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.

Q: Early growth response gene-1 (EGR1) is a multifunctional transcription factor that is implicated in viral infection. In this study, we observed that foot-and-mouth disease virus (FMDV) infection significantly triggered EGR1 expression. Overexpression of EGR1 suppressed FMDV replication in porcine cells, and knockdown of EGR1 considerably promoted FMDV replication. A previously reported FMDV mutant virus (with two amino acids mutations in SAP domain) that displays a strong type I interferon (IFN) induction activity was used in this study. We found that SAP mutant FMDV infection induced a higher expression of EGR1 than wildtype FMDV infection, and also triggered higher IFNβ and IFN-stimulated genes (ISGs) expression than wildtype FMDV infection. This implied a link between EGR1 and type I IFN signaling. Further study showed that overexpression of EGR1 resulted in Sendai virus (SeV)-induced IFN-stimulated response element (ISRE) and NF-κB promoter activation. In addition, the SeV-induced ISGs expression was impaired in EGR1 knockdown cells. EGR1 upregulation promoted type I IFN signaling activation and suppressed FMDV and Seneca Valley virus replication. Suppression of the transcriptional activity of EGR1 did not affect its antiviral effect against FMDV. This study reveals a new mechanism evolved by EGR1 to enhance type I IFN signaling and suppress FMDV replication.

A: Citation: Early Growth Response Gene-1 Suppresses Foot-and-Mouth Disease Virus Replication by Enhancing Type I Interferon Pathway Signal Transduction
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Q: This paper attempts to understand optimal ventilation rates at the national level across 26 European countries and to contrast the benefits of optimizing ventilation with filtration of outdoor air pollution and control of indoor sources. This is an important topic given the key role of the housing sector in tackling both air pollution and climate change. Although the methods used are relatively simplistic, they are appropriate for analyses performed at the scale presented in the paper. The findings and conclusions are well supported by the results. I would therefore support publication. However, I believe the manuscript would benefit from a stronger statement of the aims of the work and some clarifications regarding the methods (see below). My main concern relates to the assumption made by the authors that indoor-generated PM2.5 is equally as harmful to health as outdoor-generated PM2.5. There is little evidence to support this (though it is quite a commonly made assumption). I would like to see some form of sensitivity analysis in relation to this assumption, since it may have an impact on the final results (though probably not on the ultimate conclusions). More detailed comments can be found below. I consider the suggested revisions to be relatively minor. 1. Is the question posed original, important and well defined? The research question posed by the paper is important and I believe the methods used are appropriate to answer it. However, the aims of the paper are not currently well stated (in both the main text and in the abstract). The main statement of the aims comes towards the end of page 5, which states "This work aims to summarize the current understanding of the sources of health risks in indoor environments and their relationship to ventilation requirements". This doesn't really capture what the authors have actually done. There is a slightly better statement of the aims hidden in the Methods (top of page 7) but even this doesn't quite feel sufficient. 2. Are the data sound and well controlled? Yes, although the source of some of the input data can be made clearer in the text, especially in relation to Table 2 (see below) . 3. Is the interpretation (discussion and conclusion) well balanced and supported by the data? Yes. 4. Are the methods appropriate and well described, and are sufficient details provided to allow others to evaluate and/or replicate the work? The methods are generally well described. However, I have a few specific issues (see the additional comments below). The methods are based on relatively simplistic tools (both the mass-balance exposure model and the risk/health impact model). However, I think they are appropriate for the type of analysis presented in the paper. My main concern relates to the assumption of equal health risk associated with both outdoor-and indoor-generated PM2.5. The authors discuss this briefly in the Discussion section but this assumption is highly uncertain since almost all of the published epidemiology is based on outdoor PM2.5. The paper would benefit from greater emphasis on the sensitivity of the results to this assumption. Perhaps, the analysis (or part of it) could be repeated without the effects of indoorgenerated PM2.5 or with a reduced exposure-response coefficient? 6. Can the writing, organization, tables and figures be improved? Although the manuscript is generally well written, there are reoccurring problems, most importantly missing articles throughout the paper (e.g. a, the). For instance, in the abstract, "Based on measurements of the European Environment Agency (EEA),…" and "A framework for developing European health-based ventilation guidelines…" would be preferable. I realise that English is not the authors' first language (and, again, I should stress that most of the language used is very good). However, I think the paper would benefit from a thorough edit by a native English speaker. Also, the figures appear to be quite pixelated and may not be in an appropriate format for publication. 7. When revisions are requested. No preference. 8. Are there any ethical or competing interests issues you would like to raise? None. • I believe the abstract would benefit from a little editing. At present, the Background section feels unnecessarily long and there isn't enough detail in either the Methods or Results sections. The methods used for the health impact calculations aren't mentioned at all, despite being key to the paper. At the moment, I don't feel the main results are clearly stated in the abstract. • The paper refers throughout to "optimization". I think a mathematician might object to the use of the term because the method doesn't actually use a formal optimization process. I don't think this is too much of a problem but I do think a clear statement of what the authors mean by optimization would be helpful (e.g. in the Methods). As I understand it, the "optimal" ventilation rate is just taken to be the one for which the health burden is smallest.

A: Reducing burden of disease from residential indoor air exposures in Europe (HEALTHVENT project) Reducing burden of disease from residential indoor air exposures in Europe (HEALTHVENT project)
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Q: Background: Human cytomegalovirus (HCMV) is a virus which has the potential to alter cellular gene expression through multiple mechanisms. Objective: With the application of DNA microarrays, we could monitor the effects of pathogens on host-cell gene expression programmes in great depth and on a broad scale. Methods: Changes in mRNA expression levels of human endothelial-like ECV304 cells following infection with human cytomegalovirus AD169 strain was analyzed by a microarray system comprising 21073 60-mer oligonucleotide probes which represent 18716 human genes or transcripts. Results: The results from cDNA microarray showed that there were 559 differential expressed genes consisted of 471 upregulated genes and 88 down-regulated genes. Real-time qPCR was performed to validate the expression of 6 selected genes (RPS24, MGC8721, SLC27A3, MST4, TRAF2 and LRRC28), and the results of which were consistent with those from the microarray. Among 237 biology processes, 39 biology processes were found to be related significantly to HCMV-infection. The signal transduction is the most significant biological process with the lowest p value (p=0.005) among all biological process which involved in response to HCMV infection. Conclusion: Several of these gene products might play key roles in virus-induced pathogenesis. These findings may help to elucidate the pathogenic mechanisms of HCMV caused diseases.

A:
Global analysis of differential expressed genes in ECV304 Endothelial-like cells infected with human cytomegalovirus
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