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 Input:
A fundamental prerequisite for using degradable synthetic biopolymers as composite skin substitutes is the ability to establish vascular tissue. PEGT/PBT block-copolymer matrices have previously been shown as a favorable dermal substitute. In this study, quantitative data on neovascularization of PEGT/PBT block-copolymer matrices are presented.', 'PEGT/PBT-block-copolymer discs of three different pore diameters (1: < 75 microm, 2: 75-212 microm, 3: 250-300 microm) were implanted into dorsal skinfold chambers of balb/c mice. Histological sections were evaluated 7, 14, and 21 days post implantation by light and scanning electron microscopy. Blood vessel analysis was performed by means of digital image analysis (n = 288) of hematoxylin/eosin stained sections within apical (AOF) and basal (BOF) observation fields of the matrices.', 'Twenty-one days after implantation the density of blood vessels within the BOF of the scaffolds with a pore size of 75-212 and 250-300 microm were 4.6 +/- 0.45 and 5.8 +/- 0.62 (mean +/- S.E.M.; blood vessel profiles (BVF)), respectively. In <75 microm scaffolds, smaller numbers of BVF were found (4.2 +/- 0.39). In contrast, the evaluation within the AOF revealed significantly higher numbers of BVF in 75-212 microm group (3.5 +/- 0.49) and 250-300 microm group (4.5 +/- 0.66) as compared to the < 75 microm group (2.3 +/- 0.48).

Ex Output:
Does analysis of neovascularization of PEGT/PBT-copolymer dermis substitute in balb/c-mice?


Ex Input:
A transgenic mouse model has revealed parameters of the angiogenic switch during multistep tumorigenesis of pancreatic islets, and demonstrated efficacy of antiangiogenic therapies. Pericytes have been revealed as functionally important for tumor neovasculature, using kinase inhibitors targeting their platelet-derived growth factor receptors (PDGFRs). Additionally, vascular endothelial growth factor receptor (VEGFR) inhibitors and metronomic chemotherapy show modest benefit against early- but not late-stage disease.', 'Seeking to improve efficacy against otherwise intractable end-stage pancreatic islet tumors, two receptor tyrosine kinase inhibitors, imatinib and SU11248, were used to disrupt PDGFR-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerated dose (MTD) or metronomic chemotherapy and/or VEGFR inhibition.', 'Imatinib, despite equivocal efficacy as monotherapy, reduced pericyte coverage of tumor vessels and enhanced efficacy in combination with metronomic chemotherapy or VEGFR inhibition. A regimen involving all three was even better. MTD using cyclophosphamide caused transitory regression, but then rapid regrowth, in contrast to metronomic cyclophosphamide plus imatinib, which produced stable disease. The MTD regimen elicited apoptosis of tumor cells but not endothelial cells, whereas the other regimens increased endothelial cell apoptosis concordant with efficacy. A "chemo-switch" protocol, involving sequential MTD and then metronomic chemotherapy, overlaid with multitargeted inhibition of PDGFR and VEGFR, gave complete responses and unprecedented survival advantage in this model.

Ex Output:
Is a multitargeted , metronomic , and maximum-tolerated dose `` chemo-switch '' regimen antiangiogenic , producing objective responses and survival benefit in a mouse model of cancer?


Ex Input:
Activation of the NOP receptor by its endogenous ligand nociceptin/orphanin FQ reduces ethanol intake in genetically selected alcohol preferring Marchigian Sardinian alcohol preferring (msP) rats. Here we evaluated whether buprenorphine, a partial agonist at micro-opioid and NOP receptors, would reduce ethanol consumption in msP rats via activation of NOP receptors.', 'Marchigian Sardinian alcohol preferring rats trained to drink 10% alcohol 2 hours/day were injected with buprenorphine (.03, .3, 3.0, or 6.0 mg/kg intraperitoneally [IP]) 90 min before access to ethanol.', 'Similar to prototypical micro-agonists, the two lowest doses of buprenorphine significantly increased ethanol consumption (p < .01); in contrast, the two highest doses reduced it (p < .05). Pretreatment with naltrexone (.25 mg/kg IP) prevented the increase of ethanol intake induced by .03 mg/kg of buprenorphine (p < .001) but did not affect the inhibition of ethanol drinking induced by 3.0 mg/kg of buprenorphine. Conversely, pretreatment with the selective NOP receptor antagonist UFP-101 (10.0 or 20.0 microg/rat) abolished the suppression of ethanol drinking by 3.0 mg/kg of buprenorphine.

Ex Output:

Does buprenorphine reduce alcohol drinking through activation of the nociceptin/orphanin FQ-NOP receptor system?