Delayed Treatment with Sodium Hydrosulfide Improves Regional Blood Flow and Alleviates Cecal Ligation and Puncture (CLP)-Induced Septic Shock - Wikidata - wikimedia - TriplyDB

Delayed Treatment with Sodium Hydrosulfide Improves Regional Blood Flow and Alleviates Cecal Ligation and Puncture (CLP)-Induced Septic Shock

Delayed Treatment with Sodium Hydrosulfide Improves Regional Blood Flow and Alleviates Cecal Ligation and Puncture (CLP)-Induced Septic Shock

http://www.wikidata.org/entity/Q40797264

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Effect of endotoxemia in mice genetically deficient in cystathionine-γ-lyase, cystathionine-β-synthase or 3-mercaptopyruvate sulfurtransferase.The clinically used poly(ADP-ribose) polymerase (PARP) inhibitor olaparib improves organ function, suppresses inflammatory responses and accelerates wound healing in a murine model of third-degree burn injury.Hydrogen sulfide prevents diaphragm weakness in cecal ligation puncture-induced sepsis by preservation of mitochondrial function.S-Sulfhydration of ATP synthase by hydrogen sulfide stimulates mitochondrial bioenergetics.Pharmacologically induced reversible hypometabolic state mitigates radiation induced lethality in mice.Changes in hydrogen sulfide in rats with hepatic cirrhosis in different stages.Transduced PEP-1-Heme Oxygenase-1 Fusion Protein Attenuates Lung Injury in Septic Shock Rats.Protective effects of exogenous NaHS against sepsis-induced myocardial mitochondrial injury by enhancing the PGC-1α/NRF2 pathway and mitochondrial biosynthesis in mice.Lactate as a Potential Biomarker of Sepsis in a Rat Cecal Ligation and Puncture Model.

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P2860

Delayed Treatment with Sodium Hydrosulfide Improves Regional Blood Flow and Alleviates Cecal Ligation and Puncture (CLP)-Induced Septic Shock

http://www.wikidata.org/entity/Q40797264

description

2016 nî lūn-bûn

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2016年の論文

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2016年学术文章

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2016年学术文章

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2016年学术文章

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2016年学术文章

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2016年学术文章

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2016年學術文章

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2016年學術文章

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2016年學術文章

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Delayed Treatment with Sodium ...... ure (CLP)-Induced Septic Shock

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Akbar Ahmad

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Csaba Szabo

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Nadiya Druzhyna

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P2860

The role of H2S bioavailability in endothelial dysfunction

H2S during circulatory shock: some unresolved questions

Hydrogen sulfide donor NaHS reduces organ injury in a rat model of pneumococcal pneumosepsis, associated with improved bio-energetic status

Abandon the mouse research ship? Not just yet!

Role of hydrogen sulfide in severe burn injury-induced inflammation in mice.

Hydrogen sulfide: an endogenous mediator of resolution of inflammation and injury.

Endothelial dysfunction is a potential contributor to multiple organ failure and mortality in aged mice subjected to septic shock: preclinical studies in a murine model of cecal ligation and puncture

AP39, a novel mitochondria-targeted hydrogen sulfide donor, stimulates cellular bioenergetics, exerts cytoprotective effects and protects against the loss of mitochondrial DNA integrity in oxidatively stressed endothelial cells in vitro.

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

Reversing established sepsis with antagonists of endogenous high-mobility group box 1.

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