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: Pathological evidence supports a potential role of the pro- and anti-inflammatory cytokine network in the pathogenesis of inflammatory bowel disease (IBD). Moreover, associated studies suggest a possible involvement of cytokine-related genes in IBD susceptibility. In this study, we evaluated the effect of the anti-inflammatory interleukin-10 (IL10) gene on ulcerative colitis (UC).', 'Two functional single nucleotide polymorphisms (-1082 G/A, -819 T/C) in the IL10 promoter in 203 Italian sporadic UC patients and 391 controls were determined using high-resolution melting analysis.', 'The frequency of the -1082A allele was significantly higher in the UC patients than in controls (p=0.00003); -1082 genotype frequencies were also significantly different between UC patients and controls (p=0.0001). Allele and genotype frequencies of -819 T/C were not significantly associated with UC. Furthermore, the frequencies of haplotypes -1082A/-819C and -1082A/-819T, which have been reported to have a lower promoter activity, were significantly higher in UC patients than in controls (p=0.0004). After gender stratification, we found a significant difference in the -1082A allele (p=0.00004) and genotype (p=0.0002) frequencies only between female UC patients and controls; the same result was obtained for the -1082A/-819C and -1082A/-819T haplotypes (p=0.0006).

A: Do interleukin-10 promoter polymorphisms influence susceptibility to ulcerative colitis in a gender-specific manner?
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Q: This study investigated the isolated and combined effects of heat [temperate (22C/30% rH) vs. hot (35C/40% rH)] and hypoxia [sea level (FiO2 0.21) vs. moderate altitude (FiO2 0.15)] on exercise capacity and neuromuscular fatigue characteristics.', 'Eleven physically active subjects cycled to exhaustion at constant workload (66% of the power output associated with their maximal oxygen uptake in temperate conditions) in four different environmental conditions [temperate/sea level (control), hot/sea level (hot), temperate/moderate altitude (hypoxia) and hot/moderate altitude (hot+hypoxia)]. Torque and electromyography (EMG) responses following electrical stimulation of the tibial nerve (plantar-flexion; soleus) were recorded before and 5min after exercise.', 'Time to exhaustion was reduced (P<0.05) in hot (-3515%) or hypoxia (-3614%) compared to control (6128min), while hot+hypoxia (-5120%) further compromised exercise capacity (P<0.05). However, the effect of temperature or altitude on end-exercise core temperature (P=0.089 and P=0.070, respectively) and rating of perceived exertion (P>0.05) did not reach significance. Maximal voluntary contraction torque, voluntary activation (twitch interpolation) and peak twitch torque decreased from pre- to post-exercise (-91, -41 and -61% all trials compounded, respectively; P<0.05), with no effect of the temperature or altitude. M-wave amplitude and root mean square activity were reduced (P<0.05) in hot compared to temperate conditions, while normalized maximal EMG activity did not change. Altitude had no effect on any measured parameters.

A: Does combining heat stress and moderate hypoxia reduce cycling time to exhaustion without modifying neuromuscular fatigue characteristics?
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Q: We sought to evaluate whether improvement in ejection fraction (EF) with carvedilol therapy is accompanied by improvement in neurohumoral factors.', 'Forty-two patients with dilated cardiomyopathy were given carvedilol for 3 to 5 months. Changes in EF, plasma atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and norepinephrine levels were determined. Iodine-123 metaiodobenzylguanidine (MIBG) images were also obtained before and after carvedilol therapy. Myocardial uptake of MIBG was calculated as the heart to mediastinal activity ratio (H/M). Storage and release of MIBG was calculated as percent myocardial MIBG washout rate (WR). We divided patients into 2 groups: 27 responders whose EF increased by more than 5% and 15 nonresponders whose EF increased by 5% or less. EF of responders increased by 15 +/- 5% and that of nonresponders by 1 +/- 4%. Although MIBG image-derived indexes of nonresponders remained unchanged, the delayed H/M (1.91 +/- 0.34 v 2.24 +/- 0.53, P < .01) and WR (49 +/- 11 v 39 +/- 9%, P < .01) of responders improved, respectively. The plasma ANP (51 +/- 50 v 27 +/- 24 pg/mL, P < .01) and BNP (194 +/- 197 v 49 +/- 62 pg/mL, P < .01) levels of responders decreased. The degree of changes in the plasma BNP level correlated with changes in EF (r = -.698, P < .01).

A:
Is improvement in left ventricular function in response to carvedilol accompanied by attenuation of neurohumoral activation in patients with dilated cardiomyopathy?
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