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.

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

We investigated the ability of monoclonal B cells to restore primary and secondary T-cell dependent antibody responses in adoptive immune-deficient hosts. Priming induced B cell activation and expansion, AID expression, antibody production and the generation of IgM + IgGand IgM -IgG + antigen-experienced B-cell subsets that persisted in the lymphopenic environment by cell division. Upon secondary transfer and recall the IgM -IgG + cells responded by the production of antigen-specific IgG while the IgM + memory cells secreted mainly IgM and little IgG, but generated new B cells expressing germinal center markers. The recall responses were more efficient if the antigenic boost was delayed suggesting that a period of adaptation is necessary before the transferred cells are able to respond. Overall these findings indicate that reconstitution of a functional and complete memory pool requires transfer of all different antigen-experienced B cell subsets. We also found that the size of the memory B cell pool did not rely on the number of the responding naïve B cells, suggesting autonomous homeostatic controls for naïve and memory B cells. By reconstituting a stable memory B cell pool in immune-deficient hosts using a monoclonal high-affinity B cell population we demonstrate the potential value of B cell adoptive immunotherapy.
Regulation and Maintenance of an Adoptive T-Cell Dependent Memory B Cell Pool

or Actinomycin D (5nM) resulted in significantly decreased IE and pp65 mRNA and protein levels in human fibroblasts at early times post infection. This initially delayed replication was compensated for later during the replication process, at which stage it didn't significantly affect virus production. Pol I inhibition also reduced HSV-1 ICP0 and gB transcripts, suggesting that some herpesviruses engage Pol I for their early transcription. In contrast, inhibition of Pol I failed to affect MCMV transcription. Collectively, our results contribute to better understanding of the functional interplay between RNA Pol I-mediated nucleolar events and the Herpes viruses, particularly HCMV whose pathogenic impact ranges from congenital malformations and potentially deadly infections among immunosuppressed patients, up to HCMV's emerging oncomodulatory role in human tumors.

Human cytomegalovirus and Herpes Simplex type I virus can engage RNA polymerase I for transcription of immediate early genes