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Background Following stroke, microglia can be driven to the “classically activated” pro-inflammatory (M1) phenotype and the “alternatively activated” anti-inflammatory (M2) phenotype. Salidroside (SLDS) is known to inhibit inflammation and to possess protective effects in neurological diseases, but to date, the exact mechanisms involved in these processes after stroke have yet to be elucidated. The purpose of this study was to determine the effects of SLDS on neuroprotection and microglial polarization after stroke. Methods Male adult C57/BL6 mice were subjected to focal transient cerebral ischemia followed by intravenous SLDS injection. The optimal dose was determined by evaluation of cerebral infarct volume and neurological functions. RT-PCR and immunostaining were performed to assess microglial polarization. A transwell system and a direct-contact coculture system were used to elucidate the effects of SLDS-induced microglial polarization on oligodendrocyte differentiation and neuronal survival. Results SLDS significantly reduced cerebral infarction and improved neurological function after cerebral ischemia. SLDS treatment reduced the expression of M1 microglia/macrophage markers and increased the expression of M2 microglia/macrophage markers after stroke and induced primary microglia from M1 phenotype to M2 phenotype. Furthermore, SLDS treatment enhanced microglial phagocytosis and suppressed microglial-derived inflammatory cytokine release. Cocultures of oligodendrocytes and SLDS-treated M1 microglia resulted in increased oligodendrocyte differentiation. Moreover, SLDS protected neurons against oxygen glucose deprivation by promoting microglial M2 polarization. Conclusions These data demonstrate that SLDS protects against cerebral ischemia by modulating microglial polarization. An understanding of the mechanisms involved in SLDS-mediated microglial polarization may lead to new therapeutic opportunities after stroke.

Intracerebral hemorrhage (ICH) is a common cerebrovascular disease characterized by a high incidence, disability rate, and mortality. Epigallocatechin gallate (EGCG), a key catechin compound found in green tea, has received increasing attention for its potential neuroprotective and therapeutic effects in neurological disorders. Studies have indicated that EGCG may influence various signaling pathways and molecular targets, including the inhibition of oxidative stress, reduction of inflammatory responses, suppression of cell apoptosis, regulation of cell survival, and enhancement of autophagy. Although the exact mechanism of action of EGCG is not fully understood, it has become a focal point of research in various disciplines due to its promising potential. This study aims to investigate the effects of EGCG on oxidative stress, iron deposition, and cell apoptosis in rats with ICH, as well as to uncover the underlying mechanisms. An ICH rat model was created to simulate cerebral hemorrhage, while an in vitro model utilizing primary cortical neurons was developed. The neurons were pre-treated with EGCG before being exposed to Erastin and RSL3 to induce iron death. The levels of oxidative stress, iron deposition, and cell apoptosis were evaluated in both models. In the ICH model, EGCG was discovered to enhance the activation of the Keap1/P62/Nrf2 signaling pathway in both in vivo and in vitro studies. Furthermore, EGCG significantly elevated the levels of GPX4 and XCT proteins, as well as the nuclear expression of Nrf2. It was noted that the Nrf2 inhibitor ML385 partially decreased the expression of these proteins. Through the activation of the Keap1/P62/Nrf2 pathway, EGCG inhibits inflammation, oxidative stress and iron deposition in rats with cerebral hemorrhage. EGCG inhibits oxidative stress, iron deposition and apoptosis in rats with ICH by activating Keap1/P62/Nrf2 pathway.

Skin microcirculation provides essential insights in clinical practice. However, the specific characteristics and distribution patterns of dermal microarterioles and microvenules remain insufficiently explored. This study aimed to analyze their structural differences and distribution in the human forehead skin using an innovative intravascular dual perfusion technique combined with immunofluorescence staining to distinguish microvessel types within the dermis. Using two post-mortem cadaver specimens, lead oxide-gelatin perfusion was applied to label microarterioles, and latex was used for microvenules. Tissue sections underwent hematoxylin and eosin and immunofluorescence staining, with cluster of differentiation 31 (CD31) serving as a general vascular marker and monocarboxylate transporter 1 (MCT1) as a venule-specific marker. The analysis revealed significant structural differences between dermal layers: vessels in the deep dermis had larger diameters and thicker walls than those in the superficial layer, while microvessel density was higher in the superficial dermis. These findings demonstrate distinct patterns and significant differences in microvessel distribution between the superficial and deep dermal layers, reflecting their layer-specific functional demands. Furthermore, MCT1 was identified as a specific marker for microvenules, and a novel method combining CD31 and MCT1 immunofluorescent staining was introduced to differentiate dermal microarterioles from microvenules. These results offer valuable implications for surgical planning, skin grafting, and diagnostics related to microcirculation.

