119 research outputs found

    Equine glaucoma

    Get PDF
    Glaucoma is a group of eye diseases characterized by functional damage to the optic nerve and ganglion cells of the retina, usually due to a transient or permanent elevation in intraocular pressure (IOP). The condition occurs infrequently in horses, and is most often a complication of anterior uveitis. Its development is often insidious and can remain asymptomatic until an advanced stage associated with hydrophthalmos and blindness. In horses, an IOP greater than 30 mmHg, measured by applanation or rebound tonometry, in conjunction with compatible clinical features is consistent with a diagnosis of glaucoma. Medical and surgical treatments are directed towards reducing IOP, but glaucoma secondary to equine recurrent uveitis is generally difficult to control. This article summarises the clinical, pathogenesis, diagnostic and therapeutic data of equine glaucomaLe glaucome est une affection oculaire rĂ©sultant d’une augmentation temporaire ou permanente de la pression intraoculaire (PIO), qui entraĂźne une atteinte fonctionnelle du nerf optique et des cellules ganglionnaires de la rĂ©tine. Peu frĂ©quent chez le cheval, il reprĂ©sente le plus souvent une complication d’une uvĂ©ite antĂ©rieure. Son dĂ©veloppement est souvent insidieux et peut rester ignorĂ© jusqu’à un stade avancĂ© caractĂ©risĂ© par l’hydrophtalmie et la cĂ©citĂ©. Une PIO supĂ©rieure Ă  30 mmHg, mesurĂ©e par tonomĂ©trie Ă  aplanissement ou Ă  rebond, associĂ©e Ă  un tableau clinique Ă©vocateur est considĂ©rĂ©e comme une confirmation du diagnostic de glaucome chez le cheval. Les traitements mĂ©dicaux et chirurgicaux visent Ă  diminuer la PIO, mais le glaucome secondaire Ă  l’uvĂ©ite rĂ©currente Ă©quine est gĂ©nĂ©ralement difficile Ă  contrĂŽler. Cet article prĂ©sente une synthĂšse des donnĂ©es cliniques, pathogĂ©niques, diagnostiques et thĂ©rapeutiques sur le glaucome Ă©qui

    Forced assembly by multilayer coextrusion to create oriented graphene reinforced polymer nanocomposites

    Get PDF
    A potential advantage of platelet-like nanofillers as nanocomposite reinforcements is the possibility of achieving two-dimensional stiffening through planar orientation of the platelets. The ability to achieve improved properties through in-plane orientation of the platelets is a challenge and, here, we present the first results of using forced assembly to orient graphene nanoplatelets in poly(methyl methacrylate)/ polystyrene (PMMA/PS) and PMMA/PMMA multilayer films produced through multilayer coextrusion. The films exhibited a multilayer structure made of alternating layers of polymer and polymer containing graphene as evidenced by electron microscopy. Significant single layer reinforcement of 118% at a concentration of 2 wt % graphene was achieveddhigher than previously reported reinforcement for randomly dispersed graphene. The large reinforcement is attributed to the planar orientation of the graphene in the individual polymer layers. Anisotropy of the stiffening was also observed and attributed to imperfect planar orientation of the graphene lateral to the extrusion flow

    Counting RNA pseudoknotted structures

    Get PDF
    International audienceIn 2004, Condon and coauthors gave a hierarchical classification of exact RNA structure prediction algorithms according to the generality of structure classes that they handle. We complete this classification by adding two recent prediction algo- rithms. More importantly, we precisely quantify the hierarchy by giving closed or asymptotic formulas for the theoretical number of structures of given size n in all the classes but one. This allows to assess the tradeoff between the expressiveness and the computational complexity of RNA structure prediction algorithms

    Clinical, electroretinographic and histomorphometric evaluation of the retina in sheep with natural scrapie

