Toward a typeface for the transcription of facial actions in sign languages

International audienceNon-manual actions, and more specifically facial actions (FA) can be found in all Sign Languages (SL). Those actions involve all the different facial parts and can have various and intricate linguistic relations with manual signs. Unlike in vocal languages, FA in SL provide more meaning than simple expressions of feelings and emotions. Yet non-manual parameters are among the most unknown formal features in SL studies. During the past 30 years, some studies have started questioning the meanings and linguistic values and the relations between manual and non-manual signs (Crashborn et al. 2008; Crashborn & Bank 2014); more recently, SL corpora have been analysed, segmented, and transcribed to help study FA (Vogst-Svenden 2008; Bergman et al. 2008; Sutton-Spence & Day 2008).Moreover, to fill the lack of an annotation system for FA, a few manual annotation systems have integrated facial glyphs, such as HamNoSys (Prillwitz et al. 1989) and SignWriting (Sutton 1995). On one hand, HamNoSys has been developed to describe all existing SLs at a phonetic level; it allows a formal, linear, highly detailed and searchable description of manual parameters. As for non-manual parameters, HamNoSys offers the replacement of hands by another articulators. Non-manual parameters can be written as “eyes” or “mouth” and described by the same symbols developed for hands (Hanke 2004). Unfortunately only a limited number of manual symbols can be translated into FA and the annotation system remains incomplete. On the other hand, SignWriting describes SL with iconic symbols placed in a 2D space representing the signer’s body. Facial expressions are divided into mouth, eyes, nose, eyebrows, etc., and are drawn in a circular “head” much like emoticons. SignWriting offers a detailed description of posture and actions of non-manual parameters, but does not ensure compatibility with the most common annotation software used by SL linguists (e.g., ELAN).Typannot, a interdisciplinary project led by linguists, designers, and developers, which aims to set up a complete transcription system for SL that includes every SL parameter (handshape, localisation, movement, FA), has developed a different methodologie. As mentioned earlier, FA have various linguistic values (mouthings, adverbial mouth gestures, semantically empty, enacting, whole face) and also include prosody and emotional meanings. In this regard, they can be more variable and signer-related than manual parameters. To offer the best annotation tool, Typannot’s approach has been to define facial parameters and all their possible tangible configurations. The goal is to set up the most efficient, simple, yet complete and universal formula to describe all possible FA.This formula is based on a 3 dimensional grid. Indeed all the different configurations of FA can be described by its X, Y, Z axis position. As a result, all FA can be described and encoded using a restricted list of 39 qualifiers. Based on this model and to help reduce the annotation process, a set of generic glyphs has been developed. Each qualifier has its own symbolic “generic” glyph. This methodical decomposition of all facial components enables a precise and accurate transcription of a complex FA using only a few glyphs.This formula and its generic glyphs have gone through a series of tests and revisions. Recently, an 18m20s long FA corpus of two deaf signers has been recorded using two different cameras. The first one, RGB HQ, is used to capture a high quality image and the second, infrared Kinect, is used to captured the depth. The latter was linked with Brekel Proface 2 (Leong et al. 2015), a 3D animation software that enables an automatic recognition of FA. This corpus has been fully annotated using Typannot’s generic glyphs. These annotations have enabled the validation of the general structure of Typannot FAformula and to identify some minor corrections to be made. For instance, it has been shown that the description of the air used to puff out or suck in cheeks is too restrictive and the description of the opening and closure of the eyelids is too unnecessarily precise.When those changes are implemented, our next task will be to develop a morphological glyphic system that will combine the different generic glyphs used for each facial parameter into one unique morphological glyph. This means that for any given FA, all the information contained in Typannot descriptive formula will be contained within one legible glyph. Some early research and work has already begun on this topic, but needs further development before providing a statement on its typographic structure. When this system is completed, it will be released with its own virtual keyboard (Typannot Keyboard, currently in development for handshapes) to help transcription and improve annotation processes.Bibliography :-Chételat-Pelé, E. (2010). Les Gestes Non Manuels en Langue des Signes Française ; Annotation, analyse et formalisation : application aux mouvements des sourcils et aux clignements des yeux. Université de Provence - Aix-Marseille I.-Crasborn, O., Van Der Kooij, E., Waters, D., Woll, B., & Mesch, J. (2008). Frequency distribution and spreading behavior of different types of mouth actions in three sign languages. Sign Language & Linguistics, 11(1), 45–67.-Crasborn, O. A., & Bank, R. (2014). An annotation scheme for the linguistic study of mouth actions in sign languages. http://repository.ubn.ru.nl/handle/2066/132960-Fontana, S. (2008). Mouth actions as gesture in sign language. Gesture, 8(1), 104‑123.-Hanke, T. (2004). HamNoSys—Representing sign language data in language resources and language processing contexts. In Workshop on the Representation and Processing of Sign Languages on the occasion of the Fourth International Conference on Language Resources and Evaluation (p. 1‑6).-Leong, C. W., Chen, L., Feng, G., Lee, C. M., & Mulholland, M. (2015). Utilizing depth sensors for analyzing multimodal presentations: Hardware, software and toolkits (p. 547‑556).Presented at Proceedings of the 2015 ACM on International Conference on Multimodal Interaction, ACM.-Prillwitz, S., Leven, R., Zienert, H., Hanke, T., & Henning, J. (1989). Hamburg notation system for sign languages: An introductory guide. Signum Press, Hamburg.-Sandler, W. (2009). Symbiotic symbolization by hand and mouth in sign language. Semiotica, 2009(174), 241‑275. http://doi.org/10.1515/semi.2009.035-Sutton, V. (1995). Lessons in Sign Writing: Textbook. DAC, La Jolla (CA).-Sutton-Spence, R., & Boyes-Braem, P. (2001). The hands are the head of the mouth: The mouth as articulator in sign languages. Signum Press, Hamburg