Background Intracerebral hemorrhage (ICH) is a severe form of stroke characterized by high incidence and mortality rates. Currently, there is a significant lack of effective treatments aimed at improving clinical outcomes. Our research team has developed a three-dimensional (3D) biological scaffold that incorporates Bergenin, allowing for the sustained release of the compound. Methods This 3D biological scaffold was fabricated using a combination of photoinitiator, GEMA, silk fibroin, and decellularized brain matrix (dECM) to encapsulate Bergenin through advanced 3D bioprinting techniques. The kinetics of drug release were evaluated through both in vivo and in vitro studies. A cerebral hemorrhage model was established, and a 3D biological scaffold containing Bergenin was transplanted in situ. Levels of inflammatory response, oxidative stress, and apoptosis were quantified. The neurological function of rats with cerebral hemorrhage was assessed on days 1, 3, and 5 using the turning test, forelimb placement test, Longa score, and Bederson score. Results The 3D biological scaffold incorporating Bergenin significantly enhances the maintenance of drug concentration in the bloodstream, leading to a marked reduction in inflammatory markers such as IL-6, iNOS, and COX-2 levels in a cerebral hemorrhage model, primarily through the inhibition of the NF-κB pathway. Additionally, the scaffold effectively reduces the expression of hypoxia-inducible factor 1-alpha (HIF-1α) in primary cultured astrocytes, which in turn decreases the production of reactive oxygen species (ROS) and inhibits IL-6 production induced by hemin. Subsequent experiments reveal that the 3D biological scaffold containing Bergenin promotes the activation of the Nrf-2/HO-1 signaling pathway, both in vivo and in vitro, thereby preventing cell death. Moreover, the application of this 3D biological scaffold has been demonstrated to improve drug retention in the bloodstream. Conclusion This strategy effectively mitigates inflammation, oxidative stress, and cell death in rats with cerebral hemorrhage by inhibiting the NF-κB pathway while concurrently activating the Nrf-2/HO-1 pathway.

Background Neuroinflammation following intracerebral hemorrhage (ICH) is a critical contributor to secondary brain injury. Lactylation modification, a novel epigenetic regulatory mechanism, may participate in pathological processes by modulating inflammatory gene expression. This study investigates whether exosomes derived from human umbilical cord mesenchymal stem cells (hUCMSC-exos) alleviate ICH-induced neuroinflammation by regulating lactylation modification via the PI3K/AKT/PKM2/H3K18la axis. Methods In vivo, an ICH model was established by stereotactic injection of collagenase IV into the rat striatum. At 6 h post-ICH, hUCMSC-exos (100 μg/200 μL) were administered via tail vein. In vitro, a hemin-induced (20 μM) ICH cell model was established using primary astrocytes, followed by hUCMSC-exos treatment (20 μg/mL) at 6 h post-modeling. The expression of the PI3K/AKT/PKM2/H3K18la axis and inflammatory cytokines (TNF-α, IL-1β, and IL-10) was evaluated in both models to assess the impact of hUCMSC-exos on glycolysis, lactylation modification, and neuroinflammation. Neurological function in ICH rats was evaluated using corner turn, forelimb placement, Longa, and Bederson scores at days 1, 3, 7, and 14. Results hUCMSC-exos intervention significantly upregulated phosphorylated PI3K (p-PI3K) and AKT (p-AKT) levels, while downregulating PKM2, LDHA, and H3K18la expression. Pro-inflammatory cytokines (TNF-α and IL-1β) were markedly reduced, whereas the anti-inflammatory cytokine IL-10 was elevated. Consequently, hUCMSC-exos improved neurological recovery in ICH rats. Conclusion hUCMSC-exos attenuate ICH-induced glycolysis, lactylation modification, and excessive neuroinflammation via the PI3K/AKT/PKM2/H3K18la axis, offering a novel therapeutic strategy for ICH.

The modified nanoparticles can significantly improve the insulation characteristics of transformer oil. Currently, there is a lack of research on the actual motion state of particles in nanofluid to further understand the micro-mechanism of nanoparticles improving the insulation characteristics of transformer oil. In this study, the nanofluid containing 0.01g/L of TiO 2 with a particle size of 20nm is prepared using the thermal oscillation method. Breakdown voltage tests are carried out. The experimental test results show that adding nanoparticles can significantly reduce the breakdown probability of transformer oil. The more the water content, the less the enhancement effect of the nanofluid on breakdown voltage. The higher the temperature, the stronger the enhancement effect of the nanofluid on breakdown voltage. Finally, the polarization process of nanoparticles and the trajectory of charged particles in the transformer oil under different electric fields are simulated using COMSOL to further analyze the influence mechanism of nanoparticles on the insulation characteristics of transformer oil. The simulation results show that under the action of the electric field, nanoparticles polarize and generate charge shallow traps to adsorb electrons, reducing the high-speed free charges in the oil, and indirectly increasing the breakdown voltage.

