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BackgroundEndoscopic examination is a popular and routine procedure for the diagnosis and treatment of gastrointestinal (GI) diseases. Skilled endoscopists are in great demand in clinical practice, but the training process for beginners to become endoscopy specialists is fairly long. Convenience and a self-paced, learner-centered approach make electronic learning (e-learning) an excellent instructional prospect. ObjectiveThis study aimed to develop and apply an e-learning system in gastroscopy teaching and learning and to evaluate its effectiveness and user satisfaction. MethodsThe e-learning software Gastroscope Roaming System was developed for primary learners. The system simulates the real structure of the upper gastrointestinal (UGI) tract to teach the main characteristics of gastroscopy under both normal conditions and conditions of common UGI tract diseases. A randomized controlled trial was conducted. Participants were randomly allocated to an e-learning group (EG)or a non–e-learning control group after a pretest. On completing the training, participants undertook a posttest and gastroscopy examination. In addition, the EG completed a satisfaction questionnaire. ResultsOf the 44 volunteers, 41 (93%) completed the gastroscopy learning and testing components. No significant pretest differences were found between the intervention and control groups (mean 50.86, SD 6.12 vs mean 50.76, SD 6.88; P=.96). After 1 month of learning, the EG’s posttest scores were higher (mean 83.70, SD 5.99 vs mean 78.76, SD 7.58; P=.03) and improved more (P=.01) than those of the control group, with better performance in the gastroscopy examination (mean 91.05, SD 4.58 vs mean 84.38, SD 5.19; P

The emergence of lockers has provided convenience for the public, but the rapid development of the Internet has greatly improved the quality of life of the masses, and people are no longer satisfied with the services provided by ordinary lockers. With the rapid development of logistics and express delivery, shared lockers have also come into being, and among many shared locker brands, XiaoTie smart lockers stand out. Although XiaoTie smart lockers are more convenient than ordinary lockers, there are still problems such as a small number of storage cabinets, imperfect storage services, high charges due to the high cost of express lockers, insufficient security and high competitive pressure. In order to enhance the competitiveness of the XiaoTie brand, strengthen the professional ability of XiaoTie smart lockers, and ultimately aim to improve the revenue and market share of XiaoTie smart lockers, this paper puts forward targeted suggestions such as broadening financing channels, developing business models, and cultivating professional talents.

A short peptide termed NEMO‐binding domain (NBD) peptide has an inhibitory effect on nuclear factor kappa‐B (NF‐κB). Despite its efficacy in inhibiting inflammatory responses, the precise neuroprotective mechanisms of NBD peptide in spinal cord injury (SCI) remain unclear. This study aims to determine whether the pyroptosis‐related aspects involved in the neuroprotective effects of NBD peptide post‐SCI.Using RNA sequencing, the molecular mechanisms of NBD peptide in SCI are explored. The evaluation of functional recovery is performed using the Basso mouse scale, Nissl staining, footprint analysis, Masson's trichrome staining, and HE staining. Western blotting, enzyme‐linked immunosorbent assays, and immunofluorescence assays are used to examine pyroptosis, autophagy, lysosomal membrane permeabilization (LMP), acid sphingomyelinase (ASMase), and the NF‐κB/p38‐MAPK related signaling pathway.NBD peptide mitigated glial scar formation, reduced motor neuron death, and enhanced functional recovery in SCI mice. Additionally, NBD peptide inhibits pyroptosis, ameliorate LMP‐induced autophagy flux disorder in neuron post‐SCI. Mechanistically, NBD peptide alleviates LMP and subsequently enhances autophagy by inhibiting ASMase through the NF‐κB/p38‐MAPK/Elk‐1/Egr‐1 signaling cascade, thereby mitigating neuronal death. NBD peptide contributes to functional restoration by suppressing ASMase‐mediated LMP and autophagy depression, and inhibiting pyroptosis in neuron following SCI, which may have potential clinical application value. [ABSTRACT FROM AUTHOR]

With the rapid development of wind power generation in recent years, the demand for detecting weak signals of wind turbine faults has become more urgent. This paper introduces a novel memristor chaotic circuit constructed based on third-order magnetically memristors. The Melnikov chaotic condition of this circuit is analyzed, and its dynamical characteristics are studied through phase trajectory diagrams, bifurcation diagrams, Lyapunov exponent spectra, and Poincaré maps. Leveraging the initial value sensitivity and noise immunity of chaotic systems, the memristor chaotic circuit is employed for the detection of weak signals in wind turbine faults. Using the chaotic system state transition method, we find the threshold for the circuit state to transition from chaotic state to large-scale periodic state, adjust the parameters to make the system in a critical state, input the wind turbine fault vibration signal, and detect the fault signal based on its state transition. Subsequently, the chaotic resonance method is employed, introducing the signal under test, which contains high-intensity chaotic noise, into this novel memristive circuit. This results in chaotic resonance, causing the noise components to be concentrated toward the frequency region where the weak signal under test is located, thereby enhancing the fault signal and facilitating fault identification. The results indicate that this novel memristor chaotic circuit possesses advantages such as high accuracy, strong noise immunity, straightforward operation, and clear judgment in the field of weak signal detection. This circuit shows promising applications in the field of weak signal detection. [ABSTRACT FROM AUTHOR]

