Sarcoendoplasmic reticulum Ca(2+) ATPase. A critical target in chlorine inhalation-induced cardiotoxicity. - Test2 - elhamkhani - TriplyDB

Sarcoendoplasmic reticulum Ca(2+) ATPase. A critical target in chlorine inhalation-induced cardiotoxicity.

Sarcoendoplasmic reticulum Ca(2+) ATPase. A critical target in chlorine inhalation-induced cardiotoxicity.

http://www.wikidata.org/entity/Q35816343

about

Inhaled matters of the heart An Official American Thoracic Society Workshop Report: Chemical Inhalational Disasters. Biology of Lung Injury, Development of Novel Therapeutics, and Medical Preparedness.Hyaluronan mediates airway hyperresponsiveness in oxidative lung injury Chlorine inhalation-induced myocardial depression and failure.Respiratory syncytial virus infection increases chlorine-induced airway hyperresponsiveness Chlorine-induced cardiopulmonary injury Nitrite therapy prevents chlorine gas toxicity in rabbits.Formation of chlorinated lipids post-chlorine gas exposure.Ultraviolet Radiation-Induced Downregulation of SERCA2 Mediates Activation of NLRP3 Inflammasome in Basal Cell Carcinoma.Oxygen Administration Improves Survival but Worsens Cardiopulmonary Functions in Chlorine-exposed Rats.Cardiotoxic effects of the novel approved anti-ErbB2 agents and reverse cardioprotective effects of ranolazine.Hydrogen sulphide increases pulmonary veins and atrial arrhythmogenesis with activation of protein kinase C.Halogen Inhalation-Induced Lung Injury and Acute Respiratory Distress Syndrome.

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P2860

Sarcoendoplasmic reticulum Ca(2+) ATPase. A critical target in chlorine inhalation-induced cardiotoxicity.

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Aftab Ahmad

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Chlorine-induced injury to the airways in mice

Pharmacology at work for cardio-oncology: ranolazine to treat early cardiotoxicity induced by antitumor drugs

Mechanisms of altered Ca²⁺ handling in heart failure

Integrative assessment of chlorine-induced acute lung injury in mice

Chlorine gas exposure disrupts nitric oxide homeostasis in the pulmonary vasculature

Chlorine gas inhalation: human clinical evidence of toxicity and experience in animal models

Chlorine gas exposure causes systemic endothelial dysfunction by inhibiting endothelial nitric oxide synthase-dependent signaling

The principal eosinophil peroxidase product, HOSCN, is a uniquely potent phagocyte oxidant inducer of endothelial cell tissue factor activity: a potential mechanism for thrombosis in eosinophilic inflammatory states

Calcium signalling: dynamics, homeostasis and remodelling

Hypochlorous acid-mediated protein oxidation: how important are chloramine transfer reactions and protein tertiary structure?

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