆有利于减少烧结烟气中NOx的排放,排放浓度可以降低10%~20%。     

Efficacy of different schedules in the management of chronic hepatitis C with interferon-alpha

We have evaluated the kinetics of nitrogen dioxide production in a system for inhalation of nitric oxide. In addition to a small fraction of contamination of nitrogen dioxide in the nitric oxide stock gas, a considerable part of the total concentration of nitrogen dioxide is formed immediately after mixing of nitric oxide and oxygen. This initial build-up of nitrogen dioxide is followed by a linear, time-dependent increase in the concentration of nitrogen dioxide. An equation describing the concentration of nitrogen dioxide in the delivery system is formulated: [NO2] = kA x [NO] + kB x [NO]2 x [O2] + kC x t x [NO]2 x [O2], where nitrogen dioxide [NO2] and nitric oxide [NO] concentrations are in parts per million (ppm), oxygen concentration [O2] is expressed as a percentage and contact time (t) is in seconds. The rate constants are kA = 5.12 x 10(-3), kB = 1.41 x 10(-6) and kC = 0.86 x 10(-6). Calculated nitrogen dioxide values correlated well with measured concentrations. This new finding of an initial build-up of nitrogen dioxide has to be taken into consideration if the conversion of nitric oxide to nitrogen dioxide is to be calculated and in the safety guidelines for the use of nitric oxide.     

燃烧NOx生成机理及抑制方法

对ＮＯｘ的危害、燃烧ＮＯｘ生成机理及抑方法进行了叙述了，对降低ＮＯｘ的途径进行了探讨。     

湍流燃烧混合对NOx生成的影响

用普朗特混合理论，在湍流燃烧回流混合区的混合指数概念基础上，对气体燃烧混合影响NOx湍流生成的特性进行了理论研究。由实验结果确定了NOx湍流反应的达姆克勒准数，对现有NOx生成的湍流反应速率进行了模拟结果与实验结果的对比评价。结果表明，NOx湍流生成是扩散和反应动力学联合控制的非平衡化学反应流，为正确使用数学模型而进行数值模拟提供了理论依据。     

Selective defect in nitric oxide synthesis may explain the impaired endothelium-dependent vasodilation in patients with essential hypertension

BACKGROUND: Patients with essential hypertension have impaired endothelial NO activity, but the mechanism underlying this abnormality is unknown. METHODS AND RESULTS: To investigate whether the endothelial dysfunction of hypertensive patients is related to a selective defect in NO synthesis, we studied the forearm blood flow responses to intra-arterial infusion of acetylcholine (7.5 to 30 microg/min), an endothelial agonist linked to NO synthase through the Ca2+ signaling pathway, and isoproterenol (50 to 200 ng/min), a beta-adrenoceptor agonist that stimulates NO production by increasing intracellular cAMP, in 12 normotensive subjects and 12 hypertensive patients. The infusion of isoproterenol was repeated during the concurrent blockade of NO synthesis by NG-monomethyl-L-arginine (L-NMMA; 4 micromol/min). The vasodilator response to acetylcholine was significantly reduced in hypertensives compared with normotensives (maximum blood flow: 10.4+/-4.6 versus 14.4+/-3.7 mL x min[-1] x dL[-1]; P=.008). However, the vasodilator effect of isoproterenol was similar in normotensives and hypertensives (maximum blood flow: 14.4+/-5.4 versus 13.5+/-5 mL x min[-1] x dL[-1]; P=.56) and was significantly (both P<.01) and equally blunted by L-NMMA in both groups (maximum blood flow: 11+/-3 mL x min[-1] x dL[-1] in normotensives versus 10.8+/-3.9 mL x min[-1] x dL[-1] in hypertensives; P=.77). The vasodilator response to sodium nitroprusside (0.8 to 3.2 microg/min), an exogenous NO donor, was similar in both groups and was not modified by L-NMMA. CONCLUSIONS: Hypertensive patients have impaired endothelium-dependent vasodilation in response to acetylcholine but preserved NO activity in response to beta-adrenergic stimulation. These findings suggest that the endothelial dysfunction in essential hypertension is due to a selective abnormality of NO synthesis, probably related to a defect in the phosphatidylinositol/Ca2+ signaling pathway.     

