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This paper presents a comprehensive framework for real-time monitoring and optimization of user-side energy management systems leveraging edge computing technology. The proposed approach addresses key challenges in traditional centralized energy management by bringing computation and data processing closer to end devices. The framework encompasses three main components: an edge computing-based system architecture for data acquisition and processing, real-time monitoring methods for energy consumption and power quality, and optimization techniques for demand response and distributed energy resource coordination. Through case studies and experimental analysis, we demonstrate that the proposed framework achieves significant improvements in energy efficiency, response time, and cost reduction compared to conventional centralized approaches. The results show up to 30% increase in renewable energy utilization and 25% reduction in operating costs across various deployment scenarios. This work provides valuable insights into the application of edge computing for next-generation energy management systems while highlighting remaining challenges and future research directions.

Summary The intestine is colonized by a considerable community of microorganisms that cohabits within the host and plays a critical role in maintaining host homeostasis. Recently, accumulating evidence has revealed that the gut microbial ecology plays a pivotal role in the occurrence and development of cardiovascular disease (CVD). Moreover, the effects of imbalances in microbe–host interactions on homeostasis can lead to the progression of CVD. Alterations in the composition of gut flora and disruptions in gut microbial metabolism are implicated in the pathogenesis of CVD. Furthermore, the gut microbiota functions like an endocrine organ that produces bioactive metabolites, including trimethylamine/trimethylamine N‐oxide, short‐chain fatty acids and bile acids, which are also involved in host health and disease via numerous pathways. Thus, the gut microbiota and its metabolic pathways have attracted growing attention as a therapeutic target for CVD treatment. The fundamental purpose of this review was to summarize recent studies that have illustrated the complex interactions between the gut microbiota, their metabolites and the development of common CVD, as well as the effects of gut dysbiosis on CVD risk factors. Moreover, we systematically discuss the normal physiology of gut microbiota and potential therapeutic strategies targeting gut microbiota to prevent and treat CVD. The fundamental purpose of this review is to summarize recent studies on illustrating the complex interactions between the gut microbiota, their metabolites and the development of common CVD, as well as the effects of gut dysbiosis on CVD risk factors. Moreover, we systematically discuss the normal physiology of gut microbiota and potential therapeutic strategies targeting gut microbiota to prevent and treat CVD.

Heart failure (HF) is frequently the consequence of sustained, abnormal neurohormonal, and mechanical stress and remains a leading cause of death worldwide. The key pathophysiological process leading to HF is cardiac remodeling, a term referring to maladaptation to cardiac stress at the molecular, cellular, tissue, and organ levels. HF and many of the conditions that predispose one to HF are associated with oxidative stress. Increased generation of reactive oxygen species (ROS) in the heart can directly lead to increased necrosis and apoptosis of cardiomyocytes which subsequently induce cardiac remodeling and dysfunction. Nuclear factor-erythroid-2- (NF-E2-) related factor 2 (Nrf2) is a transcription factor that controls the basal and inducible expression of a battery of antioxidant genes and other cytoprotective phase II detoxifying enzymes that are ubiquitously expressed in the cardiovascular system. Emerging evidence has revealed that Nrf2 and its target genes are critical regulators of cardiovascular homeostasis via the suppression of oxidative stress, which is the key player in the development and progression of HF. The purpose of this review is to summarize evidence that activation of Nrf2 enhances endogenous antioxidant defenses and counteracts oxidative stress-associated cardiac remodeling and HF.

The emergence of immune checkpoint inhibitors (ICIs) have provided a new perspective for cancer immunotherapy. Immune checkpoint inhibitors significantly improve the survival prognosis of patients with various advanced cancers by inhibiting immune checkpoint molecules, thereby releasing the suppression of T cells by tumor microenvironment, such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1). Immune checkpoint inhibitor (ICI) therapy, while effective, gives rise to distinct immune-related adverse events (irAEs), including cardiovascular toxicities, necessitating focused research efforts to better understand and address these specific complications. The myocarditis-associated toxicity has been extensively studied. This article reviews the latest clinical and preclinical literature on the epidemiology and pathogenesis of ICI-related atherosclerosis, explores the pathophysiological mechanisms by which ICIs promote atherosclerosis, and discusses risk assessment, identification and monitoring methods, and intervention strategies for ICI treatment related atherosclerosis.

Acute kidney injury (AKI) is a common clinical problem, and patients who survive AKI have a high risk of chronic kidney disease (CKD). The acute protective effects of Cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors in AKI have been examined, there is still relatively little known regarding the impact of acute CDK4/6 inhibition on the chronic sequence of AKI. Therefore, we utilized the CDK4/6 inhibitor Palbociclib to examine the long-term effects of CDK4/6 inhibition in a rodent model of ischemic AKI. Palbociclib (Palb) was administered during the acute stage or post the acute stage of AKI and mice were sacrificed 21 days post injury. We found that Palb could cause renal senescence and renal fibrosis. Furthermore, dasatinib (D) plus quercetin (Q) were used to eliminate senescent cells in ischemic AKI murine model and Palb was administered post the treatment of D + Q. We found that Palb could reverse the senolytic and antifibrotic effects induced by D + Q, which indicates that the profibrotic effect of Palb could be ascribed to its pro-senescent effects. Our results demonstrate that CDK4/6 inhibitors treatment might be deleterious on the chronic sequence of AKI.

