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.

[EX Q]: Ovarian cancer (OvCa) is the most lethal gynecologic malignancy in the United States because of chemoresistant recurrent disease. Our objective was to investigate the efficacy of inhibiting the Notch pathway with a -secretase inhibitor (GSI) in an OvCa patient-derived xenograft model as a single agent therapy and in combination with standard chemotherapy.', 'Immunocompromised mice bearing xenografts derived from clinically platinum-sensitive human ovarian serous carcinomas were treated with vehicle, GSI (MRK-003) alone, paclitaxel and carboplatin (P/C) alone, or the combination of GSI and P/C. Mice bearing platinum-resistant xenografts were given GSI with or without paclitaxel. Gene transcript levels of the Notch pathway target Hes1 were analyzed using RT-PCR. Notch1 and Notch3 protein levels were evaluated. The Wilcoxon rank-sum test was used to assess significance between the different treatment groups.', 'Expression of Notch1 and 3 was variable. GSI alone decreased tumor growth in two of three platinum-sensitive ovarian tumors (p<0.05), as well as in one of three platinum-sensitive tumors (p=0.04). The combination of GSI and paclitaxel was significantly more effective than GSI alone and paclitaxel alone in all platinum-resistant ovarian tumors (all p<0.05). The addition of GSI did not alter the effect of P/C in platinum-sensitive tumors. Interestingly, although the response of each tumor to chronic GSI exposure did not correlate with its endogenous level of Notch expression, GSI did negatively affect Notch signaling in an acute setting.
[EX A]: Does inhibition of notch signaling in combination with Paclitaxel reduce platinum-resistant ovarian tumor growth?

[EX Q]: An association between obesity and otitis media with effusion (OME) has been previously reported. The aim of this study was to evaluate the association between dietary intake and OME when adjusting obesity.', 'We analyzed the differences in dietary intake between children with/without OME who were 4 through 13 years of age using data from a large population-based survey - the Korea National Health and Nutrition Examination Survey - from 2008 through 2012. Data from 4359 participants were analyzed using simple and multiple logistic regression analyses with complex sampling.', 'The BMI category, the proportion of total calorie intake, protein intake, water intake, and Na intake (intake/recommendation), and the distribution of carbohydrate intake were not associated with OME. The distribution of fat intake was associated with OME (each 10% increase of fat calories/total calories: unadjusted odds ratio [OR]=1.331, 95% confidence interval [CI]=1.016-1.744, P=0.038; age- and sex-adjusted OR=1.359, 95% CI=1.028-1.797, P=0.031; adjusted for age, sex and other factors OR=1.392, 95% CI=1.054-1.839, P=0.020). Based on BMI subgroup analysis, the distribution of fat intake was associated with OME in the healthy weight group (each 10% increase of fat calories/total calories: unadjusted OR=1.393, 95% CI=1.017-1.909, P=0.039; adjusted OR=1.470, 95% CI=1.051-2.055, P=0.024) but not in the obese group.
[EX A]: Is a high-fat diet associated with otitis media with effusion?

[EX Q]: Human inflammatory bowel disease (e.g., Crohn's disease and ulcerative colitis), is associated with leukocyte accumulation in the inflamed intestinal tissue. Recent studies strongly suggest a role of beta1 integrin receptors in regulating tissue damage and disease symptoms related to inflammatory bowel disease. The aim of this study was to investigate the role of the collagen-binding alpha2beta1 integrin (CD49b/CD29) in dextran sodium sulfate-induced colitis in mice.", 'Colitis was induced in mice through oral administration of 2% dextran sodium sulfate in drinking water. Rectal administration of anti-alpha2-monoclonal antibody (mAb) in 1 group was compared with oral treatment with betamethasone in another group and rectal administration of a control antibody in a third group. Clinical and histological signs of colitis, neutrophil infiltration into the colon mucosa, and gene expression of metalloproteinases were assessed.', 'Rectal administration of anti-alpha2-mAb was found to significantly reduce weight loss from 13.5% +/- 6.5% to 2.2% +/- 0.2% (P = 0.013 versus control mAb) and mucosal neutrophil infiltration from 47.2 +/- 10.0 to 6.6 +/- 8.0 neutrophils per counted area (P < 0.05 versus control mAb). Metalloproteinase gene expression was suppressed through anti-alpha2-mAb treatment. The protective effect against colitis seen after anti-alpha2beta1 integrin treatment was found to be favorable to the effect seen after high-dose oral betamethasone.
[EX A]:
Does integrin alpha2beta1 regulate neutrophil recruitment and inflammatory activity in experimental colitis in mice?