instruction:
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.
question:
Anxiety and depression frequently co-occur in the elderly and in patients with dementia. Prior research has shown that depression is related to the risk of dementia, but the effect of anxiety on dementia remains unclear. We studied whether anxiety symptoms and anxiety disorders are associated with the risk of dementia and cognition.', 'We studied 2,708 nondemented participants from the prospective, population-based Rotterdam Study who underwent the Hospital Anxiety and Depression Scale (HADS) (sample I, baseline 1993-1995) and 3,069 nondemented participants who underwent screening for anxiety disorders (sample II, baseline 2002-2004). In 1993-1995, anxiety symptoms were assessed using the HADS. In 2002-2004, anxiety disorders were assessed using the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. In both study samples, participants were continuously monitored for dementia until January 1, 2011. Cognition was tested in 2002-2004 and at a follow-up visit in 2009-2011 in sample II only.', 'In sample I, 358 persons developed dementia, and in sample II, 248 persons developed dementia. We did not find an association with the risk of dementia for anxiety symptoms (hazard ratio 1.05, 95% confidence interval: 0.77-1.43, Wald statistic 0.08, p\xa0= 0.77, df\xa0= 1) or for anxiety disorders (hazard ratio 0.92, 95% confidence interval: 0.58-1.45, Wald statistic 0.14, p\xa0= 0.71, df\xa0= 1). We could demonstrate an association of anxiety disorders with poor cognition cross-sectionally, but this attenuated after additional adjustments.
answer:
Is anxiety associated with the risk of dementia or cognitive decline : the Rotterdam Study?


question:
Proprotein convertase subtilisin kexin-like 9 (PCSK9) is a secreted glycoprotein that is transcriptionally regulated by cholesterol status. It modulates levels of circulating low density lipoprotein cholesterol (LDLC) by negatively regulating low density lipoprotein receptor (LDLR) levels. PCSK9 variants that result in 'gain of function' have been linked to autosomal dominant hypercholesterolemia, while significant protection from coronary artery disease has been documented in individuals who carry 'loss of function' PCSK9 variants. PCSK9 circulates in human plasma, and we previously reported that plasma PCSK9 is positively correlated with total cholesterol and LDLC in men.", 'Herein, we report the effects of two lipid-modulating therapies, namely statins and fibrates, on PCSK9 plasma levels in human subjects. We also document their effects on endogenous PCSK9 and LDLR expression in a human hepatocyte cell line, HepG2, using immunoprecipitation and immunoblot analyses. Changes in plasma PCSK9 following fenofibrate or gemfibrozil treatments (fibric acid derivatives) were inversely correlated with changes in LDLC levels (r = -0.558, p = 0.013). Atorvastatin administration (HMGCoA reductase inhibitor) significantly increased plasma PCSK9 (7.40%, p = 0.033) and these changes were inversely correlated with changes in LDLC levels (r = -0.393, p = 0.012). Immunoblot analyses of endogenous PCSK9 and LDLR expression by HepG2 cells in response to statins and fibrates showed that LDLR is more upregulated than PCSK9 by simvastatin (2.6x vs 1.5x, respectively at 10 muM), while fenofibrate did not induce changes in either.
answer:
Are plasma PCSK9 levels significantly modified by statins and fibrates in humans?


question:
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.
answer:

Is sprouty4 , a suppressor of tumor cell motility , down regulated by DNA methylation in human prostate cancer?