Local Stent-Based Release of Transforming Growth Factor-β1 Limits Arterial In-Stent Restenosis.

The long-term success of intra-arterial stenting remains limited by in-stent restenosis (ISR). Transforming growth factor-β1 (TGF-β1) can inhibit smooth muscle cell (SMC) proliferation and migration and convert SMCs into extracellular matrix (ECM)-synthesizing cells. Here, we evaluate the effects of stent-based delivery of TGF-β1 on ISR in a rabbit model.

Outcomes with retrievable inferior vena cava filters: a multicenter study.

Purpose: To retrospectively review the outcomes after placement and retrieval of retrievable inferior vena cava (IVC) filters at two academic medical centers.

Materials And Methods: All patients who underwent retrievable filter placement between May 2001 and December 2005 were included. Hospital records at both institutions were reviewed, and relevant data were collected concerning the placement and retrieval of all removable filters.

Directed migration of smooth muscle cells to engineer plaque-resistant vein grafts.

Purpose: To test the hypothesis that controlled perivascular release of tissue plasminogen activator (tPA) can generate cleaved extracellular matrix (ECM) chemotactic gradients to guide the migration of vascular smooth muscle cells (SMCs) away from the lumen, thereby limiting neointima formation.

Methods: This hypothesis was tested in rabbit models in which the perivascular surface of vein bypass grafts was treated with microspheres releasing tPA (MS-tPA), microspheres containing no drug (MS-blank), or phosphate buffered saline (PBS). Vein graft segments harvested after 7 days were then evaluated for elastin content, proliferating SMCs, intima-to-media (I/M) ratio, and inflammation; late impact on neointima formation was also examined.

Efficient inhibition of in-stent restenosis by controlled stent-based inhibition of elastase: a pilot study.

Purpose: It is proposed that local elastase inhibition could suppress the extracellular matrix (ECM) degradation and subsequent smooth muscle cell migration and limit subsequent in-stent restenosis. This study evaluated the effect of stent-based controlled elastase inhibition on restenosis after stent implantation in a rabbit model.

Materials And Methods: Biodegradable microspheres containing the potent elastase inhibitor alpha-1-antitrypsin (AAT) were prepared.

Stent-based controlled release of intravascular angiostatin to limit plaque progression and in-stent restenosis.

Purpose: To evaluate the importance of angiogenesis in plaque progression after stent placement, this study examines stent-based controlled delivery of the antiangiogenic agent, angiostatin, in a rabbit model.

Materials And Methods: Controlled release biodegradable microspheres delivering angiostatin or polymer-only microspheres (polylactic-co-glycolic-acid-polyethylene glycol; PLGA/PEG) were loaded in channeled stents, anchored, and deployed in the aorta of adult New Zealand white rabbits (n = 6 animals per group, three each per time point). The stented aortas were harvested at 7 days and 28 days and evaluated for neovascularization, local inflammation, vascular smooth muscle cell proliferation, and in-stent plaque progression.

In-stent restenosis limitation with stent-based controlled-release nitric oxide: initial results in rabbits.

Purpose: To evaluate effect of controlled stent-based release of an NO donor to limit in-stent restenosis in rabbits.

Materials And Methods: Bioerodable microspheres containing NO donor or biodegradable polymer (polylactide-co-glycolide-polyethylene glycol) were prepared and loaded in channeled stents. Daily concentrations of NO release from NO-containing microspheres were assayed in vitro.

Sonographic diagnosis of traumatic gallbladder rupture.

Gallbladder injuries after blunt abdominal trauma are rare and often follow a vague and insidious clinical course. Consequently, gallbladder injuries commonly go undiagnosed until exploratory laparotomy. Early diagnosis is essential, because trauma to the gallbladder is typically treated surgically, and delay in treatment can result in considerable mortality and morbidity.