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Genomic and cellular responses to aspirin in colonic organoids from African- and European-Americans.
Physiol Genomics
January 2025
Section of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Chicago, Chicago, Illinois.
Aspirin (ASA) is a proven chemoprotective agent for colorectal cancer (CRC), though inter-individual responses and cellular mechanisms are not well characterized. Human organoids are ideal to study treatment responses across individuals. Here, colonic organoids from African-Americans (AA) and European-Americans (EA)were used to profile genomic and cellular ASA responses.
View Article and Find Full Text PDFParadigms and Perspectives: The Evolving Prostaglandin E Story in Chronic Sinus Disease.
J Allergy Clin Immunol
January 2025
Department of Medicine, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Jeff and Penny Vinik Center for Translational Immunology Research, Boston, MA, USA 02115.
Aspirin-based PROTACs as COX-2 degraders for anti-inflammation.
Bioorg Med Chem
January 2025
Institute for Inheritance-Based Innovation of Chinese Medicine, School of Pharmacy, Shenzhen University Medical School, Shenzhen University, Shenzhen 518060, China. Electronic address:
Cyclooxygenase-2 (COX-2) is a key enzyme in the biosynthesis of prostaglandins and plays a special role in the process of inflammatory response. COX-2 is a target of non-steroidal anti-inflammatory drugs (NSAIDs), which can effectively relieve inflammation, pain and fever responses by inhibiting COX-2. Despite the significant study progress of inhibitors targeting COX-2, the development of COX-2 degraders remains insufficient.
View Article and Find Full Text PDFArachidonic acid synergizes with aspirin preventing myocardial ischemia-reperfusion injury and mitigates bleeding risk.
Cardiovasc Res
January 2025
State Key Laboratory of Cardiovascular Disease, Clinical Pharmacology Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, China.
Aims: The therapeutic efficacy of coronary revascularization is compromised by myocardial ischemia-reperfusion (MI/R) injury. Higher levels of circulating arachidonic acid (AA) are reportedly associated with lower risk of cardiovascular disease. The cyclooxygenase (COX) pathway metabolizes AA into prostaglandins (PGs) and the platelet-activating thromboxane A2 (TXA2), which is inhibited by aspirin.
View Article and Find Full Text PDFOral and intranasal aspirin desensitisation for non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease.
Cochrane Database Syst Rev
January 2025
Department of Otorhinolaryngology, Amsterdam University Medical Centre, Amsterdam, Netherlands.
Background: NSAID-exacerbated respiratory disease (N-ERD) is a hypersensitivity to non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen, accompanied by chronic rhinosinusitis (with or without nasal polyps) or asthma. The prevalence of hypersensitivity to NSAIDs is estimated to be 2%. The first line of treatment is the avoidance of NSAIDs.
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