9 research outputs found

    A Mixed Reality Approach for dealing with the Video Fatigue of Online Meetings

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    Much of the issue with video meetings is the lack of naturalistic cues, together with the feeling of being observed all the time. Video calls take away most body language cues, but because the person is still visible, your brain still tries to compute that non-verbal language. It means that you’re working harder, trying to achieve the impossible. This impacts data retention and can lead to participants feeling unnecessarily tired. This project aims to transform the way online meetings happen, by turning off the camera and simplifying the information that our brains need to compute, thus preventing ‘Zoom fatigue’. The immersive solution we are developing, iVXR, consists of cutting-edge augmented reality technology, natural language processing, speech to text technologies and sub-real-time hardware acceleration using high performance computing

    The Glucose Transporter 2 regulates CD8+ T cell function via environment sensing

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    T cell activation is associated with a profound and rapid metabolic response to meet increased energy demands for cell division, differentiation and development of effector function. Glucose uptake and engagement of the glycolytic pathway are major checkpoints for this event. Here we show that the low-affinity, concentration-dependent glucose transporter 2 (Glut2) regulates the development of CD8+ T cell effector responses in mice by promoting glucose uptake, glycolysis and glucose storage. Expression of Glut2 is modulated by environmental factors including glucose and oxygen availability and extracellular acidification. Glut2 is highly expressed by circulating, recently primed T cells, allowing efficient glucose uptake and storage. In glucose-deprived inflammatory environments, Glut2 becomes downregulated, thus preventing passive loss of intracellular glucose. Mechanistically, Glut2 expression is regulated by a combination of molecular interactions involving hypoxia-inducible factor-1 alpha, galectin-9 and stomatin. Finally, we show that human T cells also rely on this glucose transporter, thus providing a potential target for therapeutic immunomodulation

    An Extended Reality Solution for Mitigating the Video Fatigue of Online Meetings

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    Much of the issue with video meetings is the lack of naturalistic cues, together with the feeling of being observed all the time. Video calls take away most body language cues, but because the person is still visible, the brain still tries to compute that non-verbal language. It means that participants are working harder, trying to achieve the impossible. This impacts data retention and can lead to participants feeling unnecessarily tired. The solution presented in this chapter aims to transform the way online meetings happen, by turning off the camera and simplifying the information that our brains need to compute, thus preventing video fatigue. The immersive solution developed, iVXR, consists of cutting-edge augmented reality technology, natural language processing, speech-to-text technologies, and sub-real-time hardware acceleration using high-performance computing

    Investigating the reactive sites and the anomalously large changes in surface pKa values of chemically modified carbon nanotubes of different morphologies

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    Bamboo-like multiwalled (b-MWCNT), hollow-tube multiwalled (h-MWCNT) and single-walled C nanotubes (SWCNT), chem. modified with 1-anthraquinonyl (AQ) or 4-nitrophenyl (NP) groups, are characterized using voltammetric, electron microscopic and Raman spectroscopic techniques. The pKa values of the AQ-modified CNTs are shifted by >3 units when compared to the pKa values of anthrahydroquinone (AHQ, the reduced form of AQ) in aq. soln. to beyond pH 14. These large changes in the surface pKa values of the modified CNTs are explored further by comparing the pKa values of CNTs modified with an anthraquinonyl-2-carboxylic acid group. These groups are attached to the CNT surface via the formation of an amide bond with an aminophenyl spacer unit derived from the chem. redn. of NP modified CNTs. The location of reactive sites on the CNT surface is studied and their influence on the pKa of the modified materials is discussed. Comparison with modified pyrolytic graphite electrodes exposing pure edge-plane or pure basal-plane crystal faces indicates that the modifying aryl groups are predominantly located on edge-plane like defects at the tube ends of MWCNTs. The effect of polymer formation on electron transfer kinetics of b-MWCNTs and h-MWCNTs is also discussed. In contrast SWCNTs show both significant side-wall functionalization and fast electron transfer kinetics which is attributed to their different electronic structure. [on SciFinder(R)

    Loss of voltage-gated hydrogen channel 1 expression reveals heterogeneous metabolic adaptation to intracellular acidification by T cells

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    Voltage-gated hydrogen channel 1 (Hvcn1) is a voltage-gated proton channel, which reduces cytosol acidification and facilitates the production of ROS. The increased expression of this channel in some cancers has led to proposing Hvcn1 antagonists as potential therapeutics. While its role in most leukocytes has been studied in depth, the function of Hvcn1 in T cells remains poorly defined. We show that Hvcn1 plays a nonredundant role in protecting naive T cells from intracellular acidification during priming. Despite sharing overall functional impairment in vivo and in vitro, Hvcn1-deficient CD4(+) and CD8(+) T cells display profound differences during the transition from naive to primed T cells, including in the preservation of T cell receptor (TCR) signaling, cellular division, and death. These selective features result, at least in part, from a substantially different metabolic response to intracellular acidification associated with priming. While Hvcn1-deficient naive CD4(+) T cells reprogram to rescue the glycolytic pathway, naive CD8(+) T cells, which express high levels of this channel in the mitochondria, respond by metabolically compensating mitochondrial dysfunction, at least in part via AMPK activation. These observations imply heterogeneity between adaptation of naive CD4(+) and CD8(+) T cells to intracellular acidification during activation
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