Innovative tools and modeling methodology for impact prediction and assessment of the contribution of materials on indoor air quality

International audienceBackground: The combination of more and more airtight buildings and the emission of formaldehyde and other volatile organic compounds (VOCs) by building, decoration and furniture materials lead to lower indoor air quality. Hence, it is an important challenge for public health but also for the preservation of cultural heritage, as for example, artworks in museum showcases and other cultural objects. Indeed, some VOCs such as organic acids or carbonyl compounds may play a role in the degradation of some metallic objects or historic papers. Thus, simple and cost effective sampling tools are required to meet the recent and growing demand of on-site diagnostic of indoor air quality , including emission source identification and their ranking.Results: In this aim, we developed new tools based on passive sampling (Solid-Phase Micro Extraction, SPME) to measure carbonyls compounds (including formaldehyde) and other VOCs and both in indoor air and at the material/ air interface. On one hand, the coupling of SPME with a specially designed emission cell allows the screening and the quantification of the VOCs emitted by building, decoration or furniture materials. On the other hand, indoor air is simply analysed using new vacuum vial sampling combined with VOCs pre-concentration by SPME. These alternative sampling methods are energy free, compact, silent and easy to implement for on-site measurements. They show satisfactory analytical performance as detection limits range from 0.05 to 0.1 µg m −3 with an average Relative Standard Deviation (RSD) of 18 %. They already have been applied to monitoring of indoor air quality and building material emissions for a 6 months period. The data obtained were in agreement with the prediction of a physical monozonal model which considers building materials both as VOC sources and sinks and air exchange rate in one single room ("box model").Conclusion: Results are promising, even if more data are required to complete validation, and the model could be envisaged as a predictive tool for indoor air quality. This new integrated approach involving measurements and mod-eling could be easily transposed to historic environments and to the preservation of cultural heritage

Show me the numbers: a quantitative portrait of the attitudes, experiences, and values of philosophers of science regarding broadly engaged work

Philosophers of science are increasingly arguing for the importance of doing scientifically- and socially-engaged work, suggesting that we need to reduce barriers to extra-disciplinary engagement and broaden our impact. Yet, we currently lack empirical data to inform these discussions, leaving a number of important questions unanswered. How common is it for philosophers of science to engage other communities, and in what ways are they engaging? What barriers are most prevalent when it comes to broadly disseminating one’s work or collaborating with others? To what extent do philosophers of science actually value an engaged approach? Our project addresses this gap in our collective knowledge by providing empirical data regarding the state of philosophy of science today. We report the results of a survey of 299 philosophers of science about their attitudes towards and experiences with engaging those outside the discipline. Our data suggest that a significant majority of philosophers of science think it is important for non-philosophers to read and make use of their work; most are engaging with communities outside the discipline; and many think philosophy of science, as a discipline, has an obligation to ensure it has a broader impact. Interestingly, however, many of these same philosophers believe engaged work is generally undervalued in the discipline. We think these findings call for cautious optimism on the part of those who value engaged work—while there seems to be more interest in engaging other communities than many assume, significant barriers still remain

Interdisciplinarity and insularity in the diffusion of knowledge: an analysis of disciplinary boundaries between philosophy of science and the sciences

Two fundamentally different perspectives on knowledge diffusion dominate debates about academic disciplines. On the one hand, critics of disciplinary research and education have argued that disciplines are isolated silos, within which specialists pursue inward-looking and increasingly narrow research agendas. On the other hand, critics of the silo argument have demonstrated that researchers constantly import and export ideas across disciplinary boundaries. These perspectives have different implications for how knowledge diffuses, how intellectuals gain and lose status within their disciplines, and how intellectual reputations evolve within and across disciplines. We argue that highly general claims about the nature of disciplinary boundaries are counterproductive, and that research on the nature of specific disciplinary boundaries is more useful. To that end, this paper uses a novel publication and citation network dataset and statistical models of citation networks to test hypotheses about the boundaries between philosophy of science and 11 disciplinary clusters. Specifically, we test hypotheses about whether engaging with and being cited by scientific communities outside philosophy of science has an impact on one’s position within philosophy of science. Our results suggest that philosophers of science produce interdisciplinary scholarship, but they tend not to cite work by other philosophers when it is published in journals outside of their discipline. Furthermore, net of other factors, receiving citations from other disciplines has no meaningful impact—positive or negative—on citations within philosophy of science. We conclude by considering this evidence for simultaneous interdisciplinarity and insularity in terms of scientific trading theory and other work on disciplinary boundaries and communication

Assessment of VOCs Material/Air Exchanges of Building Products Using the DOSEC®-SPME Method

ACTInternational audienceUsing low emissive materials in building is an effective way to reduce indoor concentrations of pollutants such as VOCs. Material emissions are assessed by the ISO 16000-9 standard. This procedure is time-consuming and is not suitable for on-site measurements. This work aimed in assessing an alternative method, DOSEC\textregistered-SPME, for simple measurements. To validate it, emissions of 30 materials were characterized by both ISO 16000-9 and DOSEC\textregistered-SPME. A first correlation was found between the two methods for formaldehyde emissions of raw materials. This encouraging result allows considering the development of new decision making tools for the selection of healthy building materials

Mechanisms controlling the expression of the components of the exocytotic apparatus under physiological and pathological conditions

