Role of CO2 and H2O on NO Formation during Biomass Char Oxidation

The trans-2-deoxyribosylation of 4-thiouracil (4SUra) and 2-thiouracil (2SUra), as well as 6-azauracil, 6-azathymine and 6-aza-2-thiothymine was studied using dG and E. coli purine nucleoside phosphorylase (PNP) for the in situ generation of 2-deoxy-α-D-ribofuranose-1-phosphate (dRib-1P) followed by its coupling with the bases catalyzed by either E. coli thymidine (TP) or uridine (UP) phosphorylases. 4SUra revealed satisfactory substrate activity for UP and, unexpectedly, complete inertness for TP; no formation of 2’-deoxy-2-thiouridine (2SUd) was observed under analogous reaction conditions in the presence of UP and TP. On the contrary, 2SU, 2SUd, 4STd and 2STd are good substrates for both UP and TP; moreover, 2SU, 4STd and 2’-deoxy-5-azacytidine (Decitabine) are substrates for PNP and the phosphorolysis of the latter is reversible. Condensation of 2SUra and 5-azacytosine with dRib-1P (Ba salt) catalyzed by the accordant UP and PNP in Tris∙HCl buffer gave 2SUd and 2’-deoxy-5-azacytidine in 27% and 15% yields, respectively. 6-Azauracil and 6-azathymine showed good substrate properties for both TP and UP, whereas only TP recognizes 2-thio-6-azathymine as a substrate. 5-Phenyl and 5-tert-butyl derivatives of 6-azauracil and its 2-thioxo derivative were tested as substrates for UP and TP, and only 5-phenyl- and 5-tert-butyl-6-azauracils displayed very low substrate activity. The role of structural peculiarities and electronic properties in the substrate recognition by E. coli nucleoside phosphorylases is discussed.

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The role of secondary char oxidation in the transition from smoldering to flaming

Proceedings of the Combustion Institute ◽

10.1016/j.proci.2006.08.006 ◽

2007 ◽

Vol 31 (2) ◽

pp. 2669-2676 ◽

Cited By ~ 21

Author(s):

Olivier Putzeys ◽

Amnon Bar-Ilan ◽

Guillermo Rein ◽

A. Carlos Fernandez-Pello ◽

David L. Urban

Keyword(s):

Char Oxidation

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The role of H2O in NO formation and reduction during oxy-steam combustion of bituminous coal char

Combustion and Flame ◽

10.1016/j.combustflame.2021.111883 ◽

2022 ◽

Vol 237 ◽

pp. 111883

Author(s):

Shuang Yue ◽

Chunbo Wang ◽

Ziyang Xu ◽

Dong Wang ◽

Fei Zheng ◽

...

Keyword(s):

Bituminous Coal ◽

Coal Char ◽

No Formation

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eNOS-induced vascular barrier disruption in retinopathy by c-Src activation and tyrosine phosphorylation of VE-cadherin

eLife ◽

10.7554/elife.64944 ◽

2021 ◽

Vol 10 ◽

Author(s):

Takeshi Ninchoji ◽

Dominic T Love ◽

Ross O Smith ◽

Marie Hedlund ◽

Dietmar Vestweber ◽

...

Keyword(s):

No Synthase ◽

Dependent Manner ◽

Vascular Endothelial ◽

Ocular Diseases ◽

Oxygen Induced Retinopathy ◽

No Formation ◽

Therapy Development ◽

Endothelial Growth Factor ◽

Deutsche Forschungsgemeinschaft

Background:Hypoxia and consequent production of vascular endothelial growth factor A (VEGFA) promote blood vessel leakiness and edema in ocular diseases. Anti-VEGFA therapeutics may aggravate hypoxia; therefore, therapy development is needed.Methods:Oxygen-induced retinopathy was used as a model to test the role of nitric oxide (NO) in pathological neovascularization and vessel permeability. Suppression of NO formation was achieved chemically using L-NMMA, or genetically, in endothelial NO synthase serine to alanine (S1176A) mutant mice.Results:Suppression of NO formation resulted in reduced retinal neoangiogenesis. Remaining vascular tufts exhibited reduced vascular leakage through stabilized endothelial adherens junctions, manifested as reduced phosphorylation of vascular endothelial (VE)-cadherin Y685 in a c-Src-dependent manner. Treatment with a single dose of L-NMMA in established retinopathy restored the vascular barrier and prevented leakage.Conclusions:We conclude that NO destabilizes adheren junctions, resulting in vascular hyperpermeability, by converging with the VEGFA/VEGFR2/c-Src/VE-cadherin pathway.Funding:This study was supported by the Swedish Cancer foundation (19 0119 Pj ), the Swedish Research Council (2020-01349), the Knut and Alice Wallenberg foundation (KAW 2020.0057) and a Fondation Leducq Transatlantic Network of Excellence Grant in Neurovascular Disease (17 CVD 03). KAW also supported LCW with a Wallenberg Scholar grant (2015.0275). WCS was supported by Grants R35 HL139945, P01 HL1070205, AHA MERIT Award. DV was supported by grants from the Deutsche Forschungsgemeinschaft, SFB1450, B03, and CRU342, P2.

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