Solubility of hydrogen sulfide in aqueous diethanolamine solutions at high pressures

1973 ◽  
Vol 18 (1) ◽  
pp. 71-73 ◽  
Author(s):  
Jong Il Lee ◽  
Frederick D. Otto ◽  
Alan E. Mather
1953 ◽  
Vol 18 (6) ◽  
pp. 748-752 ◽  
Author(s):  
T. L. CAIRNS ◽  
A. W. LARCHAR ◽  
B. C. McKUSICK

2015 ◽  
Vol 393 ◽  
pp. 33-39 ◽  
Author(s):  
Negar Sadegh ◽  
Kaj Thomsen ◽  
Even Solbraa ◽  
Eivind Johannessen ◽  
Gunn Iren Rudolfsen ◽  
...  

2018 ◽  
Vol 20 (37) ◽  
pp. 24222-24226 ◽  
Author(s):  
Jia-Yue Yang ◽  
Ming Hu

Ultrahigh pressure greatly shortens interatomic distances and induces strong electron–phonon coupling that significantly reduces the phonon transport of superconducting H3S.


1992 ◽  
Vol 70 (1) ◽  
pp. 55-57 ◽  
Author(s):  
Yuming Xu ◽  
Lili Li ◽  
Loren G. Hepler

Partial molar volumes at infinite dilution for three acidic gases (carbon dioxide, hydrogen sulfide, and sulfur dioxide) in four physical solvents (propylene carbonate, methyl cyanoacetate, N-formyl morpholine, and Selexol) have been obtained using our new dilatometer. These partial molar volumes, in combination with the Henry's law constants obtained previously, have been used in the Krichevsky–Kasarnovsky equation for predicting the solubilities of acidic gases in physical solvents at high pressures. Keywords: partial molar volume, solubility, physical solvents.


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.


1998 ◽  
Vol 77 (4) ◽  
pp. 1063-1075
Author(s):  
W. C. Mackrodt, E.-A. Williamson, D. W

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