201 research outputs found

    Sub-kelvin temperature management in ion traps for optical clocks

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    The uncertainty of the ac Stark shift due to thermal radiation represents a major contribution to the systematic uncertainty budget of state-of-the-art optical atomic clocks. In the case of optical clocks based on trapped ions, the thermal behavior of the rf-driven ion trap must be precisely known. This determination is even more difficult when scalable linear ion traps are used. Such traps enable a more advanced control of multiple ions and have become a platform for new applications in quantum metrology, simulation and computation. Nevertheless, their complex structure makes it more difficult to precisely determine its temperature in operation and thus the related systematic uncertainty. We present here scalable linear ion traps for optical clocks, which exhibit very low temperature rise under operation. We use a finite-element model refined with experimental measurements to determine the thermal distribution in the ion trap and the temperature at the position of the ions. The trap temperature is investigated at different rf-drive frequencies and amplitudes with an infrared camera and integrated temperature sensors. We show that for typical trapping parameters for In+\mathrm{In}^{+}, Al+\mathrm{Al}^{+}, Lu+\mathrm{Lu}^{+}, Ca+\mathrm{Ca}^{+}, Sr+\mathrm{Sr}^{+} or Yb+\mathrm{Yb}^{+} ions, the temperature rise at the position of the ions resulting from rf heating of the trap stays below 700 mK and can be controlled with an uncertainty on the order of a few 100 mK maximum.Comment: 18 page

    The Effect of Perioperative Auditory Stimulation with Music on Procedural Pain: A Narrative Review.

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    PURPOSE OF REVIEW Music therapy has seen increasing applications in various medical fields over the last decades. In the vast range of possibilities through which music can relieve suffering, there is a risk that-given its efficacy-the physiological underpinnings are too little understood. This review provides evidence-based neurobiological concepts for the use of music in perioperative pain management. RECENT FINDINGS The current neuroscientific literature shows a significant convergence of the pain matrix and neuronal networks of pleasure triggered by music. These functions seem to antagonize each other and can thus be brought to fruition in pain therapy. The encouraging results of fMRI and EEG studies still await full translation of this top-down modulating mechanism into broad clinical practice. We embed the current clinical literature in a neurobiological framework. This involves touching on Bayesian "predictive coding" pain theories in broad strokes and outlining functional units in the nociception and pain matrix. These will help to understand clinical findings in the literature summarized in the second part of the review. There are opportunities for perioperative practitioners, including anesthesiologists treating acute pain and anxiety in emergency and perioperative situations, where music could help bring relieve to patients

    Analgesia for the Bayesian Brain: How Predictive Coding Offers Insights Into the Subjectivity of Pain.

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    PURPOSE OF REVIEW In order to better treat pain, we must understand its architecture and pathways. Many modulatory approaches of pain management strategies are only poorly understood. This review aims to provide a theoretical framework of pain perception and modulation in order to assist in clinical understanding and research of analgesia and anesthesia. RECENT FINDINGS Limitations of traditional models for pain have driven the application of new data analysis models. The Bayesian principle of predictive coding has found increasing application in neuroscientific research, providing a promising theoretical background for the principles of consciousness and perception. It can be applied to the subjective perception of pain. Pain perception can be viewed as a continuous hierarchical process of bottom-up sensory inputs colliding with top-down modulations and prior experiences, involving multiple cortical and subcortical hubs of the pain matrix. Predictive coding provides a mathematical model for this interplay

    Caveolin-1 protects B6129 mice against Helicobacter pylori gastritis.

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    Caveolin-1 (Cav1) is a scaffold protein and pathogen receptor in the mucosa of the gastrointestinal tract. Chronic infection of gastric epithelial cells by Helicobacter pylori (H. pylori) is a major risk factor for human gastric cancer (GC) where Cav1 is frequently down-regulated. However, the function of Cav1 in H. pylori infection and pathogenesis of GC remained unknown. We show here that Cav1-deficient mice, infected for 11 months with the CagA-delivery deficient H. pylori strain SS1, developed more severe gastritis and tissue damage, including loss of parietal cells and foveolar hyperplasia, and displayed lower colonisation of the gastric mucosa than wild-type B6129 littermates. Cav1-null mice showed enhanced infiltration of macrophages and B-cells and secretion of chemokines (RANTES) but had reduced levels of CD25+ regulatory T-cells. Cav1-deficient human GC cells (AGS), infected with the CagA-delivery proficient H. pylori strain G27, were more sensitive to CagA-related cytoskeletal stress morphologies ("humming bird") compared to AGS cells stably transfected with Cav1 (AGS/Cav1). Infection of AGS/Cav1 cells triggered the recruitment of p120 RhoGTPase-activating protein/deleted in liver cancer-1 (p120RhoGAP/DLC1) to Cav1 and counteracted CagA-induced cytoskeletal rearrangements. In human GC cell lines (MKN45, N87) and mouse stomach tissue, H. pylori down-regulated endogenous expression of Cav1 independently of CagA. Mechanistically, H. pylori activated sterol-responsive element-binding protein-1 (SREBP1) to repress transcription of the human Cav1 gene from sterol-responsive elements (SREs) in the proximal Cav1 promoter. These data suggested a protective role of Cav1 against H. pylori-induced inflammation and tissue damage. We propose that H. pylori exploits down-regulation of Cav1 to subvert the host's immune response and to promote signalling of its virulence factors in host cells
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