A Novel Approach against Vascular Intimal Hyperplasia Through the Suppression of Girdin.

Intimal hyperplasia is an impediment to patency in both arteries after percutaneous angioplasty (PTA) and veingraft. It is well known that migration and proliferation of vascular smooth muscle cells (SMCs) influence the vascular remodeling process, there are no therapies to prevent intimal hyperplasia of post-PTA arteries and vein grafts. Girdin (girders of actin filaments), also known as Gα-interacting vesicle associated protein (GIV) is a novel actin-binding Akt substrate.

Fate of ischemic limbs in patients with Buerger's disease based on our 30-year experience: does smoking have a definitive impact on the late loss of limbs?

Purpose: We herein review the long-term results of our series of critical ischemic limbs caused by Buerger's disease.

Methods: A retrospective review of 103 patients with critical limb ischemia who were diagnosed with Buerger's disease by Shionoya's criteria between 1980 and 2010.

Results: The age of onset was 38.

Role of Girdin in intimal hyperplasia in vein grafts and efficacy of atelocollagen-mediated application of small interfering RNA for vein graft failure.

Objective: Intimal hyperplasia is a major obstacle to patency in grafted veins. Although migration and proliferation of vascular smooth muscle cells (SMCs) pivotally affect the vascular remodeling process, no therapy has been established to prevent intimal hyperplasia of vein grafts. We previously reported that the actin-binding protein Girdin crucially affects arterial remodeling.

Subclavian artery aneurysm in Marfan syndrome.

We present a case of a left subclavian artery aneurysm in a 48-year-old man with Marfan syndrome. Aneurysms of the subclavian artery are rare in patients with Marfan syndrome. Resection of the aneurysm and interposition with a synthetic graft were performed through a supra- and infraclavicular incision, without resecting the clavicle.