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.

Input: Consider Input: 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?

Output: 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.


Input: Consider Input: Context: To test the hypothesis that effective pulmonary capillary blood flow can be a useful indicator for estimating appropriate oxygenation and ventilation during one-lung ventilation in lung surgery.', 'Prospective data analysis.', 'A 770-bed general teaching hospital.', '15 ASA physical status II and III patients undergoing elective lung surgery.', 'Patients received general and thoracic epidural anesthesia and underwent lung operation with one-lung ventilation.', 'We measured effective pulmonary capillary blood flow by a partial CO2 rebreathing method and oxygenation parameters during two-lung ventilation before surgery, during one-lung ventilation, and during two-lung ventilation after lung surgery.', 'The effective pulmonary capillary blood flow index significantly decreased by 31.6%, which was associated with a significant decrease in arterial oxygen tension (PaO2). The pulmonary shunt fraction increased to 46.3% during one-lung ventilation. During two-lung ventilation, after chest closure, effective pulmonary capillary blood flow index divided by heart rate (i.e., effective pulmonary blood stroke flow index) was still significantly lower than that seen during two-lung ventilation before thoracotomy. There were significant correlations between effective pulmonary capillary blood flow, pulmonary blood stroke flow index, and PaO2.\Question: Is a noninvasive partial carbon dioxide rebreathing technique for measurement of pulmonary capillary blood flow also a useful oxygenation monitor during one-lung ventilation?

Output: Effective pulmonary capillary blood flow index and effective pulmonary blood stroke flow index are useful indicators for determining appropriate oxygenation therapy during one-lung ventilation.


Input: Consider Input: Context: Targeting the energy storing white adipose tissue (WAT) by pharmacological and dietary means in order to promote its conversion to energy expending "brite" cell type holds promise as an anti-obesity approach. Present study was designed to investigate/revisit the effect of capsaicin on adipogenic differentiation with special reference to induction of "brite" phenotype during differentiation of 3T3-L1 preadipocytes.', 'Multiple techniques such as Ca2+ influx assay, Oil Red-O staining, nutrigenomic analysis in preadipocytes and matured adipocytes have been employed to understand the effect of capsaicin at different doses. In addition to in-vitro experiments, in-vivo studies were carried out in high-fat diet (HFD) fed rats treated with resiniferatoxin (RTX) (a TRPV1 agonist) and in mice administered capsaicin.', 'TRPV1 channels are expressed in preadipocytes but not in adipocytes. In preadipocytes, both capsaicin and RTX stimulate Ca2+ influx in dose-dependent manner. This stimulation may be prevented by capsazepine, a TRPV1 antagonist. At lower doses, capsaicin inhibits lipid accumulation and stimulates TRPV1 gene expression, while at higher doses it enhances accumulation of lipids and suppresses expression of its receptor. In doses of 0.1-100 µM, capsaicin promotes expression of major pro-adipogenic factor PPARγ and some of its downstream targets. In concentrations of 1 µM, capsaicin up-regulates anti-adipogenic genes. Low-dose capsaicin treatment of 3T3-L1 preadipocytes differentiating into adipocytes results in increased expression of brown fat cell marker genes. In white adipose of mice, capsaicin administration leads to increase in browning-specific genes. Global TRPV1 ablation (i.p. by RTX administration) leads to increase in locomotor activity with no change in body weight.\Question: Does capsaicin induce `` brite '' phenotype in differentiating 3T3-L1 preadipocytes?


Output: Our findings suggest the dual modulatory role of capsaicin in adipogenesis. Capsaicin inhibits adipogenesis in 3T3-L1 via TRPV1 activation and induces brown-like phenotype whereas higher doses.