    Get PDF
    Background: The retina is part of the diencephalon in a peripheral location and may be involved in prion diseases. Retinal function and structural changes were assessed in naturally scrapie-affected red face Manech ewes presenting the classical signs of the disease, and clinically healthy age-matched subjects for controls. Ophthalmic examination was done prior to electroretinography (ERG), which was carried out under conditions that allowed photopic and scotopic activities to be assessed. Histomorphometry of the inner and outer retinal layers was performed post-mortem, and retinas were also examined for evidence of abnormal prion protein (PrPSc) accumulation and glial fibrillary acidic protein (GFAP) upregulation as a marker of gliosis. Scrapie status was determined by examination of brain tissue Results: Ocular reflexes and ophthalmoscopy did not reveal any difference between scrapie affected and control animals. Although the light-and dark-adapted ERG responses of both rod-and cone-mediated functions had a similar waveform in scrapie-affected and control sheep, a significant reduction in the amplitude of the ERG a-and b-waves was observed in affected animals compared to controls. These functional alterations were correlated with a substantial loss of cells in the outer nuclear layer (ONL), lengthening and disorganization in photoreceptor segments, and substantial reduction in cellularity and thickness of the inner nuclear layer (INL). The degenerative changes in the INL and ONL were most marked in the central and paracentral areas of the scrapie retinas, and were accompanied in all scrapie retinas by PrPSc deposition in the ganglion cell and synaptic layers. GFAP immunoreactivity was mainly increased in the ganglion cell and inner plexiform layers. Conclusions: No appreciable fundoscopic changes were observed in the scrapie-affected ewes although reproducible changes in retinal function as measured by ERG were observed in these animals. The alterations in the receptoral and post-receptoral pathways corresponded to the degenerative lesions observed in the ONL and INL of the scrapie retinas. The retinal degeneration was associated with prion protein infectivity which presumably spread via the optic nerve

    Preparation and characterization of poly(ethylene terephthalate) ïŹlms coated by chitosan and vermiculite nanoclay

    Get PDF
    Chitosan (CS) layers are coated on a poly(ethylene terephthalate) (PET) film in order to decrease the oxygen permeability through the polymeric films for food packaging applications. Oxygen transmission rate (OTR) of the 130 ÎŒm PET films can be decreased from 11 to only 0.31 cm3/mÂČ.day with a coated layer of 2 ÎŒm of CS. Additional decrease is obtained with the addition of vermiculite (VMT) to CS matrix in high proportion (40 to 50 w/w%). The OTR of the coated PET films decreased to very low values, below the detection limit of commercial instrumentation (≀0.008 cm3/m2 day). This high-barrier behavior is believed to be due to the brick wall nanostructure, which produces an extremely tortuous path for oxygen molecules

    Early T Cell Signalling Is Reversibly Altered in PD-1+ T Lymphocytes Infiltrating Human Tumors

    Get PDF
    To improve cancer immunotherapy, a better understanding of the weak efficiency of tumor-infiltrating T lymphocytes (TIL) is necessary. We have analyzed the functional state of human TIL immediately after resection of three types of tumors (NSCLC, melanoma and RCC). Several signalling pathways (calcium, phosphorylation of ERK and Akt) and cytokine secretion are affected to different extents in TIL, and show a partial spontaneous recovery within a few hours in culture. The global result is an anergy that is quite distinct from clonal anergy induced in vitro, and closer to adaptive tolerance in mice. PD-1 (programmed death -1) is systematically expressed by TIL and may contribute to their anergy by its mere expression, and not only when it interacts with its ligands PD-L1 or PD-L2, which are not expressed by every tumor. Indeed, the TCR-induced calcium and ERK responses were reduced in peripheral blood T cells transfected with PD-1. Inhibition by sodium stibogluconate of the SHP-1 and SHP-2 phosphatases that associate with several inhibitory receptors including PD-1, relieves part of the anergy apparent in TIL or in PD-1-transfected T cells. This work highlights some of the molecular modifications contributing to functional defects of human TIL

    Submicroscopic Deletions at 13q32.1 Cause Congenital Microcoria.

    Get PDF
    International audienceCongenital microcoria (MCOR) is a rare autosomal-dominant disorder characterized by inability of the iris to dilate owing to absence of dilator pupillae muscle. So far, a dozen MCOR-affected families have been reported worldwide. By using whole-genome oligonucleotide array CGH, we have identified deletions at 13q32.1 segregating with MCOR in six families originating from France, Japan, and Mexico. Breakpoint sequence analyses showed nonrecurrent deletions in 5/6 families. The deletions varied from 35 kbp to 80 kbp in size, but invariably encompassed or interrupted only two genes: TGDS encoding the TDP-glucose 4,6-dehydratase and GPR180 encoding the G protein-coupled receptor 180, also known as intimal thickness-related receptor (ITR). Unlike TGDS which has no known function in muscle cells, GPR180 is involved in the regulation of smooth muscle cell growth. The identification of a null GPR180 mutation segregating over two generations with iridocorneal angle dysgenesis, which can be regarded as a MCOR endophenotype, is consistent with the view that deletions of this gene, with or without the loss of elements regulating the expression of neighboring genes, are the cause of MCOR

