William Brooks.

Thomas G. Brott, M.D., Robert W. Hobson, II, M.D., George Howard, Dr.P.H., Gary S. Roubin, M.D., Ph.D., Wayne M. Clark, M.D., William Brooks, M.D., Ariane Mackey, M.D., Michael D. Hill, M.D., Pierre P. Leimgruber, M.D., Alice J. Sheffet, Ph.D., Virginia J. Howard, Ph.D., Wesley S. Moore, M.D., Jenifer H. Voeks, Ph.D., L. Nelson Hopkins, M.D., Donald E. Cutlip, M.D., David J. Cohen, M.D., Jeffrey J. Popma, M.D., Robert D. Ferguson, M.D., Stanley N. Cohen, M.D., Joseph L. Blackshear, M.D., Frank L. Silver, M.D., J.P. Mohr, M.D., Brajesh K. Lal, M.D., and James F. Meschia, M.D. For the CREST Investigators: Stenting versus Endarterectomy for Treatment of Carotid-Artery Stenosis Carotid-artery atherosclerosis is an important cause of ischemic stroke.1 Carotid endarterectomy has been established as effective treatment for both symptomatic patients and asymptomatic patients.2-4 Carotid-artery stenting is another option for treatment.Whereas the overall ratio of nonsynonymous to synonymous mutations was 3. Furthermore, these mutations occurred solely in conserved sites across species . Four of the genes with significant mutation frequencies, TP53, ATM, MYD88, and NOTCH1, have been described previously in chronic lymphocytic leukemia. 3A in the Supplementary Appendix). 3C in the Supplementary Appendix).19 Finally, we detected a recurrent frameshift mutation in the C-terminal PEST domain of NOTCH1 in 4 patients that was identical to that recently reported in various other investigations of chronic lymphocytic leukemia.5,6 This mutation is connected with unmutated IGHV and a poor prognosis,5,6 in fact it is predicted to trigger impaired degradation of NOTCH1, leading to pathway activation.