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.

Input: Consider Input: Context: Anorectal manometry provides objective information about anorectal function, but its results depend on the examiner's skill, the type of equipment, and subject characteristics like age or gender. This single institution, prospective study was performed to investigate the effect of gender and age on the results of anorectal manometry.", 'All included subjects completed a questionnaire to assess their bowel function. The survey included 13 validated questions (eight on constipation and five on incontinence) and was used to exclude subjects with pathological constipation or incontinence. Subjects with normal bowel function underwent anorectal manometry to measure anal sphincter length (ASL), maximum resting pressure (MRP), and maximum squeeze pressure (MSP), and the results were compared by gender and age.', 'The mean age of the 154 participants (94 male and 60 female) was 59.1 years. ASL was greater in men (4.23 vs. 3.85 cm, p<0.001). MRP was not significantly different according to gender (p=0.93), but MSP was higher in men (190.18 vs. 116.49 mmHg, p<0.001). ASL did not correlate with age (p=0.707). MRP was inversely related to age in both men (R (2)=0.152, p<0.001) and women (R (2)=0.282, p<0.001), and MSP only in women (R (2)=0.210, p<0.001).
Answer: Anorectal manometric parameters are influenced by gender and age. This should be taken into consideration when interpreting manometric readings in a clinical setting.

Output: Are anorectal manometric parameters influenced by gender and age in subjects with normal bowel function?

Input: Consider Input: Context: Reactive oxygen species have been implicated as signaling molecules modulating the activity of redox-sensitive transcription factors such as nuclear factor kappa B (NF-kappaB). Recently, the transcription factor hypoxia-inducible factor-1 (HIF-1), known to mediate gene expression by hypoxia, has been found to be also activated by nonhypoxic factors in a redox-sensitive manner. We therefore aimed to elucidate the link between these 2 important redox-sensitive transcription factors.', 'In pulmonary artery smooth muscle cells, reactive oxygen species generated either by exogenous H2O2 or by a NOX4-containing NADPH oxidase stimulated by thrombin activated or induced NF-kappaB and HIF-1alpha. The reactive oxygen species-mediated HIF-1alpha induction occurred on the transcriptional level and was dependent on NF-kappaB. Transfection experiments with wild-type or mutant HIF-1alpha promoter constructs revealed the presence of a yet unidentified NF-kappaB binding element. Gel shift analyses and chromatin immunoprecipitation verified binding of NF-kappaB to this site. Furthermore, reactive oxygen species enhanced expression of plasminogen activator inhibitor-1, which was prevented by dominant-negative IkappaB or mutation of the HIF-1 binding site within the plasminogen activator inhibitor-1 promoter.
Answer: These findings show for the first time to our knowledge that reactive oxygen species directly link HIF-1alpha and NF-kappaB, implicating an important pathophysiological role of this novel pathway in disorders associated with elevated levels of reactive oxygen species.

Output: Do reactive oxygen species activate the HIF-1alpha promoter via a functional NFkappaB site?

Input: Consider Input: Context: Managing aggressive breast cancers with enhanced chromosomal instability (CIN) is a significant challenge in clinics. Previously, we described that a cell cycle-associated kinase called Tousled-like kinase 2 (TLK2) is frequently deregulated by genomic amplifications in aggressive estrogen receptor-positive (ER
Answer: Targeting TLK2 presents an attractive therapeutic strategy for the TLK2-amplified breast cancers that possess enhanced genomic instability and aggressiveness. Mol Cancer Res; 14(10); 920-7. ©️2016 AACR.
Output: Does amplification of TLK2 induce Genomic Instability via Impairing the G2-M Checkpoint?