Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis.

By John Danesh, S. Lewington, S. Thompson, G. Lowe, R. Collins, J. Kostis, A. Wilson, A. Folsom, K. Wu, M. Benderly and 105 more. Journal of the American Medical Association (JAMA), 2005

1,312 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/a4e8e304310c7ae2bd99a3e5572319d970673e5c

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1. A. Piccinini
2. R. Rückerl
3. A. Schneider
4. Annette Peters
5. S. Breitner
6. J. Cyrys
7. K. Midwood

Citations in the corpus

• Health effects of particulate air pollution: A review of epidemiological evidence (2011, background): “Several studies on animals (Nemmar et al., 2001; Nemmar et al., 2004; Oberdorster © 2011 Informa Healthcare USA, Inc. et al., 2002; Semmler et al., 2004) and humans (Mills et al., 2006; Nemmar et al., 2002) demonstrated extrapulmonary translocation of UFP.”
• Impact of C-reactive protein and fibrinogen on cardiovascular prognosis in patients with stable angina pectoris: the AtheroGene study. (2006, neutral): “In addition, a recent meta-analysis adds evidence for a moderately strong association between plasma fibrinogen levels and the risk of CHD, even after adjustment.(22) In our study, which followed up patients with Table 2 HRs for follow-up events across quartiles of C-reactive protein and fibrinogen ”
• DAMPening Inflammation by Modulating TLR Signalling (2010, background): “• Atherosclerosis [219, 220] • Multiple sclerosis [221] • Rheumatoid arthritis [106] • Sepsis [221] • Tumors inc breast [222], ostesarcoma [223] FNEDA”
• Inflammatory cytokines and risk of coronary heart disease: new prospective study and updated meta-analysis. (2014, neutral): “Int J Epidemiol 2006 Aug;35(4):935-943.”
• Immune Effector Mechanisms Implicated in Atherosclerosis: From Mice to Humans (2013, neutral): “Cholesterol crystal formation in macrophages depends on uptake, the intracellular balance between free cholesterol and cholesterol ester, and cholesterol efflux to extracellular acceptors such as apolipoproteins E or AI (Kellner-Weibel et al., 1999).”