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.

Input: Consider Input: Evodiamine is one of active alkaloids isolated from the traditional Chinese medicine Evodia rutaecarpa Bentham and has various pharmacological properties. In this study, we investigated its effects on the migration, invasion, and associated mechanism in human nasopharyngeal carcinoma (NPC) cells.', 'Cell viability was determined by MTT assay after evodiamine treatment. Wound-healing assay and Boyden transwell system were used to evaluate the inhibitory effects of evodiamine on cell migration and invasion. MMP-2/9 activity was determined using commercial detection kits. The levels of associated proteins involved in the regulation of cell migration and invasion were analyzed by Western blotting.', 'Evodiamine effectively inhibited the migration and invasion of HONE1 and CNE1 cells, and hardly affected cell proliferation, but significantly suppressed cell adhesion activity in vitro. Additionally, evodiamine treatment significantly decreased mRNA and protein levels of MMP-2 and its activity in the NPC cells, but had little effects on MMP-9 mRNA and protein levels and its activity. Further investigation revealed that evodiamine inhibited the translocation of NF-κB p65, which involves the regulation of MMP-2 expression in cancer invasion. Additionally, evodiamine treatment did not significantly affect the protein levels of JNK, p38, Akt, and their phosphorylated forms and ERK1/2, but strongly attenuated ERK1/2 phosphorylation level, which at least partly accounts for the signal pathway of evodiamine-inhibited migration and invasion of NPC cells.

Output: Does evodiamine inhibit the migration and invasion of nasopharyngeal carcinoma cells in vitro via repressing MMP-2 expression?


Input: Consider Input: Airway remodeling in asthma is the result of increased expression of connective tissue proteins, airway smooth muscle cell (ASMC) hyperplasia and hypertrophy. TGF-beta1 has been found to increase ASMC proliferation. The activation of mitogen-activated protein kinases (MAPKs), p38, ERK, and JNK, is critical to the signal transduction associated with cell proliferation. In the present study, we determined the role of phosphorylated MAPKs in TGF-beta1 induced ASMC proliferation.', 'Confluent and growth-arrested bovine ASMCs were treated with TGF-beta1. Proliferation was measured by [3H]-thymidine incorporation and cell counting. Expressions of phosphorylated p38, ERK1/2, and JNK were determined by Western analysis.', 'In a concentration-dependent manner, TGF-beta1 increased [3H]-thymidine incorporation and cell number of ASMCs. TGF-beta1 also enhanced serum-induced ASMC proliferation. Although ASMCs cultured with TGF-beta1 had a significant increase in phosphorylated p38, ERK1/2, and JNK, the maximal phosphorylation of each MAPK had a varied onset after incubation with TGF-beta1. TGF-beta1 induced DNA synthesis was inhibited by SB 203580 or PD 98059, selective inhibitors of p38 and MAP kinase kinase (MEK), respectively. Antibodies against EGF, FGF-2, IGF-I, and PDGF did not inhibit the TGF-beta1 induced DNA synthesis.

Output: Does tGF-beta1 increase proliferation of airway smooth muscle cells by phosphorylation of map kinases?


Input: Consider Input: Patients with obstructive sleep apnea (OSA) and coronary artery disease have a poor long-term prognosis. It is unknown whether the coronary blood flow (CBF) response to OSA is appropriate for myocardial metabolic requirements. Therefore, CBF was assessed during OSA, before and after the development of coronary artery endothelial dysfunction.', 'University Hospital Animal Laboratory.', 'Newborn lambs.', 'Lambs were surgically instrumented for invasive hemodynamic monitoring and sleep-wake EEG recordings. A tracheostomy was inserted to control the upper airway and model OSA during sleep. Coronary artery endothelial dysfunction was created using infusions of lipopolysaccharide (LPS). The CBF response during OSA was assessed and compared to changes in myocardial work (rate-pressure product [RPP]), O2 saturation, and cortical arousal, before and after the LPS infusions.', 'During OSA, CBF increased by 8.6% +/- 2.4% above baseline in the pre-LPS condition and 8.8% +/- 1.9% post-LPS, peaking following termination of the respiratory event. Pre-LPS, change in CBF post-apnea was independently correlated with change in RPP (R2 = 0.50), minimum SpO2 (R2 = 0.11) and the presence of cortical arousal (R2 = 0.04) (P < 0.01, forward stepwise regression analysis). Following LPS, the only predictor of CBF was degree of O2 desaturation (R2 = 0.14, P < 0.05).


Output: Does coronary blood flow become uncoupled from myocardial work during obstructive sleep apnea in the presence of endothelial dysfunction?