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Anti Inflammatory Effects of Statins in Cardiac Surgery Patients

World Journal of Cardiovascular Surgery 2012年第3期2卷 40-47页

作者： A. Raza S. Kennedy Y. Fan B. Maher M. Codd T. Murphy A. Wood W. Watson Prof. Eoin O’Malley National Centre for Cardiothoracic Surgery mater misericordiae university hospital Eccles Street Dublin Ireland ucd school of medicine and medical sciences ucd conway institute and mater misericordiae university hospital university college dublin Dublin Ireland

Objectives: Cardiac surgery with cardiopulmonary bypass provokes systemic inflammatory response, which may cause organ dysfunction. Studies have suggested that pre-operative statin therapy can reduce morbidity and mortality associated with cardiac surgery;the mechanism for this remains unclear. We hypothesise that underlying mechanism of action for these effects of statins is through inhibition of neutrophil transendothelial migration. Methods: We recruited 151 patients undergoing cardiac surgery. Of these 41 patients were on no-statin;48 patients on low-dose (10 - 30 mg) and 62 patients were on high-dose statin (40 - 80 mg). Ex vivo neutrophil migration was performed on pre-operative blood samples of 90 patients. Of these 90 patients we used 36 patients to assess the levels of TNF-α and sICAM-1. Clinical parameters of total 151 patients were assessed to analyse outcome. Results: Ex vivo neutrophil migration was decreased in high-dose statin group when compared to neutrophils isolated from no-statin or low-dose statin groups (p < 0.001). Serum TNF-α levels were lower in the high-dose statin group (p = 0.002) and sICAM-1 levels were decreased in both low (p = 0.02) and high-dose statin (p = 0.01) groups. Conclusion: Our study demonstrates that high-dose statins reduce ex-vivo transendothelial neutrophil migration, TNF-α and sICAM-1 serum levels suggesting that statins may help in decreasing the post-cardiac surgery morbidity.

关键词： Statins Neutrophils Cardiac Surgery Outcome TNF-α sICAM-1

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Exploiting autophagy in multiple myeloma

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Journal of Cancer Metastasis and Treatment 2019年第10期4卷 1-20页

作者： Matthew Ho Ashish Patel Cathal Hanley Adam Murphy Tara McSweeney Li Zhang Amanda McCann Peter O’Gorman Giada Bianchi ucd school of medicine College of Health and Agricultural SciencesUniversity College DublinBelfield DublinDublin 4Ireland ucd conway institute of Biomolecular and Biomedical Science DublinDublin 4Ireland Department of Hematology West China HospitalSichuan UniversityChengdu 610041SichuanChina Haematology Department Mater Misericordiae University HospitalDublinDublin 7Ireland LeBow institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center Department of Medical OncologyDana Farber Cancer InstituteHarvard Medical SchoolBostonMA 02215USA.

Multiple myeloma(MM)is a plasma cell cancer characterized by sustained endoplasmic reticulum(ER)stress and unfolded protein response activation in the setting of high rates of immunoglobulin ***,MM cells rely heavily on protein quality control pathways for survival as evidenced by the clinical efficacy of proteasome inhibitors(PI).Autophagy is an intracellular self-digestion mechanism that plays a role in the ER protein quality control *** then,basal levels of autophagy were recently found to confer a survival and drug-resistance benefit to MM ***,excessive induction of autophagy in MM cells leads to autophagic cell death,highlighting the double-edged nature of autophagy modulation in *** review provides an overview of the role that autophagy plays in MM pathogenesis,survival,and *** highlight the potential utility of therapeutically targeting autophagy in MM,focusing on preclinical data of autophagic modulators in combination with alkylators,anthracyclines,PI,and immunomodulatory drugs.

关键词： Multiple myeloma autophagy drug resistance hematopoiesis immunoglobulin antibody

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