Publications by authors named "Bruce Cutler"

Objective: We assessed the effect of an open vascular simulation course on the surgical skill of junior surgical residents in performing a vascular end-to-side anastomosis and determined the course length required for effectiveness. We hypothesized that a 6-week course would significantly increase the surgical skill of junior residents in performing an end-to-side anastomosis, while a 3-week course would not.

Methods: We randomized 37 junior residents (postgraduate year 1 to 3) to a course consisting of three (short course, n = 18) or six (long course, n = 19) consecutive weekly 1-hour teaching sessions.

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Objectives: Interleukin 18 (IL18) is an interferon (IFN)-gamma-inducing factor and a proinflammatory and proatherogenic cytokine. IL18 binding protein (IL18-BP) functions as an IL18 inhibitor. This study was designed to investigate whether systemic administration of IL18-BP could inhibit neointimal hyperplasia and arterial lipid deposition.

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Objectives: The goal of this study was to evaluate the ability of recombinant human thrombomodulin (rTM) to inhibit neointimal hyperplasia when bound to expanded polytetrafluoroethylene (ePTFE) stent grafts placed in a porcine balloon injured carotid artery model.

Methods: The left carotid artery of male pigs, weighing 25 to 30 Kg, was injured with an angioplasty balloon. Two weeks later either a non-coated standard ePTFE stent graft (Viabahn, 6 x 25 mm, W.

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Introduction And Objectives: Several publications document the technical feasibility of stent graft repair of aortic transection. We report our mid-term results of endovascular repair of thoracic aortic transections using covered stent grafts and compare this to a cohort undergoing open repair during the same time period to demonstrate the shift in practice pattern at our institution.

Materials And Methods: A retrospective review of patients who sustained blunt thoracic transection was undertaken.

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The success of vascular intervention including angioplasty, stenting, and arterial bypass remains limited by negative remodeling resulted in lumen restenosis. This study was to characterize the global transcription profile reflecting concurrent events along arterial remodeling and neointima formation in a rat carotid artery balloon-injury model. Expression profiling of injured and control common carotid arteries on days 4, 7, 14 post-injury that mark the major pathohistological progression stages of neointimal formation were recorded on high-density oligonucleotide arrays.

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Objective: Smooth muscle cell proliferation is a major pathophysiologic factor in injury-induced neointimal hyperplasia and recurrent stenosis. We have demonstrated that recombinant human thrombomodulin (rTM) inhibits thrombin-induced arterial smooth muscle cell proliferation in vitro. The purpose of this study was to investigate the effect of rTM on neointimal hyperplasia in vivo.

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Atherosclerosis contributing to cardiovascular disease is the leading cause of death in the United States. It is also the major cause of peripheral arterial disease (PAD). Although there is substantial evidence that aggressive treatment of hyperlipidemia improves the outcome of patients with coronary artery disease (CAD), relatively little attention has been directed toward lipid control in patients with PAD.

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Background: The success of synthetic grafts for vascular reconstruction remains limited by thrombosis and intimal hyperplasia. In addition to the well-described antithrombotic effects of thrombomodulin, we have demonstrated that recombinant human thrombomodulin (rTM) inhibits arterial smooth muscle cell proliferation induced by thrombin. This study investigated the binding of functional rTM to expanded polytetrafluoroethylene (ePTFE).

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A 48-year-old woman was admitted to our institution with angina pectoris and a systolic murmur. At cardiac catheterization, she was found to have an anomalous origin of the left anterior descending coronary artery from the pulmonary trunk. There was also an associated atrial septal defect and a bicuspid aortic valve.

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