"Triggered switching" is the theory that code-switching happens more often with words connected to both languages, such as cognates. Corpus analyses have supported this theory; however, they do not allow testing for directional causality. Here, we test the triggering hypothesis through a picture-naming task, and examine whether cognates trigger code-switches, as well as more subtle interference effects resulting in disfluencies. Forty English-Spanish bilinguals completed a picture-cued sentence production task in three conditions: English-only, Spanish-only, and mixed. Half of the pictures represented Spanish-English cognates. Unsurprisingly, participants were more likely to code-switch when asked to use both their languages compared to only their dominant or non-dominant language. However, participants were not more likely to switch languages for cognate than for non-cognate trials. Participants tended to be more fluent on cognate trials in the dominant and the non-dominant condition, and on non-cognate trials in the mixed-language condition, although these effects were not significant. These findings suggest that both language context and cognate status are important to consider when testing both overt switches and disfluencies in bilingual speech production.
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http://dx.doi.org/10.3390/languages7040264 | DOI Listing |
It is hypothesised that peripheral immune states responding to regional environmental triggers contribute to central neurodegeneration. Region-specific genetic selection pressures require this hypothesis to be assessed in an ancestry specific manner. Here we utilise genome-wide association studies and expression quantitative trait loci from African, East Asian and European ancestries to show that genes causing neurodegeneration are preferentially expressed in innate rather than adaptive immune cells, and that expression of these genes mediates the risk of neurodegenerative disease in monocytes in an ancestry-specific manner.
View Article and Find Full Text PDFJ Orthop
July 2025
Department of Surgery and Perioperative Care, Dell Medical School-The University of Texas at Austin, Austin, TX, USA.
Background: The pathophysiology of enthesopathy and tendinopathy is mucoid degeneration, which includes chondroid metaplasia. The chondroid metaplasia can be associated with calcification. Inflammation is typically absent unless calcification triggers a self-limited immune response representing acute calcific tendinitis.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Biophysics, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Neurotransmitter release is triggered in microseconds by Ca-binding to the Synaptotagmin-1 C-domains and by SNARE complexes that form four-helix bundles between synaptic vesicles and plasma membranes, but the coupling mechanism between Ca-sensing and membrane fusion is unknown. Release requires extension of SNARE helices into juxtamembrane linkers that precede transmembrane regions (linker zippering) and binding of the Synaptotagmin-1 CB domain to SNARE complexes through a "primary interface" comprising two regions (I and II). The Synaptotagmin-1 Ca-binding loops were believed to accelerate membrane fusion by inducing membrane curvature, perturbing lipid bilayers, or helping bridge the membranes, but SNARE complex binding through the primary interface orients the Ca-binding loops away from the fusion site, hindering these putative activities.
View Article and Find Full Text PDFFEBS J
January 2025
Department of Pharmacology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany.
Creatine is essential for ATP regeneration in energy-demanding cells. Creatine deficiency results in severe neurodevelopmental impairments. In the brain, creatine is synthesized locally by oligodendrocytes to supply neighboring neurons.
View Article and Find Full Text PDFBiochim Biophys Acta Biomembr
January 2025
Department of Molecular Pathobiology, New York University, New York, NY, USA. Electronic address:
Inorganic polyphosphate (polyP) is a polymer that consists of a series of orthophosphates connected by high-energy phosphoanhydride bonds, like those found in ATP. In mammalian mitochondria, polyP has been linked to the activation of the mitochondrial permeability transition pore (mPTP). However, the details of this process are not completely understood.
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