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: 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.

Answer: 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)


Question: Both antiseptic hand rubbing (AHR) using ethanol-based disinfectants (EBDs) and antiseptic hand washing (AHW) are important means of infection control to prevent seasonal influenza A virus (IAV) outbreaks. However, previous reports suggest a reduced efficacy of ethanol disinfection against pathogens in mucus. We aimed to elucidate the situations and mechanisms underlying the reduced efficacy of EBDs against IAV in infectious mucus. We evaluated IAV inactivation and ethanol concentration change using IAV-infected patients' mucus (sputum). Additionally, AHR and AHW effectiveness against infectious mucus adhering to the hands and fingers was evaluated in 10 volunteers. Our clinical study showed that EBD effectiveness against IAV in mucus was extremely reduced compared to IAV in saline. IAV in mucus remained active despite 120 s of AHR; however, IAV in saline was completely inactivated within 30 s. Due to the low rate of diffusion/convection because of the physical properties of mucus as a hydrogel, the time required for the ethanol concentration to reach an IAV inactivation level and thus for EBDs to completely inactivate IAV was approximately eight times longer in mucus than in saline. On the other hand, AHR inactivated IAV in mucus within 30 s when the mucus dried completely because the hydrogel characteristics were lost. Additionally, AHW rapidly inactivated IAV. Until infectious mucus has completely dried, infectious IAV can remain on the hands and fingers, even after appropriate AHR using EBD, thereby increasing the risk of IAV transmission. We clarified the ineffectiveness of EBD use against IAV in infectious mucus. IMPORTANCE Antiseptic hand rubbing (AHR) and antiseptic hand washing (AHW) are important to prevent the spread of influenza A virus (IAV). This study elucidated the situations/mechanisms underlying the reduced efficacy of AHR against infectious mucus derived from IAV-infected individuals and indicated the weaknesses of the current hand hygiene regimens. Due to the low rate of diffusion/convection because of the physical properties of mucus as a hydrogel, the efficacy of AHR using ethanolbased disinfectant against mucus is greatly reduced until infectious mucus adhering to the hands/fingers has completely dried. If there is insufficient time before treating the next patient (i.e., if the infectious mucus is not completely dry), medical staff should be aware that effectiveness of AHR is reduced. Since AHW is effective against both dry and nondry infectious mucus, AHW should be adopted to compensate for these weaknesses of AHR. FIG 1 Analysis of the physical properties of mucus from 19 influenza A virus-infected patients. (A) Rheological analysis: mean, maximum, and minimum viscosities of mucus (sputum) samples at different shear rates (left panel). Shown is a comparison of mucus and saline viscosities at different shear rates (right panel). (B) Average parameters measured for saline and mucus samples: contact angles, surface tension, and densities at different temperatures. (C) Time required for saline and mucus to completely dry (complete drying time). (D) Ethanol diffusion coefficients of saline and mucus exposed to an 80% ethanol concentration. Situations of Reduced Hand Hygiene Effectiveness September/October 2019 Volume 4 Issue 5 e00474-19 msphere.asm.org 3 FIG 6 Additional fluid simulation of changes in the ethanol concentrations in mucus. (A) Addition of 95 l of 80% ethanol to 5 l saline was modeled in OpenFOAM, demonstrating the disappearance over time of the region with Ͻ31% ethanol (shown in red). See also Movie S1. (B) Addition of 95 l of 80% ethanol to 5 l mucus was modeled. The simulation was performed under conditions of reduced viscosity (16.7% of the actual measurement value) because of the long time required for disappearance of the concentration region of Ͻ31%. See also Movie S2.

Answer: Situations Leading to Reduced Effectiveness of Current Hand Hygiene against Infectious Mucus from Influenza Virus- Infected Patients


Question: Poly-g-glutamic acid (g-PGA) is an anionic polypeptide secreted by Bacillus sp. that has been shown to activate immune cells through interactions with toll-like receptor 4 (TLR4). However, its ability to induce the type I interferon (IFN) response has not yet been characterized. Here, we demonstrate that g-PGA induces type I IFN signaling pathway via the TLR4 signaling pathway. The induction required both myeloid differentiation factor 2 (MD2) and the pattern-recognition receptor CD14, which are two TLR4associated accessory proteins. The g-PGA with high molecular weights (2000 and 5000 kDa) was able to activate the subsequent signals through TLR4/MD2 to result in dimerization of IRF-3, a transcription factor required for IFN gene expression, leading to increases in mRNA levels of the type I IFN-response genes, 2 0 e5 0 OAS and ISG56. Moreover, g-PGA (2000 kDa) displayed an antiviral activity against SARS coronavirus and hepatitis C virus. Our results identify high-molecular weight g-PGA as a TLR4 ligand and demonstrate that g-PGA requires both CD14 and MD2 for the activation of type I IFN responses. Our results suggest that the microbial biopolymer g-PGA may have therapeutic potential against a broad range of viruses sensitive to type I IFNs.

Answer:
The antiviral activity of poly-g-glutamic acid, a polypeptide secreted by Bacillus sp., through induction of CD14-dependent type I interferon responses