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.

Input: Consider Input: An urgent demand of assessing passengers' exposure risks in airliner cabins was raised as commercial airliners are one of the major media that carrying and transmitting infectious disease worldwide. In this study, simulations were conducted using a Boeing 737 cabin model to study the transport characteristics of airborne droplets and the associated infection risks of passengers. The numerical results of the airflow field were firstly compared against the experimental data in the literature to validate the reliability of the simulations. Airborne droplets were assumed to be released by passengers through coughing and their transport characteristics were modelled using the Lagrangian approach. Numerical results found that the particle travel distance was very sensitive to the release locations, and the impact was more significant along the longitudinal and horizontal directions. Particles released by passengers sitting next to the windows could travel much further than the others. A quantifiable approach was then applied to assess the individual infection risks of passengers. The key particle transport information such as the particle residence time yielded from the Lagrangian tracking process was extracted and integrated into the Wells-Riley equation to estimate the risks of infection. Compared to the Eulerian-based approach, the Lagrangian-based approach presented in this study is more robust as it addresses both the particle concentration and particle residence time in the breathing zone of every individual passenger.

Output: Evaluation of airborne disease infection risks in an airliner cabin using the Lagrangian-based Wells-Riley approach

Input: Consider Input: IFITM3 restricts cellular infection by multiple important viral pathogens, and is particularly critical for the innate immune response against influenza virus. Expression of IFITM3 expands acidic endolysosomal compartments and prevents fusion of endocytosed viruses, leading to their degradation. This small, 133 amino acid, antiviral protein is controlled by at least four distinct post-translational modifications. Positive regulation of IFITM3 antiviral activity is provided by Spalmitoylation, while negative regulatory mechanisms include lysine ubiquitination, lysine methylation and tyrosine phosphorylation. Herein, we describe specific insights into IFITM3 trafficking and activity that were provided by studies of IFITM3 post-translational modifications, and discuss evidence suggesting that IFITM3 adopts multiple membrane topologies involving at least one intramembrane domain in its antivirally active conformation.

Output: Regulation of the trafficking and antiviral activity of IFITM3 by post-translational modifications

Input: Consider Input: Rev DDX3 DDX5 RNA helicase RNA export a b s t r a c t RNA helicase plays an important role in host mRNA and viral mRNA transcription, transport, and translation. Many viruses utilize RNA helicases in their life cycle, while human immunodeficiency virus type 1 (HIV-1) does not encode an RNA helicase. Thus, host RNA helicase has been involved in HIV-1 replication. Indeed, DDX1 and DDX3 DEAD-box RNA helicases are known to be required for efficient HIV-1 Revdependent RNA export. However, it remains unclear whether distinct DDX RNA helicases cross-talk and cooperate to modulate the HIV-1 Rev function. In this study, we noticed that distinct DDX RNA helicases, including DDX1, DDX3, DDX5, DDX17, DDX21, DDX56, except DDX6, bound to the Rev protein and they colocalized with Rev in nucleolus or nucleus. In this context, these DEAD-box RNA helicases except DDX6 markedly enhanced the HIV-1 Rev-dependent RNA export. Furthermore, DDX3 interacted with DDX5 and synergistically enhanced the Rev function. As well, combination of other distinct DDX RNA helicases cooperated to stimulate the Rev function. Altogether, these results suggest that distinct DDX DEAD-box RNA helicases cooperate to modulate the HIV-1 Rev function. Crown
Output: Distinct DDX DEAD-box RNA helicases cooperate to modulate the HIV-1 Rev function