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: HBV covalently closed circular DNA (cccDNA), the replicative intermediate responsible for persistent HBV infection of hepatocytes, is the template for transcription of all viral mRNAs. Nuclear cccDNA accumulates as a stable episome organized into minichromosomes by histone and nonhistone proteins. In this study we investigated, by a newly developed sensitive and specific assay, the relationship between viral replication and HBV chromatin assembly, transcription, and interaction with viral and cellular regulatory proteins.', 'To achieve this aim we coupled a quantitative chromatin immunoprecipitation (ChIP) technique to an established method that allows the amplification of virion-encapsidated HBV genomes after transfection of linear HBV DNA into human hepatoma HuH7 cells. The cccDNA-ChIP technique was also applied to study HBV minichromosome transcriptional regulation in liver tissue from HBV-infected patients.', 'The use of anti-acetyl-H4/-H3 specific antibodies to immunoprecipitate transcriptionally active chromatin revealed that HBV replication is regulated by the acetylation status of the cccDNA-bound H3/H4 histones. Class I histone deacetylases inhibitors induced an evident increase of both cccDNA-bound acetylated H4 and HBV replication. Finally, histones hypoacetylation and histone deacetylase 1 recruitment onto the cccDNA in liver tissue correlated with low HBV viremia in hepatitis B patients.\Question: Is hepatitis B virus replication regulated by the acetylation status of hepatitis B virus cccDNA-bound H3 and H4 histones?

A: We developed a ChIP-based assay to analyze, in vitro and ex vivo, the transcriptional regulation of HBV cccDNA minichromosome. Our results provide new insights on the regulation of HBV replication and identify the enzymatic activities that modulate the acetylation of cccDNA-bound histones as new therapeutic targets for anti-HBV drugs.
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Q: Context: Chlorophyllin (CHL) was proved to have strong anti-inducement effect toward many mutagens and epicarcinogens. This study was to explore effect of CHL in preventing colon neoplasms in mice induced by dimethylhydrazine (DMH), and the selective inhibition on cyclooxygenase 2(COX-2).', 'The colorectal neoplasms were induced with DMH in mice and the different dose of CHL were administered in different phases, then the prevention of colorectal neoplasms by CHL was examined; The IC50 and growth curve of HT29 cells were measured with MTT method after treated with CHL; The effect of CHL on the expression of COX-1 mRNA and COX-2 mRNA in HT29 cells were measured with RT-PCR method; The effect of CHL on the expression of COX-2 protein and NF-kappaB protein were measured with western blot and immunohistochemistry methods.', 'The incidence of colon cancer, average tumor amount, and percentage of carcinoma in CHL group were significantly lower than those in DMH group (P< .05); CHL could inhibit the growth of HT29 cells. The effects were dose dependent; CHL could selectively inhibit the expression of COX-2mRNA in HT29 cells,the expression of COX-2 protein in colon neoplasms and HT29 cells, and the expression of NF-kappaB protein in colon neoplasms.\Question: Do [ CHL prevent colon neoplasms in mice and its selective inhibition on COX-2 ]?

A: CHL could prevent colon neoplasms in mice induced by DMH and the preventive effect related to selective inhibition on COX-2, furthermore, the inhibition of CHL on COX-2 was realized by inhibiting NF-kappaB protein.
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Q: Context: There is evidence that patients with bipolar disorder have working memory deficits even during periods of euthymia. The neural basis of such deficits and its relationship with genetic risk remain unclear. We utilized functional magnetic resonance imaging (fMRI) to investigate neural activity in samples of bipolar disorder patients and their unaffected first-degree relatives while performing working memory tasks of increasing difficulty.', 'Twenty remitted bipolar I disorder patients, 20 of their unaffected first-degree relatives, and 20 healthy volunteers were recruited and successfully completed scanning. Subjects participated in fMRI scans consisting of an n-back working memory task with three stages of increasing difficulty (1-back, 2-back, and 3-back), alternating with a baseline attention task. Groups were analyzed separately to produce brain activation maps, and a group-by-task analysis of variance (ANOVA) with post hoc comparisons was completed.', 'Patients performed more poorly online than control subjects and relatives on the 2-back and 3-back tasks. The group-by-task ANOVA demonstrated a significantly altered region of neural activity involving a cluster located in the left frontal pole/ventrolateral gyrus. Post hoc analyses demonstrated that this cluster was accounted for by significantly greater activation in relatives compared with control subjects for the 2-back task. Patients demonstrated a trend to significantly greater activation than control subjects in the same cluster during 1-back performance.\Question: Is genetic liability for bipolar disorder characterized by excess frontal activation in response to a working memory task?

A:
Left prefrontal hyperactivation during working memory is associated with genetic liability for bipolar disorder and represents a potential neurobiological endophenotype for the illness.
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