Implication d'une voie neuronale allant de l'aire tegmentale ventrale à l'amygdale dans l'anxiété et la peur

Mental disorders are the leading cause of disability-adjusted life years worldwide. Traumatic experiences and social stress promote the onset of mental disorders including post-traumatic stress disorders (PTSD) and anxiety disorders. A lack of understanding in the etiology of these disorders have led current therapies to aim at treating symptoms rather than the underlying dysfunctions. Hence, a major clinical challenge is to unravel how individuals control their emotions and cope with stressful events. My PhD project addresses the fundamental mechanisms that underpin mental disorders where individuals cannot cope with stressful events leading to excessive fear and anxiety. While the ventral tegmental area (VTA) is a heterogeneous brain structure well-studied for its function in reward processing, this brain region also plays a role in signaling negative valence. Indeed, subpopulations of VTA neurons respond to aversive stimuli. This functional divergence could arise from the unique properties in distinct target-specific cell populations within the VTA. However, our understanding of the inputs and outputs of the VTA that could contribute to the onset of exacerbated anxiety and fear responses is currently very limited.The central hypothesis of my PhD project is that VTA projection neurons are significant modulators of the main center of anxiety and fear: the amygdala. My project is designed to model and study these defensive behaviors in mice. Hence, my thesis addresses two distinct but overlapping aims:(i) Dissecting VTA glutamatergic projections to the amygdala and their contribution to adaptative and pathological anxiety.(ii) Assessing the inputs and outputs of VTA projection neurons regulating fear responses.For my first aim, I studied the distribution pattern of VTA glutamatergic neurons and their axonal innervation of the amygdala through histological studies. My results are consistent with a growing body of evidence depicting the VTA as a structure comprised of well-compartmentalized cell populations with different functional roles. Secondly, relying upon electrophysiological tools and the use of the chronic social defeat (CSD) paradigm to induce anxiety disorders, I found alterations of both presynaptic and post-synaptic plasticity in VTA glutamatergic neurons projecting to the amygdala. This suggests a potentiation of the neuronal transmission for these efferences to the amygdala paralleled with the appearance of anxiety following CSD. Causality was shown using optogenetic tools to chronically activate these projecting neurons. Indeed, this modulation was sufficient to increase anxiety levels and induce similar change in synaptic plasticity as in CSD. Hence, this first aim strongly suggests a role of this neuronal projection in anxiety disorders.My second aim was based upon the discovery that the laterodorsal tegmentum contribute to fear responses, namely freezing, through efferences to the VTA. I focused on unravelling the connectivity of the VTA with fear centers, and dissecting the contribution of individual cell-types to this newly discovered role. Using chemogenetic tools, I showed that activation of VTA-amygdala pathway is necessary for the manifestation of unconditionned freezing upon electric foot shock exposure. In contrast to my first aim, I showed in this second axis that VTA GABAergic projecting neurons to the amygdala, but not glutamatergic neither dopaminergic cells, are responsible for this fear response.Overall, my thesis work brings new insights into the interconnectivity of two salience centers in the brain, namely the VTA and the amygdala. Moreover, my results suggest that stress challenges on this brain connections contribute to maladaptive anxiety. I propose that future circuit-based therapies could be targeted at the VTA-amygdala pathway to alleviates anxiety symptoms.Les