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.

Ex Input:
Context: Activation of NF-kappaB signaling pathway plays a critical role in the initiation and progression of carcinogenesis. However, the role of NF-kappaB pathway in esophageal squamous cell carcinoma (ESCC) has not been fully elucidated. Studies have shown that curcumin possesses anti-infection and anti-oxidation effects. This study was to evaluate whether curcumin could induce apoptosis through inhibition of NF-kappaB signaling pathway in ESCC cells.', 'Expressions of pIkappaBalpha and Bcl-2 were detected using Western blott after incubation of ESCC cells with curcumin (50 micromol/L) at different time points. Apoptosis and the number of viable ESCC cells were analyzed using flow cytometry and MTT, respectively, after the treatment of curcumin, 5-FU, or the combination of curcumin and 5-FU.', 'In two ESCC cell lines, EC9706 and Eca109,curcumin inhibited IkappaBalpha phosphorylation and Bcl-2 in a time-dependent manner; curcumin alone increased cell apoptosis (P<0.05), and the effect became more prominent when it was combined with 5-FU (P<0.05); curcumin plus 5-FU exerted a stronger inhibition effect on cell proliferation than curcumin alone (P<0.05) or 5-FU alone (P<0.05).
Answer: Curcumin inhibits the phosphorylation of IkappaBalpha, leading to suppression of proliferation, induction of apoptosis and an increase of the sensitivity of ESCC cell lines towards 5-FU.

Ex Output:
Does [ Curcumin promote apoptosis of esophageal squamous carcinoma cell lines through inhibition of NF-kappaB signaling pathway ]?


Ex Input:
Context: Impaired spatial working memory is a core cognitive deficit observed in people with 22q11 Deletion syndrome (22q11DS) and has been suggested as a candidate endophenotype for schizophrenia. However, to date, the neuroanatomical mechanisms describing its structural and functional underpinnings in 22q11DS remain unclear. We quantitatively investigate the cognitive processes and associated neuroanatomy of spatial working memory in people with 22q11DS compared to matched controls. We examine whether there are significant between-group differences in spatial working memory using task related fMRI, Voxel based morphometry and white matter fiber tractography.', 'Multimodal magnetic resonance imaging employing functional, diffusion and volumetric techniques were used to quantitatively assess the cognitive and neuroanatomical features of spatial working memory processes in 22q11DS. Twenty-six participants with genetically confirmed 22q11DS aged between 9 and 52 years and 26 controls aged between 8 and 46 years, matched for age, gender, and handedness were recruited.', 'People with 22q11DS have significant differences in spatial working memory functioning accompanied by a gray matter volume reduction in the right precuneus. Gray matter volume was significantly correlated with task performance scores in these areas. Tractography revealed extensive differences along fibers between task-related cortical activations with pronounced differences localized to interhemispheric commissural fibers within the parietal section of the corpus callosum.
Answer: Abnormal spatial working memory in 22q11DS is associated with aberrant functional activity in conjunction with gray and white matter structural abnormalities. These anomalies in discrete brain regions may increase susceptibility to the development of psychiatric disorders such as schizophrenia. Hum Brain Mapp 37:4689-4705, 2016. © 2016 Wiley Periodicals, Inc.

Ex Output:
Does multimodal MRI reveal structural connectivity differences in 22q11 deletion syndrome related to impaired spatial working memory?


Ex Input:
Context: The literature seldom specifies the location or method of measurement of ST segment elevation (STE) for determining eligibility in reperfusion trials. The objective of this study was to assess if different methods of measurement of STE in precordial leads of patients with anterior acute myocardial infarction due to left anterior descending occlusion result in significantly different scores.', 'This was a retrospective review of diagnostic electrocardiograms (ECGs) of consecutive patients presenting to our emergency department with acute myocardial infarction who had emergent primary percutaneous coronary intervention, left anterior descending occlusion, and no bundle branch block. STE was measured at the J point and at 60 milliseconds after the J point, relative to the PR segment, in leads V1-V6. STE by the two methods was compared for each lead, as were ST scores (sum of STE in leads V1-V6) and the sum of the STE in V2-V4. Eligibility for reperfusion therapy using 1-mm and 2-mm STE criteria in two consecutive anterior leads, as well as ST scores and the sum of the STE in V2-V4, were evaluated.', 'Thirty-seven ECGs were analyzed. Mean ST measurements in every lead were significantly lower when measured at the J point versus 60 milliseconds after the J point, as were ST scores (9.7 +/- 2.14 mm vs. 14.9 +/- 2.69 mm; p < 0.00001). Fewer ECGs met enrollment criteria when based on STE at the J point versus at 60 milliseconds after the J point. Fewer ECGs met an ST score of 6 mm when measured at the J point (70% vs. 88%).
Answer: In anterior STE myocardial infarction, STE measurements produce different results depending on the method of measurement. Future clinical trials should specify the method of measurement.

Ex Output:

Does sT segment elevation differ depending on the method of measurement?