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: SOX2 and SOX9 are commonly overexpressed in glioblastoma, and regulate the activity of glioma stem cells (GSCs). Their specific and overlapping roles in GSCs and glioma treatment remain unclear.', 'SOX2 and SOX9 levels were examined in human biopsies. Gain and loss of function determined the impact of altering SOX2 and SOX9 on cell proliferation, senescence, stem cell activity, tumorigenesis and chemoresistance.', 'SOX2 and SOX9 expression correlates positively in glioma cells and glioblastoma biopsies. High levels of SOX2 bypass cellular senescence and promote resistance to temozolomide. Mechanistic investigations revealed that SOX2 acts upstream of SOX9. mTOR genetic and pharmacologic (rapamycin) inhibition decreased SOX2 and SOX9 expression, and reversed chemoresistance.
Answer: Our findings reveal SOX2-SOX9 as an oncogenic axis that regulates stem cell properties and chemoresistance. We identify that rapamycin abrogate SOX protein expression and provide evidence that a combination of rapamycin and temozolomide inhibits tumor growth in cells with high SOX2/SOX9.

Ex Output:
Does mTOR inhibition decrease SOX2-SOX9 mediated glioma stem cell activity and temozolomide resistance?


Ex Input:
Context: Observational and clinical studies suggest different responses upon sex hormone replacement therapy in ischaemic heart disease. Few studies, however, have examined the impact of oestrogen receptor-dependent mechanisms on the extent of injury after myocardial infarction (MI). Therefore, we set out to evaluate the effect of oestrogen (E2) replacement on infarct size and remodelling, and the respective role of the oestrogen receptors (ER)alpha and -beta in this process, using ERalpha- and ERbeta-deficient mice.', 'Wild type (WT) (ERalpha(+/+) and ERbeta(+/+)), ERalpha-deficient (ERalpha(-/-)) and ERbeta-deficient (ERbeta(-/-)) mice were ovariectomized and subsequently supplemented with E2 or placebo using subcutaneous 60-day release pellets. MI was induced by left coronary artery ligation. Two weeks following MI, haemodynamic function was assessed and infarct size was determined.', 'There was no significant difference in infarct size between E2- or placebo-treated WT (ERalpha(+/+) and ERbeta(+/+)) mice. Surprisingly, E2 treatment did result in smaller infarct sizes in ERalpha(-/-) mice, but increased the infarct size in ERbeta(-/-) mice. Increase of the left ventricular mass post-MI was significantly larger in the E2-treated ERalpha(-/-) animals compared with placebo-treated animals. E2 treatment also significantly increased post-MI mortality in ERalpha(+/+), ERbeta(+/+) and ERalpha(-/-) animals, but not in ERbeta(-/-) mice.
Answer: Although E2 modulates the infarct size in ERalpha(-/-), it also appears to be responsible for the higher mortality following MI. ERbeta appears to be the receptor involved in the modulating effects of E2 in the infarcted heart.

Ex Output:
Does oestrogen modulate cardiac ischaemic remodelling through oestrogen receptor-specific mechanisms?


Ex Input:
Context: Islet function is regulated by islet autonomic nerves. These nerves harbour not only the classical neurotransmitters, acetyl choline and noradrenaline, but also neuropeptides. This study examined whether the neuropeptides, pituitary adenylate cyclase activating polypeptide (PACAP) and gastrin releasing polypeptide (GRP) contribute to the regulation of insulin secretion in model experiments by using receptor gene deleted mice.', 'Anaesthetized mice with genetic deletion of one of the PACAP receptors (PAC1 receptors) or one of the GRP receptors (GRP receptor) or their wildtype counterparts were given glucose through a gastric gavage (150 mg) or intravenously (0.25, 0.50 or 1 g/kg). Blood samples were taken regularly during the following 120 min (after gastric glucose) or at 1 min (after intravenous glucose) for analysis of glucose and insulin.', 'The insulin response to gastric glucose was suppressed by 66% in PAC1 receptor gene deleted mice in association with impaired glucose elimination, whereas the insulin response to intravenous glucose was impaired by 36% only. The insulin response to glucose was suppressed in GRP receptor gene deleted mice by 24% together with impaired glucose elimination, whereas the insulin response to intravenous glucose was not significantly suppressed.
Answer: The insulin responses to gastric versus intravenous glucose in receptor gene deleted mice show that PACAP, and to a lesser extent GRP, contributes to the insulin response to gastric administration of glucose.

Ex Output:

Is the insulin response to gastric glucose reduced in PAC1 and GRP receptor gene deleted mice?