instruction:
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.
question:
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.
answer:
Does ezetimibe suppress cholesterol accumulation in lipid-loaded vascular smooth muscle cells in vitro via MAPK signaling?


question:
To determine whether cancer antigen-125 (CA-125) levels are increased in women with endometriosis, especially in those with endometriomas (OMAs), deep infiltrating lesions (DIE), and superficial endometriosis (SUP) compared with controls without endometriosis in a large cohort of operated women.', 'Cross-sectional study (Canadian Task Force classification II-2).', 'Tertiary-care university hospital.', 'Four hundred six women with histologically proven endometriosis and 279 women without endometriosis.', 'Surgical examination of the abdomino-pelvic cavity.', 'Preoperative serum CA-125 antigen levels were evaluated by electrochemoluminescence immunoassay in women with endometriosis and controls. Correlations between serum CA-125 levels and clinical and anatomical characteristics of disease severity were examined. Women with endometriosis displayed higher mean serum CA-125 levels compared with disease-free controls (50.1\xa0±\xa062.4 U/mL vs 22.5\xa0±\xa025.2 U/mL; p\xa0≤\xa0.001). CA-125 levels were significantly increased in women with OMA (60.8\xa0±\xa063.5 U/mL) and DIE (55.2\xa0±\xa068.7 U/mL) compared with women with SUP (23.2\xa0±\xa024.5 U/mL) and controls (22.5\xa0±\xa025.2 U/mL). There was no difference in CA-125 levels between patients with SUP and controls and between patients with OMA and DIE. CA-125 serum levels were correlated with DIE severity: the mean number of DIE lesions and worst DIE lesion.
answer:
Is increased serum cancer antigen-125 a marker for severity of deep endometriosis?


question:
High fructose intake has been suggested to be a key factor that induces nonalcoholic fatty liver disease (NAFLD), but the evidence from large epidemiologic studies is lacking.', 'We examined the cross-sectional association between fructose intake and NAFLD by using the Fatty Liver Index (FLI) and the NAFLD liver fat score.', 'The Helsinki Birth Cohort Study investigated 2003 Finnish men and women born in 1943-1944 in Helsinki who participated in a clinical health examination in the years 2001-2004. Trained study nurses measured weight, height, and waist circumference, and body mass index was calculated. Laboratory staff drew fasting blood for measurements of triglycerides and γ-glutamyl-transferase. The FLI and the NAFLD liver fat score were calculated on the basis of these measurements. Habitual fructose and other dietary intake over the past year were assessed by using validated and standardized 131-item food-frequency questionnaires. Data were analyzed in a cross-sectional manner by using logistic regression modeling with statistical software.', 'In a model adjusted for age, sex, and energy intake, participants in the highest fructose intake quartile (range: 29.2-88.0 g/d) had lower risk of NAFLD assessed by using the FLI (OR: 0.56; 95% CI: 0.42, 0.75; P-trend < 0.001) and NAFLD liver fat score (OR: 0.72; 95% CI: 0.53, 0.99; P-trend < 0.001) than that of the lowest intake quartile (range: 2.2-15.2 g/d). This association remained after adjustment for educational attainment, smoking, physical activity, and other dietary variables only for the FLI (OR: 0.68; 95% CI: 0.47, 0.84; P-trend < 0.05).
answer:

Is higher fructose intake inversely associated with risk of nonalcoholic fatty liver disease in older Finnish adults?