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".
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Question: Paragraph: Numerous living organisms possess biophotonic nanostructures that provide coloration and other diverse functions for survival. While such structures have been actively studied and replicated in the laboratory, it remains unclear whether they can be used for biomedical applications. Here we show a transparent photonic nanostructure inspired by the longtail glasswing (Chorinea faunus) butterfly and demonstrate its use in intraocular pressure (IOP) sensors in vivo. We exploit the phase separation between two immiscible polymers (poly(methyl methacrylate) and polystyrene) to form nanostructured features on top of a Si 3 N 4 substrate. The membrane thus formed shows good angle-independent white light transmission, strong hydrophilicity and anti-biofouling properties that prevent adhesion of proteins, bacteria, and eukaryotic cells. We then developed a microscale implantable IOP sensor using our photonic membrane as an optomechanical sensing element. Finally, we performed in vivo testing on New Zealand white rabbits and show that our Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#termsReprints and permission information is available online at www.nature.com/reprints. 
 Title: Multifunctional biophotonic nanostructures inspired by longtail glasswing butterfly for medical devices HHS Public Access Author manuscript

Answer: True


Question: Paragraph: A hallmark of disease is that most pathogens are able to infect more than one host species. However, for most pathogens, we still have a limited understanding of how this affects epidemiology, persistence and virulence of infections-including several zoonotic pathogens that reside in wild animal reservoirs and spillover into humans. In this chapter, we review the current knowledge of mallard (Anas platyrhynchos) as host for pathogens. This species is widely distributed, often occupying habitats close to humans and livestock, and is an important game bird species and the ancestor to domestic ducks-thereby being an excellent model species to highlight aspects of the wildlife, domestic animal interface and the relevance for human health. We discuss mallard as host for a range of pathogens but focus more in depth of it as a reservoir host for influenza A virus (IAV). Over the last decades, IAV research has surged, prompted in part to the genesis and spread of highly pathogenic virus variants that have been devastating to domestic poultry and caused a number of human spillover infections. The aim of this chapter is to synthesise and review the intricate interactions of virus, host and environmental factors governing IAV epidemiology and evolution. 
 Title: Of Ducks and Men: Ecology and Evolution of a Zoonotic Pathogen in a Wild Reservoir Host

Answer: False


Question: Paragraph: The mammalian reoviruses and rotaviruses have evolved specifi c mechanisms to evade the Type I interferon (IFN) antiviral response. Rotavirus likely represses the IFN response by at least 4 mechanisms. First, the rotavirus protein NSP1, most likely functioning as an E3 ligase, can induce proteasome-dependent degradation of the transcription factors IRF3, IRF5, and IRF7 to prevent their induction of IFN. Second, NSP1 can induce proteasome-dependent degradation of the ubiquitin ligase complex protein β-TrCP, resulting in stabilization of IκB and concomitant failure of virus to activate NF-κB for induction of IFN. Third, rotavirus may sequester NF-κB in viroplasms. And fourth, rotavirus can prevent STAT1 and STAT2 nuclear translocation. The predominant mechanism for rotavirus inhibition of the IFN response is likely both rotavirus strain-specifi c and cell type-specifi c. The mammalian reoviruses also display strain-specifi c differences in their modulation of the IFN response. Reovirus activates RIG-I and IPS-1 for phosphorylation of IRF3. Reovirus-induced activation of MDA5 also participates in induction if IFN-β, perhaps through activation of NF-κB. Reovirus likely inhibits the IFN response by at least 3 virus strain-specifi c mechanisms. First, the reovirus μ2 protein can induce an unusual nuclear accumulation of IRF9 and repress IFN-stimulated gene (ISG) expression, most likely by disrupting IRF9 function as part of the heterotrimeric transcription factor complex, ISGF3. Second, the reovirus σ3 protein can bind dsRNA and prevent activation of the latent antiviral effector protein PKR. And third, genetic approaches have identifi ed the reovirus λ2 and σ2 proteins in virus strain-specifi c modulation of the IFN response, but the signifi cance remains unclear. In sum, members of the family Reoviridae have evolved a variety of mechanisms to subvert the host's innate protective response. Yue Z, Shatkin AJ. 1997. Double-stranded RNA-dependent protein kinase (PKR) is regulated by reovirus structural proteins. Virology 234(2):364-371. Zurney J, Howard KE, Sherry B. 2007. Basal expression levels of IFNAR and Jak-STAT components are determinants of celltype-specifi c differences in cardiac antiviral responses. J Virol 81(24):13668-13680. Zurney J, Kobayashi T, Holm GH, Dermody TS, Sherry B. 2009. Reovirus mu2 protein inhibits interferon signaling through a novel mechanism involving nuclear accumulation of interferon regulatory factor 9. J Virol 83 (5):2178-2187. 
 Title: Rotavirus and Reovirus Modulation of the Interferon Response

Answer:
True