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: The prevention of airborne infections in emergency departments is a very important issue. This study investigated the effects of architectural features on airborne pathogen dispersion in emergency departments by using a CFD (computational fluid dynamics) simulation tool. The study included three architectural features as the major variables: increased ventilation rate, inlet and outlet diffuser positions, and partitions between beds. The most effective method for preventing pathogen dispersion and reducing the pathogen concentration was found to be increasing the ventilation rate. Installing partitions between the beds and changing the ventilation system's inlet and outlet diffuser positions contributed only minimally to reducing the concentration of airborne pathogens. 
 Title: Case Study of Airborne Pathogen Dispersion Patterns in Emergency Departments with Different Ventilation and Partition Conditions

A: False
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Q: Paragraph: The burden of vector-borne diseases (Dengue, Zika virus, yellow fever, etc.) gradually increased in the past decade across the globe. Mathematical modelling on infectious diseases helps to study the transmission dynamics of the pathogens. Theoretically, the diseases can be controlled and eventually eradicated by maintaining the effective reproduction number, (R eff ), strictly less than 1. We established a vector-host compartmental model, and derived (R eff ) for vector-borne diseases. The analytic form of the (R eff ) was found to be the product of the basic reproduction number and the geometric average of the susceptibilities of the host and vector populations. The (R eff ) formula was demonstrated to be consistent with the estimates of the 2015-2016 yellow fever outbreak in Luanda, and distinguished the second minor epidemic wave. For those using the compartmental model to study the vector-borne infectious disease epidemics, we further remark that it is important to be aware of whether one or two generations is considered for the transition ''from host to vector to host'' in reproduction number calculation. 
 Title: Distributed under Creative Commons CC-BY 4.0 Modelling the effective reproduction number of vector-borne diseases: the yellow fever outbreak in Luanda, Angola 2015-2016 as an example

A: False
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Q: Paragraph: The contribution of distinct central nervous system (CNS) resident cells to protective alpha/beta interferon (IFN-␣/␤) function following viral infections is poorly understood. Based on numerous immune regulatory functions of astrocytes, we evaluated the contribution of astrocyte IFN-␣/␤ signaling toward protection against the nonlethal glia-and neuronotropic mouse hepatitis virus (MHV) strain A59. Analysis of gene expression associated with IFN-␣/␤ function, e.g., pattern recognition receptors (PRRs) and interferon-stimulated genes (ISGs), revealed lower basal mRNA levels in brain-derived astrocytes than in microglia. Although astrocytes poorly induced Ifn␤ mRNA following infection, they upregulated various mRNAs in the IFN-␣/␤ pathway to a higher extent than microglia, supporting effective IFN-␣/␤ responsiveness. Ablation of the IFN-␣/␤ receptor (IFNAR) in astrocytes using mGFAPcre IFNAR fl/fl mice resulted in severe encephalomyelitis and mortality, coincident with uncontrolled virus replication. Further, virus spread was not restricted to astrocytes but also affected microglia and neurons, despite increased and sustained Ifn␣/␤ and ISG mRNA levels within the CNS. IFN-␥, a crucial mediator for MHV control, was not impaired in infected mGFAPcre IFNAR fl/fl mice despite reduced T cell CNS infiltration. Unexpectedly however, poor induction of IFN-␥-dependent major histocompatibility complex (MHC) class II expression on microglia supported that defective IFN-␥ signaling contributes to uncontrolled virus replication. A link between sustained elevated IFN-␣/␤ and impaired responsiveness to IFN-␥ supports the novel concept that temporally limited early IFN-␣/␤ responses are critical for effective antiviral IFN-␥ function. Overall, our results imply that IFN-␣/␤ signaling in astrocytes is not only critical in limiting early CNS viral spread but also promotes protective antiviral IFN-␥ function. 
 Title: Alpha/Beta Interferon (IFN-␣/␤) Signaling in Astrocytes Mediates Protection against Viral Encephalomyelitis and Regulates IFN-␥-Dependent Responses

A:
False
****