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.

Q: Context: The epigenetic mechanism of tumorigenesis in pancreatic intraductal papillary mucinous neoplasm (IPMN) remains largely unknown. The aim of this study is to examine the role of enhancer of zeste homologue 2 (EZH2) alteration in pancreatic IPMN progression.', 'Fifty-four surgically resected pancreatic IPMN specimens, including a total of 181 lesions (normal duct in 48, adenoma in 50, borderline atypia in 53, carcinoma in situ (CIS) in 19, and invasive carcinoma in 11) were analyzed by immunohistochemical staining (EZH2, Ki-67, p27Kip1). Using paraffin embedded sections, total RNA was successfully extracted from 20 IPMN lesions (borderline IPMN in 9, CIS in 6, invasive carcinoma in 5) and 7 pancreatic normal ducts, and then levels of EZH2 and p27Kip1 mRNA were analyzed by real time PCR.', 'In immunohistochemical analysis, cell proliferative activity revealed by Ki-67 positive nuclei was increased during IPMN progression (normal duct<adenoma<borderline atypia<CIS invasive carcinoma). EZH2 expression displayed a similar pattern (normal duct<adenoma<borderline atypia<CIS invasive carcinoma) with cell proliferative activity. EZH2 expression in malignant (CIS and invasive carcinoma) IPMNs was significantly higher than that in adenoma and borderline-atypia IPMNs. EZH2 expression level in IPMN lesions was positively correlated with the Ki-67 positive nuclear ratio (p<0.0001). EZH2-positive cells in malignant IPMN did not express p27Kip1. EZH2 mRNA expressions in malignant lesions were significantly higher than those in benign lesions (p<0.0001). In contrast, p27Kip1 mRNA in malignant lesions was significantly decreased compared to those in benign lesion (p<0.05), and there was an inverse correlation between EZH2 and p27Kip1 mRNA levels (p = 0.0109).
Answer: EZH2 is associated with the accelerated cell proliferation and malignant step in pancreatic IPMN via the downregulation of p27Kip1.

A: Is eZH2 associated with malignant behavior in pancreatic IPMN via p27Kip1 downregulation?
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Q: Context: To test the role of mast cells in gut inflammation and colitis using interleukin (IL)-10-deficient mice as an experimental model.', 'Mast cell-deficient (Kit (W-sh/W-sh) ) mice were crossbred with IL-10-deficient mice to obtain double knockout (DKO) mice. The growth, mucosal damage and colitis status of DKO mice were compared with their IL-10-deficient littermates.', 'DKO mice exhibited exacerbated colitis compared with their IL-10-deficient littermates, as shown by increased pathological score, higher myeloperoxidase content, enhanced Th1 type pro-inflammatory cytokines and inflammatory signaling, elevated oxidative stress, as well as pronounced goblet cell loss. In addition, deficiency in mast cells resulted in enhanced mucosal damage, increased gut permeability, and impaired epithelial tight junctions. Mast cell deficiency was also linked to systemic inflammation, as demonstrated by higher serum levels of tumor necrosis factor and interferon in DKO mice than that in IL-10-deficient mice.
Answer: Mast cell deficiency in IL-10-deficient mice resulted in systematic and gut inflammation, impaired gut barrier function, and severer Th1-mediated colitis when compared to mice with only IL-10-deficiency. Inflammation and impaired gut epithelial barrier function likely form a vicious cycle to worsen colitis in the DKO mice.

A: Does mast cell deficiency exacerbate inflammatory bowel symptoms in interleukin-10-deficient mice?
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Q: Context: Transannular patching (TAP) frequently accompanies primary repairs (PRs) in symptomatic neonates with tetralogy of Fallot (TOF). If a systemic-pulmonary shunt (SPS) facilitates the growth of the pulmonary valve annulus (PVA), patients with a marginally small PVA could benefit from a staged repair in terms of lowering the risk of TAP.', 'Among 216 infants with TOF who underwent surgical intervention between January 2004 and December 2013, 29 infants underwent SPS with a subsequent repair (SPS group), whereas 187 infants received a PR (PR group). Median age and the Z-score of the PVA (PVA [Z]) at SPS were 32 days and-3.5, respectively. There was one late death and one follow-up loss after SPS, and preservation of the PVA was achieved on repair in 16 patients (16 of 29; 55%).', 'Multiple regression analysis showed that performance of SPS was the only indicator of the increase in the PVA (Z) in the entire cohort (n= 216). On mixed linear regression, the PVA (Z) increased significantly after the placement of an SPS (-3.6+ 0.2*duration in months, p= 0.001), whereas the prerepair changes in the PVA (Z) were not statistically significant in the PR group (p= 0.7), with a significant intergroup difference (p < 0.001). Receiver operating characteristic curve analysis showed that placement of TAP is expected when the preshunt PVA (Z) is smaller than-4.2 (area under the curve: 0.82; 95% confidence interval: 0.62 to 1.00; sensitivity, 100%; specificity, 73%).
Answer: SPS facilitates outgrowth of the PVA over somatic growth in patients with TOF. However, preservation of the PVA may not be achieved on staged repair if the initial PVA is too small.

A:
Does systemic-Pulmonary Shunt facilitate the Growth of the Pulmonary Valve Annulus in Patients With Tetralogy of Fallot?
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