Reformation of gasoline on a rhenium-alumina catalyst treated with hydrogen sulfide. With the object of improving its octane characteristics

1961 ◽  
Vol 10 (1) ◽  
pp. 92-93
Author(s):  
Kh. M. Minachev ◽  
M. A. Ryashentseva
Keyword(s):  
Hydrogen Sulfide ◽  
Alumina Catalyst

Dissociation of dihydrogen and hydrogen sulfide over a sulfided NiMo-alumina catalyst as evidenced by D2S-H2 isotopic exchange

1995 ◽  
Vol 34 (3-4) ◽  
pp. 375-378 ◽  
Author(s):  
P. d'Araujo ◽  
C. Thomas ◽  
L. Vivier ◽  
D. Duprez ◽  
G. P�rot ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Isotopic Exchange ◽  
Alumina Catalyst

Influence of hydrogen sulfide on the hydrodesulfurization of dibenzothiophene on a sulfided cobalt-molybdenum/alumina catalyst

1982 ◽  
Vol 3 (1) ◽  
pp. 57-64 ◽  
Author(s):  
M.L. Vrinat ◽  
C.G. Gachet ◽  
G. Cavalletto ◽  
L. De Mourgues
Keyword(s):  
Hydrogen Sulfide ◽  
Alumina Catalyst

Deactivation of a Palladium-Supported Alumina Catalyst by Hydrogen Sulfide during the Oxidation of Methane

Langmuir ◽  
1994 ◽  
Vol 10 (10) ◽  
pp. 3567-3570 ◽  
Author(s):  
U. Feuerriegel ◽  
W. Klose ◽  
S. Sloboshanin ◽  
H. Goebel ◽  
J. A. Schaefer
Keyword(s):  
Hydrogen Sulfide ◽  
Alumina Catalyst ◽  
Oxidation Of Methane

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

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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