troubles mentaux sont la principale cause d'handicap au monde (OMS). Les expériences traumatiques et le stress social favorisent le développement des troubles mentaux tels que les troubles du stress post-traumatique et les troubles anxieux. Le manque de connaissance sur l'étiologie de ces troubles a conduit à ce que les thérapies ciblent les symptômes plutôt que les causes sous-jacentes de ces troubles. Ainsi, un enjeu clinique majeur est de comprendre comment les individus contrôlent leurs émotions et gèrent les situations stressantes.Mon projet de thèse vise à étudier les mécanismes fondamentaux régulant les troubles mentaux où les individus sont submergés par le stress, tel que les désordres de l'anxiété et de la peur. L'ATV est une structure hétérogène connue pour son rôle dans la sensation de plaisir mais aussi pour son implication dans la valence négative où certaines de ses sous-populations neuronales sont activées par des stimuli aversifs. Cette diversité fonctionnelle pourrait être liée aux différentes sous-populations neuronales de l'ATV ainsi qu'à leurs différentes connections afférentes et efférentes. Néanmoins, l'interaction entre l'ATV et les structures régulant les comportementaux défensifs associés à l'anxiété et la peur reste mal compris.L'hypothèse de ma thèse place l'ATV comme un important modulateur de l'activité de l'amygdale pouvant ainsi réguler l'anxiété et la peur. Mon projet est organisé sur l'utilisation d'un modèle de souris d'anxiété et de peur pour répondre à des objectifs distincts mais entrecroisé :-Disséquer les projections glutamatergiques de l'ATV vers l'amygdale ainsi que leur contribution dans l'anxiété adaptative et pathologique-Déterminer les afférences et efférences neuronales de l'ATV régulant la réponse de peur J 'ai complété mon premier objectif par des approches histologiques en cartographiant la distribution des neurones glutamatergiques de l'ATV et leurs innervations de l'amygdale. Ces résultats sont en accord avec une accumulation de preuves indiquant que l'ATV est une structure composée de populations neuronales compartimentalisées selon leurs fonctions.A l'aide de techniques d'électrophysiologie et du modèle de défaite sociale chronique (DSC) afin d'induire des troubles anxieux de longue durée, nous avons trouvé des altérations de la plasticité pré- et post-synaptique suggérant une potentialisation de la transmission neuronale glutamatergique entre l'ATV et l'amygdale suite à un DSC. Par la suite, j'ai induit une activation chronique des projections glutamatergique de l'ATV allant à l'amygdale via des techniques d'optogénétiques in vivo. Cette modulation est suffisante pour augmenter l'anxiété et causer des changements de plasticité synaptique similaires à ceux retrouvés durant le DSC. Ainsi, cet axe de ma thèse suggère fortement un rôle de cette projections neuronale dans l'induction des troubles anxieux.Mon second objectif est basé sur la découverte d'une régulation de la peur par des efférences du tegmentum latérodorsal allant à l'ATV. J'ai étudié ici la connectivité de l'ATV avec plusieurs centres de la peur où j'ai déterminé le type cellulaire et les connections responsables de cette régulation. Une modulation des projections de l'ATV allant à l'amygdale a été suffisantes pour altérer l'induction contextuelle de la peur. De plus, l'inhibition des projections GABAergiques de l'ATV vers l'amygdale ont réduit la réponse contextuelle de peur. Ainsi, le second axe de ma thèse a révélé le rôle des neurones GABAergiques de l'ATV projetant à l'amygdale dans l'induction de la peur.En conclusion, mes travaux mettent en évidence la connectivité entre deux centres cérébraux de la saillance émotionnelle, l'ATV et l'amygdale. De plus, mon étude suggère que les effets du stress sur ces connections pourrait contribuer aux troubles anxieux. De future thérapies pourraient cibler le réseau neuronal ATV-Amygdale afin de soulager les symptômes des troubles anxieux

