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: Before desflurane is advocated for patients undergoing neurosurgical procedures, it is necessary to determine the effect of desflurane on cerebral blood flow (CBF). In this study, CBF values are compared between desflurane and isoflurane at two doses. In addition, CBF reactivity to CO2 and the effect of prolonged exposure were compared between the two agents.', 'Cerebral blood flow measurements with intravenous 133Xe were performed in 24 patients undergoing craniotomy for mass lesions, randomized to receive either isoflurane or desflurane in oxygen and air. Cerebral blood flow was determined at 1 and 1.5 MAC concentrations at PaCO2 of 25 mmHg in the absence of surgical stimulation. Intraoperatively, with 1.25 MAC anesthesia, CBF was determined at target PaCO2 of 25 and 35 mmHg. In 15 patients, an additional measurement at 1.25 MAC was made before closure.', 'At 1.0 MAC, mean +/- SD CBF values for the desflurane and isoflurane groups were 18 +/- 2 and 20 +/- 3 ml x 100 g-1 x min-1, respectively. At 1.5 MAC, CBF values were the same for the two anesthetics; 17 +/- 3 ml x 100 g-1 x min-1 for isoflurane and 19 +/- 4 ml.100 g-1 x min-1 for desflurane. During 1.25 MAC anesthesia, there were no differences between groups, with CO2 reactivity 1.3 +/- 1.2 ml x 100 g-1 x min-1 x mmHg-1 for desflurane and 1.6 +/- 0.6 ml.100 g-1 x min-1 x mmHg-1 for isoflurane. There was no demonstrable decrease in CBF with prolonged exposure to either agent.
Answer: Desflurane and isoflurane are similar in terms of absolute CBF, the response to increasing doses, and the preservation of CO2 reactivity.
Example Output: Do desflurane and isoflurane have similar effects on cerebral blood flow in patients with intracranial mass lesions?

Example Input: Context: To determine the effects of endostatin on vascular growth factor receptor 2 (VEGFR2) expression in non-small cell lung cancer (NSCLC) cells and the mechanisms underlying its radiosensitizing effect.', 'VEGFR2 mRNA levels were determined in different NSCLC cell lines using qRT-PCR. RT-PCR and Western blot assays were used to assess the expression of mRNA and proteins. The radiosensitivity of the cells was determined by colony-formation assays; and cell apoptosis and cell cycle distribution were determined by flow cytometry.', 'VEGFR2 mRNA levels differed among the five NSCLC cell lines (P < 0.01), with the highest expression in Calu-1 cells and lowest in A549 cells. Endostatin significantly inhibited the growth of Calu-1 cells (P < 0.01) (IC20 = 296.5 μg/ml), and the expression of VEGFR2 and HIF-1α (P < 0.05). Phosphorylation of protein kinase B (Akt), extracellular signal-regulated kinases 1/2 (ERK1/2), and p38 were significantly lower in endostatin-treated cells than control (P < 0.05). Endostatin enhanced the radiosensitivity of Calu-1 cells to SER = 1.38 and induced apoptosis (P < 0.01) and G2/M blockage (P < 0.01). However, endostatin had limited effects on A549 cells. Compared with Calu-1 cells, there was not significantly effects on cell radiosensitivity (SER = 1.09).
Answer: Endostatin induces apoptosis and enhances radiosensitivity of the VEGFR2 high-expressing cell line Calu-1, but it has a limited effect on the VEGFR2 low-expressing cell line A549.
Example Output:
Does endostatin exert radiosensitizing effect in non-small cell lung cancer cells by inhibiting VEGFR2 expression?