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: We evaluated if interventions aimed at air travellers can delay establishment of a SARS-CoV-2 outbreak in a previously unaffected country. Methods: For countries with no sustained SARS-CoV-2 transmission and with no shared border with affected regions we simulated arriving infected air travellers. We assessed the effectiveness of syndromic screening at departure and/or arrival & traveller sensitisation to the COVID-2019-like symptoms with the aim to trigger rapid self-isolation and reporting on symptom onset to enable contact tracing. We assumed that syndromic screening would reduce the number of infected arrivals and that traveller sensitisation reduce the average number of secondary cases. We report the minimal expected delay achievable in 50% (75% & 97.5%) of simulations. In the simulations we account for uncertainty in the number of secondary cases in the absence of air traveller targeted interventions and the arrival times of infected cases and also present sensitivity analyses on arrival rates of infected travellers and the effectiveness of traveller sensitisation. Results: Under baseline assumptions exit and entry screening combined with traveller sensitisation can delay a local SARS-CoV-2 outbreak by at least 83 (75% of simulations: at least 36, 97.5% 8) days while there is no more than 1 infected traveller per week. The benefit of entry screening is small if exit screening is effective: the combination of only exit screening and traveller sensitisation can delay an outbreak by at least 76 (75%: 33, 97.5%: 7) days. With increasing rates of infected travellers, less effective sensitisation or without screening these delays shrink rapidly to a week or less. Conclusion: Syndromic screening and traveller sensitisation in combination could delay outbreaks in yet unaffected countries and support local containment efforts, but only if infected traveller numbers are very low. . CC-BY 4.0 International license It is made available under a author/funder, who has granted medRxiv a license to display the preprint in perpetuity. is the (which was not peer-reviewed) The copyright holder for this preprint . 
 Title: Title: Interventions targeting air travellers early in the pandemic may delay local outbreaks of SARS-CoV-2

A: True
****
Q: Paragraph: The development and use of numerous animal models of human autoimmune diseases have provided important advances in our understanding of pathogenic mechanisms of disease and provided robust and reliable models to test novel therapeutic strategies. However, few preclinical studies of therapeutic treatments have demonstrated efficacy in the clinic, possibly because of the biological differences between humans and other animals. Although animal models of human disease are imperfect, it is important to understand the differences between the human disease and its animal models and to design experimental studies using animal models appropriately for the questions being asked. This review provides an overview of the currently used animal models of three human neuroimmunological diseases, multiple sclerosis, Guillain-Barré syndrome, and myasthenia gravis, as well as the advantages and disadvantages of each model and how they correlate or differ from their human counterpart. 
 Title: Animal Models for the Study of Neuroimmunological Disease

A: True
****
Q: Paragraph: Ebolavirus, a member of the Filoviridae family of negative-sense RNA viruses, causes severe haemorrhagic fever leading up to 90% lethality. Ebolavirus matrix protein VP40 is involved in the virus assembly and budding process. The RNA binding pocket of VP40 is considered as the drug target site for structure based drug design. High Throughput Virtual Screening and molecular docking studies were employed to find the suitable inhibitors against VP40. Ten compounds showing good glide score and glide energy as well as interaction with specific amino acid residues were short listed as drug leads. These small molecule inhibitors could be potent inhibitors for VP40 matrix protein by blocking virus assembly and budding process. ISSN 0973-2063 (online) 0973-8894 (print) Bioinformation 9(6): 286-292 (2013) 287 © 2013 Biomedical Informatics replication [23]. C-terminal domain of VP40 is required for membrane association [24, 25]. open access ISSN 0973-2063 (online) 0973-8894 (print) Bioinformation 9(6): 286-292 (2013) 289 
 Title: Hypothesis High-throughput virtual screening and docking studies of matrix protein vp40 of ebola virus

A:
False
****