TASK DEFINITION: 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.
PROBLEM: To ascertain whether inoculation of lipopolysaccharide (LPS) into the mouse cochlea might induce enhancement of DNA binding activity of NK-kappa B and to establish a positive model of NF-kappa B activation in the cochlea.', 'Two groups of CBA mice were transtympanically injected either with 10 micrograms of LPS or an equal volume of saline. The nuclear proteins of the cochlea were extracted, quantitated and bound with 32P-radiolabeled oligonucleotide probe for NF-kappa B. The bound and free probes were separated by electrophoresis on a 4.5% native polyacrylamide gel. Supershift assays were carried out using the antibodies against NF-kappa B subunit P65 and P50.', 'The radiolabeled probe bound differently to nuclear extracts from the LPS-treated and the saline-treated mouse cochleae, showing that LPS inoculation significantly increased NF-kappa B binding activity. Supershift analysis demonstrated that the enhancement of DNA binding activity was related to both P65 and P50 subunits.

SOLUTION: Does [ Lipopolysaccharide enhance DNA binding activity of nuclear factor-kappa B in the mouse cochlea ]?

PROBLEM: Allergic airway inflammation is triggered by allergen exposure through several steps including release of IL-33, which promotes cytokine (IL-5, IL-13) production by type 2 innate lymphoid cells (ILC2s). MicroRNA (miR)-155 has recently been described to regulate adaptive responses in allergic inflammation. However, the role of miR-155 in the regulation of ILC2s remains unexplored.', 'We sought to elucidate the contribution of miR-155 in ILC2 expansion using experimental murine models of allergic airway inflammation.', 'To determine the role of miR-155 in the regulation of ILC2s in allergic airway inflammation, miR-155 deficient (miR-155', 'miR-155 was 10-fold upregulated in WT-derived ILC2s in response to IL-33. Furthermore, miR-155

SOLUTION: Is microRNA-155 a critical regulator of type 2 innate lymphoid cells and IL-33 signaling in experimental models of allergic airway inflammation?

PROBLEM: Ingested proteins are known to stimulate a rise in insulin and glucagon concentrations. In our effort to explain this effect, we have begun to measure the effect of individual amino acids.', 'The objectives were to determine the effect of lysine ingestion on insulin and glucagon concentrations and whether the effect is moderated by glucose ingestion.', 'Thirteen healthy subjects were studied on 4 occasions. Water, 25 g glucose, 1 mmol lysine/kg lean body mass, or lysine plus glucose was given on separate occasions at 0800 after a 12-h fast. Serum lysine, glucose, insulin, and glucagon were measured during a 2.5-h period. The amount of lysine provided was equivalent to that present in a 672-g (24-oz) steak.', 'Lysine ingestion resulted in an approximately 3-fold increase in lysine concentration and in a small decrease in glucose concentration. When lysine was ingested with glucose, the 2.5-h glucose area response decreased by 44% (P < 0.02). Lysine alone increased the insulin area response modestly; the insulin increase when lysine was ingested with glucose was similar to that when only glucose was ingested. Lysine stimulated an increase in glucagon (P < 0.02), whereas glucose decreased glucagon.

SOLUTION:
Does lysine ingestion markedly attenuate the glucose response to ingested glucose without a change in insulin response?