Thermodynamic properties of the aqueous sulfide and bisulfide ions and the second ionization constant of hydrogen sulfide over extended temperatures

1971 ◽  
Vol 10 (3) ◽  
pp. 619-625 ◽  
Author(s):  
James W. Cobble ◽  
Howard P. Stephens
1961 ◽  
Vol 65 (2) ◽  
pp. 264-267 ◽  
Author(s):  
H. L. Loy ◽  
D. M. Himmelblau

1970 ◽  
Vol 48 (5) ◽  
pp. 764-775 ◽  
Author(s):  
E. C. W. Clarke ◽  
D. N. Glew

An apparatus is described in which deuterium and hydrogen sulfides have been prepared by the hydrolysis of aluminum sulfide. Liquid densities have been determined at −79 °C and give the molar volumes 34.811 ± 0.003 cm3 for deuterium sulfide and 34.711 ± 0.003 for hydrogen sulfide. Vapor pressures of deuterium and hydrogen sulfides have been determined at −78 °C in a quartz–metal apparatus, and in the range −30 to +30 °C in a stainless steel apparatus. Equations are derived for the deuterium and hydrogen sulfide vapor pressures and for their ratio. An isotopic vapor pressure cross-over point is found at −48 °C, above which deuterium sulfide is more volatile than hydrogen sulfide. Gas and liquid molar volumes and enthalpy changes are evaluated for liquid vaporization at saturation. The deuterium and hydrogen sulfide vaporization standard thermodynamic function changes and their errors, together with the isotopic differences for these functions and their errors, are tabulated between −80 and +50°C.


2020 ◽  
Vol 315 ◽  
pp. 113751 ◽  
Author(s):  
Chun-Sheng Jia ◽  
Ji Li ◽  
Yu-Song Liu ◽  
Xiao-Long Peng ◽  
Xu Jia ◽  
...  

1979 ◽  
Vol 44 ◽  
pp. 349-355
Author(s):  
R.W. Milkey

The focus of discussion in Working Group 3 was on the Thermodynamic Properties as determined spectroscopically, including the observational techniques and the theoretical modeling of physical processes responsible for the emission spectrum. Recent advances in observational techniques and theoretical concepts make this discussion particularly timely. It is wise to remember that the determination of thermodynamic parameters is not an end in itself and that these are interesting chiefly for what they can tell us about the energetics and mass transport in prominences.


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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