The coupling between neurons can lead to diverse neural network architectures, with the Hopfield neural network (HNN) being particularly noteworthy for its resemblance to human brain function and its potential in modeling chaotic systems. This paper introduces a novel approach: a fractional-order HNN coupled with a hyperbolic tangent-type memristor. Initially, we propose a new model for the hyperbolic tangent-type memristor and fingerprints. Subsequently, we construct a memristor-coupled fractional-order Hopfield neural network (mFOHNN) and explore its dynamic behavior using various analytical tools, including phase diagrams, bifurcation diagrams, Lyapunov exponent diagrams, Poincaré maps, and attractor basins. Our findings reveal rich coexisting bifurcation behavior in the neural network model, influenced by different initial values of coexisting attractors. Finally, we validate the model through analysis and implementation using Multisim circuit simulation software and FPGA hardware, respectively. [ABSTRACT FROM AUTHOR]

Preventing and treating avascular necrosis at the distal end of the flaps are critical to surgery success, but current treatments are not ideal. A recent study shows that apoptotic bodies (ABs) generated near the site of apoptosis can be taken up and promote cell proliferation. The study reveals that ABs derived from fibroblast‐like cells in the subcutaneous connective tissue (FSCT cells) of skin flaps promoted ischaemic flap survival. It is also found that ABs inhibited cell death and oxidative stress and promoted M1‐to‐M2 polarization in macrophages. Transcriptome sequencing and protein level testing demonstrated that ABs promoted ischaemic flap survival in endothelial cells and macrophages by inhibiting ferroptosis via the KEAP1‐Nrf2 axis. Furthermore, microRNA (miR) sequencing data and in vitro and in vivo experiments demonstrated that ABs inhibited KEAP1 by delivering miR‐339‐5p to exert therapeutic effects. In conclusion, FSCT cell‐derived ABs inhibited ferroptosis, promoted the macrophage M1‐to‐M2 transition via the miR‐339‐5p/KEAP1/Nrf2 axis and promoted ischaemic flap survival. These results provide a potential therapeutic strategy to promote ischaemic flap survival by administering ABs. [ABSTRACT FROM AUTHOR]

Avascular necrosis frequently occurs as a complication following surgery involving the distal perforator flap. Dihydrocapsaicin (DHC) can protect tissue from ischemia–reperfusion (I/R) injury, but its specific role in multizone perforator flaps remains unclear. In this study, the prospective target of DHC in the context of I/R injury was predicted using network pharmacology analysis. Flap viability was determined through survival area analysis, laser Doppler blood flow, angiograms, and histological examination. The expressions of angiogenesis, apoptosis, NLR family pyrin domain containing 3 (NLRP3) inflammasome, oxidative stress, and molecules related to cyclic guanosine monophosphate (GMP)‐adenosine monophosphate synthase (cGAS)‐interferon gene stimulant (STING) pathway were assessed using western blotting, immunofluorescence, TUNEL staining, and dihydroethidium (DHE) staining. Our finding revealed that DHC promoted the perforator flap survival, which involves the cGAS–STING pathway, oxidative stress, NLRP3 inflammasome, apoptosis, and angiogenesis. DHC induced oxidative stress resistance and suppressed the NLRP3 inflammasome, preventing apoptosis in vascular endothelial cells. Through regulation of STING pathway, DHC controlled oxidative stress in endothelial cells and NLRP3 levels in ischemic flaps. However, activation of the cGAS–STING pathway led to the accumulation of reactive oxygen species (ROS) and NLRP3 inflammasome, thereby diminishing the protective role of DHC. DHC enhanced the survival of multidomain perforator flaps by suppressing the cGAS–STING pathway, oxidative stress, and the formation of NLRP3 inflammasome. These findings unveil a potentially novel mechanism with clinical significance for promoting the survival of multidomain perforator flaps. [ABSTRACT FROM AUTHOR]

