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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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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.
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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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Background: ISG15 is an Ubiquitin-like protein, highly induced by Type I Interferons. Upon the cooperative activity of specific Ubiquitinating enzymes, ISG15 can be conjugated to its substrates. Increasing evidence points to a role for protein ISGylation in anti-viral and anti-tumoral defense. Principal Findings: We identified ISG15 from Old World Monkeys (OWm) as a hyper-efficient protein modifier. Western blot analysis visualized more efficient conjugation of OWmISG15 relative to HuISG15 in human (Hu), monkey and mouse (Mo) cell-lines. Moreover, the substrates of OWmISG15 identified upon Tandem Affinity Purification followed by LC-MS/MS identification largely outnumbered these of HuISG15 itself. Several Ubiquitin-Conjugating enzymes were identified as novel ISGylated substrates. Introduction of a N89D mutation in HuISG15 improved its ISGylation capacity, and additional Q31K/ T33A/D133N mutations yielded a HuISG15 variant with an ISGylation efficiency comparable to OWmISG15. Homology modeling and structural superposition situate N89 in the interaction interface with the Activating enzyme. Analysis of the UbE1L residues in this interface revealed a striking homology between OWmUbE1L and HuUbE1, the Activating enzyme of Ubiquitin. In line with this observation, we found efficient activation of AgmISG15, but not HuISG15 or MoISG15, by HuUbE1, thus providing a likely explanation for OWm hyperISGylation. Conclusions: This study discloses the poor conjugation competence of HuISG15 compared to OWmISG15 and maps the critical determinants for efficient conjugation. HyperISGylation may greatly assist ISGylation studies and may enhance its function as positive regulator of Interferon-related immune responses or as anti-tumoral modulator.
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HyperISGylation of Old World Monkey ISG15 in Human Cells


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Myelin transcription factor 1 (Myt1) is a zinc-finger DNA binding protein that influences developing oligodendrocyte progenitor (OP) cell proliferation, differentiation, and myelin gene transcription in vitro. The potential of Myt1 to play a role in OP responses leading to remyelination was examined using murine hepatitis virus strain A59 (MHV) to induce spinal cord demyelination and potential relevance to human pathology was evaluated in multiple sclerosis (MS) lesions. In MHV-infected mice, the density of Myt1 expressing cells markedly increased in lesioned areas of spinal cord white matter. Myt1 expressing cells proliferated most extensively during active demyelination and subsequently accumulated to maximal levels during early remyelination. Cells with nuclear Myt1 immunoreactivity were mainly OP cells, identified by co-localization with platelet-derived growth factor alpha receptor, with additional phenotypes being either oligodendrocytes or neural stem cells, identified by CC1 antigen and Musashi1, respectively. The density of OP cells expressing Myt1 was significantly increased in white matter of MHV-infected mice during demyelination and early remyelination then as remyelination advanced the values returned to levels comparable to PBSinjected control mice. In MHV lesions, Myt1 was not expressed in astrocytes, lymphocytes, or macrophage/micro-glial cells. MS lesions demonstrated increased Myt1 expression in both the periplaque white matter adjacent to lesions and within early remyelinating lesions. These results suggest a potential role for Myt1 in the regeneration of oligodendrocyte lineage cells in response to demyelination.
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Myelin Transcription Factor 1 (Myt1) Expression in Demyelinated Lesions of Rodent and Human CNS