rome, and we suspect the same in the new syndrome," says Dietz. "Our studies so far support the idea that these patients' cells compensate for the problems in TGF-beta receptor 1 and 2, but in doing so overshoot what's normal. More work needs to be done to address this issue, which might offer a target for developing medical intervention for these patients."

The Johns Hopkins researchers were funded by the Howard Hughes Medical Institute, the National Heart, Lung and Blood Institute, the National Institute of Arthritis and Musculoskeletal and Skin Diseases and the National Marfan Foundation.

Authors on the paper are Loeys, Dietz, Junji Chen, Enid Neptune, Daniel Judge, Megan Podowski, Tammy Holm, Jennifer Meyers, Carmen Leitch, Nicholas Katsanis, Neda Sharifi, Lauren Xu, Loretha Myers, Philip Spevak and Duke Cameron of Johns Hopkins; Julie De Backer, Jan Hellemans, Paul Coucke and Anne De Paepe of Ghent University Hospital, Belgium; Yan Chen and Daniel Rifkin of New York University School of Medicine; Elaine Davis of McGill University, Montreal, Canada; Catherine Webb, Northwestern University School of Medicine; and Wolfram Kress, University of Wuerzburg, Germany.

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Contact: Joanna Downer
jdowner1@jhmi.edu
410-614-5105
Johns Hopkins Medical Institutions
30-Jan-2005

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