Nonthermal plasma technique for the removal of hydrogen sulfide from methane

2020 ◽  
Author(s):  
A. N. Ochered'ko ◽  
A. Yu. Ryabov ◽  
S. V. Kudryashov
2012 ◽  
Vol 16 ◽  
pp. 856-862 ◽  
Author(s):  
Xiaoqing Dang ◽  
Jiayu Huang ◽  
Lu Kang ◽  
Tao Wu ◽  
Qing Zhang

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Lianshui Zhang ◽  
Xiaojun Wang ◽  
Weidong Lai ◽  
Xueliang Cheng ◽  
Kuifang Zhao

Nonthermal plasma technique has drawn extensive attentions for removal of air pollutants such as NOxand SO2. The NO removal mechanism in pulse discharged plasma is discussed in this paper. Emission spectra diagnosis indicates that the higher the discharge voltage is, the more the NO are removed and transformed into O, N, N2, NO2, and so forth. Plasma electron temperatureTeis ranged from 6400 K at 2.4 kV discharge voltage to 9500 K at 4.8 kV. After establishing a zero-dimensional chemical reaction kinetic model, the major reaction paths are clarified as the electron collision dissociation of NO into N and O during discharge and followed by single substitution of N on NO to form N2during and after discharge, compared with the small fraction of NO2formed by oxidizing NO. The reaction directions can be adjusted by N2additive, and the optimal N2/NO mixing ratio is 2 : 1. Such a ratio not only compensates the disadvantage of electron competitive consumption by the mixed N2, but also heightens the total NO removal extent through accelerating the NO oxidization process.


2007 ◽  
Author(s):  
Morris Argyle ◽  
John Ackerman ◽  
Suresh Muknahallipatna ◽  
Jerry Hamann ◽  
Stanislaw Legowski ◽  
...  

2007 ◽  
Vol 62 (8) ◽  
pp. 2216-2227 ◽  
Author(s):  
Gui-Bing Zhao ◽  
Sanil John ◽  
Ji-Jun Zhang ◽  
Jerry C. Hamann ◽  
Suresh S. Muknahallipatna ◽  
...  

2012 ◽  
Vol 95 ◽  
pp. 87-92 ◽  
Author(s):  
E. Linga Reddy ◽  
V.M. Biju ◽  
Ch. Subrahmanyam

1988 ◽  
Vol 102 ◽  
pp. 243-246
Author(s):  
J.T. Costello ◽  
W.G. Lynam ◽  
P.K. Carroll

AbstractThe dual laser-produced plasma technique for the study of ionic absorption spectra has been developed by the use of two Q-switched ruby lasers to enable independent generation of the absorbing and back-lighting plasmas. Optical pulse handling is used in the coupling cicuits to enable reproducible pulse delays from 250 nsec. to 10 msec, to be achieved. At delay times > 700 nsec. spectra of essentially pure neutral species are observed. The technique is valuable, not only for obtaining the neutral spectra of highly refractory and/or corrosive materials but also for studying behaviour of ionic species as a function of time. Typical spectra are shown in Fig. 1.


2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.


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