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Sepsis is life-threatening and often leads to acute brain damage. Dexmedetomidine, an α 2 -adrenoceptor agonist, has been reported to possess neuroprotective effects against various brain injury but underlying mechanisms remain elusive. In this study, in vitro and in vivo models of sepsis were used to explore the effects of dexmedetomidine on the inflammasome activity and its associated glia pyroptosis and neuronal death. In vitro, inflammasome activation and pyroptosis were found in astrocytes following lipopolysaccharide (LPS) exposure. Dexmedetomidine significantly alleviated astrocyte pyroptosis and inhibited histone release induced by LPS. In vivo, LPS treatment in rats promoted caspase-1 immunoreactivity in astrocytes and caused an increase in the release of pro-inflammatory cytokines of IL-1β and IL-18, resulting in neuronal injury, which was attenuated by dexmedetomidine; this neuroprotective effect was abolished by α 2 -adrenoceptor antagonist atipamezole. Dexmedetomidine significantly reduced the high mortality rate caused by LPS challenge. Our data demonstrated that dexmedetomidine may protect glia cells via reducing pyroptosis and subsequently protect neurons, all of which may preserve brain function and ultimately improve the outcome in sepsis.

Objective Although growing evidence supports the benefits of physical exercise for amputees, existing studies present inconsistent findings. This systematic review and meta-analysis aimed to evaluate whether exercise interventions can effectively enhance physical performance and quality of life in individuals with lower-limb amputation. Methods Seven databases (PubMed, Cochrane Library, OVID, Scopus, PsycINFO, CINAHL, and Web of Science) were systematically searched up to April 21, 2025. Study quality was assessed using the RoB 2 tool, and meta-analyses were performed using R software (version 4.1.3). Results A total of 18 randomized controlled trials were included, with 7 studies incorporated into the meta-analysis. Evidence ranging from low to moderate quality suggests that exercise interventions yield significant benefits for individuals with limb amputation. Compared to usual care, exercise significantly improved gait speed [WMD = 0.009, 95% CI (0.03, 0.16), P  = 0.004], 2-min walk test performance [WMD = 8.81, 95% CI (1.92, 15.7), P  = 0.012], and Timed Up and Go test scores [WMD = –2.01, 95% CI (–3.90, –0.13), P  = 0.037]. No significant difference was observed in the Life-Space Community Index [WMD = –0.44, 95% CI (–2.48, 1.61), P  = 0.676]. Qualitative findings further supported the beneficial effects of exercise, although outcomes varied depending on exercise modality and assessment tools. In addition, heterogeneity in intervention protocols and participant characteristics limited the ability to conduct formal subgroup analyses or draw definitive conclusions. Conclusion Targeted exercise prescriptions can improve physical performance and quality of life in individuals with limb amputation. These findings support the integration of individualized exercise strategies into rehabilitation programs. However, heterogeneity in participant characteristics (e.g., age, gender, etiology, and amputation level) remains underexplored. Future research should address this diversity to optimize rehabilitation strategies for different subpopulations.

PurposeAlthough survival rates for patients with localized breast cancer have increased, patients with metastatic breast cancer still have poor prognosis. Understanding key factors involved in promoting breast cancer metastasis is imperative for better treatments. In this study, we investigated the role of syndecan-1 (Sdc1) in breast cancer metastasis.MethodsTo assess the role of Sdc1 in breast cancer metastasis, we silenced Sdc1 expression in the triple-negative breast cancer human MDA-MB-231 cell line and overexpressed it in the mouse mammary carcinoma 4T1 cell line. Intracardiac injections were performed in an experimental mouse metastasis model using both cell lines. In vitro transwell blood–brain barrier (BBB) and brain section adhesion assays were utilized to specifically investigate how Sdc1 facilitates brain metastasis. A cytokine array was performed to evaluate differences in the breast cancer cell secretome when Sdc1 is silenced.ResultsSilencing expression of Sdc1 in breast cancer cells significantly reduced metastasis to the brain. Conversely, overexpression of Sdc1 increased metastasis to the brain. We found that silencing of Sdc1 expression had no effect on attachment of breast cancer cells to brain endothelial cells or astrocytes, but migration across the BBB was reduced as well as adhesion to the perivascular regions of the brain. Loss of Sdc1 also led to changes in breast cancer cell-secreted cytokines/chemokines, which may influence the BBB.ConclusionsTaken together, our study demonstrates a role for Sdc1 in promoting breast cancer metastasis to the brain. These findings suggest that Sdc1 supports breast cancer cell migration across the BBB through regulation of cytokines, which may modulate the BBB. Further elucidating this mechanism will allow for the development of therapeutic strategies to combat brain metastasis.

