Given a passage with a context and an answer, 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 Input:
Context: Intestinal fibrosis is mainly associated with Crohn's disease and is defined as a progressive and excessive deposition of extracellular matrix components. No specific antifibrotic therapies are available. In this study, we evaluate the antifibrotic effect of a novel 5-ASA analog able to activate the peroxisome proliferator-activated receptor γ, named GED-0507-34 Levo.", 'Colonic fibrosis was induced in 110 C57BL/6 mice by 3 cycles of 2.5% (wt/vol) dextran sulfate sodium administration for 6 weeks. The preventive effects of oral daily GED (30 mg · kg(-1) · d(-1)) administration were evaluated using a macroscopic and histological score and also through biological endpoints. Expression of main markers of myofibroblasts activation was determined in transforming growth factor (TGF-β)-stimulated intestinal fibroblasts and epithelial cells.', 'GED improved macroscopic and microscopic intestinal lesions in dextran sulfate sodium-treated animals and reduced the profibrotic gene expression of Acta2, COL1a1, and Fn1 by 1.48-folds (P < 0.05), 1.93-folds (P < 0.005), and 1.03-fold (P < 0.05), respectively. It reduced protein levels of main markers of fibrosis (α-SMA and Collagen I-II) and the main TGF-β/Smad pathway components. GED also decreased the interleukin-13 and connective tissue growth factor expression by 1.89-folds (P < 0.05) and 2.2-folds (P < 0.005), respectively. GED inhibited TGF-β-induced activation of both fibroblast and intestinal epithelial cell lines, by regulating mRNA expression of α-SMA and fibronectin, and restoring the TGF-β-induced loss of intestinal epithelial cell markers. GED treatment also reduced the TGF-β and ACTA1 expression in primary human intestinal fibroblasts from ulcerative colitis patients.
Answer: GED ameliorates intestinal fibrosis in dextran sulfate sodium-induced chronic colitis in mice and regulates major profibrotic cellular and molecular mechanisms.

Ex Output:
Does novel PPARγ Modulator GED-0507-34 Levo ameliorate Inflammation-driven Intestinal Fibrosis?


Ex Input:
Context: Several lines of evidence suggest that the dietary isoflavone genistein (Gen) has beneficial effects with regard to cardiovascular disease and in particular on aspects related to blood pressure and angiogenesis. The biological action of Gen may be, at least in part, attributed to its ability to affect cell signalling and response. However, so far, most of the molecular mechanisms underlying the activity of Gen in the endothelium are unknown.', 'To examine the transcriptional response to 2.5 microM Gen on primary human endothelial cells (HUVEC), we applied cDNA array technology both under baseline condition and after treatment with the pro-atherogenic stimulus, copper-oxidized LDL. The alteration of the expression patterns of individual transcripts was substantiated using either RT-PCR or Northern blotting. Gen significantly affected the expression of genes encoding for proteins centrally involved in the vascular tone such as endothelin-converting enzyme-1, endothelin-2, estrogen related receptor alpha and atrial natriuretic peptide receptor A precursor. Furthermore, Gen countered the effect of oxLDL on mRNA levels encoding for vascular endothelial growth factor receptor 165, types 1 and 2.
Answer: Our data indicate that physiologically achievable levels of Gen change the expression of mRNA encoding for proteins involved in the control of blood pressure under baseline conditions and reduce the angiogenic response to oxLDL in the endothelium.

Ex Output:
Does genistein affect the expression of genes involved in blood pressure regulation and angiogenesis in primary human endothelial cells?


Ex Input:
Context: To determine how anterior advancement of the mandible (ADM) affects spontaneous breathing through the nasal route in healthy human volunteers sedated with intravenous midazolam.', 'In four subjects who exhibited nasal breathing during midazolam sedation (intravenous dose: 0.09+/-0.02 mg x kg(-1), mean +/- SD), we measured respiratory rate (RR), peak nasal inspiratory airflow rate (V(nIpeak)) peak nasal expiratory airflow rate (V(nEpeak), duty ratio (Ti/Ttot) and nasal resistance (Rn) before and after ADM. Nasal resistance was calculated by dividing the difference between nasal mask and oropharyngeal pressure by airflow rate at peak nasal inspiratory airflow.', 'The RR, V(nIpeak), and V(nEpeak) increased following ADM (P<0.001, respectively). On the contrary, Ti/Ttot decreased after ADM (P<0.001). Consequently, ADM decreased Rn from 30.4+/-40.8 to 5.0+/-5.6 (cm H2O x l(-1) x sec(-1)) (mean +/- SD) (P<0.001). In these four subjects, no respiratory airflow was observed through the oral route before and after ADM.
Answer: Advancement of the mandible decreases nasal resistance, thereby facilitating spontaneous breathing through the nasal route in normal humans sedated with midazolam.

Ex Output:

Does advancement of the mandible facilitate nasal breathing in human subjects sedated with midazolam?