Quantitative analysis of gait parameters, such as stride frequency and step speed, is essential for optimizing physical exercise for the human body. However, the current electronic sensors used in human motion monitoring remain constrained by factors such as battery life and accuracy. This study developed a self‐powered gait analysis system (SGAS) based on a triboelectric nanogenerator (TENG) fabricated electrospun composite nanofibers for motion monitoring and gait analysis for regulating exercise programs. The SGAS consists of a sensing module, a charging module, a data acquisition and processing module, and an Internet of Things (IoT) platform. Within the sensing module, two specialized sensing units, TENG‐S1 and TENG‐S2, are positioned at the forefoot and heel to generate synchronized signals in tandem with the user's footsteps. These signals are instrumental for real‐time step count and step speed monitoring. The output of the two TENG units is significantly improved by systematically investigating and optimizing the electrospun composite nanofibers' composition, strength, and wear resistance. Additionally, a charge amplifier circuit is implemented to process the raw voltage signal, consequently bolstering the reliability of the sensing signal. This refined data is then ready for further reading and calculation by the micro‐controller unit (MCU) during the signal transmission process. Finally, the well‐conditioned signals are wirelessly transmitted to the IoT platform for data analysis, storage, and visualization, enhancing human motion monitoring. Electrospun triboelectric gait sensing analysis system was fabricated by preparing PVDF/BaTiO3/CNT composite fiber membrane by electrospinningtechnique and introducing Ecoflex perforated array elastomer into TENG, which not only provided high output performance, but also ensured the robustness of output and the comfort of wearing. The quantitative gait parameters were uploaded to an IoT platform via wireless network for data visualization.

A gold immunochromatographic sensor （GICS） was developed for the rapid detection of 26 sulfonamides in honey samples. The sensor was based on a group-specific monoclonal antibody （mAb） that can recognize all 26 sulfonamides. Three haptens （hapten I with a thiazole ring, hapten 2 with a benzene ring, and hapten 3 with a straight carbon chain） were used for antigen preparation. With hybridoma technology, a group-specific mAb was screened with a 50% maximal inhibitory concentration （IC50） against sulfathizole （STZ） and the other 25 analogues ranging from 0.08 to 90.18 ng/mL. Mono-dispersed gold nanoparticles were conjugated with the mAb to develop the lateral immunochromatographic strip. A labeled antibody concentration of 0.1 pg/mL and a coating antigen concentration of 0.2 μg/mL in the test line were chosen for strip preparation. Under optimized conditions, the visual limits of detection （vLOD） for the concentrations of STZ, sulfamethoxazole, sulfamethizole, sulfadiazine, sulfamerazine, sulfadimethoxine, sulfamonomethoxine, sulfameter, sulfamethoxypyridazine, and sulfachloropyridazine were 5, 0.25, 0.25, 10, 5, 10, 25, 2.5, 5, 0.25, and 10 μg/kg, respectively. Scanner analysis in honey samples revealed good performance for detection of the 26 sulfonamides. Commercial honey samples were tested with the sensor and positive results were confirmed with high-performance liquid chromatography. The proposed strip sensor provides a convenient method for the rapid and reliable determination of sulfonamides pollutants in honey samples.

Intracerebral hemorrhage (ICH) is a severe form of stroke with high mortality, and apoptosis in the perihematomal region contributes to neurological deficits. This study aimed to investigate the role of NDRG4 in cerebral injury following ICH, focusing on apoptosis and related signaling pathways. A total of 242 male Sprague Dawley rats were used to establish a collagenase-induced ICH model and were allocated across four experiments to examine NDRG4 temporal expression, validate adenoviral overexpression, evaluate its effects on ICH outcomes, and probe PI3K/Akt/GSK3β signaling (6 rats per group). Neurological function, brain water content, TUNEL staining, Western blotting, and RT-qPCR were used to assess the effects of NDRG4 overexpression on ICH-induced brain injury and apoptosis. NDRG4 expression was significantly reduced in perihematomal brain tissue after intracerebral hemorrhage. In rats receiving adenoviral NDRG4 overexpression, neurological performance was significantly better than in ICH controls, and brain water content was significantly lower. NDRG4 overexpression was also associated with a significant reduction in TUNEL-positive cells, a significantly lower Bax/Bcl-2 ratio, and significantly decreased cleaved caspase-3 levels, while Bcl-2 levels were significantly higher. These biochemical and histological differences were accompanied by significantly increased phosphorylation of Akt (Ser473) and GSK3β (Ser9). Co-administration of wortmannin was associated with partial attenuation of these changes, suggesting that the observed effects may be related to activation of the PI3K/Akt/GSK3β signaling pathway. NDRG4 overexpression was associated with reduced perihematomal injury and improved neurological scores, partly associated with activation of the PI3K/Akt/GSK3β pathway. Further studies are warranted to delineate the specific cell types involved, the detailed mechanisms, and the translational relevance of these findings.

Aiming at the problems of the traditional planetary gear fault diagnosis method of wind turbines, such as the poor timeliness of data transmission, weak visualization effect of state monitoring, and untimely feedback of fault information, this paper proposes a planetary gear fault diagnosis method for wind turbines based on a digital twin. The method was used to build the digital twin model of wind turbines and analyze the wind turbines’ operating state utilizing virtual and real data. Empirical mode decomposition (EMD) was used, and an atom search optimization–support vector machine (ASO-SVM) model was established for planetary gear fault diagnosis. The digital twin model diagnoses faults and constantly revises the model based on the diagnostic results. The digital twin fault diagnosis system was implemented in the Unity3D platform. The experimental results demonstrate the feasibility of the proposed early-warning system for the real-time diagnosis of planetary gear faults in wind turbines.