Introduction: Dexmedetomidine is a potent, highly selective α-2 adrenoceptor agonist with sedative, analgesic, anxiolytic, and opioid-sparing properties. A large number of dexmedetomidine-related publications have sprung out in the last 2 decades. However, no bibliometric analysis for clinical research on dexmedetomidine has been published to analyze hot spots, trends, and frontiers in this field. Methods: The clinical articles and reviews related to dexmedetomidine, published from 2002 to 2021 in the Web of Science Core Collection, were retrieved on 19 May 2022, using relevant search terms. VOSviewer and CiteSpace were used to conduct this bibliometric study. Results: The results showed that a total of 2,299 publications were retrieved from 656 academic journals with 48,549 co-cited references by 2,335 institutions from 65 countries/regions. The United States had the most publications among all the countries (n = 870, 37.8%) and the Harvard University contributed the most among all institutions (n = 57, 2.48%). The most productive academic journal on dexmedetomidine was Pediatric Anesthesia and the first co-cited journal was Anesthesiology . Mika Scheinin is the most productive author and Pratik P Pandharipande is the most co-cited author. Co-cited reference analysis and keyword analysis illustrated hot spots in the dexmedetomidine field including pharmacokinetics and pharmacodynamics, intensive care unit sedation and outcome, pain management and nerve block, and premedication and use in children. The effect of dexmedetomidine sedation on the outcomes of critically ill patients, the analgesic effect of dexmedetomidine, and its organ protective property are the frontiers in future research. Conclusion: This bibliometric analysis provided us with concise information about the development trend and provided an important reference for researchers to guide future research.

The accurate prediction and analysis of emergencies in Urban Rail Transit Systems (URTS) are essential for the development of effective early warning and prevention mechanisms. This study presents an integrated perception model designed to predict emergencies and analyze their causes based on historical unstructured emergency data. To address issues related to data structuredness and missing values, we employed label encoding and an Elastic Net Regularization-based Generative Adversarial Interpolation Network (ER-GAIN) for data structuring and imputation. Additionally, to mitigate the impact of imbalanced data on the predictive performance of emergencies, we introduced an Adaptive Boosting Ensemble Model (AdaBoost) to forecast the key features of emergencies, including event types and levels. We also utilized Information Gain (IG) to analyze and rank the causes of various significant emergencies. Experimental results indicate that, compared to baseline data imputation models, ER-GAIN improved the prediction accuracy of key emergency features by 3.67% and 3.78%, respectively. Furthermore, AdaBoost enhanced the accuracy by over 4.34% and 3.25% compared to baseline predictive models. Through causation analysis, we identified the critical causes of train operation and fire incidents. The findings of this research will contribute to the establishment of early warning and prevention mechanisms for emergencies in URTS, potentially leading to safer and more reliable URTS operations.

An acoustic imaging method for detecting and locating gas leaks based on a virtual ultrasonic sensor array is proposed and experimentally demonstrated. A scanning sensor array of only two sensors is used to collect the acoustic signals generated by the leakage hole. The matrix of the leakage signal is processed by the cross-power spectrum method to achieve time consistency, afterward, the location of the leakage source can be calculated by the virtual beamforming method. The influence of the number of sensors and the distance between adjacent sensors on the effect of the proposed method are compared and discussed. To verify the effectiveness and operability of the detection and localization method, several experiments were carried out. Furthermore, a series of experiments were conducted to assess the accuracy and stability of this method. The experimental results demonstrate that the proposed method based on a virtual sensor array can achieve highly accurate localization of gas leaks and performs well regarding stability.

Endophytic plant growth promoting rhizobacteria (PGPRs) could replace chemical fertilizers in sustainable agriculture. Unfortunately, they are susceptible to harsh environmental conditions. Here, we proposed a polymeric hydrogel (PMH) consisting of carboxymethyl chitosan, sodium alginate, and calcium chloride for loading and protecting endophytic PGPR. This hydrogel can load endophytic PGPRs to not only boost its growth-promoting efficiency, but also help them adapt more effectively to environments. Using endophytic PGPR Ensifer C5 as model bacteria and Brasscia napus as host, we demonstrate that the PMH facilitate the colonization of endophytic PGPRs in the apical and lateral root primordia regions. Further analysis indicates that the PMH modulate suberin deposition of the endodermal cell layers and regulate the accumulation of auxin at the root tip. Meanwhile, PMH enhances the antioxidant capacity and disease resistance properties of plants by increasing the content of arachidonic acid metabolism intermediates in the plant. Importantly, the combination of PMH and endophytic PGPRs increases the yields of B. napus by approximately 30% in the field. Furthermore, PMH attenuates the loss of endophytic PGPR activity in the acidic environments. Overall, this microbial encapsulation strategy is a promising way to protect fragile endophytic microorganisms, providing attractive avenues in sustainable agriculture. Plant growth promoting rhizobacteria can replace chemical fertilizers, but they are susceptible to harsh environmental conditions. Here, the authors report on a protective hydrogel for promoting rhizobacteria colonization to enhance growth and improve adaptability of plants to acidic soil.

