Valérie Thuries

Hôpital La Pitié Salpêtrière (Groupe Hospitalier "La Pitié Salpêtrière - Charles Foix"), Lutetia Parisorum, Île-de-France, France

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Publications (3)17.55 Total impact

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    ABSTRACT: AIMS: Although demyelination is an important cause of neurological deficits in Multiple Sclerosis (MS), recently axonal pathology and concomitant involvement of sodium channels (Nav) have become a focus of major interest. Studies in experimental autoimmune encephalomyelitis and MS have shown a diffuse distribution of the expression of two channels, Nav1.6 and Nav1.2, along the demyelinated axons. However, the relationship between the expression of these channels by the axon and its environment are not yet known. The aim of this study was to identify the stage and the neuropathological characteristics of the plaque associated with the changes in sodium channel axonal expression. METHODS: We analysed the expression of Nav1.6 and Nav1.2 along demyelinated axons in 64 plaques from 12 MS cases (compared to 6 control cases) characterized according to the Vienna consensus. We used Bodian silver impregnation combined with Luxol fast blue stain and immunohistochemistry for myelin basic protein, microglia/macrophages, B and T cells, neurofilaments and glial fibrillary acidic protein performed on sections of formalin fixed, paraffin embedded tissue. RESULTS: The presence of axonal diffuse expression of Nav1.6 was more frequent in inflammatory plaques with no active demyelination, and particularly within plaques with T cells and activated microglia. On the other hand, Nav1.2 expression seemed to be independent of the stage and the neuropathological environment of the plaque. CONCLUSIONS: The cellular environment of the axon influences the differential expression of Nav channels. A better understanding on the influence of inflammation on the sodium channels mediated axonal degeneration could offer therapeutic perspectives.
    Neuropathology and Applied Neurobiology 05/2013; DOI:10.1111/nan.12059 · 4.97 Impact Factor
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    ABSTRACT: Fluorescence in situ hybridization is an indispensable technique used in routine pathology and for theranostic purposes. Because fluorescence in situ hybridization techniques require sophisticated microscopic workstations and long procedures of image acquisition with sometimes subjective and poorly reproducible results, we decided to test a whole-slide imaging system as an alternative approach. In this study, we used the latest generation of Pannoramic 250 Flash digital microscopes (P250 Flash digital microscopes; 3DHISTECH, Budapest, Hungary) to digitize fluorescence in situ hybridization slides of diffuse large B cells lymphoma cases for detecting MYC rearrangement. The P250 Flash digital microscope was found to be precise with better definition of split signals in cells containing MYC rearrangement with fewer truncated signals as compared to traditional fluorescence microscopy. This digital technique is easier thanks to the preview function, which allows almost immediate identification of the tumor area, and the panning and zooming functionalities as well as a shorter acquisition time. Moreover, fluorescence in situ hybridization analyses using the digital technique appeared to be more reproducible between pathologists. Finally, the digital technique also allowed prolonged conservation of photos. In conclusion, whole-slide imaging technologies represent rapid, robust, and highly sensitive methods for interpreting fluorescence in situ hybridization slides with break-apart probes. In addition, these techniques offer an easier way to interpret the signals and allow definitive storage of the images for pathology expert networks or e-learning databases.
    Human pathology 03/2013; 44(8). DOI:10.1016/j.humpath.2012.12.009 · 2.81 Impact Factor
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    ABSTRACT: A K17I mutation in the ANG gene encoding angiogenin has been identified in a case that we previously published as ALS with neuronal intranuclear protein inclusions (Seilhean et al. in Acta Neuropathol 108:81-87, 2004). These inclusions were immunoreactive for smooth muscle alpha-actin but not for angiogenin. Moreover, they were not labeled by anti-TDP-43 antibodies, while numerous cytoplasmic inclusions immunoreactive for ubiquitin, p62 and TDP-43 were detected in both oligodendrocytes and neurons in various regions of the central nervous system. In addition, expression of smooth muscle alpha-actin was increased in the liver where severe steatosis was observed. This is the first neuropathological description of a case with an ANG mutation. Angiogenin is known to interact with actin. Like other proteins involved in ALS pathogenesis, such as senataxin, TDP-43 and FUS/TLS, it plays a role in RNA maturation.
    Acta Neuropathologica 06/2009; 118(4):561-73. DOI:10.1007/s00401-009-0545-9 · 9.78 Impact Factor

Publication Stats

30 Citations
17.55 Total Impact Points


  • 2009
    • Hôpital La Pitié Salpêtrière (Groupe Hospitalier "La Pitié Salpêtrière - Charles Foix")
      • Département de Neuropathologie
      Lutetia Parisorum, Île-de-France, France