Background and Purpose: Ischaemia–reperfusion (I/R) injury is a major contributor to skin flap necrosis, which presents a challenge in achieving satisfactory therapeutic outcomes. Previous studies showed that cathelicidin‐BF (BF‐30) protects tissues from I/R injury. In this investigation, BF‐30 was synthesized and its role and mechanism in promoting survival of I/R‐injured skin flaps explored. Experimental Approach: Survival rate analysis and laser Doppler blood flow analysis were used to evaluate I/R‐injured flap viability. Western blotting, immunofluorescence, TdT‐mediated dUTP nick end labelling (TUNEL) and dihydroethidium were utilized to examine the levels of apoptosis, pyroptosis, oxidative stress, transcription factor EB (TFEB)‐mediated autophagy and molecules related to the adenosine 5′‐monophosphate‐activated protein kinase (AMPK)–transient receptor potential mucolipin 1 (TRPML1)–calcineurin signalling pathway. Key Results: The outcomes revealed that BF‐30 enhanced I/R‐injured island skin flap viability. Autophagy, oxidative stress, pyroptosis and apoptosis were related to the BF‐30 capability to enhance I/R‐injured flap survival. Improved autophagy flux and tolerance to oxidative stress promoted the inhibition of apoptosis and pyroptosis in vascular endothelial cells. Activation of TFEB increased autophagy and inhibited endothelial cell oxidative stress in I/R‐injured flaps. A reduction in TFEB level led to a loss of the protective effect of BF‐30, by reducing autophagy flux and increasing the accumulation of reactive oxygen species (ROS) in endothelial cells. Additionally, BF‐30 modulated TFEB activity via the AMPK–TRPML1–calcineurin signalling pathway. Conclusion and Implications: BF‐30 promotes I/R‐injured skin flap survival by TFEB‐mediated up‐regulation of autophagy and inhibition of oxidative stress, which may have possible clinical applications. [ABSTRACT FROM AUTHOR]

A disposable electrochemical sensor based on silver nanoparticle-embedded cellulose hydrogel composites was developed for sensitive detection of sulfamethoxazole residues in meat samples. Scanning electron microscopy confirmed the porous structure of the cellulose matrix anchored with 20–50 nm silver nanoparticles (AgNPs). Fourier transform infrared spectroscopy and X-ray diffraction verified that the metallic AgNPs coordinated with the amorphous cellulose chains. At an optimum 0.5% loading, the nanocomposite sensor showed a peak-to-peak separation of 150 mV, diffusion-controlled charge transfer kinetics, and an electron transfer coefficient of 0.6 using a ferro/ferricyanide redox probe. Square-wave voltammetry was applied for sensing sulfamethoxazole based on its two-electron oxidation peak at 0.72 V vs. Ag/AgCl in Britton–Robinson buffer of pH 7.0. A linear detection range of 0.1–100 μM sulfamethoxazole was obtained with a sensitivity of 0.752 μA/μM and limit of detection of 0.04 μM. Successful recovery between 86 and 92% and less than 6% RSD was achieved from spiked meat samples. The key benefits of the proposed disposable sensor include facile fabrication, an antifouling surface, and a reliable quantification ability, meeting regulatory limits. This research demonstrates the potential of novel cellulose–silver nanocomposite materials towards developing rapid, low-cost electroanalytical devices for decentralized on-site screening of veterinary drug residues to ensure food safety. [ABSTRACT FROM AUTHOR]

We present a technique that utilizes cascaded resonant cylindrical piezoelectric ceramics and multimode optical fibers wound around them to effectively mitigate laser speckle. By precisely driving the ceramics at their resonant frequencies and inducing comprehensive mode scrambling within the multimode fiber, we achieve a remarkable speckle suppression efficiency of up to 94%. To the best of our knowledge, this sets a new benchmark among various methods aimed at suppressing the speckle of a coherent light. Our study thoroughly explores variables influencing efficiency, including the cascading number of piezoelectric ceramics, driving voltage, fiber core diameter, and more. This method has significant promise for diverse applications that require efficient and fast control of speckle contrast. [ABSTRACT FROM AUTHOR]

The clinical efficacy for treating of celastrol rheumatoid arthritis (RA) has been well-documented, but its mechanism of action remains unclear. Here we explored through what proteins and processes celastrol may act in activated fibroblast-like synoviocytes (FLS) from RA patients. Differential expression of genes and proteins after celastrol treatment of FLS was examined using RNA sequencing, label-free relatively quantitative proteomics and molecular docking. In this paper, expression of 26,565 genes and 3,372 proteins was analyzed. Celastrol was associated with significant changes in genes that respond to oxidative stress and oxygen levels, as well as genes that stabilize or synthesize components of the extracellular matrix. These results identify several potential mechanisms through which celastrol may inhibit inflammation in RA.

Extracellular vesicles (EVs) are membrane‐enclosed nanovesicles secreted by cells into the extracellular space and contain functional biomolecules, e.g. signaling receptors, bioactive lipids, nucleic acids, and proteins, which can serve as biomarkers. Neurons and glial cells secrete EVs, contributing to various physiological and pathological aspects of brain diseases. EVs confer their role in the bidirectional crosstalk between the central nervous system (CNS) and the periphery owing to their distinctive ability to cross the unique blood–brain barrier (BBB). Thus, EVs in the blood, cerebrospinal fluid (CSF), and urine can be intriguing biomarkers, enabling the minimally invasive diagnosis of CNS diseases. Although there has been an enormous interest in evaluating EVs as promising biomarkers, the lack of ultra‐sensitive approaches for isolating and detecting brain‐derived EVs (BDEVs) has hindered the development of efficient biomarkers. This review presents the recent salient findings of exosomal biomarkers, focusing on brain disorders. We summarize highly sensitive sensors for EV detection and state‐of‐the‐art methods for single EV detection. Finally, the prospect of developing advanced EV analysis approaches for the non‐invasive diagnosis of brain diseases is presented. [ABSTRACT FROM AUTHOR]