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Background: As an important component of accelerated rehabilitation surgery, goal-directed fluid therapy (GDT) is one of the optimized fluid therapy strategies and is closely related to perioperative complications and mortality. This article aimed to study the effect of combining plasma colloid osmotic pressure (COP) with stroke volume variation (SVV) as a target for intraoperative GDT for postoperative pulmonary complications in older patients undergoing major abdominal surgery. Methods: In this study, older patients (n = 100) undergoing radical resection of gastroenteric tumors were randomized to three groups: Group C (n1 = 31) received a conventional infusion regimen, Group S1 (n2 = 34) received GDT based on SVV, and Group S2 (n3 = 35) received GDT based on SVV and COP. The results were recorded, including the lung injury score (LIS); PaO2/FiO2 ratio; lactic acid value at the times of beginning (T0) and 1 h (T1), 2 h (T2), and 3 h (T3) after liquid infusion in the operation room; the total liquid infusion volume; infusion volumes of crystalline and colloidal liquids; urine production rate; pulmonary complications 7 days after surgery; and the severity grading of postoperative pulmonary complications. Results: The patients in the S2 group had fewer postoperative pulmonary complications than those in the C group (P < 0.05) and the proportion of pulmonary complications of grade 1 and higher than grade 2 in S2 group was significantly lower than that in C group (P <0.05); the patients in the S2 group had a higher PaO2/FiO2 ratio than those in the C group (P < 0.05), lower LIS than those in the S1 and C groups (P < 0.05), less total liquid infusion than those in the C group (P < 0.05), and more colloidal fluid infusion than those in the S1 and C groups (P < 0.05). Conclusion: The findings of our study show that intraoperative GDT based on COP and SVV can reduce the incidence of pulmonary complications and conducive to shortening the hospital stay in older patients after gastrointestinal surgery. Trial registration: Chinese Clinical Trial. no. ChiCTR2100045671. Registry at www.chictr.org.cn on April 20, 2021. [ABSTRACT FROM AUTHOR]

This study explored the structures of three polysaccharides from Bupleurum chinense DC. (BCPRs), and evaluated their antioxidant and anti-aging properties. The HPGPC and ion chromatography analyses revealed that the molecular weights of the BCPRs ranged from 12.05 to 21.20 kDa, and were primarily composed of rhamnose, arabinose, xylose, galactose, glucose and galacturonic acid. Methylation and NMR studies identified 10 PMAAs, establishing the various backbones of BCPRs 1–3. BCPR-3 demonstrated potent antioxidant activities, including DPPH, ABTS, hydroxy, and superoxide radicals scavenging in vitro. At concentrations between 125 and 500 μg/mL, BCPR-3 increased T-AOC, SOD and GSH-Px activities, while decreasing MDA levels in H 2 O 2 -induced SH-SY5Y cells. In addition, RNA-seq results indicated that BCPR-3 considerably downregulated the expression of 49 genes and upregulated five genes compared with the control group. KEGG analysis suggested that these differentially expressed genes (DEGs) were predominantly involved in the TNF and PI3K/Akt signaling pathways. Furthermore, in vivo experiment with Drosophila melanogaster showed that BCPR-3 could extend the average lifespan of flies. In conclusion, polysaccharides from B. chinense exhibited potential antioxidant and anti-aging activities, which could be developed as new ingredients to combat oxidative stress damage and slow the aging process. [Display omitted] • Three acid polysaccharides were isolated from the roots of Bupleurum chinense DC. • BCPR-1, BCPR-2 and BCPR-3 possessed antioxidant activities. • BCPR-3 had a protective effect on SH-SY5Y cell injury induced by H 2 O 2. • BCPR-3 exerts antioxidant effect by regulating TNF and PI3K/Akt signaling pathways. • BCPR-3 could relatively prolong the life span of Drosophila melanogaster. [ABSTRACT FROM AUTHOR]

