By Helena Kuivaniemi MD, PhD, Gerard Tromp PhD, David J. Carey PhD, James R. Elmore MD (auth.), Jonathon W. Homeister, Monte S. Willis (eds.)
Molecular and Translational Vascular Medicine will function a cutting-edge source for physicians and translational clinical researchers alike who're drawn to the quickly evolving box of vascular drugs. The textual content offers new perception into the elemental mechanisms of vintage vascular pathophysiologic tactics like angiogenesis, atherosclerosis, thrombosis, and vasculitis. additionally, it covers new parts of research together with the function of the ubiquitin proteasome procedure in vascular disorder, endothelial progenitor cells for ailment therapy, and the genetic foundation of thoracic aortic aneurysms. finally, this quantity contains sections at the newly rising box of healing angiogenesis, and the constructing know-how of nanoparticle-based imaging and healing therapy of the diseased vasculature. All chapters are written by way of demonstrated specialists of their fields, together with pathologists, cardiovascular surgeons, and internists in addition to translational biomedical researchers in a variety of disciplines. whereas entire, the cloth is gifted in a fashion that simplifies the advanced pathophysiologic mechanisms that underlie universal vascular illnesses.
Molecular and Translational Vascular Medicine may be of significant worth to a large viewers together with internists, cardiovascular and vascular surgeons, pathologists, citizens and fellows, in addition to translational biomedical researchers.
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94. Shimizu K, Shichiri M, Libby P, Lee RT, Mitchell RN. Th2-predominant inflammation and blockade of IFN-gamma signaling induce aneurysms in allografted aortas. J Clin Invest. 2004;114:300–8. 95. Thompson RW, Curci JA, Ennis TL, Mao D, Pagano MB, Pham CT. Pathophysiology of abdominal aortic aneurysms: insights from the elastase-induced model in mice with different genetic backgrounds. Ann N Y Acad Sci. 2006;1085:59–73. 96. Pyo R, Lee JK, Shipley JM, et al. Targeted gene disruption of matrix metalloproteinase-9 (gelatinase B) suppresses development of experimental abdominal aortic aneurysms.
This new definition provides sensitivity and specificity for classification of HSP (using other forms of vasculitis as controls) of 100% and 87%, respectively [8]. Pathogenesis As many as 50% of occurrences in paediatric patients are preceded by an upper respiratory tract infection [4, 9]. Several agents have been implicated, including group A streptococci, varicella, hepatitis B, Epstein–Barr virus, parvovirus B19, Mycoplasma, Campylobacter, and Yersinia [4]. Of note, Masuda et al. showed that nephritis-associated plasmin receptor (NAPlr), a group A streptococcal antigen, may have a pathogenetic role in a subset of patients with HSP nephritis [10].