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: We describe an evidence-based approach to enhancing the resilience of healthcare workers in preparation for an influenza pandemic, based on evidence about the stress associated with working in healthcare during the SARS outbreak. SARS was associated with significant long-term stress in healthcare workers, but not with increased mental illness. Reducing pandemic-related stress may best be accomplished through interventions designed to enhance resilience in psychologically healthy people. Applicable models to improve adaptation in individuals include Folkman and Greer's framework for stress appraisal and coping along with psychological first aid. Resilience is supported at an organizational level by effective training and support, development of material and relational reserves, effective leadership, the effects of the characteristics of "magnet hospitals," and a culture of organizational justice. Evidence supports the goal of developing and maintaining an organizational culture of resilience in order to reduce the expected stress of an influenza pandemic on healthcare workers. This recommendation goes well beyond the provision of adequate training and counseling. Although the severity of a pandemic is unpredictable, this effort is not likely to be wasted because it will also support the health of both patients and staff in normal times. 
 Title: Applying the Lessons of SARS to Pandemic Influenza An Evidence-based Approach to Mitigating the Stress Experienced by Healthcare Workers

Answer: True


Question: Paragraph: Despite the wide use of Caenorhabditis elegans as a model organism, the first virus naturally infecting this organism was not discovered until six years ago. The Orsay virus and its related nematode viruses have a positive-sense RNA genome, encoding three proteins: CP, RdRP, and a novel δ protein that shares no homology with any other proteins. δ can be expressed either as a free δ or a CP-δ fusion protein by ribosomal frameshift, but the structure and function of both δ and CP-δ remain unknown. Using a combination of electron microscopy, X-ray crystallography, computational and biophysical analyses, here we show that the Orsay δ protein forms a~420-Å long, pentameric fiber with an N-terminal α-helical bundle, a β-stranded filament in the middle, and a C-terminal head domain. The pentameric nature of the δ fiber has been independently confirmed by both mass spectrometry and analytical ultracentrifugation. Recombinant Orsay capsid containing CP-δ shows protruding long fibers with globular heads at the distal end. Mutant viruses with disrupted CP-δ fibers were generated by organism-based reverse genetics. These viruses were found to be either non-viable or with poor infectivity according to phenotypic and qRT-PCR analyses. Furthermore, addition of purified δ proteins to worm culture greatly reduced Orsay infectivity in a sequence-specific manner. Based on the structure resemblance between the Orsay CP-δ fiber and the fibers from reovirus and adenovirus, we propose that CP-δ functions as a cell attachment protein to mediate Orsay entry into worm intestine cells. Orsay, the only virus known to naturally infect the nematode Caenorhabditis elegans, expresses a capsid-δ fusion protein. We have demonstrated that the Orsay fusion protein is incorporated into Orsay capsid and forms a~420-Å long fiber protruding from the PLOS Pathogens | 
 Title: Structure of a pentameric virion-associated fiber with a potential role in Orsay virus entry to host cells

Answer: False


Question: Paragraph: Intracerebral inoculation of Theiler's murine encephalomyelitis virus (TMEV) into susceptible mouse strains produces a chronic demyelinating disease in which mononuclear cell-rich infiltrates in the central nervous system (CNS) are prominent. Current evidence strongly supports an immune-mediated basis for myelin breakdown, with an effector role proposed for TMEV-specific, major histocompatibility complex (MHC) class II-restricted delayed-type hypersensitivity (DTH) responses in which lymphokine-activated macrophages mediate bystander demyelination. The present study examined the possibility that concomitant or later-appearing neuroantigen-specific autoimmune T cell responses, such as those demonstrated in chronic-relapsing experimental allergic encephalomyelitis (R-EAE), may contribute to the demyelinating process following TMEV infection. T cell responses against intact, purified major myelin proteins (myelin 10 basic protein (MBP) and proteohpid protein (PLP)), and against altered myelin constituents were readily demonstrable in SJL//J mice with R-EAE, but were not detectable in SJL//J mice with TMEV-induced demyehnating disease. TMEV-infected mice also did not display T cell responses against the peptide fragments of MBP(91-104) and PLP(139-151) recently shown to be encephalitogenic in SJL/J mice. In addition, induction of neuroantigen-specific tolerance to a heterogeneous mixture of CNS antigens, via the i.v. injection of syngeneic SJL//J splenocytes covalently coupled with mouse spinal cord homogenate, resulted in significant suppression of clinical and histologic signs of R-EAE and the accompanying MBPand PLP-specific DTH responses. In contrast, neuroantigen-specific tolerance failed to alter the development of clinical and histologic signs of TMEV-induced demyelinating disease or the accompanying virus-specific DTH and humoral immune responses. These findings demonstrate that TMEV-induced demyelinating disease can occur in the apparent absence of neuroantigen-specific autoimmune responses. The relationship of the present results to the immunopathology of multiple sclerosis is discussed. 
 Title: Class II-restricted T cell responses in Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease III. Failure of neuroantigen-specific immune tolerance to affect the clinical course of demyelination

Answer:
False