METHODS: Radiation arteriopathy in the common carotid arteries of 171 wild-type mice was examined with doses of 25, 80, 120, or 200 Gy (Experiment 1). Radiation arteriopathy in 68 wild-type arteriovenous fistulae was examined histologically and morphometrically with preoperative radiation doses of 0, 25, or 200 Gy (Experiment 2). Radiation arteriopathy

in 51 transgenic arteriovenous fistulae (36 ENG and 15 eNOS knockout fistulae) was examined using preoperative radiation doses of 0, 25, or 200 Gy (Experiment 3).

RESULTS: High-dose radiation (200 Gy) of mouse common carotid arteries induced only Protein Tyrosine Kinase inhibitor mild arteriopathy (mean score, 0.66) without intimal hyperplasia and with high mortal- ity Epigenetics inhibitor (68%). Radiation arteriopathy in wild-type arteriovenous fistulae was severe (mean score, 3.5 at 200 Gy), with intimal hyperplasia and medial disruption at 3 months, decreasing luminal areas with increasing dose, and no mortality. Arteriopathy was robust in transgenic genic arteriovenous fistulae with ENG +/- and with eNOS +/- with thick intimal hyperplasia in the former and distinct smooth muscle cell proliferation in the latter.

CONCLUSION: The transgenic arteriovenous

fistula model can be adapted to rapidly reproduce radiation arteriopathy observed in resected brain arteriovenous malformations after radiosurgery. High radiation doses accelerate the progression of arteriopathy to fit the 4-month time limitation of the model, allowing transgenic tissues to retain their phenotypes throughout the experimental window.

Modified radiation responses in ENG and eNOS knock-out fistulae indicate that arteriopathy after arteriovenous malformation radiosurgery might potentially be enhanced by altered gene expression.”
“A highly effective attenuated equine infectious anemia virus (EIAB) vaccine (EIAV(D9)) capable of protecting 100% of horses from disease induced by a homologous Env challenge strain (EIAV(PV)) was recently tested in ponies to determine the level of protection against divergent Env challenge strains (J. K. Craigo, B. S. Zhang, S. Barnes, T. L. Tagmyer, S. J. Cook, C. J. Issel, and R. C. Montelaro, Histidine ammonia-lyase Proc. Natl. Acad. Sci. USA 104:15105-15110, 2007). An inverse correlation between challenge strain Env variation and vaccine protection from disease was observed. Given the striking differences in protective immunity, we hypothesized that analysis of the Immoral and cellular immune responses to the Env protein could reveal potential determinants of vaccine protection. Neutralization activity against the homologous Env or challenge strain-specific Env in immune sera from the vaccinated ponies did not correlate with protection from disease.