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.

Example Input: n-3 Fatty acids lower plasma triacylglycerols not only in the fasting state but also in the postprandial state. However, it is not known whether chylomicrons, chylomicron remnants, and VLDLs are all affected equally or whether some lipoprotein species are lowered preferentially.', 'Lipoproteins, including large and small chylomicron remnants, were determined specifically with the aid of a newly developed method involving a combination of size-exclusion chromatography and fluorometric determination of retinyl palmitate, which served as a marker for exogenous fat.', 'Twelve hypertriacylglycerolemic men were treated for 6 wk with 4 capsules containing 85% fish-oil concentrate/d; each capsule contained 850 mg n-3 fatty acid ethyl esters (49.1% eicosapentaenoic acid by wt and 32.2% docosahexaenoic acid by wt). Oral-fat-tolerance tests were performed before and after the treatment. Blood samples were drawn in the fasting state and until 8 h postprandially.', 'Treatment with n-3 fatty acids reduced the fasting VLDL-triacylglycerol concentration by 44% (P < 0.05) and postprandial chylomicrons and VLDLs at 4, 6, and 8 h (P < 0.05) by 49-64% and 36-43%, respectively. Chylomicron remnants were reduced only in the late postprandial phase: large chylomicron remnants by 19% at 6 h and by 43% at 8 h (P < 0.05) and small chylomicron remnants by 31% at 8 h (P < 0.05).
Example Output: Are postprandial chylomicrons and VLDLs in severe hypertriacylglycerolemia lowered more effectively than are chylomicron remnants after treatment with n-3 fatty acids?

Example Input: Hypoxemia is a common complication of chronic obstructive pulmonary disease and a major factor in patients' prognosis and quality of life. The response to exercise has been evaluated by various means but no standardization has been accepted.", 'To suggest a simple outpatient technique for evaluating the response of arterial oxygen saturation to exercise for use as a marker of disease severity.', 'Ninety-six patients with various degrees of COPD were divided into three groups: mild (forced expiratory volume in 1 sec > 65%), moderate (FEV1 between 50 and 65%), and severe (FEV1 < 50%). Using continuous oximeter recording we measured oxygen saturation during 15 steps of climbing, and quantified oxygen desaturation by measuring the "desaturation area," defined as the area under the curve of oxygen saturation from the beginning of exercise through the lowest desaturation point and until after recovery to the baseline level of oxygen percent saturation. Desaturation was correlated to spirometry, lung gas volumes, blood gas analysis, and 6 min walking distance.', 'A good correlation was found between severity of COPD and baseline SaO2, lowest SaO2, recovery time, and desaturation area. A negative correlation was found between desaturation area and FEV1 (r = -0.65), FEV1/forced vital capacity (r = -0.58), residual volume to total lung capacity (r = 0.52), and diffusing lung capacity for carbon monoxide (r = -0.52). In stepwise multiple regression analysis only FEV1 correlated significantly to desaturation area. A good correlation was noted between 6 min walking distance and desaturation area with the 15 steps technique (r = 0.56).
Example Output: Do quantitative 15 steps exercise oximetry as a marker of disease severity in patients with chronic obstructive pulmonary disease?

Example Input: Fetal hypoxia is an important determinant of neonatal encephalopathy caused by birth asphyxia, in which hypoxia-induced free radical formation plays an important role.', 'Maternal treatment with allopurinol, will cross the placenta during fetal hypoxia (primary outcome) and reduce S-100B and free radical formation (secondary outcome).', 'In a randomized, double-blind feasibility study, 53 pregnant women in labor (54 fetuses) with a gestational age of >36 weeks and fetal hypoxia, as indicated by abnormal/nonreassuring fetal heart rate tracing or fetal scalp pH of <7.20, received 500 mg of allopurinol or placebo intravenously. Severity of fetal hypoxia, brain damage and free radical formation were assessed by arterial cord blood lactate, S-100B and non-protein-bound-iron concentrations, respectively. At birth, maternal and cord blood concentrations of allopurinol and its active metabolite oxypurinol were determined.', 'Allopurinol and oxypurinol concentrations were within the therapeutic range in the mother (allopurinol > 2 mg/L and/or oxypurinol > 4 mg/L) but not always in arterial cord blood. We therefore created 3 groups: a placebo (n = 27), therapeutic allopurinol (n = 15), and subtherapeutic allopurinol group (n = 12). Cord lactate concentration did not differ, but S-100B was significantly lower in the therapeutic allopurinol group compared with the placebo and subtherapeutic allopurinol groups (P < .01). Fewer therapeutic allopurinol cord samples had measurable non-protein-bound iron concentrations compared with placebo (P < .01).
Example Output:
Does maternal allopurinol during fetal hypoxia lower cord blood levels of the brain injury marker S-100B?