This study explored the structures of three polysaccharides from Bupleurum chinense DC. (BCPRs), and evaluated their antioxidant and anti-aging properties. The HPGPC and ion chromatography analyses revealed that the molecular weights of the BCPRs ranged from 12.05 to 21.20 kDa, and were primarily composed of rhamnose, arabinose, xylose, galactose, glucose and galacturonic acid. Methylation and NMR studies identified 10 PMAAs, establishing the various backbones of BCPRs 1–3. BCPR-3 demonstrated potent antioxidant activities, including DPPH, ABTS, hydroxy, and superoxide radicals scavenging in vitro. At concentrations between 125 and 500 μg/mL, BCPR-3 increased T-AOC, SOD and GSH-Px activities, while decreasing MDA levels in H 2 O 2 -induced SH-SY5Y cells. In addition, RNA-seq results indicated that BCPR-3 considerably downregulated the expression of 49 genes and upregulated five genes compared with the control group. KEGG analysis suggested that these differentially expressed genes (DEGs) were predominantly involved in the TNF and PI3K/Akt signaling pathways. Furthermore, in vivo experiment with Drosophila melanogaster showed that BCPR-3 could extend the average lifespan of flies. In conclusion, polysaccharides from B. chinense exhibited potential antioxidant and anti-aging activities, which could be developed as new ingredients to combat oxidative stress damage and slow the aging process. [Display omitted] • Three acid polysaccharides were isolated from the roots of Bupleurum chinense DC. • BCPR-1, BCPR-2 and BCPR-3 possessed antioxidant activities. • BCPR-3 had a protective effect on SH-SY5Y cell injury induced by H 2 O 2. • BCPR-3 exerts antioxidant effect by regulating TNF and PI3K/Akt signaling pathways. • BCPR-3 could relatively prolong the life span of Drosophila melanogaster. [ABSTRACT FROM AUTHOR]

Background: Increasing evidence indicates that leucine-rich-alpha-2-glycoprotein 1 (LRG1) is associated with multiple malignancies, but whether it participates in gastric cancer (GC) angiogenesis remains unclear. Methods: The expression levels of LRG1 were assessed in GC samples. Endothelial tube formation analysis, HUVEC migration assay, chorioallantoic membrane assay (CAM), and xenograft tumor model were used to investigate the effect of LRG1 on angiogenesis in gastric cancer. The involvement of activating transcription factor 3 (ATF3) was analyzed by chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assay. Western blot and enzyme-linked immunosorbent assay were performed to measure the SRC/STAT3/VEGFA pathway. Results: LRG1 was overexpressed in GC tissues and associated with cancer angiogenesis. In addition, LRG1 markedly promoted GC cell proliferation in vitro and in vivo. Moreover, overexpression of LRG1 could stimulate GC angiogenesis in vitro and in vivo. Then, we identified ATF3 promotes the transcription of LRG1 and is a positive regulator of angiogenesis. Additionally, LRG1 could activate VEGFA expression via the SRC/STAT3/ VEGFA pathway in GC cells, thus contributing to the angiogenesis of GC. Conclusions: The present study suggests LRG1 plays a crucial role in the regulation of angiogenesis in GC and could be a potential therapeutic target for GC. [ABSTRACT FROM AUTHOR]

Bone marrow-derived stem/progenitor cells have been utilized for cardiac or vascular repair after ischemic injury, but they are subject to apoptosis and immune rejection in the ischemic site. Multiple scaffolds were used as delivery tools to transplant stem/progenitor cells; however, these scaffolds did not show intrinsically antiapoptotic or anti-inflammatory properties. Decellularized aortic scaffolds that facilitate cell delivery and tissue repair were prepared by removing cells of patient-derived aortic tissues. Scanning electron microscopy (SEM) showed cells attached well to the scaffold after culturing for 5 days. Live/dead staining showed most seeded cells survived at day 7 on a decellularized aortic scaffold. Ki67 staining demonstrated that decellularized aortic scaffold promoted proliferation of bone marrow-derived CD34+ progenitor cells. Apoptosis of CD34+ progenitor cells induced by H2O2 at high concentration was significantly alleviated in the presence of decellularized aortic scaffolds, demonstrating a protective effect against oxidative stress-induced apoptosis. Furthermore, decellularized aortic scaffolds significantly reduced