Metastasis is the most common cause of mortality in breast cancer patients worldwide. To identify improved mouse models for breast cancer growth and spontaneous metastasis, we examined growth and metastasis of both estrogen receptor positive (T47D) and negative (MDA-MB-231, SUM1315, and CN34BrM) human breast cancer cells in nude and NSG mice. Both primary tumor growth and spontaneous metastases were increased in NSG mice compared to nude mice. In addition, a pattern of metastasis similar to that observed in human breast cancer patients (metastases to the lungs, liver, bones, brain, and lymph nodes) was found in NSG mice. Furthermore, there was an increase in the metastatic burden in NSG compared to nude mice that were injected with MDA-MB-231 breast cancer cells in an intracardiac experimental metastasis model. This data demonstrates that NSG mice provide a better model for studying human breast cancer metastasis compared to the current nude mouse model.

Dexmedetomidine in combination with opioids has been used for postoperative analgesia. The purpose of this study was to investigate the impacts of dexmedetomidine supplemented intravenous analgesia on morphine consumption and subjective sleep quality in elderly patients after open abdominal surgery. This was a pilot randomized controlled trial. 58 elderly patients (age ≥ 60 years) who underwent open abdominal surgery were randomized to receive either dexmedetomidine supplemented morphine analgesia (0.5 mg/ml morphine plus 2 μg/ml dexmedetomidine in 100 ml normal saline, DEX group) or morphine analgesia (0.5 mg/ml morphine in 100 ml normal saline, CTRL group) for 72 hours after surgery. Patient-controlled analgesia pump was programmed to deliver a 2ml bolus with a lockout interval of 8 minutes and a background infusion at a rate of 1 ml/h. The primary endpoint was 72-hour morphine consumption. Secondary endpoints included pain intensity, subjective sleep quality, and 30-day complications and mortality after surgery. The 72-hour morphine consumption was lower in the DEX group than in the CTRL group (median 39.0 mg [interquartile range 37.3, 41.0] in the DEX group vs. 49.0 mg [45.5, 50.0] in the CTRL group; median difference -9.0 mg [95% CI -10.0, -6.0], P < 0.001). The intensity of pain within 48 hours was lower (P<0.001 at 4, 12 and 48 hours, P = 0.007 at 24 hours) whereas the subjective quality of sleep was higher (P = 0.031 during the night of surgery and P<0.001 during the 1st night after surgery, respectively) in the DEX group than in the CTRL group. The incidence of 30-day complications did not differ significantly between groups, but it was slightly lower in the DEX group (P = 0.060). There were no significant differences between groups regarding 30-day mortality and the incidences of adverse events. For elderly patients after open abdominal surgery, dexmedetomidine supplemented analgesia decreases morphine consumption, improves analgesic effects and subjective sleep quality without increasing adverse events. Chinese Clinical Trial Registry ChiCTR-IPR-14005620.

Background Bladder Cancer (BCa) is a severe genitourinary tract disease with an uncertain pathology. Increasing evidence indicates that the tumor microenvironment plays a decisive role with respect to cancer progression, and that this is driven by tumor cell interactions with stromal components. Tenascin-C (TN-C) is an important extracellular matrix (ECM) component, which has been reported to be involved in other types of cancer, such as breast cancer. The expression of TN-C in BCa tissue has been reported to be positively associated with the BCa pathological grade, yet the presence of urine TN-C is considered as an independent risk factor for BCa. However, the role of TN-C in BCa progression is still unknow. Thus, the object of the present investigation is to determine the role of TN-C in BCa progression and the involved mechanism. Methods In this study, expression of TN-C in BCa tissue of Chinese local people was determined by IHC. Patients corresponding to tumor specimens were flowed up by telephone call to get their prognostic data and analyzed by using SPSS 19.0 statistic package. In vitro mechanistic investigation was demonstrated by QT-qPCR, Western Blot, Plasmid transfection to establishment of high/low TN-C-expression stable cell line, Boyden Chamber Assay, BrdU incorporation, Wound Healing, laser scanning confocal microscopy (LSCM) and ELISA. Results TN-C expression in BCa tissue increases with tumor grade and is an independent risk factor for BCa patient. The in vitro investigation suggested that TN-C enhances BCa cell migration, invasion, proliferation and contributes to the elevated expression of EMT-related markers by activating NF-κB signaling, the mechanism of which involving in syndecan-4. Conclusions Expression of TN-C in BCa tissues of Chinese local people is increased according to tumor grade and is an independent risk factor. TN-C mediates BCa cell malignant behavior via syndecan-4 and NF-κB signaling. Although the mechanisms through which syndecan-4 is associated with the activation of NF-κB signaling are unclear, the data presented herein provide a foundation for future investigations into the role of TN-C in BCa progression.