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: Ranavirus cross-species infections have been documented, but the viral proteins involved in the interaction with cell receptors have not yet been identified. Here, viral cell-binding proteins and their cognate cellular receptors were investigated using two ranaviruses, Andrias davidianus ranavirus (ADRV) and Rana grylio virus (RGV), and two different cell lines, Chinese giant salamander thymus cells (GSTC) and Epithelioma papulosum cyprinid (EPC) cells. The heparan sulfate (HS) analog heparin inhibited plaque formation of ADRV and RGV in the two cell lines by more than 80% at a concentration of 5 g/mL. In addition, enzymatic removal of cell surface HS by heparinase I markedly reduced plaque formation by both viruses and competition with heparin reduced virus-cell binding. These results indicate that cell surface HS is involved in ADRV and RGV cell binding and infection. Furthermore, recombinant viral envelope proteins ADRV-58L and RGV-53R bound heparin-Sepharose beads implying the potential that cell surface HS is involved in the initial interaction between ranaviruses and susceptible host cells. To our knowledge, this is the first report identifying cell surface HS as ranavirus binding factor and furthers understanding of interactions between ranaviruses and host cells.

Output: Ranaviruses Bind Cells from Different Species through Interaction with Heparan Sulfate

Input: Consider Input: In the current COVID-19 crisis, the US and many countries in the world are suffering acute shortages of modern ventilators to care for desperately ill patients. Since modern ICU ventilators are powerful devices that can deliver very high gas flow rates and pressures, multiple physicians have attempted to ventilate more than one patient on a single ventilatorso-called "vent splitting". Early applications of this approach have utilized simple concatenations of ventilator tubing and T-pieces, to provide flow to more than one patient. Additional approaches using custom flow splitters -sometimes made using 3D printing technologies -have also advanced into the clinic with FDA approval. However, heretofore there has been less progress made on controlling individual ventilatory pressures for patients with severe lung disease. Given the inherent variability and instability of lung compliance amongst patients with COVID-19, there remains an important need to provide a means of extending ventilator usefulness to more than one patient, but in a way that provides more tailored pressures that can be titrated over time. In this descriptive report, we provide the basis for a ventilator circuit that can support two patients with individualized peak inspiratory and end-expiratory pressures. The circuit is comprised of exclusively "off the shelf" materials and is inexpensive to produce. The circuit can be used with typical ICU ventilators, and with anesthesia ventilators used in operating rooms. Inspiratory and end-expiratory pressures for each patient can be titrated over time, without changes for one patient affecting the ventilation parameters of the other patient. Using in-line spirometry, individual tidal volumes can be measured for each patient. This Pressure-Regulated Ventilator Splitting (PReVentS) Yale University protocol operates under a pressure-control ventilatory mode, and may function optimally when patients are not triggering breaths from the ventilator. This method has been tested thus far only in the laboratory with mock lungs, and has not yet been deployed in animals or in patients. However, given the novelty and potential utility of this approach, we deemed it appropriate to provide this information to the broader critical care community at the present time. In coming days and weeks, we will continue to characterize and refine this approach, using large animal models and proof-of-principle human studies.

Output: Pressure-Regulated Ventilator Splitting (PReVentS) - A COVID-19 Response Paradigm from Yale University

Input: Consider Input: Introduction. Cytosolic pattern recognition receptors (PRR) have been shown to detect nucleic acids from RNA and DNA viruses in order to launch a type I interferon mediated antiviral state [1]. Here we show that RNA of the facultative intracellular bacterium Salmonella typhimurium is a ligand for RIG-I, triggers production of type-I interferons and contributes to pathogenicity in vivo. Methods. We use RIG-IA/A MEFs [2] or human epithelial cells depleted of RIG-I by lentiviral shRNA transduction for transfection and infection experiments. IFNbeta production was measured by 293T IFNbeta-reporter cells or qPCR. Intracellular bacterial titers were determined by gentamycin protection assay. In vivo infection experiments were performed as described [3] using SL1344 or SL1344 aroA deficient Salmonella strains in RIG-I+/+ and RIG-IA/A mice [4]. Results. Infection of fibroblasts and epithelial cells with S. typhimurium, but not with non-invasive E. coli, triggers IFNbeta transcription, suggesting that intracellular replication is required. RIG-I dependent recognition of bacterial RNA is dominant in non-phagocytic cells, as shown in RIG-I knockout and knockdown model cells. Despite presence of other pathogen-associated patterns (PAMP), like LPS or flagellin, no IFNbeta was produced in fibroblasts and epithelial cells lacking RIG-I upon S. typhimurium infection. In contrast, in macrophages TLR dependent recognition of bacterial PAMPs through TRIF/Myd88 overcomes RIG-I deficiency and leads to robust induction of type I interferon. We observed higher bacterial titers at early time points after infection in the cecum of S. typhimurium infected RIG-IA/A mice, when compared to wild type animals. However, at later stages of infection, S. typhimurium overcomes the innate response leading to similar weight loss and mortality in wildtype and RIG-IA/A mice. Conclusion. In summary, our data implicate a role of RIG-I mediated innate immune recognition of bacterial RNA in early control of bacterial replication, most likely mediated by non-phagocytic intestinal epithelial cells targeted by S. typhimurium. Disclosure of interest: None declared. Combined action of type I and type III IFN restricts initial replication of SARScoronavirus in the lung but fails to inhibit systemic virus spread
Output: P133 RIG-I mediates recognition of Salmonella RNA in non-phagocytic cells and con- tributes to early bacterial replication in vivo P135 Defining the intracellular innate immune synapse