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]: Our previous in-vivo and in-vitro studies demonstrated that inflammation accelerated the progression of atherosclerosis via the dysregulation of the low-density lipoprotein receptor (LDLr) pathway. The current study aimed to investigate the effects and their underlying mechanisms of inflammation on lipid accumulation in the radial arteries of endstage renal disease (ESRD) patients with arteriovenostomy.', '30 ESRD patients with arteriovenostomy were included. The patients were divided into two groups based on their plasma levels of C-reactive protein: a control (n = 16) and an inflamed group (n = 14). The expression of tumor necrosis factor-alpha (TNF-alpha) and monocyte chemotactic protein-1 of the radial arteries were increased in the inflamed group. Foam cell formation and lipid droplet accumulation were examined by hematoxylin and eosin (H & E) and Oil Red O staining. Intracellular cholesterol trafficking-related proteins were examined by immunohistochemistry and immunofluorescent staining.', 'There was significant lipid accumulation in the radial arteries of the inflamed group compared with the control. Further analysis demonstrated that this accumulation was correlated with the increased protein expression of LDLr, sterol regulatory element-binding protein-2 (SREBP-2), and SREBP cleavageactivating protein (SCAP). Confocal microscopy showed that inflammation enhanced the translocation of SCAP escorting SREBP-2 from the endoplasmic reticulum to the Golgi, thereby activating LDLr gene transcription. Interestingly, upregulated LDLr expression was positively associated with the increased protein expression of mammalian target of rapamycin (mTOR), which had enhanced coexpression with SREBP-2. This finding suggests that the activation of mTOR may be involved in LDLr pathway disruption through the upregulation of SREBP-2 expression.
[A]: 0


[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]: Simvastatin has lung vascular-protective effects via augmentation of endothelial barrier function. Accordingly, on the basis of our previous study, we hypothesized that endothelial cell (EC) protection by simvastatin is dependent on the stabilization on cytoskeletons.', 'Sixty C57BL/6 mice were divided into two experimental groups: LPS group (L group) and LPS+simvastatin treated group (L+S group). All mice in these two groups received an intraperitoneal injection of LPS (10\u200amg/kg/d). Simvastatin was administered intraperitoneally immediately after the LPS injection in animals of the L+S group at a dose of 20\u200amg/kg/day. Lung injury degree and the protective effects of simvastatin against LPS-induced lung injury were assessed at the time-points of 24, 48 and 72\u200ah post-injection. Serum alanine transaminase (ALT), serum creatinine (Scr) were identified to assess the hepatic and renal side-effects of simvastatin.', 'LPS inhibited the cytoskeletal regulating proteins of Cdc42 and PAK4, and was accompanied by an increased circulating endothelial microparticles (EMPs) level. The adherent junction (AJ) protein of VE-cadherin was also decreased by LPS, and was accompanied by a thickening alveolar wall, increased lung W/D values and high albumin concentration in bronchoalveolar lavage (BAL). Protective effects of simvastatin against LPS-induced lung injury were illustrated by regulating and stabilizing cytoskeletons, as well as intercellular AJs. The values of ALT and Scr were all lower than the common upper limits according to assay kits.
[A]:
0