Abstract The last decade has witnessed spectacular progress in the identification of the protein apparatus required for exocytosis of neurotransmitters, peptide hormones and other bioactive products. In striking contrast, our knowledge of the mechanisms determining the expression of the components of the secretory machinery has remained rudimentary. Since modifications in secretory functions are associated with several physiological processes and contribute to the development of human pathologies, a better knowledge of the control of the expression of the genes involved in exocytosis is urgently needed. Recent studies have led to the identification of transcription factors and other regulatory molecules such as microRNAs that modulate the cellular level of key controllers of the exocytotic process. These findings furnish a new perspective for understanding how secretory functions can adapt to normal physiological conditions and shed light on the mechanisms involved in the development of important human diseases such as diabetes mellitus characterized by defective release of bioactive compounds. The molecular machinery underlying the process of exocytosis Convergence of data obtained in different model systems including yeast, Caenorhabditis elegans, Drosophila and mammals led to the identification of numerous components of the protein apparatus governing exocytosis. These components include members of the SNARE (soluble N-ethylmaleimidesensitive fusion protein attachment protein receptor) and Rab families. The SNAREs constitute a group of evolutionarily conserved proteins characterized by the presence of amino acid sequences, referred to as SNARE motifs, which allow them to form thermodynamically favourable complexes. There is now compelling evidence that the assembly of these complexes represents one of the key events driving fusion of secretory vesicles with their target compartment

Role for inducible cAMP early repressor in promoting pancreatic beta cell dysfunction evoked by oxidative stress in human and rat islets

Aims/hypothesis: Pro-atherogenic and pro-oxidant, oxidised LDL trigger adverse effects on pancreatic beta cells, possibly contributing to diabetes progression. Because oxidised LDL diminish the expression of genes regulated by the inducible cAMP early repressor (ICER), we investigated the involvement of this transcription factor and of oxidative stress in beta cell failure elicited by oxidised LDL. Methods: Isolated human and rat islets, and insulin-secreting cells were cultured with human native or oxidised LDL or with hydrogen peroxide. The expression of genes was determined by quantitative real-time PCR and western blotting. Insulin secretion was monitored by EIA kit. Cell apoptosis was determined by scoring cells displaying pycnotic nuclei. Results: Exposure of beta cell lines and islets to oxidised LDL, but not to native LDL raised the abundance of ICER. Induction of this repressor by the modified LDL compromised the expression of important beta cell genes, including insulin and anti-apoptotic islet brain 1, as well as of genes coding for key components of the secretory machinery. This led to hampering of insulin production and secretion, and of cell survival. Silencing of this transcription factor by RNA interference restored the expression of its target genes and alleviated beta cell dysfunction and death triggered by oxidised LDL. Induction of ICER was stimulated by oxidative stress, whereas antioxidant treatment with N-acetylcysteine or HDL prevented the rise of ICER elicited by oxidised LDL and restored beta cell functions. Conclusions/interpretation: Induction of ICER links oxidative stress to beta cell failure caused by oxidised LDL and can be effectively abrogated by antioxidant treatmen

Endoplasmic Reticulum Stress Links Oxidative Stress to Impaired Pancreatic Beta-Cell Function Caused by Human Oxidized LDL.

Elevated plasma concentration of the pro-atherogenic oxidized low density lipoprotein cholesterol (LDL) triggers adverse effects in pancreatic beta-cells and is associated with type 2 diabetes. Here, we investigated whether the endoplasmic reticulum (ER) stress is a key player coupling oxidative stress to beta-cell dysfunction and death elicited by human oxidized LDL. We found that human oxidized LDL activates ER stress as evidenced by the activation of the inositol requiring 1α, and the elevated expression of both DDIT3 (also called CHOP) and DNAJC3 (also called P58IPK) ER stress markers in isolated human islets and the mouse insulin secreting MIN6 cells. Silencing of Chop and inhibition of ER stress markers by the chemical chaperone phenyl butyric acid (PBA) prevented cell death caused by oxidized LDL. Finally, we found that oxidative stress accounts for activation of ER stress markers induced by oxidized LDL. Induction of Chop/CHOP and p58IPK/P58IPK by oxidized LDL was mimicked by hydrogen peroxide and was blocked by co-treatment with the N-acetylcystein antioxidant. As a conclusion, the harmful effects of oxidized LDL in beta-cells requires ER stress activation in a manner that involves oxidative stress. This mechanism may account for impaired beta-cell function in diabetes and can be reversed by antioxidant treatment

Role for inducible cAMP early repressor in promoting pancreatic beta cell dysfunction evoked by oxidative stress in human and rat islets

AIMS/HYPOTHESIS: Pro-atherogenic and pro-oxidant, oxidised LDL trigger adverse effects on pancreatic beta cells, possibly contributing to diabetes progression. Because oxidised LDL diminish the expression of genes regulated by the inducible cAMP early repressor (ICER), we investigated the involvement of this transcription factor and of oxidative stress in beta cell failure elicited by oxidised LDL. METHODS: Isolated human and rat islets, and insulin-secreting cells were cultured with human native or oxidised LDL or with hydrogen peroxide. The expression of genes was determined by quantitative real-time PCR and western blotting. Insulin secretion was monitored by EIA kit. Cell apoptosis was determined by scoring cells displaying pycnotic nuclei. RESULTS: Exposure of beta cell lines and islets to oxidised LDL, but not to native LDL raised the abundance of ICER. Induction of this repressor by the modified LDL compromised the expression of important beta cell genes, including insulin and anti-apoptotic islet brain 1, as well as of genes coding for key components of the secretory machinery. This led to hampering of insulin production and secretion, and of cell survival. Silencing of this transcription factor by RNA interference restored the expression of its target genes and alleviated beta cell dysfunction and death triggered by oxidised LDL. Induction of ICER was stimulated by oxidative stress, whereas antioxidant treatment with N-acetylcysteine or HDL prevented the rise of ICER elicited by oxidised LDL and restored beta cell functions. CONCLUSIONS/INTERPRETATION: Induction of ICER links oxidative stress to beta cell failure caused by oxidised LDL and can be effectively abrogated by antioxidant treatment