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:
Retrospective analysis of prospectively collected, nonrandomized radiographical data.', 'To examine the relationship between the presence of preoperative metabolically active facet arthropathy (FA) and the amount of indirect foraminal decompression gained after extreme lateral interbody fusion (XLIF).', 'Although evidence of significant radiographical indirect decompression after XLIF has been shown, the relationship between the extent of indirect decompression and the presence of potentially attenuating, FA is yet to be studied.', 'A prospective database of consecutive patients undergoing XLIF was retrospectively analyzed. Posterior disc height, foraminal height, and cross-sectional foraminal area were measured on computed tomographic scans obtained preoperatively and 2 days postoperatively. The selected radiographical parameters were examined with respect to the presence of FA based on preoperative computed tomographic and bone scans.', 'Fifty-two consecutive patients underwent 79 levels of XLIF without direct decompression. Average age was 66.4 years and 34 (65.4%) were females. Surgery resulted in significant increases in posterior disc height 3.0 to 5.7 mm (89.0% increase), P<0.0001; foraminal height 1.4 to 1.7 cm (38.0% increase), P<0.0001; and foraminal area 1.1 to 1.4 cm (45.1% increase), P<0.0001. These increases were independent of the presence of metabolically active arthropathy.

Ex Output:
Is indirect foraminal decompression independent of metabolically active facet arthropathy in extreme lateral interbody fusion?

Ex Input:
To investigate the inhibition of amyloid beta-protein 42 (Abeta42) production in M146L cells by gamma-schisandrin.', 'M146L cells which can produce considerable Abeta42 in vitro were treated with gamma-schisandrin (1.67, 5.00 and 15.00 microg x mL(-1)), beta-secretase inhibitor (S4562, 100.00 microg x mL(-1)) and gamma-secretase inhibitor (S2188, 13.68 microg x mL(-1)), separately. Cell counting kit-8 (CCK-8) was used to assess cell viability. Enzyme-linked immunosorbent assay (ELISA) was carried out to determine the amount of Abeta42. Western blotting was used to examine C99, an intermediary product of APP cleaved by beta-secretase. beta-Secretase and gamma-secretase activities were assayed by commercial kits.', 'The CCK-8 assay indicated that different concentrations of gamma-schisandrin had no neurotoxicity on the cultured M146L. And the ELISA test showed that the amount of Abeta42 secreted by M146L cells treated with gamma-schisandrin (5.00 and 15.00 microg x mL(-1)) decreased obviously as compared with solvent control. The results of Western blotting test indicated that there was no change of C99 contents and beta-secretase activity in gamma-schisandrin treated cells, while gamma-secretase activity decreased obviously.

Ex Output:
Does [ Gamma-Schisandrin inhibit production of amyloid beta-protein 42 in M146L cells ]?

Ex Input:
Portal hypertension is associated with arterial hypotension and vascular hypocontractility, which persists despite elevated plasma levels of vasoconstrictors. We investigated the role of the RhoA/Rho-kinase pathway in vascular smooth muscle hypocontractility of rats with secondary biliary cirrhosis.', 'Aortic expressions of RhoA and Rho-kinase were analyzed in sham-operated and BDL rats by reverse-transcription polymerase chain reaction (RT-PCR) and immunoblots. Activation of aortic RhoA was examined by pull down of guanosine triphosphate (GTP)-RhoA and membrane translocation of RhoA. Rho-kinase activity was assessed as phosphorylation of its substrate, moesin. Contractility of isolated aortic rings was determined myographically. The hemodynamic effect of the Rho-kinase inhibitor (R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide (Y-27632) was determined in vivo by measuring changes in mean arterial pressure and systemic vascular resistance (SVR) (microspheres).', 'Contraction of aortic rings from BDL rats was impaired in response to the alpha(1)-adrenergic receptor agonist methoxamine but not to high molar KCl. Aortic expression of RhoA was unchanged in cirrhotic rats, whereas Rho-kinase was down-regulated posttranscriptionally. Methoxamine-induced activation of RhoA as well as basal and methoxamine-induced phosphorylation of moesin were strongly reduced in aortas from cirrhotic rats. Aortic rings from cirrhotic rats precontracted with methoxamine showed an increased sensitivity to relaxation with Y-27632. The drop in SVR induced by Y-27632 was larger in cirrhotic rats than in sham-operated rats.

Ex Output:
Does defective RhoA/Rho-kinase signaling contribute to vascular hypocontractility and vasodilation in cirrhotic rats?