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.

Q: Hypoglycaemic sulphonylureas are thought to stimulate insulin release by binding to a sulphonylurea receptor, closing K(ATP) channels and inducing electrical activity. However, the fact that these drugs stimulate insulin release at high glucose concentrations where K(ATP) channels are closed suggests additional ionic actions. The aim of this study was to test the hypothesis that sulphonylureas influence the current of the glucose- and volume-regulated anion channel.', 'Electrical and ion-channel activity were recorded in isolated rat beta cells using the patch-clamp technique. (86)Rb(+) efflux was measured using intact islets. Beta cell volume was measured using a video-imaging technique.', "In the absence of glucose, tolbutamide (100 micromol/l) transiently depolarised the cells. In the presence of glucose (5 mmol/l), tolbutamide evoked a sustained period of electrical activity, whilst at 10 mmol/l glucose, the drug evoked a pronounced 'silent' depolarisation. In the absence of glucose, tolbutamide inhibited (86)Rb(+) efflux. However, at 10 mmol/l glucose, tolbutamide induced a transient stimulation of efflux. Tolbutamide potentiated the whole-cell volume-regulated anion conductance in a glucose-dependent manner with an EC(50) of 85 micromol/l. In single channel recordings, tolbutamide increased the channel-open probability. Tolbutamide caused beta cell swelling in the presence of glucose, but not in its absence.

A: Does tolbutamide potentiate the volume-regulated anion channel current in rat pancreatic beta cells?
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Q: Is weight-training exercise intervention harmful to women with or at risk of breast cancer-related lymphoedema?', 'Systematic review with meta-analysis of randomised trials.', 'Women with or at risk of breast cancer-related lymphoedema.', 'Progressive weight-training exercise.', 'The primary outcomes were severity (volume difference) and incidence of arm lymphoedema. Secondary outcomes included muscle strength of the upper and lower limbs, quality of life and body mass index.', 'Eleven studies from eight trials involving 1091 women were included. Weight-training exercise of low to moderate intensity with relatively slow progression significantly improved the upper limb strength (SMD 0.93, 95% CI 0.73 to 1.12) and lower limb strength (SMD 0.75, 95% CI 0.47 to 1.04) without increasing the arm volume (SMD -0.09, 95% CI -0.23 to 0.05) or incidence of breast cancer-related lymphoedema (RR 0.77, 95% CI 0.52 to 1.15). No significant effects were noted for body mass index (SMD -0.10, 95% -0.31 to 0.11). Some aspects of quality of life may improve with weight training. PARTICIPANTS in all trials used pressure garments and received supervision; no trials used high-intensity weight training.

A: Is weight training harmful for women with breast cancer-related lymphoedema : a systematic review?
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Q: Nociceptin/orphanin FQ (N/OFQ) receptor (NOP) agonists produce anxiolytic-like effects in rodents while antagonists promote antidepressant-like effects. The aim of this study was to investigate the effect on anxiety and depression of NOP receptor partial agonists such as the peptides [F/G]N/OFQ(1-13)NH2 and UFP-113 and the non-peptide AT-090.', 'Invitro AT-090, UFP-113, and [F/G]N/OFQ(1-13)NH2 were tested for their ability to promote NOP/G-protein and NOP/-arrestin 2 interaction, using a bioluminescence resonance energy transfer assay. Invivo, they were tested in mice in the elevated plus maze (EPM) and in the forced swim (FST) tests. NOP partial agonists effects were systematically compared to those of full agonists (N/OFQ and Ro 65-6570) and antagonists (UFP-101 and SB-612111).', 'Invitro, AT-090, UFP-113, and [F/G]N/OFQ(1-13)NH2 promoted NOP/G protein interaction, with maximal effects lower than those evoked by N/OFQ and Ro 65-6570. AT-090 behaved as a NOP partial agonist also in inducing -arrestin 2 recruitment, while UFP-113 and [F/G]N/OFQ(1-13)NH2 were inactive in this assay. Invivo, AT-090 induced anxiolytic-like effects in the EPM but was inactive in the FST. Opposite results were obtained with UFP-113 and [F/G]N/OFQ(1-13)NH2.

A:
Does beta-arrestin 2 rather than G protein efficacy determine the anxiolytic-versus antidepressant-like effects of nociceptin/orphanin FQ receptor ligands?
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