the expression of proinflammatory cytokines (IL-8, GM-CSF, MIP-1β, GRO-α, Entoxin, and GRO) concurrently with an increase in anti-inflammatory cytokines (IL-2 and TGF-β) released from CD34+ progenitor cells when exposed to H2O2 at low concentration. Finally, neovascularization was observed by H&E and immunohistochemical staining 14 days after the decellularized aortic scaffolds were subcutaneously implanted in nude mice. This preclinical study demonstrates that the use of a decellularized aortic scaffold possessing antiapoptotic and anti-inflammatory properties may represent a promising strategy for cardiovascular repair after ischemic injury. [ABSTRACT FROM AUTHOR]

This paper studies mobile edge computing (MEC) networks where multiple wireless devices (WDs) choose to offload their computation tasks to an edge server. To conserve energy and maintain quality of service for WDs, the optimization of joint offloading decision and bandwidth allocation is formulated as a mixed integer programming problem. However, the problem is computationally limited by the curse of dimensionality, which cannot be solved by general optimization tools in an effective and efficient way, especially for large-scale WDs. In this paper, we propose a distributed deep learning-based offloading (DDLO) algorithm for MEC networks, where multiple parallel DNNs are used to generate offloading decisions. We adopt a shared replay memory to store newly generated offloading decisions which are further to train and improve all DNNs. Extensive numerical results show that the proposed DDLO algorithm can generate near-optimal offloading decisions in less than one second. [ABSTRACT FROM AUTHOR]

Purpose: Esophageal squamous cell carcinoma (ESCC) is an aggressive disease with a poor prognosis, caused by the inactivation of critical cell growth regulators that lead to uncontrolled proliferation and increased malignancy. Although Serine/Threonine Kinase 3 (STK3), also known as Mammalian STE20-like protein kinase 2 (MST2), is a highly conserved kinase of the Hippo pathway, plays a critical role in immunomodulation, organ development, cellular differentiation, and cancer suppression, its phenotype and function in ESCC require further investigation. In this study, we report for the first time on the role of STK3 kinase and its activation condition in ESCC, as well as the mechanism and mediators of kinase activation.In this study, we investigated the expression and clinical significance of STK3 in ESCC. We first used bioinformatics databases and immunohistochemistry to analyze STK3 expression in the ESCC patient cohort and conducted survival analysis. In vivo, we conducted a tumorigenicity assay using nude mouse models to demonstrate the phenotypes of STK3 kinase. In vitro, we conducted Western blot analysis, qPCR analysis, CO-IP, and immunofluorescence (IF) staining analysis to detect molecule expression, interaction, and distribution. We measured proliferation, migration, and apoptosis abilities in ESCC cells in the experimental groups using CCK-8 and transwell assays, flow cytometry, and EdU staining. We used RNA-seq to identify genes that were differentially expressed in ESCC cells with silenced STK3 or FOXO1. We demonstrated the regulatory relationship of the TP53INP1/P21 gene medicated by the STK3-FOXO1 axis using Western blotting and ChIP in vitro.We demonstrate high STK3 expression in ESCC tissue and cell lines compared to esophageal epithelium. Cellular ROS induces STK3 autophosphorylation in ESCC cells, resulting in upregulated p-STK3/4. STK3 activation inhibits ESCC cell proliferation and migration by triggering apoptosis and suppressing the cell cycle. STK3 kinase activation phosphorylates FOXO1Ser212, promoting nuclear translocation, enhancing transcriptional activity, and upregulating TP53INP1 and P21. We also investigated TP53INP1 and P21’s phenotypic effects in ESCC, finding that their knockdown significantly increases tumor proliferation, highlighting their crucial role in ESCC tumorigenesis.STK3 kinase has a high expression level in ESCC and can be activated by cellular ROS, inhibiting cell proliferation and migration. Additionally, STK3 activation-mediated FOXO1 regulates ESCC cell