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: Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a member of growth factors that have been implicated in skin patho-physiology. Although endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) appear to be involved in mitogenesis and chemotaxis in epidermal keratinocytes, the activation of eNOS and VEGF production induced by HB-EGF and its signaling mechanism remains undefined.', 'We examined possible signal transduction pathways by which HB-EGF leads to eNOS activation and VEGF production in human epidermal keratinocyte cell line (HaCaT cells).', 'The phosphorylation of epidermal growth factor receptor (EGFR), mitogen-activated protein kinase (MAPK; p42/p44 MAPK), Akt and eNOS were examined by Western blotting analysis. VEGF production was determined by enzyme-linked immunosorbent assay. Various inhibitors were utilized to investigate the signaling mechanisms of eNOS activation and VEGF production.', 'HB-EGF-induced phosphorylation of EGFR with maximum phosphorylation at 1h. HB-EGF-induced phosphorylation of p42/p44 MAPK in a few minutes. It activated Akt with maximum phosphorylation at 1h and eNOS with maximum phosphorylation at 3h. The HB-EGF-induced eNOS activation was significantly blocked by the p42/p44 MAPK inhibitor U0126 and the phosphatidylinositol 3-kinase (P13K) inhibitor LY294002. HB-EGF increased VEGF production. The HB-EGF-induced VEGF production was blocked by U0126 and LY294002. Finally, the HB-EGF-induced activation of Akt and eNOS was suppressed by VEGF competitive antagonist, CBO-P11.
Answer: These results demonstrate that HB-EGF-induced eNOS activation depends on p42/p44 MAPK, PI3K/Akt pathways and endogenous VEGF in HaCaT cells.
[A]: Do hB-EGF-induced VEGF production and eNOS activation depend on both PI3 kinase and MAP kinase in HaCaT cells?


[Q]: Context: Ovarian cancer is a well-known disease with a poor prognosis. Due to the relatively small number of cases in Taiwan, the outcome and prognostic factors of patients with primary epithelial ovarian carcinoma are unknown.', "We retrospectively studied patients with proven surgical and pathologic (Federation Internationale de Gynecologie et d'Obstetrique) FIGO IIIC primary epithelial ovarian carcinoma. All patients underwent standard staging surgery, including washing cytology, total abdominal hysterectomy, bilateral salpingo-oophorectomy, retroperitoneal lymphadenectomy, infracolic omentectomy and excisional biopsy of all suspicious lesions followed by adjuvant chemotherapy with four to 12 courses of cyclophosphamide, epirubicin and cisplatin (CEP) or cyclophosphamide, adriamycin and cisplatin (CAP) intravenously, every three weeks. To avoid the coeffects of chemotherapy and surgical procedures upon the outcome, patients who received paclitaxel-based regimens or underwent incomplete surgery were excluded. Ninety-eight patients from 1990 to 1996 were identified.", 'The mean follow-up time was 28.7 months, ranging from 5.4 months to 105.9 months. The cumulative five-year disease-free survival rate for all patients was 31.6%. Optimal debulking surgery was completed in 41.8% of patients, which contributed to long-term patient survival (54% vs 16%, p < 0.0001), compared to patients without optimal debulking surgery. Optimal debulking surgery was the only statistically significant independent prognostic factor for five-year disease-free survival using multivariate analysis.
Answer: To improve survival of patients with FIGO stage IIIC epithelial ovarian carcinoma, optimal debulking surgery should be performed as the initial form of surgical intervention.
[A]: Is optimal debulking surgery an independent prognostic factor in patients with FIGO IIIC primary epithelial ovarian carcinoma?


[Q]: Context: It has recently been found that detrusor smooth muscle cells and myofibroblasts are coupled via gap junctions. However, gap junctions cannot account for strong physical interaction between cells, which has prompted the search for intercellular adhesion molecules. Cadherin-11 is a candidate for such a molecule, since it mediates the interaction of dermal myofibroblasts in contractile wound granulation tissue. We therefore hypothesised that the physical adhesion between detrusor smooth muscle cells and myofibroblasts is mediated by cadherin-11. The aim of this study was to test this hypothesis.', 'Bladder biopsies from eight radical cystectomy specimens were snap-frozen, sectioned, and stained for E-cadherin; cadherin-11; alpha-catenin; beta-catenin; gamma-catenin; and smooth muscle cell/myofibroblast markers connexin-43, vimentin, desmin, smooth muscle actin, and smoothelin. Specimens were analysed by using binocular epifluorescent and confocal laser-scanning microscopy.', 'Specific positive membranous expression of all adhesion complex molecules except E-cadherin was detected in detrusor suburothelial tissue. All biopsies showed a similar punctate pattern of expression for cadherin-11 within bundles of smooth muscle cells and a suburothelial layer of cells. Cadherin-11 was specifically located at the cell membrane, in distinct linear domains.
Answer: To our knowledge this is the first time evidence has been provided for cadherin-mediated smooth muscle and suburothelial myofibroblast cell-cell interaction in the human bladder. Cadherin-11 most probably plays an important role in the intercellular physical coupling of detrusor smooth muscle cells and also of myofibroblasts.
[A]:
Is cadherin-11 expressed in detrusor smooth muscle cells and myofibroblasts of normal human bladder?