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: Background: Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS) are two coronaviruses with demonstrated potential to generate significant nosocomial outbreaks. In particular, MERS continues to pose a significant threat in the Middle East since 2012. Currently, no licensed vaccine or drug treatment is available to treat patients infected with either coronavirus. However, there are some MERS vaccines in the preclinical stage of development. We sought to evaluate the potential impact of targeted vaccination strategies for mitigating SARS and MERS outbreaks in healthcare settings using simple mathematical models and detailed historic transmission trees describing the progression of past nosocomial outbreaks of SARS and MERS. Results: Our findings suggest that vaccination strategies targeting patients and healthcare workers, which have been disproportionately affected during past outbreaks, and assuming two vaccination coverage levels at 50 and 75% have the potential to avert nearly 50% or more of MERS or SARS cases. Conclusion: Our modeling results informed by historic outbreak data for SARS and MERS suggest that vaccination strategies targeting patients could be an effective measure to mitigate and prevent outbreaks in the healthcare setting.

Answer: Evaluating the potential impact of targeted vaccination strategies against severe acute respiratory syndrome coronavirus (SARS- CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) outbreaks in the healthcare setting

Question: doi: bioRxiv preprint 65 required for the antiviral activity of both IFITM3 and IFITM1 [9]. The subcellular localization of 66 IFITMs is a key determinant of their antiviral profile. When expressed singly, IFITM3 and IFITM2 67 preferentially localize to early and late endosomes and lysosomes, and restrict viruses that enter via 68 these endo-lysosomal compartments. In contrast, IFITM1 primarily localizes at the cell surface and 69 can restrict viruses that enter through the plasma membrane [11-14]. Indeed, mutants of IFITM3 70 that lack an N-terminal endocytic sorting motif 20 YEML 23 localize to the plasma membrane and lose 71 their ability to inhibit influenza A virus (IAV), alphavirus and coronavirus infection by endosomal 72 routes [14-18]. 73 74 Studies focusing on IFITM3 restriction of IAV and Semliki Forest Virus (SFV) indicate that virus 75 internalization is unaffected by IFITM3 expression and, for SFV at least, the viral envelope 76 . CC-BY-NC-ND 4.0 International license author/funder. It is made available under a The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/737841 doi: bioRxiv preprint 109 knockout mice show enhanced morbidity after infection with IAV, alphaviruses and flaviviruses [33-110 .

Answer: Comparative analysis reveals adaptive evolution of bat IFITMs and a novel 1 antiviral determinant

Question: with the pathological structure of BPD, as seen in the lungs of preterm infants who died and in animal models (3, 7). As the authors note, this study was limited in that the subjects with BPD were stable outpatients younger than 3 years who did not require oxygen therapy at the time of the study. Whether their findings hold true in infants with persistent severe BPD, including those with chronic ventilator-dependent hypoxemic respiratory failure, is not clear. In addition, BPD classification was based on clinical decision making, rather than a physiologic assessment such as the oxygen reduction test (11). In an earlier article, members of this group studied DL CO and its components, DM and Vc, in full-term infants without lung disease and showed that DL CO and Vc (but not DM) correlated with the level of proangiogenic circulating hematopoietic stem/progenitor cells (pCHSPCs) (12). However, this study did not include preterm infants with or without BPD. Both pCHSPCs, also referred to as circulating progenitor cells, as well as late-outgrowth endothelial colony-forming cells, are decreased in the cord blood of preterm infants who later develop moderate or severe BPD (13, 14) . Together, these findings suggest that early disruptions in the number and function of angiogenic progenitor cells, possibly by maternal complications of pregnancy known to be associated with BPD risk, may lead to impaired development of the pulmonary vasculature and sustained impaired gas exchange in preterm infants with BPD. This study shows how a physiologic assessment, such as infant pulmonary function testing, may be used in the clinical setting to provide an estimation of impaired gas exchange in preterm infants with varying degrees of lung injury. Combining functional assays such as this with measurement of pCHSPCs and other angiogenic biomarkers in the cord blood, as well as novel imaging techniques such as quantitative pulmonary magnetic resonance imaging (15), will lead to improved disease phenotyping of preterm infants at risk for BPD. Given the spectrum of disease severity among infants with severe BPD (as determined by the currently accepted diagnostic criteria), novel methods such as these will help identify preterm neonates more accurately, permit targeted therapies for the most severely affected infants, and provide quantitative evidence of the efficacy of these interventions in young children after preterm birth (16). n

Answer:
Jobe AH, Bancalari E. Bronchopulmonary dysplasia