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 Q]: Context: Severe mitral regurgitation (MR) reduces left atrial thrombus formation in patients with mitral stenosis (MS) and atrial fibrillation (AF). Plasma D-dimer levels represent a biochemical marker for fibrinolytic activity in prothrombotic states. The prothrombotic burden in patients with mitral valve disease and/or AF was assessed using plasma D-dimer levels.', 'The study population included 89 patients with mitral valve disease, 21 with AF but normal valves, and 15 healthy controls. The mitral valve group was subdivided into patients with MS (n = 27), severe MR (n = 26), and MS with concomitant with severe MR (MS/MR; n = 36). These subgroups were further subdivided according to the atrial rhythm (sinus rhythm (SR)+AF).', 'The mean left atrial size was increased in all groups with cardiac disease. D-dimer levels were highest in the MS+AF subgroup (527 +/- 134 microg/l). Patients with MS+AF, MS+SR, and nonvalvular AF had significantly higher D-dimer levels than controls (p < 0.01, by ANOVA). Patients with MR had normal levels of D-dimer. The atrial rhythm did not influence D-dimer levels in the MS/MR subgroup, or in the pure MR subgroup (p = NS).
Answer: Plasma D-dimer levels correlated with the embolic risk in mitral valve disease and non-valvular AF. The highest levels were found in patients with MS+AF and non-valvular AF. Severe MR decreased the D-dimer levels in MS and/or AF to control levels.
[EX A]: Does mitral regurgitation reduce systemic coagulation activity in patients with rheumatic heart disease?

[EX Q]: Context: Hyperoxia increases oxidative stress through the generation of reactive oxygen species and may therefore enhance inflammation in the lungs. The aim of this study was to investigate whether short term supplementary oxygen (28%) increases oxidative stress and inflammation in the airways by measuring 8-isoprostane and interleukin 6 (IL-6) concentrations in exhaled breath condensate.', 'Twenty three healthy subjects (12 men, mean (SD) age 48 (7) years) and 23 patients with chronic obstructive pulmonary disease (COPD; 15 men, mean (SD) age 56 (5) years) were studied. 8-isoprostane and IL-6 concentrations were measured by immunoassay.', 'Increased concentrations of 8-isoprostane and IL-6 were found in all subjects after breathing 28% oxygen for 1 hour. In healthy subjects the concentrations of 8-isoprostane and IL-6 were 10.9 (2.9) pg/ml and 4.9 (0.8) pg/ml, respectively, compared with baseline concentrations of 6.1 (1.3) pg/ml and 2.9 (0.6) pg/ml, and in patients with COPD the concentrations were 27.9 (3.1) pg/ml and 8.3 (1.2) pg/ml), respectively, compared with baseline concentrations of 18.9 (3.6) pg/ml and 6.3 (0.6) pg/ml. By contrast, breathing air through the same face mask for 1 hour had no significant effects on 8-isoprostane or IL-6 concentrations in normal subjects or those with COPD.
Answer: These findings suggest that short term supplementary oxygen may enhance oxidative stress and inflammation in the airways. Whether this happens with long term oxygen therapy needs to be determined.
[EX A]: Does supplementary oxygen in healthy subjects and those with COPD increase oxidative stress and airway inflammation?

[EX Q]: Context: To assess whether the free radical scavenger, edaravone, could provide protection from oxidative stress and hearing loss induced by noise exposure.', 'Forty-eight guinea pigs were divided into six groups and exposure to a stationary noise at 125 dB SPL for 2 h only once. Group A: measured hearing and reactive oxygen species (ROS) level without noise exposure. Group B: intratympanic saline injection. Group C: intratympanic edaravone injection. Group D: exposed to noise for 2 h. Group E: intravenous edaravone injection after noise exposure. Group F: intratympanic edaravone injection after noise exposure. All animals of group D, E and F were measured hearing with ABR before noise exposure, immediately after noise exposure and at 2, 6, 12, 24, 48, 72 h after noise exposure, and then were decapitated for ROS measurement with electron spin resonance technology.', "After noise exposure, the ABR threshold of group D increased immediately after acute acoustic trauma and did not get right finally, while group F came back about 10 dB SPL. The normal level of ROS in the cochlea of guinea pigs was about 21.68 (cm/g) and significantly increased after acute acoustic trauma, reaching its peak in 2h, and didn't return to normal after 72 h. Group E did not inhibit free radicals, while group F showed significant effect on inhibiting production of free radicals.
Answer: The level of ROS in cochlea were decreased significantly after intratympanic edaravone injection. The mechanism may due to its effective clearance of the ROS in cochlea.
[EX A]:
Does [ Edaravone protect hearing from acute acoustic trauma in guinea pigs ]?