apoptosis and cell cycle arrest by targeting TP53INP1/P21. Our research underscores the anti-tumor function of STK3 in ESCC and elucidates the mechanism underlying its anti-tumor effect on ESCC.Methods: Esophageal squamous cell carcinoma (ESCC) is an aggressive disease with a poor prognosis, caused by the inactivation of critical cell growth regulators that lead to uncontrolled proliferation and increased malignancy. Although Serine/Threonine Kinase 3 (STK3), also known as Mammalian STE20-like protein kinase 2 (MST2), is a highly conserved kinase of the Hippo pathway, plays a critical role in immunomodulation, organ development, cellular differentiation, and cancer suppression, its phenotype and function in ESCC require further investigation. In this study, we report for the first time on the role of STK3 kinase and its activation condition in ESCC, as well as the mechanism and mediators of kinase activation.In this study, we investigated the expression and clinical significance of STK3 in ESCC. We first used bioinformatics databases and immunohistochemistry to analyze STK3 expression in the ESCC patient cohort and conducted survival analysis. In vivo, we conducted a tumorigenicity assay using nude mouse models to demonstrate the phenotypes of STK3 kinase. In vitro, we conducted Western blot analysis, qPCR analysis, CO-IP, and immunofluorescence (IF) staining analysis to detect molecule expression, interaction, and distribution. We measured proliferation, migration, and apoptosis abilities in ESCC cells in the experimental groups using CCK-8 and transwell assays, flow cytometry, and EdU staining. We used RNA-seq to identify genes that were differentially expressed in ESCC cells with silenced STK3 or FOXO1. We demonstrated the regulatory relationship of the TP53INP1/P21 gene medicated by the STK3-FOXO1 axis using Western blotting and ChIP in vitro.We demonstrate high STK3 expression in ESCC tissue and cell lines compared to esophageal epithelium. Cellular ROS induces STK3 autophosphorylation in ESCC cells, resulting in upregulated p-STK3/4. STK3 activation inhibits ESCC cell proliferation and migration by triggering apoptosis and suppressing the cell cycle. STK3 kinase activation phosphorylates FOXO1Ser212, promoting nuclear translocation, enhancing transcriptional activity, and upregulating TP53INP1 and P21. We also investigated TP53INP1 and P21’s phenotypic effects in ESCC, finding that their knockdown significantly increases tumor proliferation, highlighting their crucial role in ESCC tumorigenesis.STK3 kinase has a high expression level in ESCC and can be activated by cellular ROS, inhibiting cell proliferation and migration. Additionally, STK3 activation-mediated FOXO1 regulates ESCC cell apoptosis and cell cycle arrest by targeting TP53INP1/P21. Our research underscores the anti-tumor function of STK3 in ESCC and elucidates the mechanism underlying its anti-tumor effect on ESCC.Results: Esophageal squamous cell carcinoma (ESCC) is an aggressive disease with a poor prognosis, caused by the inactivation of critical cell growth regulators that lead to uncontrolled proliferation and increased malignancy. Although Serine/Threonine Kinase 3 (STK3), also known as Mammalian STE20-like protein kinase 2 (MST2), is a highly conserved kinase of the Hippo pathway, plays a critical role in immunomodulation, organ development, cellular differentiation, and cancer suppression, its phenotype and function in ESCC require further investigation. In this study, we report for the first time on the role of STK3 kinase and its activation condition in ESCC, as well as the mechanism and mediators of kinase activation.In this study, we investigated the expression and clinical significance of STK3 in ESCC. We first used bioinformatics databases and immunohistochemistry to analyze STK3 expression in the ESCC patient cohort and conducted survival analysis. In vivo, we conducted a tumorigenicity assay using nude mouse models to demonstrate the phenotypes of STK3 kinase. In vitro, we conducted Western blot analysis, qPCR analysis, CO-IP, and immunofluorescence (IF) staining analysis to detect molecule expression, interaction, and distribution. We measured proliferation, migration, and