In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".

[Q]: Paragraph: Background: The hepatitis B virus (HBV) is a major etiological factor of inflammation and damage to the liver resulting in hepatocellular carcinoma. Transcription factors play important roles in the disordered gene expression and liver injury caused by HBV. However, the molecular mechanisms behind this observation have not been defined. Results: In this study, we observed that circulating prostaglandin (PGE) 2 synthesis was increased in patients with chronic hepatitis B infection, and detected elevated cyclooxygenase (COX)-2 expression in HBV-and HBxexpressing liver cells. Likewise, the association of HBx with C/EBPβ contributed to the induction of COX-2. The COX-2 promoter was hypomethylated in HBV-positive cells, and specific demethylation of CpG dinucleotides within each of the two NF-AT sites in the COX-2 promoter resulted in the increased binding affinity of NF-AT to the cognate sites in the promoter, followed by increased COX-2 expression and PGE2 accumulation. The DNA methylatransferase DNMT3B played a key role in the methylation of the COX-2 promoter, and its decreased binding to the promoter was responsible for the regional demethylation of CpG sites, and for the increased binding of transcription factors in HBV-positive cells. Our results indicate that upregulation of COX-2 by HBV and HBx is mediated by both demethylation events and recruitment of multiple transcription factors binding to the promoter. 
 Title: Induction of Cyclooxygenase-2 Expression by Hepatitis B Virus Depends on Demethylation- associated Recruitment of Transcription Factors to the Promoter
[A]: False


[Q]: Paragraph: We characterized DBD by measuring concentrations of reactive species and ions. The inactivation efficiency was deduced using aerosol-and colony-counting methods. Susceptibility constant (Z) was introduced for performance evaluation of DBD. Modified Z was suggested for evaluation of DBD reactors of different sizes. Our methodology will be used for design optimization and performance evaluation. Dielectric barrier discharge (DBD) is a promising method to remove contaminant bioaerosols. The collection efficiency of a DBD reactor is an important factor for determining a reactor's removal efficiency. Without considering collection, simply defining the inactivation efficiency based on colony counting numbers for DBD as on and off may lead to overestimation of the inactivation efficiency of the DBD reactor. One-pass removal tests of bioaerosols were carried out to deduce the inactivation efficiency of the DBD reactor using both aerosol-and colony-counting methods. Our DBD reactor showed good performance for removing test bioaerosols for an applied voltage of 7.5 kV and a residence time of 0.24 s, with Á CFU , Á Number , and Á Inactivation values of 94%, 64%, and 83%, respectively. Additionally, we introduce the susceptibility constant of bioaerosols to DBD as a quantitative parameter for the performance evaluation of a DBD reactor. The modified susceptibility constant, which is the ratio of the susceptibility constant to the volume of the plasma reactor, has been successfully demonstrated for the performance evaluation of different sized DBD reactors under different DBD operating conditions. Our methodology will be used for design optimization, performance evaluation, and prediction of power consumption of DBD for industrial applications. 
 Title: Susceptibility constants of airborne bacteria to dielectric barrier discharge for antibacterial performance evaluation
[A]: False


[Q]: Paragraph: Nullbasic, a mutant of the HIV-1 Tat protein, has anti-HIV-1 activity through mechanisms that include inhibition of Rev function and redistribution of the HIV-1 Rev protein from the nucleolus to the nucleoplasm and cytoplasm. Here we investigate the mechanism of this effect for the first time, establishing that redistribution of Rev by Nullbasic is not due to direct interaction between the two proteins. Rather, Nullbasic affects subcellular localization of cellular proteins that regulate Rev trafficking. In particular, Nullbasic induced redistribution of exportin 1 (CRM1), nucleophosmin (B23) and nucleolin (C23) from the nucleolus to the nucleus when Rev was coexpressed, but never in its absence. Inhibition of the Rev:CRM1 interaction by leptomycin B or a non-interacting RevM10 mutant completely blocked redistribution of Rev by Nullbasic. Finally, Nullbasic did not inhibit importin bor transportin 1-mediated nuclear import, suggesting that cytoplasmic accumulation of Rev was due to increased export by CRM1. Overall, our data support the conclusion that CRM1dependent subcellular redistribution of Rev from the nucleolus by Nullbasic is not through general perturbation of either nuclear import or export. Rather, Nullbasic appears to interact with and disrupt specific components of a Rev trafficking complex required for its nucleocytoplasmic shuttling and, in particular, its nucleolar accumulation. 
 Title: Nullbasic, a Potent Anti-HIV Tat Mutant, Induces CRM1- Dependent Disruption of HIV Rev Trafficking
[A]:
True