86 research outputs found

    A 1-D modelling of streaming potential dependence on water content during drainage experiment in sand

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    The understanding of electrokinetics for unsaturated conditions is crucial for numerous of geophysical data interpretation. Nevertheless, the behaviour of the streaming potential coefficient C as a function of the water saturation Sw is still discussed. We propose here to model both the Richards' equation for hydrodynamics and the Poisson's equation for electrical potential for unsaturated conditions using 1-D finite element method. The equations are first presented and the numerical scheme is then detailed for the Poisson's equation. Then, computed streaming potentials (SPs) are compared to recently published SP measurements carried out during drainage experiment in a sand column. We show that the apparent measurement of DV / DP for the dipoles can provide the SP coefficient in these conditions. Two tests have been performed using existing models for the SP coefficient and a third one using a new relation. The results show that existing models of unsaturated SP coefficients C(Sw) provide poor results in terms of SP magnitude and behaviour. We demonstrate that the unsaturated SP coefficient can be until one order of magnitude larger than Csat, its value at saturation. We finally prove that the SP coefficient follows a non-monotonous behaviour with respect to water saturation. Key words: Electrical properties; Electromagnetic theory; Hydrogeophysics; Hydrology; Permeability and porosity; electrokinetic; streaming potential; self-potential; water content; water saturation; unsaturated condition; finite element modelin

    Biodiversity, Species Protection, and Animal Welfare Under International Law

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    The chapter explores the influence of the concept of animal welfare on international biodiversity law. A close examination of the recent evolution of this branch of international law shows that animal welfare has an ambivalent place in biodiversity-related agreements. Indeed, while welfare is only a faint consideration in the development of international regimes dealing with biodiversity as a whole, the concept has become an essential element for agreements dealing with the conservation of specific endangered species. Despite its role in these agreements, the place of animal welfare in international biodiversity law highlights that this corpus of rules is currently insufficient to be an effective tool for the protection of wildlife welfare. The last section of this study suggests that the adoption of international rules aiming at ensuring the protection of wild animals’ welfare could serve the double purpose of strengthening the conservation purpose of biodiversity regimes while also filling the welfare gap of international biodiversity law

    Loss-of-Function Mutations in WDR73 Are Responsible for Microcephaly and Steroid-Resistant Nephrotic Syndrome: Galloway-Mowat Syndrome

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    Galloway-Mowat syndrome is a rare autosomal-recessive condition characterized by nephrotic syndrome associated with microcephaly and neurological impairment. Through a combination of autozygosity mapping and whole-exome sequencing, we identified WDR73 as a gene in which mutations cause Galloway-Mowat syndrome in two unrelated families. WDR73 encodes a WD40-repeat-containing protein of unknown function. Here, we show that WDR73 was present in the brain and kidney and was located diffusely in the cytoplasm during interphase but relocalized to spindle poles and astral microtubules during mitosis. Fibroblasts from one affected child and WDR73-depleted podocytes displayed abnormal nuclear morphology, low cell viability, and alterations of the microtubule network. These data suggest that WDR73 plays a crucial role in the maintenance of cell architecture and cell survival. Altogether, WDR73 mutations cause Galloway-Mowat syndrome in a particular subset of individuals presenting with late-onset nephrotic syndrome, postnatal microcephaly, severe intellectual disability, and homogenous brain MRI features. WDR73 is another example of a gene involved in a disease affecting both the kidney glomerulus and the CNS

    Genetic and Chemical Modifiers of a CUG Toxicity Model in Drosophila

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    Non-coding CUG repeat expansions interfere with the activity of human Muscleblind-like (MBNL) proteins contributing to myotonic dystrophy 1 (DM1). To understand this toxic RNA gain-of-function mechanism we developed a Drosophila model expressing 60 pure and 480 interrupted CUG repeats in the context of a non-translatable RNA. These flies reproduced aspects of the DM1 pathology, most notably nuclear accumulation of CUG transcripts, muscle degeneration, splicing misregulation, and diminished Muscleblind function in vivo. Reduced Muscleblind activity was evident from the sensitivity of CUG-induced phenotypes to a decrease in muscleblind genetic dosage and rescue by MBNL1 expression, and further supported by the co-localization of Muscleblind and CUG repeat RNA in ribonuclear foci. Targeted expression of CUG repeats to the developing eye and brain mushroom bodies was toxic leading to rough eyes and semilethality, respectively. These phenotypes were utilized to identify genetic and chemical modifiers of the CUG-induced toxicity. 15 genetic modifiers of the rough eye phenotype were isolated. These genes identify putative cellular processes unknown to be altered by CUG repeat RNA, and they include mRNA export factor Aly, apoptosis inhibitor Thread, chromatin remodelling factor Nurf-38, and extracellular matrix structural component Viking. Ten chemical compounds suppressed the semilethal phenotype. These compounds significantly improved viability of CUG expressing flies and included non-steroidal anti-inflammatory agents (ketoprofen), muscarinic, cholinergic and histamine receptor inhibitors (orphenadrine), and drugs that can affect sodium and calcium metabolism such as clenbuterol and spironolactone. These findings provide new insights into the DM1 phenotype, and suggest novel candidates for DM1 treatments

    Effects of eight neuropsychiatric copy number variants on human brain structure

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