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排序方式: 共有596条查询结果,搜索用时 15 毫秒
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Toru Suzuki Yoshiyuki Yazaki Adriaan A. Voors Donald J.L. Jones Daniel C.S. Chan Stefan D. Anker John G. Cleland Kenneth Dickstein Gerasimos Filippatos Hans L. Hillege Chim C. Lang Piotr Ponikowski Nilesh J. Samani Dirk J. van Veldhuisen Faiez Zannad Aeilko H. Zwinderman Marco Metra Leong L. Ng 《European journal of heart failure》2019,21(7):877-886
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Rayan Jo Rachwan Javed Butler Sean P. Collins Gad Cotter Beth A. Davison Stefanie Senger Justin A. Ezekowitz Gerasimos Filippatos Phillip D. Levy Marco Metra Piotr Ponikowski John R. Teerlink Adriaan A. Voors Rudolf A. de Boer David G. Soergel G. Michael Felker Peter S. Pang 《European journal of heart failure》2019,21(12):1561-1570
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P Barlas TD Hernndez KL McFadden 《Focus on Alternative and Complementary Therapies》2010,15(3):225-226
McFadden KL, Hernández TD. Cardiovascular benefits of acupressure (Jin Shin) following stroke. Complement Ther Med 2010; 18: 42–8. 相似文献
79.
L Moreno SK McMaster T Gatheral LK Bailey LS Harrington N Cartwright PCJ Armstrong TD Warner M Paul-Clark JA Mitchell 《British journal of pharmacology》2010,160(8):1997-2007
Background and purpose:
Gram-negative bacteria contain ligands for Toll-like receptor (TLR) 4 and nucleotide oligomerization domain (NOD) 1 receptors. Lipopolysaccharide (LPS) activates TLR4, while peptidoglycan products activate NOD1. Activation of NOD1 by the specific agonist FK565 results in a profound vascular dysfunction and experimental shock in vivo.Experimental approach:
Here, we have analysed a number of pharmacological inhibitors to characterize the role of key signalling pathways in the induction of NOS2 following TLR4 or NOD1 activation.Key results:
Vascular smooth muscle (VSM) cells expressed NOD1 mRNA and protein, and, after challenge with Escherichia coli or FK565, NOS2 protein and activity were induced. Macrophages had negligible levels of NOD1 and were unaffected by FK565, but responded to E. coli and LPS by releasing increased NO and expression of NOS2 protein. Classic pharmacological inhibitors for NF-κB (SC-514) and mitogen-activated protein kinase (SB203580, PD98059) signalling pathways inhibited responses in both cell types regardless of agonist. While TLR4-mediated responses in macrophages were specifically inhibited by the pan-caspase inhibitor z-VAD-fmk and the PKC inhibitor Gö6976, NOD1-mediated responses in VSM cells were inhibited by the Rip2 inhibitor PP2.Conclusions and implications:
Our findings suggest a selective role for NOD1 in VSM cells, and highlight NOD1 as a potential novel therapeutic target for the treatment of vascular inflammation. 相似文献80.
Effects of levosimendan on right ventricular function in patients with advanced heart failure 总被引:2,自引:0,他引:2
Parissis JT Paraskevaidis I Bistola V Farmakis D Panou F Kourea K Nikolaou M Filippatos G Kremastinos D 《The American journal of cardiology》2006,98(11):1489-1492
Right ventricular (RV) dysfunction frequently complicates advanced left ventricular heart failure and contributes to an unfavorable prognosis. Levosimendan is a novel inodilator that beneficially affects hemodynamics and left ventricular systolic and diastolic function in patients with advanced heart failure. However, its effects on RV function have not yet been properly assessed in these patients. In this randomized trial, the impact of levosimendan or placebo on various echocardiographic parameters of RV systolic and diastolic function was investigated in 54 patients with advanced heart failure due to left ventricular systolic dysfunction. Tissue Doppler imaging maximal systolic tricuspid annular velocity (S wave) increased significantly only in the levosimendan group (8.2 +/- 3.2 vs 9.0 +/- 3.0 cm/s, p <0.03). Tissue Doppler imaging RV early diastolic velocity (E wave) and the ratio of early to late diastolic velocities (E/A) also increased significantly after levosimendan administration (p <0.01 and p <0.05, respectively). Systolic pulmonary arterial pressure decreased significantly (54 +/- 11 vs 43 +/- 11 mm Hg, p <0.01) in the levosimendan-treated patients. Levosimendan beneficially modulated neurohormonal and inflammatory status by decreasing B-type natriuretic peptide levels (p <0.05) and by altering the ratio of interleukin-6 to interleukin-10 in favor of the latter (p <0.05). In conclusion, levosimendan could offer further therapeutic advantages in patients with advanced heart failure by improving systolic and diastolic RV function. 相似文献