Detecting Eating Episodes with an Ear-mounted Sensor

In this paper, we propose Auracle, a wearable earpiece that can automatically recognize eating behavior. More specifically, in free-living conditions, we can recognize when and for how long a person is eating. Using an off-the-shelf contact microphone placed behind the ear, Auracle captures the sound of a person chewing as it passes through the bone and tissue of the head. This audio data is then processed by a custom analog/digital circuit board. To ensure reliable (yet comfortable) contact between microphone and skin, all hardware components are incorporated into a 3D-printed behind-the-head framework. We collected field data with 14 participants for 32 hours in free-living conditions and additional eating data with 10 participants for 2 hours in a laboratory setting. We achieved accuracy exceeding 92.8% and F1 score exceeding 77.5% for eating detection. Moreover, Auracle successfully detected 20-24 eating episodes (depending on the metrics) out of 26 in free-living conditions. We demonstrate that our custom device could sense, process, and classify audio data in real time. Additionally, we estimateAuracle can last 28.1 hours with a 110 mAh battery while communicating its observations of eating behavior to a smartphone over Bluetooth

An objective validation of polyp and instrument segmentation methods in colonoscopy through Medico 2020 polyp segmentation and MedAI 2021 transparency challenges

Automatic analysis of colonoscopy images has been an active field of research motivated by the importance of early detection of precancerous polyps. However, detecting polyps during the live examination can be challenging due to various factors such as variation of skills and experience among the endoscopists, lack of attentiveness, and fatigue leading to a high polyp miss-rate. Deep learning has emerged as a promising solution to this challenge as it can assist endoscopists in detecting and classifying overlooked polyps and abnormalities in real time. In addition to the algorithm's accuracy, transparency and interpretability are crucial to explaining the whys and hows of the algorithm's prediction. Further, most algorithms are developed in private data, closed source, or proprietary software, and methods lack reproducibility. Therefore, to promote the development of efficient and transparent methods, we have organized the "Medico automatic polyp segmentation (Medico 2020)" and "MedAI: Transparency in Medical Image Segmentation (MedAI 2021)" competitions. We present a comprehensive summary and analyze each contribution, highlight the strength of the best-performing methods, and discuss the possibility of clinical translations of such methods into the clinic. For the transparency task, a multi-disciplinary team, including expert gastroenterologists, accessed each submission and evaluated the team based on open-source practices, failure case analysis, ablation studies, usability and understandability of evaluations to gain a deeper understanding of the models' credibility for clinical deployment. Through the comprehensive analysis of the challenge, we not only highlight the advancements in polyp and surgical instrument segmentation but also encourage qualitative evaluation for building more transparent and understandable AI-based colonoscopy systems

Disease-Associated Mutations That Alter the RNA Structural Ensemble

Genome-wide association studies (GWAS) often identify disease-associated mutations in intergenic and non-coding regions of the genome. Given the high percentage of the human genome that is transcribed, we postulate that for some observed associations the disease phenotype is caused by a structural rearrangement in a regulatory region of the RNA transcript. To identify such mutations, we have performed a genome-wide analysis of all known disease-associated Single Nucleotide Polymorphisms (SNPs) from the Human Gene Mutation Database (HGMD) that map to the untranslated regions (UTRs) of a gene. Rather than using minimum free energy approaches (e.g. mFold), we use a partition function calculation that takes into consideration the ensemble of possible RNA conformations for a given sequence. We identified in the human genome disease-associated SNPs that significantly alter the global conformation of the UTR to which they map. For six disease-states (Hyperferritinemia Cataract Syndrome, β-Thalassemia, Cartilage-Hair Hypoplasia, Retinoblastoma, Chronic Obstructive Pulmonary Disease (COPD), and Hypertension), we identified multiple SNPs in UTRs that alter the mRNA structural ensemble of the associated genes. Using a Boltzmann sampling procedure for sub-optimal RNA structures, we are able to characterize and visualize the nature of the conformational changes induced by the disease-associated mutations in the structural ensemble. We observe in several cases (specifically the 5′ UTRs of FTL and RB1) SNP–induced conformational changes analogous to those observed in bacterial regulatory Riboswitches when specific ligands bind. We propose that the UTR and SNP combinations we identify constitute a “RiboSNitch,” that is a regulatory RNA in which a specific SNP has a structural consequence that results in a disease phenotype. Our SNPfold algorithm can help identify RiboSNitches by leveraging GWAS data and an analysis of the mRNA structural ensemble

