Ecoacoustics and multispecies semiosis: naming, semantics, semiotic characteristics, and competencies

Biosemiotics to date has focused on the exchange of signals between organisms, in line with bioacoustics; consideration of the wider acoustic environment as a semiotic medium is under-developed. The nascent discipline of ecoacoustics, that investigates the role of environmental sound in ecological processes and dynamics, fills this gap. In this paper we introduce key ecoacoustic terminology and concepts in order to highlight the value of ecoacoustics as a discipline in which to conceptualise and study intra- and interspecies semiosis. We stress the inherently subjective nature of all sensory scapes (vivo-, land-, vibro- and soundscapes) and propose that they should always bear an organismic attribution. Key terms to describe the sources (geophony, biophony, anthropophony, technophony) and scales (sonotopes, soundtopes, sonotones) of soundscapes are described. We introduce epithets for soundscapes to point to the degree to which the global environment is implicated in semiosis (latent, sensed and interpreted soundscapes); terms for describing key ecological structures and processes (acoustic community, acoustic habitat, ecoacoustic events) and examples of ecoacoustic events (choruses and noise) are described. The acoustic eco-field is recognized as the semiotic model that enables soniferous species to intercept core resources like food, safety and roosting places. We note that whilst ecoacoustics to date has focused on the critical task of the development of metrics for application in conservation and biodiversity assessment, these can be enriched by advancing conceptual and theoretical foundations. Finally, the mutual value of integrating ecoacoustic and biosemiotics perspectives is considered

Genome-wide association reveals contribution of MRAS to painful temporomandibular disorder in males

Painful temporomandibular disorders (TMDs) are the leading cause of chronic orofacial pain, but its underlying molecular mechanisms remain obscure. Although many environmental factors have been associated with higher risk of developing painful TMD, family and twin studies support a heritable genetic component as well. We performed a genome-wide association study assuming an additive genetic model of TMD in a discovery cohort of 999 cases and 2031 TMD-free controls from the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study. Using logistic models adjusted for sex, age, enrollment site, and race, we identified 3 distinct loci that were significant in combined or sex-segregated analyses. A single-nucleotide polymorphism on chromosome 3 (rs13078961) was significantly associated with TMD in males only (odds ratio = 2.9, 95% confidence interval: 2.02-4.27, P = 2.2 x 10(-8)). This association was nominally replicated in a meta-analysis of 7 independent orofacial pain cohorts including 160,194 participants (odds ratio - 1.16, 95% confidence interval: 1.0-1.35, P = 2.3 x 10(-2)). Functional analysis in human dorsal root ganglia and blood indicated this variant is an expression quantitative trait locus, with the minor allele associated with decreased expression of the nearby muscle RAS oncogene homolog (MRAS) gene (beta = -0.51, P = 2.43 x 10(-5)). Male mice, but not female mice, with a null mutation of Mras displayed persistent mechanical allodynia in a model of inflammatory pain. Genetic and behavioral evidence support a novel mechanism by which genetically determined MRAS expression moderates the resiliency to chronic pain. This effect is male-specific and may contribute to the lower rates of painful TMD in men1603579591National Institute of Dental and Craniofacial Research (NIDCR)United States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Dental & Craniofacial Research (NIDCR) [U01DE017018]; NIDCRUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Dental & Craniofacial Research (NIDCR) [U01DE017018, HHSN268201200008I]; Canadian Excellence Research Chairs (CERC) Program grant [CERC09]; US Cancer Pain Relief Committee (Career Development Award "Neurochemistry and Physiology of Human Pain-Processing Nuclei"); Federal Ministry of Education and ResearchFederal Ministry of Education & Research (BMBF) [01ZZ9603, 01ZZ0103, 01ZZ0403, 03ZIK012]; Ministry of Cultural Affairs; Social Ministry of the Federal State of Mecklenburg-West Pomerania; network "Greifswald Approach to Individualized Medicine (GANI_MED)" - Federal Ministry of Education and Research [03IS2061A]; Siemens Healthcare (Erlangen, Germany); Federal State of Mecklenburg-West Pomerania; Academy of FinlandAcademy of Finland [104781, 120315, 129269, 1114194, 24300796]; University Hospital Oulu; University of Oulu [75617]; NHLBI grant through the STAMPEED program [5R01HL087679-02, 1RL1MH083268-01]; NIH/National Institute of Mental Health (NIMH) [5R01MH63706: 02]; ENGAGE project; EUEuropean Union (EU) [277849]; Medical Research CouncilMedical Research Council UK (MRC) [G0500539, G0600705, G1002319]; MRC, Centenary Early Career Award; Academy of Finland EGEAproject [285547]; Biocentrum Helsinki; European Commission (EURO-BLCS)European Commission Joint Research Centre [QLG1-CT-2000-01643]; Sigrid Juselius FoundationSigrid Juselius Foundation; US National Institute of Mental HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Mental Health (NIMH) [5R01 MH 63706: 02]; Sao Paulo Research FoundationFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2006/56019-8R, 2009/02520-6]; Canadian Excellence Research Chairs (CERC) Program [CERC09]; NIH/National Institute of Neurological Disorders and Stroke (NINDS)United States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Neurological Disorders & Stroke (NINDS) [NS045685]; National Heart, Lung, and Blood Institute (NHLBI)United States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Heart Lung & Blood Institute (NHLBI) [HHSN268201300001I/N01-HC-65233, HHSN268201300004I/N01-HC-65234, HHSN268201300002I/N01-HC-65235, HHSN268201300003I/N01-HC-65236 Northwestern Univ, HHSN268201300005I/N01-HC-65237]; ENGAGE grant [HEALTH-F4-2007-201413]; Intramural Research Program of the NIH, National Institute of Environmental Health SciencesUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Environmental Health Sciences (NIEHS); Biocenter; [K12DE022793]; [H2020-633595

Genome-wide association reveals contribution of MRAS to painful temporomandibular disorder in males

Abstract Painful temporomandibular disorders (TMDs) are the leading cause of chronic orofacial pain, but its underlying molecular mechanisms remain obscure. Although many environmental factors have been associated with higher risk of developing painful TMD, family and twin studies support a heritable genetic component as well. We performed a genome-wide association study assuming an additive genetic model of TMD in a discovery cohort of 999 cases and 2031 TMD-free controls from the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study. Using logistic models adjusted for sex, age, enrollment site, and race, we identified 3 distinct loci that were significant in combined or sex-segregated analyses. A single-nucleotide polymorphism on chromosome 3 (rs13078961) was significantly associated with TMD in males only (odds ratio = 2.9, 95% confidence interval: 2.02–4.27, P = 2.2 × 10⁻⁸). This association was nominally replicated in a meta-analysis of 7 independent orofacial pain cohorts including 160,194 participants (odds ratio = 1.16, 95% confidence interval: 1.0–1.35, P = 2.3 × 10⁻²). Functional analysis in human dorsal root ganglia and blood indicated this variant is an expression quantitative trait locus, with the minor allele associated with decreased expression of the nearby muscle RAS oncogene homolog (MRAS) gene (beta = −0.51, P = 2.43 × 10⁻⁵). Male mice, but not female mice, with a null mutation of Mras displayed persistent mechanical allodynia in a model of inflammatory pain. Genetic and behavioral evidence support a novel mechanism by which genetically determined MRAS expression moderates the resiliency to chronic pain. This effect is male-specific and may contribute to the lower rates of painful TMD in men