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".

Input: Consider Input: Paragraph: Despite garnering minimal attention from the medical community overall, olfaction is indisputably critical in the manner in which we as humans interact with our surrounding environment. As the initial anatomical structure in the olfactory pathway, the nasal airway plays a crucial role in the transmission and perception of olfactory stimuli. The goal of this chapter is to provide a comprehensive overview of olfactory disturbances as it pertains to the sinonasal airway. This comprises an in-depth discussion of clinically relevant nasal olfactory anatomy and physiology, classification systems of olfactory disturbance, as well as the various etiologies and pathophysiologic mechanisms giving rise to this important disease entity. A systematic clinical approach to the diagnosis and clinical workup of olfactory disturbances is also provided in addition to an extensive review of the medical and surgical therapeutic modalities currently available. 
 Title: Diseases of the nasal cavity

Output: True


Input: Consider Input: Paragraph: As simple organisms with a parasite nature, viruses have become masters in manipulating and subvert cellular components, including host proteins and organelles, to improve viral replication. Therefore, the understanding of viral strategies to manipulate cell function disrupting plant defenses and enhancing viral infection cycles is fundamental to the production of virus-resistant plant lines. After invading susceptible plants, viruses create conditions that favor local and systemic infections by suppressing multiple layers of innate host defenses while use cellular machinery to own benefit. Viral interference in interlinked essential cellular functions results in phenotypic changes and disease symptoms, which debilitates plants favoring infection establishment. Herein in this review, the novelty it will be the discussion about the strategies used by (+) single strand RNA viruses to affect cellular processes and components to improve viral replication, in parallel to overcome plant defenses, favoring disease establishment by applying in one action using the same viral protein to coordinate viral replication and breaking down plant defense. This focus on plant-virus interaction was never done before, and this knowledge has the potential to help in the development of new strategies to produce resistant plants. 
 Title: Killing two birds with one stone: How do Plant Viruses Break Down Plant Defenses and Manipulate Cellular Processes to Replicate Themselves?

Output: True


Input: Consider Input: Paragraph: Interferon-γ (IFN-γ) 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-γ induced STAT1-dependent transcription of many genes responsible for IFN-γ immune responses. However, no proteins encoded by herpesviruses have been reported to interact with Nmi and inhibit Nmi-mediated activation of IFN-γ immune responses to achieve immune evasion from IFN-γ 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-γ stimulated genes, and (b) decreased levels of the induction of the transcription of IFN-γ stimulated genes. UL23-deficient HCMV mutants induced higher transcription of IFN-γ stimulated genes and exhibited lower titers than parental and control revertant viruses expressing functional UL23 in IFN-γ 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-γ induced responses and an increase of viral resistance to IFN-γ. Our results further highlight the roles of UL23-Nmi interactions in facilitating PLOS Pathogens | https://doi. 
 Title: Human cytomegalovirus UL23 inhibits transcription of interferon-γ stimulated genes and blocks antiviral interferon-γ responses by interacting with human N-myc interactor protein


Output: True