Search for the doubly heavy baryon Ξbc+\it{\Xi}_{bc}^{+} decaying to J/ψΞc+J/\it{\psi} \it{\Xi}_{c}^{+}

A first search for the $\it{\Xi}_{bc}^{+}\to J/\it{\psi}\it{\Xi}_{c}^{+}$ decay is performed by the LHCb experiment with a data sample of proton-proton collisions, corresponding to an integrated luminosity of $9\,\mathrm{fb}^{-1}$ recorded at centre-of-mass energies of 7, 8, and $13\mathrm{\,Te\kern -0.1em V}$. Two peaking structures are seen with a local (global) significance of $4.3\,(2.8)$ and $4.1\,(2.4)$ standard deviations at masses of $6571\,\mathrm{Me\kern -0.1em V\!/}c^2$ and $6694\,\mathrm{Me\kern -0.1em V\!/}c^2$, respectively. Upper limits are set on the $\it{\Xi}_{bc}^{+}$ baryon production cross-section times the branching fraction relative to that of the $B_{c}^{+}\to J/\it{\psi} D_{s}^{+}$ decay at centre-of-mass energies of 8 and $13\mathrm{\,Te\kern -0.1em V}$, in the $\it{\Xi}_{bc}^{+}$ and in the $B_{c}^{+}$ rapidity and transverse-momentum ranges from 2.0 to 4.5 and 0 to $20\,\mathrm{Ge\kern -0.1em V\!/}c$, respectively. Upper limits are presented as a function of the $\it{\Xi}_{bc}^{+}$ mass and lifetime.Comment: All figures and tables, along with machine-readable versions and any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-005.html (LHCb public pages

Passacaglia, violin, viola, G minor

score and parts. 32 cm

The pro to toxin LYPD6B modulates heteromeric a3β4‐containing nicotinic acetylcholine receptors, but not α7 homomers

Prototoxins are a diverse family of membrane-tethered molecules expressed in the nervous system that modulate nicotinic cholinergic signaling, but their functions and specificity have yet to be completely explored. We tested the selectivity and efficacy of leukocyte antigen, PLAUR (plasminogen activator, urokinase receptor) domain-containing (LYPD)-6B on α3β4-, α3α5β4-, and α7-containing nicotinic acetylcholine receptors (nAChRs). To constrain stoichiometry, fusion proteins encoding concatemers of human α3, β4, and α5 (D and N variants) subunits were expressed in Xenopus laevis oocytes and tested with or without LYPD6B. We used the 2-electrode voltage-clamp method to quantify responses to acetylcholine (ACh): agonist sensitivity (EC(50)), maximal agonist-induced current (I(max)), and time constant (τ) of desensitization. For β4–α3–α3–β4–α3 and β4–α3–β4–α3–α3, LYPD6B decreased EC(50) from 631 to 79 μM, reduced I(max) by at least 59%, and decreased τ. For β4–α3–α5D–β4–α3 and β4–α3–β4–α–α5D, LYPD6B decreased I(max) by 63 and 32%, respectively. Thus, LYPD6B acted only on (α3)(3)(β4)(2) and (α3)(2)(α5D)(β4)(2) and did not affect the properties of (α3)(2)(β4)(3), α7, or (α3)(2)(α5N)(β4)(2) nAChRs. Therefore, LYPD6B acts as a mixed modulator that enhances the sensitivity of (α3)(3)(β4)(2) nAChRs to ACh while reducing ACh-induced whole-cell currents. LYPD6B also negatively modulates α3β4 nAChRs that include the α5D common human variant, but not the N variant associated with nicotine dependence.—Ochoa, V., George, A. A., Nishi, R., Whiteaker, P. The prototoxin LYPD6B modulates heteromeric α3β4-containing nicotinic acetylcholine receptors, but not α7 homomers