Involvement of a ventral tegmental area-Amygdala pathway in anxiety and fear

Les troubles mentaux sont la principale cause d'handicap au monde (OMS). Les expériences traumatiques et le stress social favorisent le développement des troubles mentaux tels que les troubles du stress post-traumatique et les troubles anxieux. Le manque de connaissance sur l'étiologie de ces troubles a conduit à ce que les thérapies ciblent les symptômes plutôt que les causes sous-jacentes de ces troubles. Ainsi, un enjeu clinique majeur est de comprendre comment les individus contrôlent leurs émotions et gèrent les situations stressantes.Mon projet de thèse vise à étudier les mécanismes fondamentaux régulant les troubles mentaux où les individus sont submergés par le stress, tel que les désordres de l'anxiété et de la peur. L'ATV est une structure hétérogène connue pour son rôle dans la sensation de plaisir mais aussi pour son implication dans la valence négative où certaines de ses sous-populations neuronales sont activées par des stimuli aversifs. Cette diversité fonctionnelle pourrait être liée aux différentes sous-populations neuronales de l'ATV ainsi qu'à leurs différentes connections afférentes et efférentes. Néanmoins, l'interaction entre l'ATV et les structures régulant les comportementaux défensifs associés à l'anxiété et la peur reste mal compris.L'hypothèse de ma thèse place l'ATV comme un important modulateur de l'activité de l'amygdale pouvant ainsi réguler l'anxiété et la peur. Mon projet est organisé sur l'utilisation d'un modèle de souris d'anxiété et de peur pour répondre à des objectifs distincts mais entrecroisé :-Disséquer les projections glutamatergiques de l'ATV vers l'amygdale ainsi que leur contribution dans l'anxiété adaptative et pathologique-Déterminer les afférences et efférences neuronales de l'ATV régulant la réponse de peur J 'ai complété mon premier objectif par des approches histologiques en cartographiant la distribution des neurones glutamatergiques de l'ATV et leurs innervations de l'amygdale. Ces résultats sont en accord avec une accumulation de preuves indiquant que l'ATV est une structure composée de populations neuronales compartimentalisées selon leurs fonctions.A l'aide de techniques d'électrophysiologie et du modèle de défaite sociale chronique (DSC) afin d'induire des troubles anxieux de longue durée, nous avons trouvé des altérations de la plasticité pré- et post-synaptique suggérant une potentialisation de la transmission neuronale glutamatergique entre l'ATV et l'amygdale suite à un DSC. Par la suite, j'ai induit une activation chronique des projections glutamatergique de l'ATV allant à l'amygdale via des techniques d'optogénétiques in vivo. Cette modulation est suffisante pour augmenter l'anxiété et causer des changements de plasticité synaptique similaires à ceux retrouvés durant le DSC. Ainsi, cet axe de ma thèse suggère fortement un rôle de cette projections neuronale dans l'induction des troubles anxieux.Mon second objectif est basé sur la découverte d'une régulation de la peur par des efférences du tegmentum latérodorsal allant à l'ATV. J'ai étudié ici la connectivité de l'ATV avec plusieurs centres de la peur où j'ai déterminé le type cellulaire et les connections responsables de cette régulation. Une modulation des projections de l'ATV allant à l'amygdale a été suffisantes pour altérer l'induction contextuelle de la peur. De plus, l'inhibition des projections GABAergiques de l'ATV vers l'amygdale ont réduit la réponse contextuelle de peur. Ainsi, le second axe de ma thèse a révélé le rôle des neurones GABAergiques de l'ATV projetant à l'amygdale dans l'induction de la peur.En conclusion, mes travaux mettent en évidence la connectivité entre deux centres cérébraux de la saillance émotionnelle, l'ATV et l'amygdale. De plus, mon étude suggère que les effets du stress sur ces connections pourrait contribuer aux troubles anxieux. De future thérapies pourraient cibler le réseau neuronal ATV-Amygdale afin de soulager les symptômes des troubles anxieux.Mental disorders are the leading cause of disability-adjusted life years worldwide. Traumatic experiences and social stress promote the onset of mental disorders including post-traumatic stress disorders (PTSD) and anxiety disorders. A lack of understanding in the etiology of these disorders have led current therapies to aim at treating symptoms rather than the underlying dysfunctions. Hence, a major clinical challenge is to unravel how individuals control their emotions and cope with stressful events. My PhD project addresses the fundamental mechanisms that underpin mental disorders where individuals cannot cope with stressful events leading to excessive fear and anxiety. While the ventral tegmental area (VTA) is a heterogeneous brain structure well-studied for its function in reward processing, this brain region also plays a role in signaling negative valence. Indeed, subpopulations of VTA neurons respond to aversive stimuli. This functional divergence could arise from the unique properties in distinct target-specific cell populations within the VTA. However, our understanding of the inputs and outputs of the VTA that could contribute to the onset of exacerbated anxiety and fear responses is currently very limited.The central hypothesis of my PhD project is that VTA projection neurons are significant modulators of the main center of anxiety and fear: the amygdala. My project is designed to model and study these defensive behaviors in mice. Hence, my thesis addresses two distinct but overlapping aims:(i) Dissecting VTA glutamatergic projections to the amygdala and their contribution to adaptative and pathological anxiety.(ii) Assessing the inputs and outputs of VTA projection neurons regulating fear responses.For my first aim, I studied the distribution pattern of VTA glutamatergic neurons and their axonal innervation of the amygdala through histological studies. My results are consistent with a growing body of evidence depicting the VTA as a structure comprised of well-compartmentalized cell populations with different functional roles. Secondly, relying upon electrophysiological tools and the use of the chronic social defeat (CSD) paradigm to induce anxiety disorders, I found alterations of both presynaptic and post-synaptic plasticity in VTA glutamatergic neurons projecting to the amygdala. This suggests a potentiation of the neuronal transmission for these efferences to the amygdala paralleled with the appearance of anxiety following CSD. Causality was shown using optogenetic tools to chronically activate these projecting neurons. Indeed, this modulation was sufficient to increase anxiety levels and induce similar change in synaptic plasticity as in CSD. Hence, this first aim strongly suggests a role of this neuronal projection in anxiety disorders.My second aim was based upon the discovery that the laterodorsal tegmentum contribute to fear responses, namely freezing, through efferences to the VTA. I focused on unravelling the connectivity of the VTA with fear centers, and dissecting the contribution of individual cell-types to this newly discovered role. Using chemogenetic tools, I showed that activation of VTA-amygdala pathway is necessary for the manifestation of unconditionned freezing upon electric foot shock exposure. In contrast to my first aim, I showed in this second axis that VTA GABAergic projecting neurons to the amygdala, but not glutamatergic neither dopaminergic cells, are responsible for this fear response.Overall, my thesis work brings new insights into the interconnectivity of two salience centers in the brain, namely the VTA and the amygdala. Moreover, my results suggest that stress challenges on this brain connections contribute to maladaptive anxiety. I propose that future circuit-based therapies could be targeted at the VTA-amygdala pathway to alleviates anxiety symptoms

