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.

[EX Q]: Successful treatment of oesophageal cancer is hampered by recurrent drug resistant disease. We have previously demonstrated the importance of apoptosis and autophagy for the recovery of oesophageal cancer cells following drug treatment. When apoptosis (with autophagy) is induced, these cells are chemosensitive and will not recover following chemotherapy treatment. In contrast, when cancer cells exhibit only autophagy and limited Type II cell death, they are chemoresistant and recover following drug withdrawal.', 'MicroRNA (miRNA) expression profiling of an oesophageal cancer cell line panel was used to identify miRNAs that were important in the regulation of apoptosis and autophagy. The effects of miRNA overexpression on cell death mechanisms and recovery were assessed in the chemoresistant (autophagy inducing) KYSE450 oesophageal cancer cells.', 'MiR-193b was the most differentially expressed miRNA between the chemosensitive and chemoresistant cell lines with higher expression in chemosensitive apoptosis inducing cell lines. Colony formation assays showed that overexpression of miR-193b significantly impedes the ability of KYSE450 cells to recover following 5-fluorouracil (5-FU) treatment. The critical mRNA targets of miR-193b are unknown but target prediction and siRNA data analysis suggest that it may mediate some of its effects through stathmin 1 regulation. Apoptosis was not involved in the enhanced cytotoxicity. Overexpression of miR-193b in these cells induced autophagic flux and non-apoptotic cell death.
[EX A]: Does miR-193b promote autophagy and non-apoptotic cell death in oesophageal cancer cells?

[EX Q]: Hypoxemia is a common complication of chronic obstructive pulmonary disease and a major factor in patients' prognosis and quality of life. The response to exercise has been evaluated by various means but no standardization has been accepted.", 'To suggest a simple outpatient technique for evaluating the response of arterial oxygen saturation to exercise for use as a marker of disease severity.', 'Ninety-six patients with various degrees of COPD were divided into three groups: mild (forced expiratory volume in 1 sec > 65%), moderate (FEV1 between 50 and 65%), and severe (FEV1 < 50%). Using continuous oximeter recording we measured oxygen saturation during 15 steps of climbing, and quantified oxygen desaturation by measuring the "desaturation area," defined as the area under the curve of oxygen saturation from the beginning of exercise through the lowest desaturation point and until after recovery to the baseline level of oxygen percent saturation. Desaturation was correlated to spirometry, lung gas volumes, blood gas analysis, and 6 min walking distance.', 'A good correlation was found between severity of COPD and baseline SaO2, lowest SaO2, recovery time, and desaturation area. A negative correlation was found between desaturation area and FEV1 (r = -0.65), FEV1/forced vital capacity (r = -0.58), residual volume to total lung capacity (r = 0.52), and diffusing lung capacity for carbon monoxide (r = -0.52). In stepwise multiple regression analysis only FEV1 correlated significantly to desaturation area. A good correlation was noted between 6 min walking distance and desaturation area with the 15 steps technique (r = 0.56).
[EX A]: Do quantitative 15 steps exercise oximetry as a marker of disease severity in patients with chronic obstructive pulmonary disease?

[EX Q]: Stem cell factor (SCF) has well-known proliferative effects on hematopoietic cells. SCF also has effects on differentiation and proliferation in other cell types. Interleukin-6 (IL-6) and tumor necrosis factor (TNF)-alpha have proliferative effects in the liver. Recent studies in our laboratory have linked SCF's hepatoproliferative actions to those of IL-6, demonstrating that IL-6-induced hepatocyte proliferation depends, at least in part, on SCF. We now hypothesize that TNF-alpha's hepatoproliferative effects are also dependent on SCF.", 'In vitro studies using primary mouse hepatocytes show that SCF is induced by TNF-alpha; anti-SCF antibody treatment in this system inhibits TNF-alpha-induced hepatocyte proliferation, suggesting that TNF-alpha-induced hepatocyte proliferation is also SCF dependent. Additional in vivo experiments were performed in which wild type and/or TNF-alpha receptor-1 knockout mice (TNFR1(-/-)) were subjected to 70% hepatectomy or sham laparotomy. TNFR1(-/-) mice are known to have delayed hepatic regeneration after partial hepatectomy. Initial experiments demonstrated that the SCF receptor, c-kit, is upregulated after partial hepatectomy in wild-type mice, further emphasizing the importance of this system in the restoration of hepatic mass. SCF administration to TNFR1(-/-) mice in the context of partial hepatectomy restores hepatocyte proliferation to normal. Further, SCF administration to TNFR1(-/-) mice before hepatectomy increases phosphotyrosine signal transducer and activator (p-stat-3) levels, suggesting that SCF-induced increases in hepatocyte proliferation may also be stat-3 mediated.
[EX A]:
Are stem cell factor and its receptor , c-kit , important for hepatocyte proliferation in wild-type and tumor necrosis factor receptor-1 knockout mice after 70 % hepatectomy?