Stent-based controlled release of NO donor significantly reduces in-stent restenosis and is associated with increase in vascular cGMP and suppression of proliferation.
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. With sonography emerging as a first-line modality for evaluation of intra-abdominal trauma, sonographers may wish to become more familiar with the appearance of gallbladder injury on sonography to facilitate earlier diagnosis and to improve treatment and prognosis. We report a case of gallbladder perforation after blunt abdominal trauma diagnosed on the basis of computed tomography (CT) and sonography.
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. Channeled stents loaded with TGF-β1 or control microspheres were deployed in rabbit aortas. Stented aortas were harvested at 7 and 28 d and evaluated for Ki-67-positive cells, collagenous ECM production, and intima-to-media (I/M) ratio. At 7 d, the TGF-β1 group exhibited fewer Ki-67-positive cells were found for the TGF-β1 group (17.87 ± 2.18 cells per mm 2 ) relative to control (25.07 ± 2.65 cells per mm 2 , p = 0.04), but increased collagen content (31.4 ± 2.5 percentage area) compared with control (29.3 ± 1.2 percentage area, p = 0.019). The I/M ratio in the TGF-β1 group was reduced by 50% and 9.1% versus control at 7 d (0.13 ± 0.02 vs. 0.26 ± 0.02, p = 0.0001) and 28 d (1.80 ± 0.05 vs. 1.98 ± 0.08, p = 0.0038), respectively. Stent-based controlled release of TGF-β1 limits ISR and is associated with inhibition of SMC proliferation but an increase in ECM production.
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