Hyperactive and anxiolytic‐like behaviors result from loss of COUP‐TFI/Nr2f1 in the mouse cortex

International audienceThe nuclear receptor COUP TFI (also known as Nr2f1) plays major roles in specifying distinct neuronal subtypes during patterning of the neocortical motor and somatosensory cortex, as well as in regulating the longitudinal growth of the hippocampus during development. In humans, mutations in the NR2F1 gene lead to a global developmental delay and intellectual disabilities. While more than 30% of patients show behavioral features of autism spectrum disorder, 16% of haploinsufficient children show signs of hyperactivity and impulsivity. Loss of COUP-TFI in the cortical mouse primordium results in altered area organization and serotonin distribution, abnormal coordination of voluntary movements and learning and memory deficits. Here, we asked whether absence of COUP-TFI affects locomotor activity, anxiety, as well as depression. Mice mutant for COUP-TFI have normal motor coordination, but significant traits of hyperactivity, which does not seem to respond to N-Methyl-D-aspartate (NMDA) antagonists. However, no changes in anxiety, despite increased locomotor performances, were observed in the open field task. On the contrary, elevated plus maze and dark-light test explorations indicate a decreased anxiety-like behavior in COUP-TFI mutant mice. Finally, significantly reduced immobility in the forced swim test and no changes in anhedonia in the sucrose preference task suggest no particular depressive behaviors in mutant mice. Taken together, our study shows that loss of COUP-TFI leads to increased locomotor activity but less anxiety and contributes in further deciphering the pathophysiology of patients haploinsufficient for NR2F1

