Nature Medicine - AOP - nature.com science feeds Nature Medicine is the premier journal for biomedical research. Respected internationally for the quality of its papers on areas ranging from infectious disease to cancer and neurodegeneration, Nature Medicine aims to bridge the gap between basic research and medical advances and is consistently ranked the number one journal by the Institute of Scientific Investigation in the Medicine, Research and Experimental category. http://www.nature.com/nm/current_issue/ Nature Publishing Group en © Nature Publishing Group Nature Medicine 1078-8956 1546-170X © Nature Publishing Group permissions@nature.com Nature Medicine http://www.nature.com/includes/rj_globnavimages/nm_logo.gif http://www.nature.com/nm/ Synovial fibroblasts spread rheumatoid arthritis to unaffected joints http://feeds.nature.com/~r/nm/rss/aop/~3/Zv2Lbx-e-aI/nm.2050 Rheumatoid arthritis usually begins in one joint but spreads to other joints as the disease progresses. Elena Neumann and her colleagues show that rheumatoid arthritis synovial fibroblasts (RASFs) may be key mediators of this process. They show, using a SCID mouse model, that human RASFs can migrate long distances through the bloodstream from diseased cartilage to unaffected cartilage, where they can mount a new attack. Advertisment

Synovial fibroblasts spread rheumatoid arthritis to unaffected joints

Nature Medicine. doi:10.1038/nm.2050

Authors: Stephanie Lefèvre, Anette Knedla, Christoph Tennie, Andreas Kampmann, Christina Wunrau, Robert Dinser, Adelheid Korb, Eva-Maria Schnäker, Ingo H Tarner, Paul D Robbins, Christopher H Evans, Henning Stürz, Jürgen Steinmeyer, Steffen Gay, Jürgen Schölmerich, Thomas Pap, Ulf Müller-Ladner & Elena Neumann

]]> Synovial fibroblasts spread rheumatoid arthritis to unaffected joints Stephanie Lefèvre Anette Knedla Christoph Tennie Andreas Kampmann Christina Wunrau Robert Dinser Adelheid Korb Eva-Maria Schnäker Ingo H Tarner Paul D Robbins Christopher H Evans Henning Stürz Jürgen Steinmeyer Steffen Gay Jürgen Schölmerich Thomas Pap Ulf Müller-Ladner Elena Neumann doi:10.1038/nm.2050 Nature Medicine 2009-11-08 Nature Medicine 2009-11-08 10.1038/nm.2050 http://dx.doi.org/10.1038/nm.2050 Article http://dx.doi.org/10.1038/nm.2050 Identification of miR-145 and miR-146a as mediators of the 5q– syndrome phenotype http://feeds.nature.com/~r/nm/rss/aop/~3/Tkv_mvOz7eI/nm.2054 For myelodysplastic syndromes caused by deletion of chromosome 5q, Daniel Starczynowski et al. provide evidence that decreased expression of two miRNAs in this region—miR-145 and miR-146a—contributes to abnormal megakaryocyte differentiation and platelet production and progression of the disease to either bone marrow failure or leukemia. The authors also provide a mechanistic explanation for these effects by which loss of these two miRNAs leads to derepression of innate immune signaling. Identification of miR-145 and miR-146a as mediators of the 5q– syndrome phenotype

Nature Medicine. doi:10.1038/nm.2054

Authors: Daniel T Starczynowski, Florian Kuchenbauer, Bob Argiropoulos, Sandy Sung, Ryan Morin, Andrew Muranyi, Martin Hirst, Donna Hogge, Marco Marra, Richard A Wells, Rena Buckstein, Wan Lam, R Keith Humphries & Aly Karsan

]]> Identification of miR-145 and miR-146a as mediators of the 5q– syndrome phenotype Daniel T Starczynowski Florian Kuchenbauer Bob Argiropoulos Sandy Sung Ryan Morin Andrew Muranyi Martin Hirst Donna Hogge Marco Marra Richard A Wells Rena Buckstein Wan Lam R Keith Humphries Aly Karsan doi:10.1038/nm.2054 Nature Medicine 2009-11-08 Nature Medicine 2009-11-08 10.1038/nm.2054 http://dx.doi.org/10.1038/nm.2054 Article http://dx.doi.org/10.1038/nm.2054