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.

Q: Context: Cognitive impairment is a common feature of late-life bipolar disorder (BD). Yet, there is limited information on the biological mechanisms associated with this process. It is uncertain whether cognitively impaired patients with BD may present the Alzheimer's disease (AD) bio-signature in the cerebrospinal fluid (CSF), defined as a combination of low concentrations of the amyloid-beta peptide (Aβ1-42 ) and high concentrations of total tau (T-tau) and tau phosphorylated at threonine 181 (P-tau). In this study, we sought to determine whether cognitive impairment in elderly patients with BD is associated with the AD CSF bio-signature.", 'Seventy-two participants were enrolled in the study. The test group comprised older adults with BD and mild cognitive impairment (BD-MCI; n\xa0=\xa016) and the comparison groups comprised patients with dementia due to AD (n\xa0=\xa017), patients with amnestic MCI (aMCI; n\xa0=\xa014), and cognitively healthy older adults (control group; n\xa0=\xa025). CSF samples were obtained by lumbar puncture and concentrations of Aβ1-42 , T-tau and P-tau were determined.', 'CSF concentrations of all biomarkers were significantly different in the AD group compared to all other groups, but did not differentiate BD-MCI subjects from aMCI subjects and controls. BD-MCI patients had a non-significant reduction in CSF Aβ1-42 compared to controls, but this was still higher than in the AD group. Concentrations of T-tau and P-tau in BD-MCI patients were similar to those in controls, and significantly lower than those in AD.\Question: Is cognitive impairment in late-life bipolar disorder associated with Alzheimer 's disease pathological signature in the cerebrospinal fluid?

A: Cognitively impaired patients with BD do not display the so-called AD bio-signature in the CSF. We therefore hypothesize that cognitive deterioration in BD is not associated with the classical pathophysiological mechanisms observed in AD, i.e., amyloid deposition and hyperphosphorylation of microtubule-associated tau protein.
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Q: 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?

A: 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.
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Q: Context: Earlier studies regarding the risk of colorectal cancer in women with a prior diagnosis of breast cancer yielded conflicting results.', 'A retrospective cohort study was performed using the General Practitioner Research Database of the United Kingdom. Women with a prior diagnosis of breast cancer were compared with female control patients without a prior history of breast cancer. The primary outcome was an incident diagnosis of colorectal cancer. Poisson regression analysis was utilized to assess the effects of potential confounder variables.', 'The study included 17,415 breast cancer patients and 69,660 matched control patients with follow-up time in person years of 52,914 and 331,480, respectively. The relative rate of colorectal cancer among breast cancer patients was 0.80 (95% CI 0.56-1.15). The relative rate of colorectal cancer among women exposed and unexposed to tamoxifen were 0.73 (95% CI 0.49-1.08) and 1.81 (95% CI 0.85-3.85), respectively.\Question: Are women with a prior diagnosis of breast cancer at an increased risk for subsequent colorectal cancer?

A:
Women with a prior diagnosis of breast cancer are not at an increased risk of colorectal cancer; these women can follow average risk screening guidelines for colorectal cancer.
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