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Generation driven understanding of localized 3D scenes with 3D diffusion model
Author Correction: Deep reinforcement learning for active flow control in a turbulent separation bubble
Predicting outcomes following open abdominal aortic aneurysm repair using machine learning
Photoactuating artificial muscle from supramolecular assembly of an overcrowded alkene-derived molecular switch
Abstract The amplification of molecular motion along length scales for macroscopic muscle-like functions, based on supramolecular polymers, provides attractive opportunities ranging from soft actuators to responsive biomedical materials. Taking the challenge to reveal dynamic assembly parameters governing muscle functions, we present the design of a photoswitch amphiphile based on an overcrowded alkene-derived core, and developed supramolecular artificial muscles. Going from molecular motor amphiphile (MA) to switch amphiphile (SA), taking advantage of high thermal stability of the switch core, a self-recovering of bent SA artificial muscle is observed in post-photoactuation without external intervention. Eliminating molecular motions in SA artificial muscle during the post-photoactuation and aging process enables us to identify correlations between dynamic assembly transformations and macroscopic actuating functions. These findings provide insights into photoactuation and subsequent self-recovery mechanisms from the aspect of dynamic assembly process, which offers new opportunities for developing amphiphile-based supramolecular artificial muscles.
TCAINet an RGB T salient object detection model with cross modal fusion and adaptive decoding
TRIM52 maintains cellular fitness and is under tight proteolytic control by multiple giant E3 ligases
Abstract Tripartite motif 52 (TRIM52) exhibits strong positive selection in humans, yet is lost in many other mammals. In contrast to what one would expect for such a non-conserved factor, TRIM52 loss compromises cell fitness. We set out to determine the cellular function of TRIM52. Genetic and proteomic analyses revealed TRIM52 physically and functionally interacts with the DNA repair machinery. Our data suggest that TRIM52 limits topoisomerase 2 adducts, thereby preventing cell-cycle arrest. Consistent with a fitness-promoting function, TRIM52 is upregulated in various cancers, prompting us to investigate its regulatory pathways. We found TRIM52 to be targeted for ultra-rapid proteasomal degradation by the giant E3 ubiquitin ligases BIRC6, HUWE1, and UBR4/KCMF1. BIRC6 mono-ubiquitinates TRIM52, with subsequent extension by UBR4/KCMF1. These findings suggest a role for TRIM52 in maintaining genome integrity, and regulation of its own abundance through multi-ligase degradation.
An intelligent federated learning boosted cyberattack detection system for Denial-Of-Wallet attack using advanced heuristic search with multimodal approaches
Coherent energy transfer in coupled nonlinear microelectromechanical resonators
Chemogenetic inhibition of prefrontal cortex inputs to dorsal raphe reduces anxiety behaviors in male rat model of fetal alcohol spectrum disorder
Combined dynamical-deep learning ENSO forecasts
Comparing neural responses to cutaneous heat and pressure pain in healthy participants
Abstract Even though acute pain comes in many different shapes and forms, a lot of experimental pain studies predominantly employ cutaneous heat pain. This makes a comparison between different pain types and the link between findings from these experimental studies to clinical pain difficult. To bridge this gap, we investigated both cuff pressure pain and cutaneous heat pain using a within-subject design in combination with functional magnetic resonance imaging (fMRI). Noxious stimuli were applied with a 17-s duration at three different intensities above the pain threshold using a thermode and a computer-controlled cuff pressure device. Both pain modalities led to contralateral activation in the anterior insula and parietal operculum. Heat pain showed greater activation in the precentral gyrus, pontine reticular nucleus, and dorsal posterior insula, whilst pressure pain showed greater activation in the primary somatosensory cortex and bilateral superior parietal lobules. Most importantly, the time course of the fMRI signal changes differed between modalities, with pressure pain peaking in the first stimulus half, whereas heat pain led to a prolonged and increasing response across the stimulus duration with a peak in the second stimulus half. Our findings suggest that pressure and heat pain lead to common as well as different (temporal) activation patterns in key pain processing regions.
Thick-panel origami structures forming seamless surfaces
Innovative approach for experimental investigation and monitoring and warning of the evolutionary patterns of dam body failure in earth dams
Coxiella burnetii manipulates the lysosomal protease cathepsin B to facilitate intracellular success
Abstract The obligate intracellular bacterium Coxiella burnetii establishes an intracellular replicative niche termed the Coxiella-containing vacuole (CCV), which has been characterised as a bacterially modified phagolysosome. How C. burnetii withstands the acidic and degradative properties of this compartment is not well understood. We demonstrate that the key lysosomal protease cathepsin B is actively and selectively removed from C. burnetii-infected cells through a mechanism involving the Dot/Icm type IV-B secretion system effector CvpB. Overexpression of cathepsin B leads to defects in CCV biogenesis and bacterial replication, indicating that removal of this protein represents a strategy to reduce the hostility of the intracellular niche. In addition, we show that C. burnetii infection of mammalian cells induces the secretion of a wider cohort of lysosomal proteins, including cathepsin B, to the extracellular milieu via a mechanism dependent on retrograde traffic. This study reveals that C. burnetii is actively modulating the hydrolase cohort of its replicative niche to promote intracellular success and demonstrates that infection incites the secretory pathway to maintain lysosomal homoeostasis.