apoptosis abilities in ESCC cells in the experimental groups using CCK-8 and transwell assays, flow cytometry, and EdU staining. We used RNA-seq to identify genes that were differentially expressed in ESCC cells with silenced STK3 or FOXO1. We demonstrated the regulatory relationship of the TP53INP1/P21 gene medicated by the STK3-FOXO1 axis using Western blotting and ChIP in vitro.We demonstrate high STK3 expression in ESCC tissue and cell lines compared to esophageal epithelium. Cellular ROS induces STK3 autophosphorylation in ESCC cells, resulting in upregulated p-STK3/4. STK3 activation inhibits ESCC cell proliferation and migration by triggering apoptosis and suppressing the cell cycle. STK3 kinase activation phosphorylates FOXO1Ser212, promoting nuclear translocation, enhancing transcriptional activity, and upregulating TP53INP1 and P21. We also investigated TP53INP1 and P21’s phenotypic effects in ESCC, finding that their knockdown significantly increases tumor proliferation, highlighting their crucial role in ESCC tumorigenesis.STK3 kinase has a high expression level in ESCC and can be activated by cellular ROS, inhibiting cell proliferation and migration. Additionally, STK3 activation-mediated FOXO1 regulates ESCC cell apoptosis and cell cycle arrest by targeting TP53INP1/P21. Our research underscores the anti-tumor function of STK3 in ESCC and elucidates the mechanism underlying its anti-tumor effect on ESCC.Conclusion: Esophageal squamous cell carcinoma (ESCC) is an aggressive disease with a poor prognosis, caused by the inactivation of critical cell growth regulators that lead to uncontrolled proliferation and increased malignancy. Although Serine/Threonine Kinase 3 (STK3), also known as Mammalian STE20-like protein kinase 2 (MST2), is a highly conserved kinase of the Hippo pathway, plays a critical role in immunomodulation, organ development, cellular differentiation, and cancer suppression, its phenotype and function in ESCC require further investigation. In this study, we report for the first time on the role of STK3 kinase and its activation condition in ESCC, as well as the mechanism and mediators of kinase activation.In this study, we investigated the expression and clinical significance of STK3 in ESCC. We first used bioinformatics databases and immunohistochemistry to analyze STK3 expression in the ESCC patient cohort and conducted survival analysis. In vivo, we conducted a tumorigenicity assay using nude mouse models to demonstrate the phenotypes of STK3 kinase. In vitro, we conducted Western blot analysis, qPCR analysis, CO-IP, and immunofluorescence (IF) staining analysis to detect molecule expression, interaction, and distribution. We measured proliferation, migration, and apoptosis abilities in ESCC cells in the experimental groups using CCK-8 and transwell assays, flow cytometry, and EdU staining. We used RNA-seq to identify genes that were differentially expressed in ESCC cells with silenced STK3 or FOXO1. We demonstrated the regulatory relationship of the TP53INP1/P21 gene medicated by the STK3-FOXO1 axis using Western blotting and ChIP in vitro.We demonstrate high STK3 expression in ESCC tissue and cell lines compared to esophageal epithelium. Cellular ROS induces STK3 autophosphorylation in ESCC cells, resulting in upregulated p-STK3/4. STK3 activation inhibits ESCC cell proliferation and migration by triggering apoptosis and suppressing the cell cycle. STK3 kinase activation phosphorylates FOXO1Ser212, promoting nuclear translocation, enhancing transcriptional activity, and upregulating TP53INP1 and P21. We also investigated TP53INP1 and P21’s phenotypic effects in ESCC, finding that their knockdown significantly increases tumor proliferation, highlighting their crucial role in ESCC tumorigenesis.STK3 kinase has a high expression level in ESCC and can be activated by cellular ROS, inhibiting cell proliferation and migration. Additionally, STK3 activation-mediated FOXO1 regulates ESCC cell apoptosis and cell cycle arrest by targeting TP53INP1/P21. Our research underscores the anti-tumor function of STK3 in ESCC and elucidates the mechanism underlying its anti-tumor effect on ESCC. [ABSTRACT FROM AUTHOR]