固定源NOx的排放控制及DeNOx催化剂的应用

对减少固定源排放ＮＯｘ的技术进行了全面的综述,介绍了目前用于这一领域的几类催化剂的特点和应用情况。讨论了在我院控制来自钢铁厂、发电厂、垃圾焚烧炉等各种固定源ＮＯｘ排放可能采用的方法。     

降低火力发电厂NOx排放技术及燃烧调整试验

介绍了煤燃烧过程中NOx产生的机理和危害以及火力发电厂中降低NOx排放的技术,并且针对安阳电厂10#号锅炉进行了低NOx燃烧调整试验,在实际运行中取得了较好的结果.     

Estrogen receptor alpha and beta expression in upper gastrointestinal tract with regulation of trefoil factor family 2 mRNA levels in ovariectomized rats

STUDY OBJECTIVE: To investigate the effect of short-term inhalation of nitric oxide (NO) on transpulmonary angiotensin II formation in patients with severe ARDS. DESIGN: Prospective, clinical study. SETTING: Anesthesiology ICU of a university hospital. PATIENTS: Ten ARDS patients who responded to inhalation of 100 ppm NO by decreasing their pulmonary vascular resistance (PVR) by at least 20 dyne x s x cm(-5) were included in the study. INTERVENTIONS AND MEASUREMENTS: In addition to standard treatment, the patients inhaled 0, 1, and 100 ppm NO in 20-min intervals. Fraction of inspired oxygen was 1.0. Hemodynamics were measured and recorded online. Mixed venous (pulmonary arterial catheter) and arterial (arterial catheter) blood samples were taken simultaneously for hormonal analyses at the end of each inhalation period. RESULTS: Pulmonary arterial pressure decreased from 33+/-2 mm Hg (0 ppm NO, mean+/-SEM) to 29+/-2 mm Hg (1 ppm NO, p<0.05), and to 27+/-2 mm Hg (100 ppm NO, p<0.05, vs 0 ppm). PVR decreased from 298+/-56 (0 ppm NO) to 243+/-45 dyne x s x cm(-5) (1 ppm NO, not significant [NS]), and to 197+/-34 dyne x s x cm(-5) (100 ppm NO, p<0.05, vs 0 ppm). Arterial oxygen pressure increased from 174+/-23 mm Hg (0 ppm NO) to 205+/-26 mm Hg (1 ppm NO, NS), and to 245+/-25 mm Hg (100 ppm NO, p <0.05, vs 0 ppm). Mean plasma angiotensin II concentrations were 85+/-20 (arterial) and 57+/-13 pg/mL (mixed venous) during 0 ppm NO and did not change during inhalation of 1 and 100 ppm NO. Mean transpulmonary plasma angiotensin II concentration gradient (=difference between arterial and mixed venous blood values) was 28+/-8 pg/mL (range, 0 to 69) during 0 ppm NO and did not change during inhalation of 1 and 100 ppm NO. Mean transpulmonary angiotensin II formation (transpulmonary angiotensin II gradient multiplied with the cardiac index) was 117+/-39 ng/min/m2 (range, 0 to 414) during 0 ppm NO and did not change during inhalation of 1 and 100 ppm NO. Mean arterial plasma cyclic guanosine monophosphate concentration was 11+/-2 pmol/mL (0 ppm NO), did not change during 1 ppm NO, and increased to 58+/-8 pmol/mL (100 ppm NO, p<0.05). Arterial plasma concentrations of aldosterone (142+/-47 pg/mL), atrial natriuretic peptide (114+/-34 pg/mL), angiotensin-converting enzyme (30+/-5 U/L), and plasma renin activity (94+/-26 ng/mL/h of angiotensin I) did not change. CONCLUSION: The decrease of PVR by short-term NO inhalation in ARDS patients was not accompanied by changes in transpulmonary angiotensin II formation. Our results do not support any relationship between transpulmonary angiotensin II formation and the decrease in PVR induced by inhaled NO.     

