In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
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Question: Foot-and-mouth disease GIS OpenFOAM Livestock infectious diseases, such as foot-and-mouth disease (FMD), cause substantial economic damage to livestock farms and their related industries. Among various causes of disease spread, airborne dispersion has previously been considered to be an important factor that could not be controlled by preventive measures to stop the spread of disease that focus on direct and indirect contact. Forecasting and predicting airborne virus spread are important to make time for developing strategies and to minimise the damage of the disease. To predict the airborne spread of the disease a modelling approach is important since field experiments using sensors are ineffective because of the rarefied concentrations of virus in the air. The simulation of airborne spread during past outbreaks required improvement both for farmers and for policy decision makers. In this study a free license computational fluid dynamics (CFD) code was used to simulate airborne virus spread. Forecasting data from the Korea Meteorological Administration (KMA) was directly connected in the developed model for real-time forecasting for 48 h in three-hourly intervals. To reduce computation time, scalar transport for airborne virus spread was simulated based on a database for the CFD computed airflow in the investigated area using representative wind conditions. The simulation results, and the weather data were then used to make a database for a web-based forecasting system that could be accessible to users. ScienceDirect jo urnal homepage: www .e lsev ie r.com/ locate/issn/153 75110 b i o s y s t e m s e n g i n e e r i n g 1 2 9 ( 2 0 1 5 ) 1 6 9 e1 8 4 http://dx.

Answer: Web-based forecasting system for the airborne spread of livestock infectious disease using computational fluid dynamics


Question: Redirecting the splicing machinery through the hybridization of high affinity, RNase H-incompetent oligonucleotide analogs such as phosphoramidate morpholino oligonucleotides (PMO) might lead to important clinical applications. Chemical conjugation of PMO to arginine-rich cell penetrating peptides (CPP) such as (R-Ahx-R) 4 (with Ahx standing for 6-aminohexanoic acid) leads to sequencespecific splicing correction in the absence of endosomolytic agents in cell culture at variance with most conventional CPPs. Importantly, (R-Ahx-R) 4 -PMO conjugates are effective in mouse models of various viral infections and Duchenne muscular dystrophy. Unfortunately, active doses in some applications might be close to cytotoxic ones thus presenting challenge for systemic administration of the conjugates in those clinical settings. Structureactivity relationship studies have thus been undertaken to unravel CPP structural features important for the efficient nuclear delivery of the conjugated PMO and limiting steps in their internalization pathway. Affinity for heparin (taken as a model heparan sulfate), hydrophobicity, cellular uptake, intracellular distribution and splicing correction have been monitored. Spacing between the charges, hydrophobicity of the linker between the Arg-groups and Arg-stereochemistry influence splicing correction efficiency. A significant correlation between splicing correction efficiency, affinity for heparin and ability to destabilize model synthetic vesicles has been observed but no correlation with cellular uptake has been found. Efforts will have to focus on endosomal escape since it appears to remain the limiting factor for the delivery of these splice-redirecting ON analogs.

Answer: Delivery of steric block morpholino oligomers by (R-X-R) 4 peptides: structure-activity studies


Question: Without viral envelope proteins, viruses cannot enter cells to start infection. As the major viral proteins present on the surface of virions, viral envelope proteins are a prominent target of the host immune system in preventing and ultimately eliminating viral infection. In addition to the well-appreciated adaptive immunity that produces envelope protein-specific antibodies and T cell responses, recent studies have begun to unveil a rich layer of host innate immune mechanisms restricting viral entry. This review focuses on the exciting progress that has been made in this new direction of research, by discussing various known examples of host restriction of viral entry, and diverse viral countering strategies, in particular, the emerging role of viral envelope proteins in evading host innate immune suppression. We will also highlight the effective cooperation between innate and adaptive immunity to achieve the synergistic control of viral infection by targeting viral envelope protein and checking viral escape. Given that many of the related findings were made with HIV-1, we will use HIV-1 as the model virus to illustrate the basic principles and molecular mechanisms on host restriction targeting HIV-1 envelope protein.

Answer:
HIV-1 Envelope Glycoprotein at the Interface of Host Restriction and Virus Evasion