Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Q: Prevention of intraabdominal abscess formation constitutes an important goal in treatment of secondary peritonitis. Fibrinolytic therapy may be effective in this respect. The efficacy of recombinant tissue plasminogen activator (rtPA) and urokinase is compared in a preclinical model for surgical treatment of peritonitis.', 'Peritonitis was induced by intraperitoneal bacterial challenge in male Wistar rats. After 1 hour, surgery was performed. Four groups (n = 20) were treated with one of the following: rtPA, urokinase, streptokinase (a negative protein control), or saline. Blood cultures were taken at 6 and 24 hours; cell counts and cytokine measurements were performed in peritoneal fluid at 1, 3 and 5 days. After 5 days, animals were killed and intraperitoneal abscess formation was analyzed.', 'Both rtPA and urokinase strongly (> 75%) and significantly (P < .05) reduced abscess formation without negative side effects. No bleeding complications were observed. Fibrinolytic therapy altered the intraperitoneal cellular distribution (less neutrophils and more macrophages) but did not essentially alter the courses of interleukin-6 and interleukin-10 (decreasing in time) or tumor necrosis factor-* (increasing in time) levels.

A: Do both tissue-type plasminogen activator and urokinase prevent intraabdominal abscess formation after surgical treatment of peritonitis in the rat?
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Q: To investigate the mechanisms of anti-atherosclerotic action of ezetimibe in rat vascular smooth muscle cells (VSMCs) in vitro.', 'VSMCs of SD rats were cultured in the presence of Chol:MβCD (10 μg/mL) for 72 h, and intracellular lipid droplets and cholesterol levels were evaluated using Oil Red O staining, HPLC and Enzymatic Fluorescence Assay, respectively. The expression of caveolin-1, sterol response element-binding protein-1 (SREBP-1) and ERK1/2 were analyzed using Western blot assays. Translocation of SREBP-1 and ERK1/2 was detected with immunofluorescence.', 'Treatment with Chol:MβCD dramatically increased the cellular levels of total cholesterol (TC), cholesterol ester (CE) and free cholesterol (FC) in VSMCs, which led to the formation of foam cells. Furthermore, Chol:MβCD treatment significantly decreased the expression of caveolin-1, and stimulated the expression and nuclear translocation of SREBP-1 in VSMCs. Co-treatment with ezetimibe (3 μmol/L) significantly decreased the cellular levels of TC, CE and FC, which was accompanied by elevation of caveolin-1 expression, and by a reduction of SREBP-1 expression and nuclear translocation. Co-treatment with ezetimibe dose-dependently decreased the expression of phosphor-ERK1/2 (p-ERK1/2) in VSMCs. The ERK1/2 inhibitor PD98059 (50 μmol/L) altered the cholesterol level and the expression of p-ERK1/2, SREBP-1 and caveolin-1 in the same manner as ezetimibe did.

A: Does ezetimibe suppress cholesterol accumulation in lipid-loaded vascular smooth muscle cells in vitro via MAPK signaling?
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Q: Prostasomes are small (40-500 nm), granule-like bodies, found in normal epithelial cells of the prostate and secreted into the prostate duct system. Also poorly differentiated prostate cancer cells are producing prostasomes, since we could isolate and purify prostasomes from vertebral metastases with biochemical methods. To find out whether these prostasomes are secreted into extracellular sites of the metastases, we used electron microscopy.', 'Small biopsies from vertebral metastases of prostate cancer, taken directly from the operating field at surgery, were immediately fixated, embedded in plastic and processed for electron microscopy.', 'We found that prostasomes could be identified extracellularly in the interstitial tissues as well as in the cytoplasm of the metastatic cells.

A:
Are prostasomes secreted from poorly differentiated cells of prostate cancer metastases?
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