In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Context: Hypercholesterolemia is a well-established risk factor for the development of kidney injury. Considering that female sex hormones may play a preventative role in both cardiovascular and renal diseases, the aim of the present study was to evaluate the effects of female sex hormones on hypercholesterolemia-induced renal dysfunction.', "Apolipoprotein E-deficient (ApoE) and C57 control female mice underwent an ovariectomy (OVX) or sham surgery and after 2 months, creatinine clearance, uremia and proteinuria were determined. Renal oxidative stress and lipid deposition were also quantified. Values are presented as mean\u2009±\u2009SEM. Statistical analyses were performed using Two-way ANOVA followed by Tukey's post hoc test.", 'Creatinine clearance (μL/min) was similar between C57 (171\u2009±\u200917) and ApoE (140\u2009±\u200926) mice underwent sham surgery. OVX resulted in a reduced glomerular filtration rate in both C57 (112\u2009±\u20098, ~\u2009-\u200935%, p\u2009<\u20090.05) and ApoE (61\u2009±\u200910, ~\u2009-\u200956%, p\u2009<\u20090.05) animals. Plasma levels of urea (mg/dL) were higher in both ApoE groups (Sham: 73\u2009±\u20097; OVX: 73\u2009±\u20098, p\u2009<\u20090.05) when compared to C57 animals (Sham: 49\u2009±\u20093; OVX: 60\u2009±\u20094), with no changes among ovariectomized groups. Proteinuria levels (mg/24 h) were similar between C57 (Sham: 25.1\u2009±\u20095.7; OVX: 33.7\u2009±\u20094.7) and ApoE sham animals (26.4\u2009±\u20093.5), however, 24-h urine protein excretion was augmented in ApoE OVX animals (49.6\u2009±\u20095.8, p\u2009<\u20090.05). Histological kidney analysis demonstrated that the absence of female sex hormones resulted in increased oxidative stress, which was more severe in ApoE mice (C57 Sham: 9.2\u2009±\u20090.4; C57 OVX: 22.9\u2009±\u20091.0; ApoE Sham: 13.9\u2009±\u20090.7; ApoE OVX: 34.0\u2009±\u20091.4 au x 103, p\u2009<\u20090.05). As expected, ApoE mice presented higher lipid deposition, which was not affected by OVX (C57 Sham: 0\u2009±\u20090; C57 OVX: 0\u2009±\u20090; ApoE Sham: 6.8\u2009±\u20091.6; ApoE OVX: 5.2\u2009±\u20090.8% x 10-2, p\u2009<\u20090.05). Ovariectomy resulted in a similar reduction in ER-α protein expression in the renal cortex (C57: 0.78\u2009±\u20090.04; ApoE: 0.81\u2009±\u20090.04 au, p\u2009<\u20090.05) when compared to sham animals (C57:1.00\u2009±\u20090.04; ApoE: 1.03\u2009±\u20090.03 au).\Question: Do endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice?
Taken together these data indicate that female sex hormones may delay hypercholesterolemia-induced renal dysfunction and emphasizes the importance of plasma cholesterol control in post-menopausal women.

Context: For the majority of congenital heart diseases (CHDs), the full complexity of the causative molecular network, which is driven by genetic, epigenetic, and environmental factors, is yet to be elucidated. Epigenetic alterations are suggested to play a pivotal role in modulating the phenotypic expression of CHDs and their clinical course during life. Candidate approaches implied that DNA methylation might have a developmental role in CHD and contributes to the long-term progress of non-structural cardiac diseases. The aim of the present study is to define the postnatal epigenome of two common cardiac malformations, representing epigenetic memory, and adaption to hemodynamic alterations, which are jointly relevant for the disease course.', 'We present the first analysis of genome-wide DNA methylation data obtained from myocardial biopsies of Tetralogy of Fallot (TOF) and ventricular septal defect patients. We defined stringent sets of differentially methylated regions between patients and controls, which are significantly enriched for genomic features like promoters, exons, and cardiac enhancers. For TOF, we linked DNA methylation with genome-wide expression data and found a significant overlap for hypermethylated promoters and down-regulated genes, and vice versa. We validated and replicated the methylation of selected CpGs and performed functional assays. We identified a hypermethylated novel developmental CpG island in the promoter of SCO2 and demonstrate its functional impact. Moreover, we discovered methylation changes co-localized with novel, differential splicing events among sarcomeric genes as well as transcription factor binding sites. Finally, we demonstrated the interaction of differentially methylated and expressed genes in TOF with mutated CHD genes in a molecular network.\Question: Does comparative DNA methylation and gene expression analysis identify novel genes for structural congenital heart diseases?
By interrogating DNA methylation and gene expression data, we identify two novel mechanism contributing to the phenotypic expression of CHDs: aberrant methylation of promoter CpG islands and methylation alterations leading to differential splicing.

Context: Obsessive-compulsive disorder (OCD) is a neuropsychiatric disorder with onset in childhood and is characterized by obsessions (recurrent, intrusive, persistent thoughts, impulses and/or ideas that often cause anxiety or distress) and compulsions (ritualized and stereotypic behaviours or mental acts that are often performed to relieve anxiety or distress associated with obsessions). Although OCD is a heritable disorder, its complex molecular etiology is poorly understood.', 'We combined enrichment analyses and an elaborate literature review of the top-ranked genes emerging from the 2 published genome-wide association studies of OCD and candidate genes implicated through other evidence in order to identify biological processes that, when dysregulated, increase the risk for OCD.', 'The resulting molecular protein landscape was enriched for proteins involved in regulating postsynaptic dendritic spine formation - and hence synaptic plasticity - through insulin-dependent molecular signalling cascades.\Question: Does an integrated molecular landscape implicate the regulation of dendritic spine formation through insulin-related signalling in obsessive-compulsive disorder?

This study is a first attempt to integrate molecuar information from different sources in order to identify biological mechanisms underlying OCD etiology. Our findings are constrained by the limited information from hypothesis-free studies and the incompleteness and existing limitations of the OCD literature and the gene function annotations of gene enrichment tools. As this study was solely based on in silico analyses, experimental validation of the provided hypotheses is warranted.