Dopamine and glutamate receptors control social stress-induced striatal ERK1/2 activation

International audienceStress has been acknowledged as one of the main risk factors for the onset of psychiatric disorders. Social stress is the most common type of stressor encountered in our daily lives. Uncovering the molecular determinants of the effect of stress on the brain would help understanding the complex maladaptations that contribute to pathological stress-related mental states. We examined molecular changes in the reward system following social defeat stress in mice, as increasing evidence implicates this system in sensing stressful stimuli. Following acute or chronic social defeat stress, the activation (i.e. phosphorylation) of extracellular signal-regulated kinases ERK1 and ERK2 (pERK1/2), markers of synaptic plasticity, was monitored in sub-regions of the reward system. We employed pharmacological antagonists and inhibitory DREADD to dissect the sequence of events controlling pERK1/2 dynamics. The nucleus accumbens (NAc) showed marked increases in pERK1/2 following both acute and chronic social stress compared to the dorsal striatum. Increases in pERK1/2 required dopamine D1 receptors and GluN2B-containing NMDA receptors. Paraventricular thalamic glutamatergic inputs to the NAc are required for social stress-induced pERK1/2. The molecular adaptations identified here could contribute to the long-lasting impact of stress on the brain and may be targeted to counteract stress-related psychopathologies

Progettare un set di caratteri per trascrivere le mouth action nelle LS: il sistema tipografico Typannot

ISBN 978-2-487055-05-3 & eISBN 978-2-487055-07-0AnvurCollana E267955International audienceThe Typannot project aims at creating a complete typographic system to transcribe all sign language parameters. If handshapes have been widely studied by the linguistic community, the same is not true for mouth actions. Today research on mouth actions is still scarce in comparison with other parameters, yet the mouth carries extensive meaningful linguistic information. In this article, we will introduce our work to set up a comprehensive typographic system for mouth actions. After setting the context, we will present our goals, approach and methodology to structure the typographic system as well as explain our processes to design the typeface.Le projet Typannot a pour objectif l'élaboration d'un système typographique complet pour l'intégralité des paramètres des langues des signes. Si les configurations manuelles ont été très largement étudiées par la communauté linguistique, on ne peut pas en dire autant des mouth actions : aujourd'hui les recherches sur ces dernières restent rares en comparaison des travaux effectués sur les autres paramètres. Pourtant le bas du visage, et plus spécifiquement la bouche, transmettent des informations linguistiques majeures. Dans cet article, est introduit notre travail d'élaboration du système typographique pour la transcription des mouth actions. Après avoir présenté le contexte, seront énoncés les objectifs, notre approche et nos méthodologies pour mettre en place la structure du système. Sera présenté ensuite nos processus d'expérimentation et de design typographique avant d'évoquer les usages présents et futurs de la fonte.Il progetto Typannot mira a sviluppare un sistema tipografico completo per tutti i parametri delle lingue dei segni. Se le configurazioni manuali sono state ampiamente studiate dalla comunità linguistica, lo stesso non si può dire delle azioni della bocca: oggi le ricerche su queste ultime restano rare rispetto al lavoro svolto sugli altri parametri. Eppure, la faccia inferiore, e più specificamente la bocca, trasmette importanti informazioni linguistiche. In questo articolo viene introdotto il lavoro sullo sviluppo del sistema tipografico per la trascrizione delle azioni della bocca. Dopo aver presentato il contesto, vengono illustrati gli obiettivi, l’approccio utilizzato e le metodologie per impostare la struttura del sistema. Vengono poi presentati i processi di sperimentazione e progettazione tipografica prima di discutere gli usi presenti e futuri dei caratteri