    Le test de Schirmer chez le cheval

    No full text
    TOULOUSE3-BU Santé-Centrale (315552105) / SudocTOULOUSE-EN Vétérinaire (315552301) / SudocSudocFranceF

    IntĂ©rĂȘt de l'acide epsilon-aminocaproĂŻque dans le traitement des ulcĂšres Ă©pithĂ©liaux chroniques de la cornĂ©e chez le chien

    No full text
    L'activitĂ© protĂ©olytique liĂ©e Ă  la plasmine a Ă©tĂ© dĂ©crite dans le film lacrymal prĂ©-cornĂ©en des chiens atteints d'ulcĂšres cornĂ©ens Ă©pithĂ©liaux chroniques et contribuerait Ă  retarder la cicatrisation Ă©pithĂ©liale. L'efficacitĂ© clinique de l'acide epsilon-aminocaproĂŻque (AEAC), dĂ©jĂ  dĂ©crite dans le traitement de cette affection chez des modĂšles lagomorphes, a Ă©tĂ© explorĂ©e dans l'espĂšce canine grĂące Ă  cette Ă©tude rĂ©trospective. Les dossiers mĂ©dicaux des chiens atteints de dĂ©ficits Ă©pithĂ©liaux entre Octobre 1997 et Mars 2003 ont Ă©tĂ© analysĂ©s. Le diagnostic a reposĂ© sur la prĂ©sence d'une perte de substance Ă©pithĂ©liale Ă©voluant depuis plus de 10 jours sans cause sous-jacente apparente. A la premiĂšre consultation, le lambeau Ă©pithĂ©lial marginal non adhĂ©rent a Ă©tĂ© dĂ©bridĂ© sous anesthĂ©sie locale sur tous les yeux au moyen d'un coton-tige stĂ©rile. Sur 34 yeux (28 chiens), un traitement adjuvant consistant en l'instillation locale trois fois par jour d'un collyre Ă  base d'AEAC Ă  35.7 mg/ml (groupe AEAC) a Ă©tĂ© rĂ©alisĂ©. Dix-sept yeux (16 chiens) ayant reçu uniquement un collyre de gentamicine Ă  3 mg/ml aprĂšs desĂ©pithĂ©lialisation ont Ă©tĂ© inclus pour servir de groupe contrĂŽle. AprĂšs le dĂ©but du traitement, des suivis cliniques ont Ă©tĂ© rĂ©alisĂ©s chaque semaine pendant trois semaines. Les deux groupes de traitement avaient approximativement la mĂȘme distribution raciale et ne prĂ©sentaient pas de diffĂ©rence statistique significative (P>0.05) pour l'Ăąge, le genre, le cĂŽtĂ© affectĂ© et la durĂ©e d'Ă©volution de l'ulcĂšre. Les rĂ©sultats ont montrĂ© qu'Ă  la fin de la pĂ©riode de suivi (J21), le taux global de guĂ©rison Ă©tait significativement plus Ă©levĂ© (P=0.0001) dans le groupe AEAC (32/34= 94.1%) que dans le groupe contrĂŽle (7/17=41.2%). Aucun effet secondaire n'a Ă©tĂ© notĂ© pendant la pĂ©riode d'observation. Cette Ă©tude suggĂšre que l'utilisation locale d'AEAC semble bĂ©nĂ©fique dans le traitement des pertes Ă©pithĂ©liales cornĂ©ennes idiopathiques chez le chien et confirme indirectement que le systĂšme activateur du plasminogĂšne / plasmine, inhibĂ© par l'AEAC, est impliquĂ© dans la pathogĂ©nie de cette affection.TOULOUSE3-BU SantĂ©-Centrale (315552105) / SudocTOULOUSE-EN VĂ©tĂ©rinaire (315552301) / SudocSudocFranceF
    • 

    corecore