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]: Alterations of fibroblast growth factors (FGFs) and their receptors contribute to prostate cancer progression by enhancing cellular proliferation, survival, and motility. The Sprouty gene family negatively regulates FGF signaling and may limit the ability of FGFs to enhance tumor progression. Sprouty1 is down regulated in human prostate cancers and Sprouty1 expression can markedly inhibit prostate cancer proliferation in vitro. Sprouty4 has been shown to negatively regulate both proliferation and cell migration in other systems. We therefore examined whether Sprouty4 expression was altered in prostate cancer.', 'Expression of Sprouty4 was examined by in situ hybridization and quantitative RT-PCR. Methylation of the Sprouty4 gene promoter was assessed using bisulfite modification and sequencing. The effect of Sprouty4 expression on cell migration was determined using an in vitro wounding assay.', "By in situ hybridization Sprouty4 is expressed in normal prostatic epithelial cells and is decreased in a subset of prostate cancers. Quantitative RT-PCR confirms that Sprouty4 expression is decreased in approximately one half of prostate cancers. Analysis of the 5'-regulatory region revealed a CpG island approximately 1 kb upstream of the transcription initiation site, the proximal portion of which was preferentially methylated in prostate cancer tissues. More than one half of all prostate cancer DNAs were methylated in this region and methylation was significantly correlated with decreased Sprouty4 expression as determined by quantitative RT-PCR. When overexpressed in prostate cancer cell lines, Sprouty4 did not inhibit cell proliferation but did inhibit cell migration.
[A]: 1

[Q]: Immunosuppressant agents modulate the activity of the immune system and control adipose tissue inflammatory responses associated with obesity. Controlling adipose tissue inflammation represents an interesting option for inhibiting the low-grade inflammatory state in obese subjects and for preventing obesity-associated pathologies. In this work, we assessed the effects of thalidomide on the inflammatory response in adipose tissue as well as on systemic inflammatory marker expression in the well-established high-fat diet-induced obesity mouse model.', 'Swiss male mice were fed a high-fat diet (60% kcal from fat) for 12 weeks and received thalidomide for the last 10 days (100 mg.kg-1). Adipokine levels were measured in serum and adipose tissue by EIA and real-time quantitative PCR, respectively. Adipose tissue infiltrating macrophages were identified by immunohistochemistry and western blot analysis of F4/80 marker expression. Other inflammatory markers, such as c-Jun N-terminal kinase (JNK) phosphorylation and monocyte chemoattractant protein-1 (MCP-1) production, were also evaluated by western blot analysis. In vitro assays using 3T3-L1 adipocytes were also conducted to evaluated adipokine release.', 'In obese mice, thalidomide administration induced a reduction in adiposity accompanied by a reduction of tumor necrosis factor- (TNF-), leptin and MCP-1 adipose tissue production, macrophage infiltration and JNK activation. TNF- and leptin serum levels were also reduced by thalidomide treatment in obese mice. In vitro, the release of basal TNF- and lipopolysaccharide (LPS)-induced MCP-1 was inhibited in 3T3-L1 cells.
[A]: 0

[Q]: We sought to study the contribution of potassium channels in the effect of forskolin and 1,9-dideoxyforskolin on uterine contractility in the pregnant rat.', 'Rings taken from the middle portions of uterine horns from rats at 16 days of gestation were positioned in organ chambers containing physiologic salt solution bubbled with 5% carbon dioxide in air (37 degrees C, pH approximately 7.4) for isometric tension recording under 2 g passive tension. The effects of cumulative concentrations of forskolin and 1,9-dideoxyforskolin in the absence or presence of an adenylate cyclase inhibitor (MDL-12,330A, 10(-5) mol/L), a nonselective potassium channel blocker (tetrabutylammonium, 10(-4) mol/L), or an adenosine triphosphate-dependent potassium channel blocker (glibenclamide 10(-5) mol/L) were studied.', 'Both forskolin and, to a lesser extent, 1,9-dideoxyforskolin inhibit uterine contractions. Tetrabutylammonium, glibenclamide, and MDL-12, 330A attenuated the effects of forskolin, whereas glibenclamide was less effective against 1,9-dideoxyforskolin.
[A]:
1