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.

Q: Context: Humans can easily restore a speech signal that is temporally masked by an interfering sound (e.g., a cough masking parts of a word in a conversation), and listeners have the illusion that the speech continues through the interfering sound. This perceptual restoration for human speech is affected by prior experience. Here we provide evidence for perceptual restoration in complex vocalizations of a songbird that are acquired by vocal learning in a similar way as humans learn their language.', "European starlings were trained in a same/different paradigm to report salient differences between successive sounds. The birds' response latency for discriminating between a stimulus pair is an indicator for the salience of the difference, and these latencies can be used to evaluate perceptual distances using multi-dimensional scaling. For familiar motifs the birds showed a large perceptual distance if discriminating between song motifs that were muted for brief time periods and complete motifs. If the muted periods were filled with noise, the perceptual distance was reduced. For unfamiliar motifs no such difference was observed.
Answer: The results suggest that starlings are able to perceptually restore partly masked sounds and, similarly to humans, rely on prior experience. They may be a suitable model to study the mechanism underlying experience-dependent perceptual restoration.

A: Does stimulus familiarity affect perceptual restoration in the European starling ( Sturnus vulgaris )?
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Q: Context: Expression of CINCs was regulated differentially in lipopolysaccharide-stimulated rat macrophages. We examined whether the expression of CINCs in lipopolysaccharide-stimulated rat macrophages is similarly inhibited by anti-inflammatory drugs.', 'Rat peritoneal macrophages were stimulated by lipopolysaccharide in the presence of anti-inflammatory steroids (dexamethasone, prednisolone and hydrocortisone) or non-steroidal anti-inflammatory drugs (indomethacin and piroxicam). The production and mRNA expression of three types of CINCs were measured using enzyme-linked immunosorbent assay and northern hybridization.', 'Anti-inflammatory steroids; dexamethasone, prednisolone and hydrocortisone, dose-dependently inhibited the production of CINC-1, -2 and -3, whose inhibitory patterns were similar to each other. Furthermore mRNA expression of each CINC was inhibited by dexamethasone in a dose-dependent manner. In contrast, non-steroidal anti-inflammatory drugs, indomethacin and piroxicam were without effect. Expression of each CINC was regulated differently; the production of CINC-1 reached a maximum at 12 h and then slightly decreased after lipopolysaccharide stimulation, whereas that of CINC-2 and CINC-3 increased up to 24 h. Dexamethasone inhibited the CINCs production and mRNA expression at 9 h after lipopolysaccharide stimulation.
Answer: These results indicate no difference among CINC-1, -2 and -3 in the inhibition of production and mRNA expression of CINCs by anti-inflammatory steroids, although lipopolysaccharide differentially induces expression of each CINC expression in culture of rat macrophages.

A: Is the expression of three types of CINCs by lipopolysaccharide-stimulated rat macrophages inhibited similarly by anti-inflammatory steroids?
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Q: Context: Myocardial scarring leads to cardiac dysfunction and poor prognosis. The prevalence of and factors associated with unrecognized myocardial infarction and scar have not been previously defined using contemporary methods in a multiethnic US population.', 'To determine prevalence of and factors associated with myocardial scar in middle- and older-aged individuals in the United States.', 'The Multi-Ethnic Study of Atherosclerosis (MESA) study is a population-based cohort in the United States. Participants were aged 45 through 84 years and free of clinical cardiovascular disease (CVD) at baseline in 2000-2002. In the 10th year examination (2010-2012), 1840 participants underwent cardiac magnetic resonance (CMR) imaging with gadolinium to detect myocardial scar. Cardiovascular disease risk factors and coronary artery calcium (CAC) scores were measured at baseline and year 10. Logistic regression models were used to estimate adjusted odds ratios (ORs) for myocardial scar.', 'Cardiovascular risk factors, CAC scores, left ventricle size and function, and carotid intima-media thickness.', 'Myocardial scar detected by CMR imaging.', 'Of 1840 participants (mean [SD] age, 68 [9] years, 52% men), 146 (7.9%) had myocardial scars, of which 114 (78%) were undetected by electrocardiogram or by clinical adjudication. In adjusted models, age, male sex, body mass index, hypertension, and current smoking at baseline were associated with myocardial scar at year 10. The OR per 8.9-year increment was 1.61 (95% CI, 1.36-1.91; P <\u2009.001); for men vs women: OR, 5.76 (95% CI, 3.61-9.17; P <\u2009.001); per 4.8-SD body mass index: OR, 1.32 (95% CI, 1.09-1.61, P =\u2009.005); for hypertension: OR, 1.61 (95% CI, 1.12-2.30; P =\u2009.009); and for current vs never smokers: 2.00 (95% CI, 1.22-3.28; P =\u2009.006). Age-, sex-, and ethnicity-adjusted CAC scores at baseline were also associated with myocardial scar at year 10. Compared with a CAC score of 0, the OR for scores from 1 through 99 was 2.4 (95% CI, 1.5-3.9); from 100 through 399, 3.0 (95% CI, 1.7-5.1), and 400 or higher, 3.3 (95% CI, 1.7-6.1) (P ≤ .001). The CAC score significantly added to the association of myocardial scar with age, sex, race/ethnicity, and traditional CVD risk factors (C statistic, 0.81 with CAC vs 0.79 without CAC, P =\u2009.01).
Answer: The prevalence of myocardial scars in a US community-based multiethnic cohort was 7.9%, of which 78% were unrecognized by electrocardiography or clinical evaluation. Further studies are needed to understand the clinical consequences of these undetected scars.

A:
Does prevalence and correlate of Myocardial Scar in a US Cohort?
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