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.

Example Input: 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.
Example Output: 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)

Example Input: Objective: Coronavirus disease 2019 (COVID-19) is an escalating global epidemic caused by SARS-CoV-2, with a high mortality in critical patients. Effective indicators for predicting disease severity in SARS-CoV-2 infected patients are urgently needed. Methods: In this study, 43 COVID-19 patients admitted in Chongqing Public Health Medical Center were involved. Demographic data, clinical features, and laboratory examinations were obtained through electronic medical records. Peripheral blood specimens were collected from COVID-19 patients and examined for lymphocyte subsets and cytokine profiles by flow cytometry. Potential contributing factors for prediction of disease severity were further analyzed. Results: A total of 43 COVID-19 patients were included in this study, including 29 mild patients and 14 sever patients. Severe patients were significantly older (61.9±9.4 vs 44.4±15.9) and had higher incidence in co-infection with bacteria compared to mild group (85.7%vs27.6%). Significantly more severe patients had the clinical symptoms of anhelation (78.6%) and asthma (71.4%). For laboratory examination, 57.1% severe cases showed significant reduction in lymphocyte count. The levels of Interluekin-6 (IL6), IL10, erythrocyte sedimentation rate (ESR) and D-Dimer (D-D) were significantly higher in severe patients than mild patients, while the level of albumin (ALB) was remarkably All rights reserved. No reuse allowed without permission. the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. : medRxiv preprint lower in severe patients. Further analysis demonstrated that ESR, D-D, age, ALB and IL6 were the major contributing factors for distinguishing severe patients from mild patients. Moreover, ESR was identified as the most powerful factor to predict disease progression of COVID-19 patients. : Age and the levels of ESR, D-D, ALB and IL6 are closely related to the disease severity of COVID-19 patients. ESR can be used as a valuable indicator for distinguishing severe COVID-19 patients in early stage, so as to increase the survival of severe patients.
Example Output: Potential Factors for Prediction of Disease Severity of COVID-19 Patients

Example Input: In contrast to adult mice, young AI] mice, developed an acute hepatitis following infection with Mouse Hepatitis virus type 3. 100 % of the young animals died 4 to 5 days after the infection and high levels of virus were found in the liver and peritoneal exudate. Very low levels of IFN-y were found in the serum and peritoneal exudate of infected young mice. This was in contrast to the levels observed in adult mice. Spleen cells and macrophage cultures from young AI] mice, again in contrast to adult AI] mice, were shown to be unable to synthesize IFN-y and IFN-Ct/~ respectively. Macrophages from either young or adult AI] mice were able to be activated with exogenous recombinant IFN-y or IFN-a/~, enabling both sets of cells to restrict MHV3 replication. The results indicate that the ability of the immune system to synthesize IFN-y and IFN-a/~ may playa major role in the age-dependent resistance of AI] mice to MHV3.
Example Output:
A Major Role of Macrophage Activation by Interferon- Gamma During Mouse Hepatitis Virus Type 3 Infection. II. Age-Dependent Resistance