Taohe-Chengqi decoction (THCQ), a classical traditional Chinese medicinal (TCM) formula, has been extensively used for treating chronic kidney disease (CKD). However, the biological activity and mechanisms of action of its constituents against renal fibrosis have not yet been investigated thoroughly. This study was aimed at devising an integrated strategy for investigating the bioactivity constituents and possible pharmacological mechanisms of the n-butanol extract of THCQ (NE-THCQ) against renal fibrosis. The n-butanol extract of THCQ was prepared by the solvent extraction method. The components of NE-THCQ were analyzed using UPLC-Q/TOF-MS/MS techniques and applied for screening the active components of NE-THCQ according to their oral bioavailability and drug-likeness index. Then, we speculated the potential molecular mechanisms of NE-THCQ against renal fibrosis through pharmacological network analysis. Based on data mining techniques and topological parameters, gene ontology, and pathway enrichment, we established compound-target (C-T), protein-protein interaction (PPI) and compound-target-pathway (C-T-P) networks by Cytoscape to identify the hub targets and pathways. Finally, the potential molecular mechanisms of NE-THCQ against renal fibrosis, as predicted by the network pharmacology analyses, were validated experimentally in renal tubular epithelial cells (HK-2) and against unilateral ureteral obstruction models in the rat . We identified 26 components in NE-THCQ and screened seven bioactive ingredients. A total of 118 consensus potential targets associated with renal fibrosis were identified by the network pharmacology approach. The experimental validation results demonstrated that NE-THCQ might inhibit the inflammatory processes, reduce ECM deposition and reverse EMT PI3K/AKT/mTOR and HIF-1α/VEGF signaling pathways to exert its effect against renal fibrosis. This study identified the potential ingredients of the NE-THCQ by UPLC-Q/TOF-MS/MS and explained the possible mechanisms of NE-THCQ against renal fibrosis by integrating network pharmacology and experimental validation.

A colorimetric method is presented for the determination of the antibiotic ofloxacin (OFL) in aqueous solution. It is based on the use of an aptamer and gold nanoparticles (AuNPs). In the absence of OFL, the AuNPs are wrapped by the aptamer and maintain dispersed even at the high NaCl concentrations. The solution with colloidally dispersed AuNPs remains red and has an absorption peak at 520 nm. In the presence of OFL, it will bind to the aptamer which is then released from the AuNPs. Hence, AuNPs will aggregate in the salt solution, and color gradually turns to blue, with a new absorption peak at 650 nm. This convenient and specific colorimetric assay for OFL has a linear response in the 20 to 400 nM OFL concentration range and a 3.4 nM detection limit. The method has a large application potential for OFL detection in environmental and biological samples. Graphical abstract Schematic of a sensitive and simple colorimetric aptasensor for ofloxacin (OFL) detection in tap water and synthesic urine. The assay is based on the salt-induced aggregation of gold nanoparticles which results in a color change from red to purple.

To circumvent the computational bottlenecks associated with the intermediate steps (e.g., least squares fitting) in conventional sine wave similarity principles and directly acquire the energy metrics required for stabilized sinusoidal waveform characterization, this study leverages time domain probability distribution theory. From a complementary advantage perspective, a novel transformer inrush current identification criterion is developed using the Wasserstein distance metric. The methodology employs feature discretization to extract target/template signals, transforming them into state vectors for sample labelling. By quantifying inter-signal energy distribution disparities through this framework, it achieves a precise waveform similarity assessment in sinusoidal regimes. The theoretical analysis and simulations demonstrate that the approach eliminates frequency domain computations while maintaining implementation simplicity. Compared with conventional sine wave similarity methods, the solution streamlines protection logic and significantly enhances practical applicability with accelerated response times. Furthermore, tests conducted on field-recorded circuit breaker closing waveforms using MATLAB R2022a confirm the effectiveness of the proposed method in improving transformer protection performance.

When a transformer is in a long-term heavy load operation state, the oil temperature reaches the alarm temperature; if a slight fault occurs inside the transformer, traditional inverse time current protection and other protections that react to phase current may not operate due to insufficient sensitivity or they may operate for too long. Based on this, this article proposes a new principle of accelerating inverse time overcurrent protection based on transformer oil temperature. The proposed method uses transformer oil temperature to accelerate the action time of traditional inverse-time overcurrent protection, then introduces the transformer oil temperature factor and acceleration index to optimize the inverse time characteristic curve, and establishes a mathematical model to optimize the adjustment for the complexity of adjustment of the protection action equation and the risk of mismatch of the protection after the acceleration of oil temperature. The existing theoretical analysis and simulation verification results show that the proposed new overcurrent protection scheme based on the transformer oil temperature acceleration inverse time can effectively improve the protection of the rapidity and sensitivity, providing a new research idea for the combination of non-electrical and electrical quantity protection.