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".

[EX Q]: Paragraph: The recent Ebola virus disease outbreak emphasized the potential misuse of personal protective equipment (PPE) by health care workers (HCWs) during such an event. We aimed to compare selfperceived proficiency of PPE use and objective performance, and identify predictors of low compliance and PPE misuse. Methods: An observational study combined with subjective questionnaires were carried out during a bioterror simulation drill. Forty-two observers evaluated performance under PPE. Mistakes were recorded and graded using a structured observational format and were correlated with the subjective questionnaires and with demographic parameters. Results: One hundred seventy-eight HCWs from community clinics and hospitals were included. The mean self-perceived proficiency was high (6.1 out of 7), mean level of comfort was moderate (4.0 out of 7), and mean objective performance was intermediate (9.5 out of 13). There was no correlation between comfort and objective performance scores. Self-perceived proficiency was in correlation with donning and continuous performance with PPE but not with doffing. Clinic personnel performed better than personnel in hospitals (40.3% vs 67.8% with 3 or more mistakes, respectively; P = .001). Demographic characteristics had no correlation with objective or self-perceived performance. Conclusions: Self-perceived proficiency is a poor predictor of appropriate PPE use. The results suggest poor awareness of the possibility of PPE misuse.
Title: The association between self-perceived proficiency of personal protective equipment and objective performance: An observational study during a bioterrorism simulation drill
[EX A]: False

[EX Q]: Paragraph: A novel series of (3-diethoxyphosphoryl)isoxazolidines substituted at C5 with various quinazolinones have been synthesized by the 1,3-dipolar cycloaddition of N-methyl-C-(diethoxyphosphoryl)nitrone with N3-substitued 2-vinyl-3H-quinazolin-4-ones. All isoxazolidines were assessed for antiviral activity against a broad range of DNA and RNA viruses. Isoxazolidines trans-11f/cis-11f (90:10), trans-11h and trans-11i/cis-11i (97:3) showed weak activity (EC 50 = 6.84, 15.29 and 9.44 M) toward VZV (TK + strain) which was only one order of magnitude lower than that of acyclovir used as a reference drug. Phosphonates trans-11b/cis-11b (90:10), trans-11c, trans-11e/cis-11e (90:10) and trans-11g appeared slightly active toward cytomegalovirus (EC 50 = 27-45 M). Compounds containing benzyl substituents at N3 in the quinazolinone skeleton exhibited slight antiproliferative activity towards the tested immortalized cells with IC 50 in the 21-102 M range.
Title: molecules New Isoxazolidine-Conjugates of Quinazolinones-Synthesis, Antiviral and Cytostatic Activity
[EX A]: True

[EX Q]: Paragraph: Interferon- (IFN-) represents one of the most important innate immunity responses in a host to combat infections of many human viruses including human herpesviruses. Human N-myc interactor (Nmi) protein, which has been shown to interact with signal transducer and activator of transcription (STAT) proteins including STAT1, is important for the activation of IFN- induced STAT1-dependent transcription of many genes responsible for IFN- immune responses. However, no proteins encoded by herpesviruses have been reported to interact with Nmi and inhibit Nmi-mediated activation of IFN- immune responses to achieve immune evasion from IFN- responses. In this study, we show strong evidence that the UL23 protein of human cytomegalovirus (HCMV), a human herpesvirus, specifically interacts with Nmi. This interaction was identified through a yeast two-hybrid screen and co-immunoprecipitation in human cells. We observed that Nmi, when bound to UL23, was not associated with STAT1, suggesting that UL23 binding of Nmi disrupts the interaction of Nmi with STAT1. In cells overexpressing UL23, we observed (a) significantly reduced levels of Nmi and STAT1 in the nuclei, the sites where these proteins act to induce transcription of IFN- stimulated genes, and (b) decreased levels of the induction of the transcription of IFN- stimulated genes. UL23-deficient HCMV mutants induced higher transcription of IFN- stimulated genes and exhibited lower titers than parental and control revertant viruses expressing functional UL23 in IFN- treated cells. Thus, UL23 appears to interact directly with Nmi and inhibit nuclear translocation of Nmi and its associated protein STAT1, leading to a decrease of IFN- induced responses and an increase of viral resistance to IFN-. Our results further highlight the roles of UL23-Nmi interactions in facilitating PLOS Pathogens | https://doi.
Title: Human cytomegalovirus UL23 inhibits transcription of interferon- stimulated genes and blocks antiviral interferon- responses by interacting with human N-myc interactor protein
[EX A]:
True