147 research outputs found

    Prosody and synchronization in cognitive neuroscience

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    We introduce our methodological study with a short review of the main literature on embodied language, including some recent studies in neuroscience. We investigated this component of natural language using Recurrence Quantification Analysis (RQA). RQA is a relatively new statistical methodology, particularly effective in complex systems. RQA provided a reliable quantitative description of recurrences in text sequences at the orthographic level. In order to provide examples of the potential impact of this methodology, we used RQA to measure structural coupling and synchronization in natural and clinical verbal interactions. Results show the efficacy of this methodology and possible implications

    Profils épidémiologiques cliniques et bactériologiques des infections du tractus urinaire dans le service des maladies infectieuses et tropicales de l’hôpital Tenon de Paris: « étude préliminaire ».

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    Objectif : décrire les caractéristiques épidémiologiques, cliniques et bactériologiques des infections du tractus urinaire(ITU) dans le service des maladies infectieuses et tropicales du CHU de Ténon à Paris. Patients et méthodes : Il s’est agi d’une étude rétrospective réalisée le 25 Octobre 2016 dans le service des maladies infectieuses et tropicales du CHU de Ténon à Paris. Etaient inclus tous les patients hospitalisés, ayant à l’examen cytobactériologique des urines(ECBU) une leucocyturie significative et une uroculture positives. Résultats : Quatre patients avaient été recensés sur un total de 28 patients hospitalisés, soit une prévalence hospitalière de 14%. Leurs âges variaient entre 22 ans et 82 ans. Les signes urinaires étaient présents chez un seul patient, et étaient représentés par une dysurie et une douleur lombaire évoluant dans un contexte fébrile. Les bactéries isolées à l’examen cytobactériologique des urines(ECBU) étaient représentées par E. coli (2) dont 1 productrice de bétalactamase à spectre élargi(BLSE), P. aeruginosa(1), et K. pneumoniae (1) de phénotype sauvage tous les deux. Conclusion : Les ITU semblent relativement fréquentes au service des maladies infectieuses de l’hôpital Tenon. Ces infections évoluaient presque toujours avec d’autres comorbidités chez tous les patients. Elles s’accompagnaient rarement de signes d’appel urinaire d’où l’intérêt de leur recherche systématique dans le cadre de tout bilan infectieux

    The definition of HIV-associated neurocognitive disorders: are we overestimating the real prevalence?

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    <p>Abstract</p> <p>Background</p> <p>A substantial prevalence of mild neurocognitive disorders has been reported in HIV, also in patients treated with combination antiretroviral therapy (cART). This includes a new disorder that has been termed <it>asymptomatic neurocognitive impairment </it>(ANI).</p> <p>Discussion</p> <p>ANI is identified by performance on formal neuropsychological testing that is at least 1 SD below the mean of normative scores in at least two cognitive domains out of at least five examined in patients without associated symptoms or evident functional impairment in daily living. While two tests are recommended to assess each domain, only one is required to fulfill this diagnostic criterion. Unfortunately, this definition necessitates that about 20% of the cognitively normal HIV-infected population is classified as suffering ANI. This liberal definition raises important ethical concerns and has as well diagnostic and therapeutic implications. Since neither its biological substrate, prognostic significance nor therapeutic implications are clearly established, we recommend that this diagnosis be modified or applied cautiously.</p> <p>Summary</p> <p>The diagnoses of less severe forms of neurocognitive disorders in HIV relies on the outcomes of neuropsychological testing, and a high proportion of HIV-infected patients with effective cART may be classified as neurocognitively abnormal using the current criteria. The definition of ANI is not stringent, and results in approximately 20% of the population being classified as abnormal. To us this seems an unacceptable false-positive rate.</p

    Asymptomatic neurocognitive disorders in patients infected by HIV: fact or fiction?

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    Neurocognitive disorders are emerging as a possible complication in patients infected with HIV. Even if asymptomatic, neurocognitive abnormalities are frequently detected using a battery of tests. This supported the creation of asymptomatic neurocognitive impairment (ANI) as a new entity. In a recent article published in BMC Infectious Diseases, Magnus Gisslén and colleagues applied a statistical approach, concluding that there is an overestimation of the actual problem. In fact, about 20% of patients are classified as neurocognitively impaired without a clear impact on daily activities. In the present commentary, we discuss the clinical implications of their findings. Although a cautious approach would indicate a stricter follow-up of patients affected by this disorder, it is premature to consider it as a proper disease. Based on a review of the data in the current literature we conclude that it is urgent to conduct more studies to estimate the overall risk of progression of the asymptomatic neurocognitive impairment. Moreover, it is important to understand whether new biomarkers or neuroimaging tools can help to identify better the most at risk population

    Pathogenesis of HIV in the Central Nervous System

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    HIV can infect the brain and impair central nervous system (CNS) function. Combination antiretroviral therapy (cART) has not eradicated CNS complications. HIV-associated neurocognitive disorders (HAND) remain common despite cART, although attenuated in severity. This may result from a combination of factors including inadequate treatment of HIV reservoirs such as circulating monocytes and glia, decreased effectiveness of cART in CNS, concurrent illnesses, stimulant use, and factors associated with prescribed drugs, including antiretrovirals. This review highlights recent investigations of HIV-related CNS injury with emphasis on cART-era neuropathological mechanisms in the context of both US and international settings

    Leukotrienes inhibit early stages of HIV-1 infection in monocyte-derived microglia-like cells

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    <p>Abstract</p> <p>Background</p> <p>Microglia are one of the main cell types to be productively infected by HIV-1 in the central nervous system (CNS). Leukotriene B<sub>4 </sub>(LTB<sub>4</sub>) and cysteinyl-leukotrienes such as LTC<sub>4 </sub>are some of the proinflammatory molecules produced in infected individuals that contribute to neuroinflammation. We therefore sought to investigate the role of leukotrienes (LTs) in HIV-1 infection of microglial cells.</p> <p>Methods</p> <p>To evaluate the role of LTs on HIV-1 infection in the CNS, monocyte-derived microglial-like cells (MDMis) were utilized in this study. Leukotriene-treated MDMis were infected with either fully replicative brain-derived HIV-1 isolates (YU2) or R5-tropic luciferase-encoding particles in order to assess viral production and expression. The efficacy of various steps of the replication cycle was evaluated by means of p24 quantification by ELISA, luciferase activity determination and quantitative real-time polymerase chain reaction (RT-PCR).</p> <p>Results</p> <p>We report in this study that virus replication is reduced upon treatment of MDMis with LTB<sub>4 </sub>and LTC<sub>4</sub>. Additional experiments indicate that these proinflammatory molecules alter the pH-independent entry and early post-fusion events of the viral life cycle. Indeed, LT treatment induced a diminution in integrated proviral DNA while reverse-transcribed viral products remained unaffected. Furthermore, decreased C-C chemokine receptor type 5 (CCR5) surface expression was observed in LT-treated MDMis. Finally, the effect of LTs on HIV-1 infection in MDMis appears to be mediated partly via a signal transduction pathway involving protein kinase C.</p> <p>Conclusions</p> <p>These data show for the first time that LTs influence microglial cell infection by HIV-1, and may be a factor in the control of viral load in the CNS.</p
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