{'fraction_non_alphanumeric': 0.022222222222222223, 'fraction_numerical': 0.0044444444444444444, 'mean_word_length': 5.723880597014926, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
inhibitor reduces intimal hyperplasia in aortocoronary saphenous vein grafts

T Objective: Approximately 50% of aortocoronary saphenous vein grafts are occluded 10 years after coronary revascularization surgery. Intimal hyperplasia, a critical component in saphenous vein graft failure, is defined by vascular smooth muscle cell proliferation, which is mediated in part by subunits of heterotrimeric G proteins (G ) and downstream effectors such as mitogen-activated protein kinases. A peptide consisting of the carboxyl-terminus of the -adrenergic receptor kinase ( ARKct) binds G , thereby inhibiting G signaling. Utilizing a recombinant adenovirus containing the coding sequence for the ARKct peptide (Ad ARKct), this study investigates whether treatment of the vein graft with Ad ARKct reduces intimal hyperplasia in a large animal model of aortocoronary saphenous vein graft intimal hyperplasia.