Given a passage classify if the passage has a definite objective/aim/goal or not. Output '1' if the passage has a defininte objective/aim/goal and output '0' if the passage does not have a definite objective/aim/goal.

[Q]: The hepatitis B virus X protein (HBx) plays critical roles in cell survival via modulation of signaling pathways. In our previous studies, we reported that HBx inhibited the growth of CCL13-HBx-stable cells (Chang-HBx cells) in vitro and tumor formation in vivo in CCL13-HBx-cell-injected nude mice; however, this inhibition mechanism is unclear.', 'To investigate the role of HBx in Wnt-3/beta-catenin signaling pathways, we focused on the key molecules GSK-3beta and beta-catenin, and analyzed by Western blotting and immunofluorescence staining.', 'Results indicated that following HBx induction, GSK-3beta activity was up-regulated, the expression and accumulation of beta-catenin in the nucleus were decreased, and cell proliferation was suppressed. Inhibition of GSK-3beta activity by pharmacological inhibitors rescued the expression and accumulation of beta-catenin in the nucleus and facilitated cell proliferation and growth following HBx induction. The localization of beta-catenin, which is involved in cell proliferation, and mediated by GSK-3beta activation was also demonstrated.
[A]: 1


[Q]: Cardiac surgery produces a proinflammatory response characterized by cytokine production. Proinflammatory cytokines such as interleukin 6 (IL-6) may contribute to morbidity and mortality after cardiopulmonary bypass (CPB). Elderly patients undergoing CPB are at increased risk of morbidity and mortality. We hypothesized that patients aged >70 y produce more IL-6 during CPB.', 'Twenty-three patients (ages 23-80) undergoing cardiac surgery had blood sampled from the ascending aorta and coronary sinus on initial cannulation for bypass, at 30 min of aortic cross-clamp time, on release of the aortic cross-clamp, and at 20 min after reperfusion. Group 1 patients (n = 8) were aged <60 y, group 2 patients (n = 7) were aged between 60 and 70 y, and group 3 patients (n = 8) were aged >70 y. Plasma levels of tumor necrosis factor-alpha, IL-1, and IL-6 were analyzed.', 'The three groups did not differ with respect to preoperative ejection fraction, New York Heart Association classification, mean aortic cross-clamp time, or mean CPB time. IL-6 levels rose throughout myocardial ischemia and reperfusion in all three age groups. The increase in IL-6 during ischemia and reperfusion in the age group >70 was greater than the increase in younger patients. IL-6 was similar in the coronary sinus and the ascending aorta.
[A]: 0


[Q]: High levels of wild-type alpha-synuclein are found in autopsied brain samples of idiopathic Parkinson's disease (PD), some familial PD, some Alzheimer's disease (AD) and Down's syndrome with dementia. Therefore, we have investigated whether overexpression of wild-type alpha-synuclein causes degeneration during adenosine, 3',5'-cyclic monophosphate (cAMP)-induced differentiation of murine neuroblastoma (NB) cells in culture. We have also studied whether selenomethionine can modify the effect of overexpression of alpha-synuclein during differentiation of NB cells.", 'To study these issues, we established a murine neuroblastoma (NB) clone (NBP2-PN54-C20) that expressed high levels of wild-type human alpha-synuclein as determined by real time PCR and Western blot. We have utilized RO20-1724, an inhibitor of cyclic nucleotide phosphodiesterase, and prostaglandin A1 (PGA1), a stimulator of adenylate cyclase, or RO20-1724 and dibutyryl cAMP to induce terminal differentiation in over 95% of the cell population by elevating the intracellular levels of cAMP in NB cells. The viability of cells was determined by MTT assay and LDH leakage assay, and the degeneration was documented by photomicrographs.', 'The results showed that overexpression of human wild-type alpha-synuclein decreased viability and increased degenerative changes in comparison to those observed in vector control cells, when differentiation was induced by treatment with RO20-1724 and PGA1, but not with RO20-1724 and dibutyryl cAMP. When selenomethionine was added to NB cells overexpressing alpha-synuclein immediately after the addition of RO20-1724 and PGA1, the viability and degenerative changes were markedly reduced, suggesting the involvement of increased oxidative stress in the mechanism of action of alpha-synuclein. This protective effect was not observed after treatment with sodium selenite or methionine.
[A]:
1