Il sistema di trascrizione Typannot applicato ai gesti della bocca

International audienceResearch on sign languages (SLs) requires dedicated, efficient and comprehensive transcription systems to analyze and compare the sign parameters; at present, many transcription systems focus on manual parameters, relegating the non-manual component to a lesser role. This article presents Typannot, a formal transcription system, and in particular its application to mouth gestures: 1) first, exposing its kinesiological approach, i.e. an intrinsic articulatory description anchored in the body; 2) then, showing its conception to integrate linguistic, graphic and technical aspects within a typeface; 3) finally, presenting its application to a corpus in French Sign Language (LSF) recorded with motion capture.La recherche sur les langues des signes (LS) nécessite des systèmes de transcription dédiés, efficaces et complets pour analyser et comparer les paramètres des signes; à l'heure actuelle, de nombreux systèmes de transcription se concentrent sur les paramètres manuels, reléguant la composante non manuelle à un rôle moindre. Cet article présente Typannot, un système de transcription formelle, et en particulier son application aux gestes de la bouche: 1) d'abord, il expose son approche kinésiologique, c'est-à-dire une description articulatoire intrinsèque ancrée dans le corps; 2) puis, il montre sa conception pour intégrer les aspects linguistiques, graphiques et techniques au sein d'une police de caractères; 3) enfin, il présente son application à un corpus en Langue des Signes Française (LSF) enregistré en motion capture.La ricerca sulle lingue dei segni (SL) richiede sistemi di trascrizione dedicati, efficienti e completi per analizzare e confrontare i parametri dei segni; attualmente molti sistemi di trascrizione si concentrano sui parametri manuali, relegando la componente non manuale ad un ruolo minore. Questo articolo presenta Typannot, un sistema di trascrizione formale, e in particolare la sua applicazione ai gesti della bocca: 1) in primo luogo, esponendo il suo approccio kinesiologico, cioè una descrizione articolatoria intrinseca ancorata al corpo; 2) poi, mostrando la sua concezione per integrare gli aspetti linguistici, grafici e tecnici all'interno di un carattere tipografico; 3) infine, presentando la propria applicazione ad un corpus in Lingua dei Segni Francese (LSF) registrato con motion capture

Correlare linguaggi e corpo: l’approccio Typannot per la trascrizione delle lingue dei segni

International audienceSign Languages (SLs) linguistics traditionally follows a parametric approach based on the shapes that characterize the gesture (handshape, orientation and trajectory of the hand, facial expression…). Those shapes are actually the result of specific organizations of the body happening at a sub-parametric level. TYPANNOT (Boutet et al., 2018) aims at developing a typographic system that allows the description of this lower level of organization. Its goal is to show how the shapes are actually formed in order to eventually understand the role of the body in SLs meaning structuration.Parting away from the parametric model initiated by Stokoe (1960 until today), we adopt a kinesiological approach (Boutet, 2018) to describe the way SLs gesture is organized. Adopting this approach would allow linguists to articulate two levels of structuration that are intrinsically linked: (1) a physical level describing the way the body’s different degrees of freedom (DoF) are dynamically organized; and (2) a linguistic level describing how those specific organizations can form meaningful structures. Because of the inherent complexity of the body, TYPANNOT has to push the technological boundaries of existing transcription systems.TYPANNOT provides a typographic system that can encode the articulatory organization of the different body parts at a phonetic level (1). The system exploits OpenType font features to display transcriptions in two forms: a generic form using a string of indexable symbols (i.e., DoF of each finger), and a composed form using a synthetic visualization that can be read as a parametric translation (e.g., handshape). To implement such a detailed transcription approach, TYPANNOT has to develop intuitive graphical user interfaces.By promoting a kinesiological model, TYPANNOT is also a practical reflection on the integration of motion capture into SLs linguistic studies. Its design is finally the ground of a research linking to the emerging field of grapholinguistic.BIBLIOGRAPHIEBoutet D. 2018. Pour une approche kinésiologique de la gestualité. Habilitation à diriger des recherches, Université de Rouen-Normandie.Boutet D., Doan P., Bianchini C.S., Danet C., Goguely T., Rébulard M. 2018. Systèmes graphématiques et écritures des langues signées. in J. M. Klinkenberg & S. Polis (eds) “Signature (essais en) sémiotiques de l’écriture”. Signata, 9: 391-426