instruction:
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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Paragraph: For the purpose of this work, insect biotechnology, which is also known as yellow biotechnology, is the use of insects as well as insect-derived cells or molecules in medical (red biotechnology), agricultural (green biotechnology), and industrial (white) biotechnology. It is based on the application of biotechnological techniques on insects or their cells to develop products or services for human use. Such products are then applied in agriculture, medicine, and industrial biotechnology. Insect biotechnology has proven to be a useful resource in diverse industries, especially for the production of industrial enzymes including chitinases and cellulases, pharmaceuticals, microbial insecticides, insect genes, and many other substances. Insect cells (ICs), and particularly lepidopteran cells, constitute a competitive strategy to mammalian cells for the manufacturing of biotechnology products. Among the wide range of methods and expression hosts available for the production of biotech products, ICs are ideal for the production of complex proteins requiring extensive posttranslational modifi cation. The progress so far made in insect biotechnology essentially derives from scientifi c breakthroughs in molecular biology, especially with the advances in techniques that allow genetic manipulation of organisms and cells. Insect biotechnology has grown tremendously in the last 30 years. 
 Title: Insect Biotechnology
answer:
False


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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
answer:
True


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Paragraph: Background: Bovine herpesvirus type 1 (BHV-1) is an important pathogen in cattle that is responsible for substantial economic losses. Previous studies suggest that BHV-1 may induce apoptosis in Madin-Darby bovine kidney (MDBK) cells via a mechanism only involving caspases and p53. However, the mechanism for BHV-1-induced MDBK cell apoptosis still requires more research. Methods: MDBK was used as a model to study the precise signaling pathways of apoptosis induced by BHV-1 infection. Results: BHV-1 infection activated a Fas/FasL-mediated apoptotic pathway, resulting in activation of caspase-8 and cleavage of Bid. In addition, BHV-1 infection down-regulated Bcl-2 and up-regulated Bax expression, thereby initiating the release of cytochrome c followed by caspase-9 activation. The combined activation of the extrinsic and intrinsic pathways resulted in activation of downstream effecter caspase-3 and poly ADP-ribose polymerase (PARP), leading to apoptosis. Furthermore, blocking apoptosis using caspase inhibitors improved BHV-1-infected MDBK cell viability to different extent. BHV-1 infection did not induce significant DNA fragmentation in MDBK cells pretreated with ammonium chloride (NH 4 Cl) or cells infected with UV-inactivated BHV-1. Blocking caspases activation increased BHV-1 replication. Conclusions: BHV-1 induces apoptosis in MDBK cells through extrinsic and intrinsic pathways and there might be cross-talk between the two pathways. In addition, BHV-1 replication may be necessary for the induction of apoptosis in BHV-1-infected cells, and prolonged cell viability benefits BHV-1 replication. 
 Title: Bovine herpes virus type 1 induces apoptosis through Fas-dependent and mitochondria- controlled manner in Madin-Darby bovine kidney cells
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False