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Controversy mapping

The economic inequities, the environmental crises, the bioethical conundrums and all the issues troubling modern societies are imbroglios of politics, ethics and technologies impossible to disentangle. In these hybrid situations, public participation becomes more and more difficult. To navigate a world of uncertainties, future citizens need to be equipped with tools to explore and visualize the complexity of public debate . The purpose of mapping controversy is to contribute to the development of these tools through the creative use of digital technologies.

For a few examples of the works realized by the students of the controversy mapping course, see: the archive of the controversy websites ( http://controverses.sciences-po.fr/archiveindex/ ).

Introduced by Bruno Latour more than fifteen years ago, the cartography of controversies is currently taught in several European and American universities (Paris, Copenhagen, Milan, Manchester, Amsterdam, Liège, Lausanne, Dublin, Oslo, Padova, Trento, Cambridge, Mass., São Paulo, Rio de Janeiro, Buenos Aires…).

Characterized by a radically experimental approach , controversy mapping is developed through several research projects – MACOSPOL (mapping controversies on science for politics) 2007-09 – MEDEA (mapping environmental debate on adaptation) 2011-14 – EMAPS (electronic maps to assist public science) 2011-14 – FORCCAST (formation à la cartographie des controverses pour l’analyse de sciences et des techniques) 2012-20 Download the syllabus of the course

The course team

Tommaso Venturini (responsible of the course) tommaso.venturini@sciences-po.fr / 01 45 49 53 71 / médialab, Sciences Po, 13, rue de l’Université Mathieu Jacomy (teaching assistant) / mathieu.jacomy@sciences-po.org Thomas Tari (teaching assistant) / thomas.tari@univ-paris-est.fr Axel Meunier (teaching assistant) / axel.meunier@sciences-po.fr Nicolas Baya-Laffite (teaching assistant) / nicolas.bayalaffite@sciences-po.fr

The course in a nutshell

Understand the junction between science and society, observe it through the case study of a specific controversy and make the results of this analysis public.

Benefits for the students

Aims of the course

The most important task of the course is the analysis of a socio-technical controversy . Achieving this task implies understanding some crucial notions of STS (Science and Technology Studies) and mastering a number of traditional and digital investigation techniques. The course is meant to teach all that is necessary to accomplish this task.

Course schedule

The course alternates master lectures and practical workshops. – The master lectures are meant to introduce and discuss the theoretical notions and the methodological tools necessary for controversy mapping. – The practical workshops (in smaller groups) are meant to assure a constant and personalized support until the final exam and to provide a space for sharing and confrontation among the students.

Course organization

groups of 6 students

Primary Ciliary Dyskinesia (PCD, OMIM #242650 ) or Immotile Cilia Syndrome (ICS) is an hereditary condition affecting the motility of ciliary and spermatozoa flagella. The disorder, transmitted in an autosomal recessive mode, has an incidence of 16,000-30,000. Dysmotility to complete immotility of cilia and flagella results in multisystemic disease of varying severity, characterized by infections of the upper respiratory tract, bronchiectasis, and male sterility. When heterotaxia (situs inversus) is associated, as in in up to half of patients, PCD is also referred to as Kartagener syndrome ( OMIM #244400 ). The condition is most often associated with ultrastructural defects of axoneme, the skeleton of cilia and flagella, which is constituted of several families of proteins including dyneins, kinesin and microtubule-associated proteins (MAPs).

Our recent genome-wide linkage studies in over 30 families identified several chromosomal regions which may anchor genes linked to the phenotype, suggesting that the disease is genetically highly heterogeneous1. These results, were compatible with the localization of several dynein genes, long standing candidates for PCD since roughly half of the structural defects are in the dynein arm. Indeed, in the last few months, we and others have found mutations in 3 distinct axonemal dynein genes (DNAI1, DNAH11, DNAH5) in Kartagener syndrome. Since each of these mutations was observed in only few families thusfar, other genes, probably including additional isoforms of dynein, must also be responsible for PCD. Multiple dynein proteins are encoded by a family of distinct genes mapping to different chromosomes.

( Blouin et al. 2000 )

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Periodical Bulletin on the scientific research on Primary Ciliary Dyskinesia at Medical Genetics

Study of the genetic etiology of Primary Ciliary Dyskinesia : A summary of progress in the identification of disease-causing genes, November 2001. This bulletin was sent to physicians who collaborated to our research project on PCD. This document provide informations also that physicians are encouraged to forward to the patients and families who where included in the study.

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on Kartagener Syndrome Project by the group.

