1. A new method of destroying thrombi in blood vessels by ultrasound and simultaneously removing them is reported.2. Experiments were performed in twenty dogs with artificial thrombi in the iliac and femoral arteries and veins, The length of the thrombi ranged from 4 to 5 cm and the age from 12 h to 10 days. The unit used consisted of a generator, a frequency counter, an ultrasonic transducer with the hollow waveguide and a vacuum pump. For protection of the vessel wall the guide is surrounded by a plastic tube. The ultrasonic frequency is 26-5 kHz, the amplitude 25-30 pm. The time needed to destroy the thrombus by ultrasound and suck out the thrombotic material ranged from 2.5 to 5 min.3. To check side effects, experiments were performed in forty-four dogs. No significant changes were seen in the fibrinolytic system or microscopic structure of the vessel wall after ultrasound.

Hepatic stellate cell transdifferentiation, epithelial-mesenchymal cell transition, and the ductular reaction each contribute to the development of hepatic fibrosis in cholestatic liver diseases. Inhibitors of mammalian target of rapamycin have antifibrotic properties. We evaluated the hypothesis that the antifibrotic action of rapamycin is due to attenuated myofibroblast proliferation in addition to an inhibitory effect on epithelial-mesenchymal transition and the ductular reaction. Hepatic fibrosis was induced by bile duct ligation, and rodents received 1.5 mg/kg/day rapamycin by subcutaneous infusion for 21 days. The expression of various markers of hepatic fibrosis, stellate cell transactivation, epithelial-mesenchymal transition, and the ductular reaction was compared between treated and untreated animals. Hepatic fibrosis, hepatic procollagen type 1 messenger RNA, and alpha-smooth muscle actin expression were significantly reduced in treated animals. Hepatic stellate cell procollagen expression and proliferation were also reduced by rapamycin. The following markers of epithelial-mesenchymal transition--vimentin protein expression, S100 calcium binding protein A4 and transforming growth factor beta 1 messenger RNA, and the mothers against decapentaplegic homolog signaling pathway--were all reduced after rapamycin treatment. The intensity of the ductular reaction was reduced by rapamycin as assessed by histopathological scoring and by reduced cytokeratin 19 expression. Rapamycin caused a reduction in hepatic progenitor cell proliferation. Together, these data show that multiple profibrogenic pathways are activated in an animal model of cholestasis and that rapamycin attenuates epithelial-mesenchymal transition and the ductular reaction as well as hepatic stellate cell activation.

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