|1.||Gaston, Benjamin: 9 articles (01/2015 - 11/2005)|
|2.||Zaman, Khalequz: 4 articles (01/2015 - 05/2006)|
|3.||Palmer, Lisa A: 4 articles (02/2013 - 08/2003)|
|4.||Patel, Rakesh P: 4 articles (10/2010 - 05/2005)|
|5.||Stamler, Jonathan S: 4 articles (07/2009 - 02/2004)|
|6.||Gaston, B: 4 articles (10/2001 - 10/2000)|
|7.||Murphy, Michael P: 3 articles (07/2014 - 06/2009)|
|8.||Lewis, Stephen J: 3 articles (01/2014 - 08/2009)|
|9.||Gladwin, Mark T: 3 articles (06/2008 - 05/2005)|
|10.||Sun, Fei: 2 articles (01/2015 - 01/2014)|
|1.||Cardiovascular Diseases (Cardiovascular Disease)
01/20/2013 - "Despite enhanced insight into S-nitrosothiol biochemistry, translating these advances into beneficial pharmacotherapies for patients with cardiovascular diseases remains a primary as-yet unmet goal for investigators within the field."
04/14/2009 - "Despite substantial evidence that nitric oxide (NO) and/or endogenous S-nitrosothiols (SNOs) exert protective effects in a variety of cardiovascular diseases, the molecular details are largely unknown. "
12/01/2000 - "S-Nitrosothiols are a class of chemical compounds that decompose to release nitric oxide and show promise in the treatment of a variety of cardiovascular diseases. "
01/20/2013 - "Recent analyses using modern S-nitrosothiol detection techniques have revealed the mechanistic significance of S-nitrosylation to the pathophysiology of numerous cardiovascular diseases, including essential hypertension, pulmonary hypertension, ischemic heart disease, stroke, and congestive heart failure, among others. "
06/10/2008 - "The specific aims of this study were (1) to assess the efficacy of nitrite in reducing necrosis and apoptosis in canine myocardial infarction and (2) to determine the relative role of nitrite versus chemical intermediates, such as S-nitrosothiols. "
10/01/2007 - "This study demonstrates that exposure to CysNO before ischemia increases tissue S-nitrosothiol levels, improves postischemic contractile dysfunction, and attenuates necrosis. "
03/01/2010 - "Plasma levels of tumour necrosis factor-alpha, interleukin-6, and nitrite and total s-nitrosothiols were determined. "
06/01/2003 - "In addition NO can be converted to a number of reactive derivatives such as peroxynitrite, NO2, N2O3, and S-nitrosothiols that can kill cells in part by inhibiting mitochondrial respiration or activation of mitochondrial permeability transition, triggering neuronal apoptosis or necrosis."
09/01/2007 - "In this study, we focused on the role of S-nitrosothiols (RSNO) in the susceptibility of a cerebellar cell line R2 to NO. Our results showed the following: (i) S-nitrosoglutathione (GSNO) induced a burst of RSNO in GSH-depleted R2 cells, the majority of which were primarily contributed by the S-nitrosylation of proteins (Pro-SNOs), and was followed by severe neuronal necrosis; (ii) the elevation in the level of Pro-SNOs resulted from a dysfunction of S-nitroglutathione reductase (GSNOR) as a result of its substrate, GSNO, being unavailable in GSH-depleted cells. "
01/01/2010 - "This study was aimed to investigate the role of NO and S-nitrosothiol (SNO) homeostasis in the development of hepatocellular injury during cholestasis induced by bile duct ligation (BDL) in rats. "
01/01/2010 - "Inhibition of nitric oxide synthesis during induced cholestasis ameliorates hepatocellular injury by facilitating S-nitrosothiol homeostasis."
03/15/2007 - "Formation and role of plasma S-nitrosothiols in liver ischemia-reperfusion injury."
10/25/2007 - "In addition, S-nitrosothiols could elicit pharmacological preconditioning effect and protect against myocardial ischemia-reperfusion injury. "
01/01/2013 - "S-Nitrosothiols increased significantly in plasma, confirming in vivo sodium nitrite reduction to NO and encouraging its use against vasospasm and ischemia-reperfusion injury to the brain, kidneys, liver, and heart."
06/30/2009 - "A mitochondria-targeted S-nitrosothiol modulates respiration, nitrosates thiols, and protects against ischemia-reperfusion injury."
04/17/2012 - "This decrease was paralleled by a S-nitrosothiol-MIF- but not Cys81 serine (Ser)-MIF mutant-dependent reduction of infarct size in an in vivo model of myocardial ischemia/reperfusion injury. "
|1.||Nitric Oxide (Nitrogen Monoxide)
|2.||Glutathione (Reduced Glutathione)
|3.||Adenosine A2B Receptor
|5.||soluble guanylyl cyclase
|9.||Interleukin-6 (Interleukin 6)
|10.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|3.||Drug Therapy (Chemotherapy)