49 research outputs found

    Response Bias Modulates the Speech Motor System during Syllable Discrimination

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    Recent evidence suggests that the speech motor system may play a significant role in speech perception. Repetitive transcranial magnetic stimulation (TMS) applied to a speech region of premotor cortex impaired syllable identification, while stimulation of motor areas for different articulators selectively facilitated identification of phonemes relying on those articulators. However, in these experiments performance was not corrected for response bias. It is not currently known how response bias modulates activity in these networks. The present functional magnetic resonance imaging experiment was designed to produce specific, measureable changes in response bias in a speech perception task. Minimal consonant-vowel stimulus pairs were presented between volume acquisitions for same-different discrimination. Speech stimuli were embedded in Gaussian noise at the psychophysically determined threshold level. We manipulated bias by changing the ratio of same-to-different trials: 1:3, 1:2, 1:1, 2:1, 3:1. Ratios were blocked by run and subjects were cued to the upcoming ratio at the beginning of each run. The stimuli were physically identical across runs. Response bias (criterion, C) was measured in individual subjects for each ratio condition. Group mean bias varied in the expected direction. We predicted that activation in frontal but not temporal brain regions would co-vary with bias. Group-level regression of bias scores on percent signal change revealed a fronto-parietal network of motor and sensory-motor brain regions that were sensitive to changes in response bias. We identified several pre- and post-central clusters in the left hemisphere that overlap well with TMS targets from the aforementioned studies. Importantly, activity in these regions covaried with response bias even while the perceptual targets remained constant. Thus, previous results suggesting that speech motor cortex participates directly in the perceptual analysis of speech should be called into question

    FORUM:Remote testing for psychological and physiological acoustics

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    Acoustics research involving human participants typically takes place in specialized laboratory settings. Listening studies, for example, may present controlled sounds using calibrated transducers in sound-attenuating or anechoic chambers. In contrast, remote testing takes place outside of the laboratory in everyday settings (e.g., participants' homes). Remote testing could provide greater access to participants, larger sample sizes, and opportunities to characterize performance in typical listening environments at the cost of reduced control of environmental conditions, less precise calibration, and inconsistency in attentional state and/or response behaviors from relatively smaller sample sizes and unintuitive experimental tasks. The Acoustical Society of America Technical Committee on Psychological and Physiological Acoustics launched the Task Force on Remote Testing (https://tcppasa.org/remotetesting/) in May 2020 with goals of surveying approaches and platforms available to support remote testing and identifying challenges and considerations for prospective investigators. The results of this task force survey were made available online in the form of a set of Wiki pages and summarized in this report. This report outlines the state-of-the-art of remote testing in auditory-related research as of August 2021, which is based on the Wiki and a literature search of papers published in this area since 2020, and provides three case studies to demonstrate feasibility during practice

    A tyrosine-rich amelogenin peptide promotes neovasculogenesis in vitro and ex vivo

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    H.D.A. is grateful for the financial support provided by a Dorothy Hodgkin Postgraduate Award (jointly funded by the Engineering and Physical Sciences Research Council, UK and the Institut Straumann, Switzerland) and the Research Discretionary Funds of the Periodontology Unit, UCL Eastman Dental Institute. Financial support was also provided by the NIHR Comprehensive Biomedical Research Centre, UK and the WCU Program of the National Research Foundation of Korea (NRF), funded by the Ministry of Education, Science and Technology, South Korea (No. R31-10069)

    A Dedicated Promoter Drives Constitutive Expression of the Cell-Autonomous Immune Resistance GTPase, Irga6 (IIGP1) in Mouse Liver

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    Background: In general, immune effector molecules are induced by infection. Methodology and Principal Findings: However, strong constitutive expression of the cell-autonomous resistance GTPase, Irga6 (IIGP1), was found in mouse liver, contrasting with previous evidence that expression of this protein is exclusively dependent on induction by IFNc. Constitutive and IFNc-inducible expression of Irga6 in the liver were shown to be dependent on transcription initiated from two independent untranslated 59 exons, which splice alternatively into the long exon encoding the full-length protein sequence. Irga6 is expressed constitutively in freshly isolated hepatocytes and is competent in these cells to accumulate on the parasitophorous vacuole membrane of infecting Toxoplasma gondii tachyzoites. Conclusions and Significance: The role of constitutive hepatocyte expression of Irga6 in resistance to parasites invading from the gut via the hepatic portal system is discussed

    Loss of the interferon-γ-inducible regulatory immunity-related GTPase (IRG), Irgm1, causes activation of effector IRG proteins on lysosomes, damaging lysosomal function and predicting the dramatic susceptibility of Irgm1-deficient mice to infection

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    The interferon-γ (IFN-γ)-inducible immunity-related GTPase (IRG), Irgm1, plays an essential role in restraining activation of the IRG pathogen resistance system. However, the loss of Irgm1 in mice also causes a dramatic but unexplained susceptibility phenotype upon infection with a variety of pathogens, including many not normally controlled by the IRG system. This phenotype is associated with lymphopenia, hemopoietic collapse, and death of the mouse.Deutscher Akademischer Austausch Dienst (DAAD); International Graduate School in Development Health and Disease (IGS-DHD); Deutsche For-schungsgemeinschaft (SFBs 635, 670, 680); Max-Planck-Gesellschaft (Max Planck Fellowship)

    High-level Gpr56 expression is dispensable for the maintenance and function of hematopoietic stem and progenitor cells in mice

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    AbstractBlood formation by hematopoietic stem cells (HSCs) is regulated by a still incompletely defined network of general and HSC-specific regulators. In this study, we analyzed the role of G-protein coupled receptor 56 (Gpr56) as a candidate HSC regulator based on its differential expression in quiescent relative to proliferating HSCs and its common targeting by core HSC regulators. Detailed expression analysis revealed that Gpr56 is abundantly expressed by HSPCs during definitive hematopoiesis in the embryo and in the adult bone marrow, but its levels are reduced substantially as HSPCs differentiate. However, despite enriched expression in HSPCs, Gpr56-deficiency did not impair HSPC maintenance or function during steady-state or myeloablative stress-induced hematopoiesis. Gpr56-deficient HSCs also responded normally to physiological and pharmacological mobilization signals, despite the reported role of this GPCR as a regulator of cell adhesion and migration in neuronal cells. Moreover, Gpr56-deficient bone marrow engrafted with equivalent efficiency as wild-type HSCs in primary recipients; however, their reconstituting ability was reduced when subjected to serial transplantation. These data indicate that although GPR56 is abundantly and selectively expressed by primitive HSPCs, its high level expression is largely dispensable for steady-state and regenerative hematopoiesis

    Materials and data for: The Role of Multisensory Temporal Covariation in Audiovisual Speech Recognition in Noise

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    Materials and data for Experiments 1 and 2 in "The Role of Multisensory Temporal Covariation in Audiovisual Speech Recognition in Noise.
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