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.

[EX Q]: Rhinovirus (RV) infection in asthma induces varying degrees of airway inflammation (e.g. neutrophils), but the underlying mechanisms remain unclear.', 'The major goal was to determine the role of genetic variation [e.g. single nucleotide polymorphisms (SNPs)] of Toll-interacting protein (Tollip) in airway epithelial responses to RV in a type 2 cytokine milieu.', 'DNA from blood of asthmatic and normal subjects was genotyped for Tollip SNP rs5743899 AA, AG and GG genotypes. Human tracheobronchial epithelial (HTBE) cells from donors without lung disease were cultured to determine pro-inflammatory and antiviral responses to IL-13 and RV16. Tollip knockout and wild-type mice were challenged with house dust mite (HDM) and infected with RV1B to determine lung inflammation and antiviral response.', 'Asthmatic subjects carrying the AG or GG genotype (AG/GG) compared with the AA genotype demonstrated greater airflow limitation. HTBE cells with AG/GG expressed less Tollip. Upon IL-13 and RV16 treatment, cells with AG/GG (vs. AA) produced more IL-8 and expressed less antiviral genes, which was coupled with increased NF-κB activity and decreased expression of LC3, a hallmark of the autophagic pathway. Tollip co-localized and interacted with LC3. Inhibition of autophagy decreased antiviral genes in IL-13- and RV16-treated cells. Upon HDM and RV1B, Tollip knockout (vs. wild-type) mice demonstrated higher levels of lung neutrophilic inflammation and viral load, but lower levels of antiviral gene expression.
[EX A]: Does tollip SNP rs5743899 modulate human airway epithelial responses to rhinovirus infection?

[EX Q]: To investigate the relationship between mean platelet volume (MPV) and glycometabolic indices, to compare MPV according to HbA1c levels, and to analyse the difference in MPV between patients with and without microvascular complications.', 'This retrospective study was conducted on 60 Type 2 diabetic patients and 50 age- and sex-matched non-diabetic controls. We obtained demographic, clinical and laboratory data including MPV, platelet count, fasting and postprandial blood glucose (FBG and PBG), haemoglobin A1c (HbA1c), lipid profile, creatinine, systolic and diastolic blood pressure (BP) in patient and control groups, and diabetic microvascular complications including nephropathy, neuropathy, and retinopathy in the patient group. All analyses were performed using SPSS version 15.0 for Windows.', 'Mean platelet volume in the diabetic group was higher than in the control group (p = 0.001). Mean platelet volume was positively correlated with FBG and HbA1c levels (p = 0.03 and p < 0.001, respectively). It was also negatively related to platelet count (p < 0.001). Mean platelet volume in patients with HbA1c > 7% was significantly higher than those with HbA1c ≤ 7% (p < 0.001). Mean platelet volume was significantly increased in patients with retinopathy compared to those without retinopathy (p = 0.04).
[EX A]: Is mean platelet volume associated with glycaemic control and retinopathy in patients with type 2 diabetes mellitus?

[EX Q]: Allelic losses [loss of heterozygosity (LOH)] at the 17p13 locus are frequent (85%) in adrenocortical cancers. The tumor suppressor gene TP53 is located at 17p13. The aim of the study was to determine the frequency of TP53 somatic inactivating mutations in adrenocortical tumors with 17p13 LOH and their clinico-biological correlations.', 'TP53 somatic mutations, intragenic LOH (VNTR1 marker), and p53 overexpression were studied in 36 adrenocortical tumors with 17p13 LOH determined by Southern blot.', 'TP53 mutations were detected in 33% of the tumors, and VNTR1 LOH was present in 44% of the cases and did not always correlate with the presence of a TP53 mutation. Only the TP53-mutant tumors exhibit a strong nuclear immunoreactivity. TP53-mutant tumors were significantly larger than wild-type TP53 tumors (median tumor weight: 640 versus 185 g; P=0.02), were associated with a more advanced stage of tumor progression (MacFarlane stage IV; P=0.01), and had a shorter disease-free survival (P=0.03).
[EX A]:
Are somatic TP53 mutations relatively rare among adrenocortical cancers with the frequent 17p13 loss of heterozygosity?