A gene that contributes to heart laterality and is responsible for some cases of Kartagener syndrome, was identified by researchers in the Division of Medical Genetics of the University of Geneva Medical School and collaborators.

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Table 2. Overlap of FCHL modules with FCHL differentially expressed gene list.

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Integrating the co-expression modules with genetic data provides insight into the function and regulation of each module. The turquoise and tan MEs were associated with the rs3737787 genotypes (turquoise ME correlation = 0.28, p-value = 0.02; tan ME correlation = 0.33, p-value = 0.006) ( Roberto Cavalli ribbed off shoulder sweater Cheap Lowest Price tl8wdunT
). We observed a significant overlap between the rs3737787 correlated genes and both the turquoise and tan module genes ( Table 3 ). The tan module was the only module to be associated with FCHL, the FCHL component trait signature, and rs3737787 genotypes. To emphasize the biological implications of the tan module, we renamed it as the USF1 -regulated FCHL-associated (URFA) module. The turquoise module was not significantly associated with FCHL, suggesting that while the expression of turquoise module genes depends on rs3737787 genotypes, the gene functions of the turquoise module are less likely to be related to FCHL ( Figure 1 , Table S5 ). These results demonstrate that rs3737787 genotypes predict the expression of many genes, some of which predispose to FCHL.

Table 3. Overlap of rs3737787 modules with genes differentially expressed by the rs3737787 genotypes.

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We should point out that our sample size of 70 individuals provides 80% power to detect a significant association (p-value≤0.05) with correlation coefficient = 0.33, and only limited power to rule out associations with a correlation coefficient<0.33. To have 80% power to detect a significant association (p-value≤0.05) when the true correlation coefficient = 0.2 requires 194 individuals, and when the true correlation coefficient = 0.1 requires 783 individuals. Therefore our sample size does not permit us to rule out associations of smaller magnitude (correlation coefficient<0.33). However, our sample size of 70 individuals provides enough power to detect significant moderate correlations (correlation coefficient≥0.33) between eigengenes, SNPs, and clinical traits.

The URFA module contains 504 co-expressed genes that are enriched for the gene ontology (GO) Biological Process categories of Cellular Lipid Metabolic Processes and Lipid Metabolic Processes (p-values = 1.0×10 −5 and 9.3×10 −6 ; Benjamini-Hochberg multiple comparison corrected p-values = 0.022 and 0.039) ( Table S5 ). The URFA ME accounts for 10% of the variation of FCHL, 6% of TC, 17% of TG, and 9% of ApoB ( Dsquared2 logo printed dress Marketable For Sale KPZrdyncer
). The fact that the URFA ME was associated with rs3737787 reflects the fact that most module genes are at least partially regulated by this SNP. To evaluate whether the module causally affects FCHL component traits, we utilized the Network Edge Orienting (NEO) R software package Givenchy small Nobile bag Discount New Styles Sale Discount Footlocker Finishline Sale Online Discount Fashion Style Dz314FuXxx
which takes SNP genotypes as input into structural equation models that compute causal edge orienting scores (referred to as LEO.NB scores). Since we are only considering a single SNP (rs3737787) we computed LEO.NB. SingleMarker scores for the causal orientation of a ME→trait. The LEO.NB. SingleMarker score is a relative model fitting index for the causal model (rs3737787→ME→trait) relative to alternative causal models, and the larger the value for the LEO.NB. SingleMarker score the stronger the evidence that this causal orientation is correct. We required that the our causal model fit at least two times better than the next best alternative model, which equates to a LEO.NB. SingleMarker score of 0.3 [28] (please see the Materials and Methods for a detailed description). We found sufficient evidence to infer a causal relationship between the URFA ME and fasting plasma TGs levels (LEO.NB. SingleMarker score = 0.31), the key component trait of FCHL. The LEO.NB. SingleMarker score for the URFA ME to FCHL was 0.25. We then used the NEO software to prioritize genes inside the URFA module by calculating the LEO.NB. SingleMarker scores evaluating the causal model (rs3737787→gene expression→trait). We identified 18 causal candidate genes for FCHL, and 171 causal candidate genes for fasting plasma TGs levels ( Frame Denim le crop bell flared jeans Buy Sale Online Low Cost Cheap Price Cheap Sale Pre Order New Arrival Sale Online zD1qgWaw
). We observed 13 causal candidate genes for both FCHL and TG. None of the URFA module genes showed evidence for causally affecting TC or ApoB. Since our interest was in FCHL disease status, we characterized the 18 causal candidate genes for FCHL disease status as potential candidate genes for genetic association studies in Mexican FCHL families ( Table 4 ).

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