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.

Example Input: Context: Nonasthmatic eosinophilic bronchitis (EB) has emerged as a useful tool to study the structural and inflammatory mechanisms of airway hyperresponsiveness (AHR) in asthma. We have previously shown that vascular remodeling and reticular basement membrane (RBM) thickening are present in EB. However, it is not known whether other features of structural remodeling including increased airway smooth muscle (ASM) mass, matrix deposition, and glandular hyperplasia are also present in EB.', 'We sought to determine whether structural remodeling occurs in EB and is associated with AHR and airflow limitation.', 'Forty-two patients with asthma, 21 patients with EB, and 19 healthy volunteers were recruited. ASM area, RBM thickness, collagen 3 deposition, glandular area, mast cells, and granulocytes were assessed in bronchial biopsy samples.', 'Nonasthmatic eosinophilic bronchitis and asthma were associated with a significant increase in ASM mass and RBM thickness compared with healthy subjects. In contrast, we did not observe any significant differences in collagen 3 deposition in the lamina propria and ASM or the % area of glands in the lamina propria. Univariate analysis demonstrated that mast cell numbers in the ASM were the only feature of remodeling associated with AHR (beta = -0.51; P = .004). Stepwise linear regression revealed that a combination of mast cell numbers in the ASM (beta = -0.43) and disease duration (beta = -0.25; model-adjusted R(2) = 0.26; P = .027) best modeled AHR.
Answer: Mast cell localization to the ASM bundle, but not structural remodeling of the airway wall, is associated with AHR in asthma.
Example Output: Is airway hyperresponsiveness dissociated from airway wall structural remodeling?

Example Input: Context: High sensitivity C-reactive protein (hsCRP) is more sensitive than standard C-reactive protein (CRP) assay in evaluating the risk of coronary heart disease and other atherosclerotic events. By this time, there are several reports that type 2 diabetic subjects have higher serum levels of hsCRP than those of non-diabetic subjects. However, there are few reports about factors which have influence upon the level of serum hsCRP in type 2 diabetic subjects. We had evaluated the association of serum hsCRP level with risk factors of cardiovascular diseases and carotid intima-media thickness (IMT) in type 2 diabetic subjects.', 'One hundred and five patients (59 men and 46 women) with type 2 diabetes were recruited. Subjects with severe cardiovascular diseases were excluded. All subjects were undergone carotid ultrasonography for evaluation of carotid IMT. Serum hsCRP concentrations were measured.', 'Serum hsCRP level was correlated with mean left IMT (r = 0.366, P = 0.003), maximal left IMT (r = 0.370, P = 0.002), mean right IMT (r = 0.281, P = 0.023) and maximal right IMT (r = 0.370, P = 0.002), body mass index (r = 0.377, P < 0.001), waist circumference (r = 0.342, P < 0.001), waist-hip ratio (r = 0.229, P = 0.020), serum total cholesterol (r = 0.202, P = 0.024), serum triglyceride (r = 0.292, P = 0.022) and serum low-density lipoprotein (r = 0.133, P = 0.044).
Answer: Our result shows that serum hsCRP level is correlated with carotid IMT and the risk factors of cardiovascular diseases and may be useful to predict accelerated atherosclerotic process in type 2 diabetic subjects.
Example Output: Is serum high sensitivity C-reactive protein associated with carotid intima-media thickness in type 2 diabetes?

Example Input: Context: Biological evidence reported in the literature supports the role of CELSR1 as being essential for valvular function in murine lymphatics. Yet thus far, there have been no variants in CELSR1 associated with lymphatic dysfunction in humans.', 'In this report, a rare early inactivating mutation in CELSR1 is found to be causal for non-syndromic, lower extremity lymphedema in a family across three generations. Near-infrared fluorescence lymphatic imaging shows that instead of being propelled within the lumen of well-defined lymphatic vessels, lymph moved in regions of both legs in an unusual fashion and within sheet-like structures.
Answer: CELSRI may be responsible for primary, non-syndromic lymphedema in humans.
Example Output:
Is a novel mutation in CELSR1 associated with hereditary lymphedema?