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| http://dx.doi.org/10.3390/molecules23071592 | DOI Listing |
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Pharmacological myeloperoxidase (MPO) inhibition in an obese/hypertensive mouse model attenuates obesity and liver damage, but not cardiac remodeling.
Sci Rep
December 2019
Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Lifestyle factors are important drivers of chronic diseases, including cardiovascular syndromes, with low grade inflammation as a central player. Attenuating myeloperoxidase (MPO) activity, an inflammatory enzyme associated with obesity, hypertension and heart failure, could have protective effects on multiple organs. Herein, the effects of the novel oral available MPO inhibitor AZM198 were studied in an obese/hypertensive mouse model which displays a cardiac phenotype.
View Article and Find Full Text PDFNovel 2-Thioxanthine and Dipyrimidopyridine Derivatives: Synthesis and Antimicrobial Activity.
Molecules
June 2018
Medical Chemistry Division, Faculty of Medicine, Jazan University, Jazan 82621, Saudi Arabia.
The authors wish to make the following changes to their paper [1].[..
View Article and Find Full Text PDFNovel 2-Thioxanthine and Dipyrimidopyridine Derivatives: Synthesis and Antimicrobial Activity.
Molecules
October 2015
Medical Chemistry Division, Faculty of Medicine, Jazan University, Jazan 82621, Saudi Arabia.
Several fused imidazolopyrimidines were synthesized starting from 6-amino-1-methyl-2-thiouracil (1) followed by nitrosation, reduction and condensation with different aromatic aldehydes to give Schiff's base. The dehydrocyclization of Schiff's bases using iodine/DMF gave Compounds 5a-g. The methylation of 5a-g using a simple alkylating agent as dimethyl sulfate ((CH₃)₂SO₄) gave either monoalkylated imidazolopyrimidine 6a-g at room temperature or dialkylated derivatives 7a-g on heating 6a-g with ((CH₃)₂SO₄).
View Article and Find Full Text PDFLate intervention with a myeloperoxidase inhibitor stops progression of experimental chronic obstructive pulmonary disease.
Am J Respir Crit Care Med
January 2012
Department of Pathology and UBC James Hogg Research Centre, Institute for Heart and Lung Health, University of British Columbia, Vancouver, British Columbia, Canada.
Rationale: Inflammation and oxidative stress are linked to the deleterious effects of cigarette smoke in producing chronic obstructive pulmonary disease (COPD). Myeloperoxidase (MPO), a neutrophil and macrophage product, is important in bacterial killing, but also drives inflammatory reactions and tissue oxidation.
Objectives: To determine the role of MPO in COPD.
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