243 research outputs found

    Introduction: an overview of the acquisition of reference

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    Language is a social tool that allows us to speak to others about the world. In doing so we need words that pick out those entities that we want to talk about. Linguistic expressions that identify such entities are known as referential or referring expressions, including proper names (Laura), natural kind terms (water, gold, tiger), indexicals (you, I, she), and definite descriptions (the dog, the smallest positive number). The mechanisms of reference have been the subject of intense speculation, and the debate over descriptive (Frege 1892/1948; Searle, 1958) vs. causal (Kripke, 1972/1980) or hybrid theories of reference (Evans, 1973) is still rife in the semantics literature (Genone & Lombrozo, 2012; Lam, 2010; Martí, 2014). Whatever the theoretical approach to reference, from a developmental perspective the three key questions are the following: What is the trajectory of language learners’ comprehension and production of referential expressions? To what extent, and in which contexts, do children abide by the same linguistic constraints as adults in their referential choices? How do cross-linguistic differences shape the process of referential choice acquisition

    Plant yourself where language blooms: Direct experience of nature changes how parents and children talk about nature.

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    The current study investigated the affordances of direct and indirect experience of nature on parent-child talk. Parents and children produced a wider range of nature words when exploring a park (direct experience) than when exploring a thematically matched indoor visitor center (indirect experience). Parents and children also produced more plant-related nature word types when exploring the park compared to the visitor center. Findings suggest that direct experience of nature increases the diversity and specificity of parent-child talk about nature, and mitigates the phenomenon of “plant blindness” (cf. Wandersee & Schussler, 1999). Direct experience of nature provides an optimal context for children to learn the language of nature and consequently to cultivate children's status as custodians of the natural world

    SARS-CoV-2 and Guillain-Barré syndrome: AIDP variant with a favourable outcome.

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    The spectrum of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 infection (SARS-CoV-2), includes different neurologic manifestations of the central and peripheral nervous system. From March through April 2020, in two university hospitals located in western Switzerland, we examined three patients with Guillain-Barré syndrome (GBS) following SARS-CoV-2. These cases were characterized by a primary demyelinating electrophysiological pattern (Acute inflammatory demyelinating polyneuropathy or AIDP) and a less severe disease course compared to recently published case series. Clinical improvement was observed in all patients at week five. One patient was discharged from hospital after full recovery with persistence of minor neurological signs (areflexia). Two of the three patients remained hospitalized: one was able to walk and the other could stand up with assistance. We report three cases of typical GBS (AIDP) occurring after SARS-CoV-2 infection and presenting with a favourable clinical course. Given the interval between COVID-19-related symptoms and neurological manifestations (mean of 15 days) we postulate a secondary immune-mediated mechanism rather than direct viral damage

    Exogenous LRRK2G2019S induces parkinsonian-like pathology in a nonhuman primate

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    Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease among the elderly. To understand pathogenesis and to test therapies, animal models that faithfully reproduce key pathological PD hallmarks are needed. As a prelude to developing a model of PD, we tested the tropism, efficacy, biodistribution, and transcriptional impact of canine adenovirus type 2 (CAV-2) vectors in the brain of Microcebus murinus, a nonhuman primate that naturally develops neurodegenerative lesions. We show that introducing helper-dependent (HD) CAV-2 vectors results in long-term, neuron-specific expression at the injection site and in afferent nuclei. Although HD CAV-2 vector injection induced a modest transcriptional response, no significant adaptive immune response was generated. We then generated and tested HD CAV-2 vectors expressing LRRK2 (leucine-rich repeat kinase 2) and LRRK2 carrying a G2019S mutation (LRRK2G2019S), which is linked to sporadic and familial autosomal dominant forms of PD. We show that HD-LRRK2G2019S expression induced parkinsonian-like motor symptoms and histological features in less than 4 months

    Acute TNFα levels predict cognitive impairment 6-9 months after COVID-19 infection.

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    A neurocognitive phenotype of post-COVID-19 infection has recently been described that is characterized by a lack of awareness of memory impairment (i.e., anosognosia), altered functional connectivity in the brain's default mode and limbic networks, and an elevated monocyte count. However, the relationship between these cognitive and brain functional connectivity alterations in the chronic phase with the level of cytokines during the acute phase has yet to be identified. Determine whether acute cytokine type and levels is associated with anosognosia and functional patterns of brain connectivity 6-9 months after infection. We analyzed the predictive value of the concentration of acute cytokines (IL-1RA, IL-1β, IL-6, IL-8, IFNγ, G-CSF, GM-CSF) (cytokine panel by multiplex immunoassay) in the plasma of 39 patients (mean age 59 yrs, 38-78) in relation to their anosognosia scores for memory deficits via stepwise linear regression. Then, associations between the different cytokines and brain functional connectivity patterns were analyzed by MRI and multivariate partial least squares correlations for the whole group. Stepwise regression modeling allowed us to show that acute TNFα levels predicted (R <sup>2</sup> = 0.145; β = -0.38; p = .017) and were associated (r = -0.587; p < .001) with scores of anosognosia for memory deficits observed 6-9 months post-infection. Finally, high TNFα levels were associated with hippocampal, temporal pole, accumbens nucleus, amygdala, and cerebellum connectivity. Increased plasma TNFα levels in the acute phase of COVID-19 predict the presence of long-term anosognosia scores and changes in limbic system functional connectivity

    A new phenotype of mitochondrial disease characterized by familial late-onset predominant axial myopathy and encephalopathy

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    Axial myopathy is a rare neuromuscular disease that is characterized by paraspinal muscle atrophy and abnormal posture, most notably camptocormia (also known as bent spine). The genetic cause of familial axial myopathy is unknown. Described here are the clinical features and cause of late-onset predominant axial myopathy and encephalopathy. A 73-year-old woman presented with a 10-year history of severe paraspinal muscle atrophy and cerebellar ataxia. Her 84-year-old sister also developed late-onset paraspinal muscle atrophy and generalized seizures with encephalopathy. Computed tomography showed severe atrophy and fatty degeneration of their paraspinal muscles. Their mother and maternal aunt also developed bent spines. The existence of many ragged-red fibers and cytochrome c oxidase-negative fibers in the biceps brachii muscle of the proband indicated a mitochondrial abnormality. No significant abnormalities were observed in the respiratory chain enzyme activities; however, the activities of complexes I and IV were relatively low compared with the activities of other complexes. Sequence analysis of the mitochondrial DNA from the muscle revealed a novel heteroplasmic mutation (m.602C>T) in the mitochondrial tRNAPhe gene. This familial case of late-onset predominant axial myopathy and encephalopathy may represent a new clinical phenotype of a mitochondrial disease
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