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


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Dendritic cells (DCs) are recognized as highly potent antigen-presenting cells that are able to stimulate cytotoxic T lymphocyte (CTL) responses with antitumor activity. Consequently, DCs have been explored as cellular vaccines in cancer immunotherapy. To that end, DCs are modified with tumor antigens to enable presentation of antigen-derived peptides to CTLs. In this review we discuss the use of viral vectors for in situ modification of DCs, focusing on their clinical applications as anticancer vaccines. Among the viral vectors discussed are those derived from viruses belonging to the families of the Poxviridae, Adenoviridae, Retroviridae, Togaviridae, Paramyxoviridae, and Rhabdoviridae. We will further shed light on how the combination of viral vector-based vaccination with T-cell supporting strategies will bring this strategy to the next level. Since their discovery in 1973, it was clear that dendritic cells (DCs) stood out above the immune cell pack (1, 2). They are morphologically distinct from all other immune cell types and are gifted with an unparalleled capacity to take up, process and present self and foreign antigens to both CD4 + and CD8 + T cells. DCs are critical intermediaries between the innate and adaptive immune systems, as they stimulate, regulate, and shape both immunity and tolerance in all its disguises. Ralph Steinmann, who discovered these cells, was awarded the Nobel Prize for Medicine in 2011, because the discovery of DCs changed medicine (3). Dendritic cells in both humans and mice represent a population of at least four different subtypes with distinct phenotypical and functional characteristics (4-7). These subsets are: plasmacytoid DCs (pDCs), two subsets of conventional DCs (cDC1 and cDC2), and inflammatory DCs. The latter represent a monocyte-derived subset that appears during inflammatory responses (Table 1) . Recently, additional types of human blood DCs, monocytes, and progenitors were revealed using single cell RNA-sequencing. The group of Prof. Nir Hacohen identified pDCs next to cDC progenitor-derived cDC1 (Clec9A + ) and two types of CD1c + cDC2, of which one can also be derived from CD14 + DCs. Furthermore they found a CD141 − CD1c − CD11c + DC subset derived from CD16 + monocytes and an AXL + Siglec6 + subset (8). Future research will have to unravel a possible murine representative for the human cDC2 and AXL + Siglec6 + DC subset. Also, Langerhans cells have been considered an important DC subset for vaccination as they are localized in the epidermis (HLA-DR + CD11c + CD1a + CD207 + ). However, recent evidence suggests that they are related to macrophages, another antigen-presenting cell (APC) type with potential antitumor activity (9).
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The Journey of in vivo Virus Engineered Dendritic Cells From Bench to Bedside: A Bumpy Road


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Porcine epidemic diarrhea virus (PEDV) invades porcine intestinal epithelial cells (IECs) and causes diarrhea and dehydration in pigs. In the present study, we showed a suppression of PEDV infection in porcine jejunum intestinal epithelial cells (IPEC-J2) by an increase in autophagy. Autophagy was activated by rapamycin at a dose that does not affect cell viability and tight junction permeability. The induction of autophagy was examined by LC3I/LC3II conversion. To confirm the autophagic-flux (entire autophagy pathway), autophagolysosomes were examined by an immunofluorescence assay. Pretreatment with rapamycin significantly restricted not only a 1 h infection but also a longer infection (24 h) with PEDV, while this effect disappeared when autophagy was blocked. Co-localization of PEDV and autophagosomes suggests that PEDV could be a target of autophagy. Moreover, alleviation of PEDVinduced cell death in IPEC-J2 cells pretreated with rapamycin demonstrates a protective effect of rapamycin against PEDV-induced epithelial cell death. Collectively, the present study suggests an early prevention against PEDV infection in IPEC-J2 cells via autophagy that might be an effective strategy for the restriction of PEDV, and opens up the possibility of the use of rapamycin in vivo as an effective prophylactic and prevention treatment.
answer:

Rapamycin-induced autophagy restricts porcine epidemic diarrhea virus infectivity in porcine intestinal epithelial cells