Prognostic factors for disease progression in advanced Hodgkin''s disease: an analysis of patients aged under 60 years showing no progression in the first 6 months after starting primary chemotherapy

Cell and tissue concentrations of NO2- and NO3- are important indicators of nitric oxide synthase activity and crucial in the regulation of many metabolic functions, as well as in nonenzymatic nitric oxide release. We adapted the capillary electrophoresis technique to quantify NO2- and NO3- levels in single identified buccal neurons and ganglia in the opisthobranch mollusc Pleurobranchaea californica, a model system for the study of the chemistry of neuron function. Neurons were injected into a 75-microm separation capillary and the NO2- and NO3- were separated electrophoretically from other anions and detected by direct ultraviolet absorbance. The limits of detection for NO2- and NO3- were <200 fmol (<4 microM in the neurons under study). The NO2- and NO3- levels in individual neurons varied from 2 mM (NO2-) and 12 mM (NO3-) in neurons histochemically positive for NADPH-diaphorase activity down to undetectable levels in many NADPH-diaphorase-negative cells. These results affirm the correspondence of histochemical NADPH-diaphorase activity and nitric oxide synthase in molluscan neurons. NO2- was not detected in whole ganglion homogenates or in hemolymph, whereas hemolymph NO3- averaged 1.8 +/- 0.2 x 10(-3) M. Hemolymph NO3- in Pleurobranchaea was appreciably higher than values measured for the freshwater pulmonate Lymnaea stagnalis (3.2 +/- 0.2 x 10(-5) M) and for another opisthobranch, Aplysia californica (3.6 +/- 0.7 x 10(-4) M). Capillary electrophoresis methods provide utility and convenience for monitoring NO2-/NO3- levels in single cells and small amounts of tissue.     

高温陶瓷窑炉内影响N0x生成若干因素分析

简要分析了燃料燃烧过程中NOx的生成机理,从陶瓷工艺角度着重讨论了燃料特性、过剩空气系数、一次风率、二次风率、燃烧温度以及烟气停留时间等若干因素对NOx生成的影响.     

Forearm nitric oxide balance, vascular relaxation, and glucose metabolism in NIDDM patients

Endothelium-dependent and -independent vascular responses were assessed in 10 NIDDM patients and 6 normal subjects with no evidence of atherosclerotic disease. Changes in forearm blood flow and arteriovenous (AV) serum nitrite/nitrate (NO2-/NO3-) concentrations were measured in response to intra-arterial infusion of acetylcholine (ACh) (7.5, 15, 30 microg/min, endothelium-dependent response) and sodium nitroprusside (SNP) (0.3, 3, 10 microg/min, endothelium-independent response). Insulin sensitivity (determined by minimal model intravenous glucose tolerance test) was lower in NIDDM patients (0.82 +/- 0.20 vs. 2.97 +/- 0.29 10(4) min x microU(-1) x ml(-1); P < 0.01). Baseline forearm blood flow (4.8 +/- 0.3 vs. 4.4 +/- 0.3 ml x 100 ml(-1) tissue x min(-1); NS), mean blood pressure (100 +/- 4 vs. 92 +/- 4 mmHg; NS), and vascular resistance (21 +/- 1 vs. 21 +/- 1 units; NS), as well as their increments during ACh and SNP, infusion were similar in both groups. No difference existed in baseline NO2-/NO3- concentrations (4.09 +/- 0.33 [NIDDM patients] vs. 5.00 +/- 0.48 micromol/l [control subjects]; NS), their forearm net balance (0.31 +/- 0.08 [NIDDM patients] vs. 0.26 +/- 0.08 micromol/l x 100 ml(-1) tissue x min(-1); NS), and baseline forearm glucose uptake. During ACh infusion, both NO2- and NO3- concentrations and net balance significantly increased in both groups, whereas glucose uptake increased only in control subjects. When data from NIDDM and control groups were pooled together, a correlation was found between the forearm AV NO2- and NO3- differences and blood flow (r = 0.494, P = 0.024). On the contrary, no correlation was evident between NO2- and NO3- concentrations or net balance and insulin sensitivity. In summary, 1) no difference existed in basal and ACh-stimulated NO generation and endothelium-dependent relaxation between uncomplicated NIDDM patients and control subjects; 2) in both NIDDM and control groups, forearm NO2- and NO3- net balance following ACh stimulation was related to changes in the forearm blood flow; and 3) ACh-induced increase in forearm blood flow was associated with an increase in glucose uptake only in control subjects but not in NIDDM patients. In conclusion, our results argue against a role of impaired NO generation and blood flow regulation in determining the insulin resistance of uncomplicated NIDDM patients; rather, it supports an independent insulin regulation of hemodynamic and metabolic effects.