To address the environmental and food contamination issues caused by plastics and microorganisms, antimicrobial films using natural polymers has attracted enormous attention. In this work, we proposed a green, convenient and fast approach to prepare antimicrobial films from chitosan (CS), bacterial cellulose (BC) and ε-polylysine (ε-PL). The effects of different concentrations of ε-PL (0 %, 0.25 %, 0.5 %, 0.75 %, 1 %, w / v) on the physicochemical properties and antibacterial activity of composite films (CS-DABC-x%PL) were systematically investigated. Furthermore, a comprehensive comparison with purely physically mixed CS-BC-x%PL films provides a deeper understanding of the subject matter. Characterization tests of the films were conducted using scanning electron microscope (SEM), X-ray diffraction (XRD) and thermogravimetric analysis (TGA). The results suggested that the incorporation of 0.5 % ε-PL reduced the water solubility of the composite film by 19.82 %, along with improved the tensile strength and thermal stability by 37.31 % and 28.54 %. As ε-PL concentration increased to 1 %, the antibacterial performance of the films gradually enhanced. Additionally, the CS-DABC-0.5%PL film demonstrated effectiveness in delaying the deterioration of tilapia. These findings imply that this novel green packaging material holds significant potential in food preservation due to its promising antibacterial properties. [ABSTRACT FROM AUTHOR]

D-dimer level and platelet count (PC) have been reported separately as significant independent predictors of Acute Ischemic Stroke (AIS). Here, we aimed to investigate the combined prognostic value of abnormal D-dimer level and PC as defined for specific in-hospital and long-term outcomes in AIS patients. A total of 1468 patients admitted for ischemic stroke within 24 h of symptom onset from April 1, 2016 to November 31, 2019 at the Department of Neurology, the First Affiliated Hospital of Harbin Medical University were included in the final analysis. Eligible subjects were divided into four groups in terms of their levels of D-dimer and PC: DD−PC− (normal D-dimer level and normal PC), DD−PC+ (normal D-dimer level and abnormal PC), DD+PC− (higher D-dimer level and normal PC), and DD+PC+ (higher D-dimer level and abnormal PC). Logistic regression model and multinomial logit model were used to estimate the combined effect of D-dimer level and PC on in-hospital outcomes including discharge outcome and early neurological changes, and poor outcomes at 3, 6 and 12 months. DD+PC+ was found to be associated with the risk of in-hospital mortality (adjusted odds ratio [OR], 6.904; 95% confidence interval [CI], 2.781–17.144) and 3-month mortality (adjusted OR, 5.455; 95% CI, 2.019–14.743) compared with DD−PC−. Combination of the two indicators significantly improved the independent predictive value for functional outcomes, including early neurological deterioration (END) (OR, 3.622; 95% CI, 1.732–7.573) with threshold of at least 4-point increase on NIHSS, discharge outcome (OR, 2.713; 95% CI, 1.421–5.177); mRS of 0–1 point (OR, 0.409; 95% CI, 0.211–0.792), mRS of 0–2 points (OR, 0.234; 95% CI, 0.118, 0.461), and higher mRS-shift (OR, 2.379; 95% CI, 1.237–4.576) at 3 months; unfavorable outcome at 3 months (OR, 4.280; 95% CI, 2.169–8.446), 6 months (OR, 3.297; 95% CI, 1.452–7.488) and 12 months (OR, 4.157; 95% CI, 1.598–10.816). While comparatively weaker statistical significance was shown in DD+PC− and no correlation was found between adverse outcomes and DD−PC+. Similarly, patients with abnormal D-dimer level and PC were less likely to reach the status of stable or improving. Combination of D-dimer level and PC may have more significant prognostic value on END, in-hospital mortality, discharge outcome, and long-term outcomes than either index of D-dimer level or PC alone in AIS patients. • D-dimer and platelet are biomarkers in acute ischemic stroke. • Co-existing abnormal D-dimer level and platelet count indicates significantly higher risk. • Outcomes include functional dependence, a modified Rankin Scale shift and mortality. • The prediction of early neurological deterioration, or the status of stable or improving. [ABSTRACT FROM AUTHOR]

This study discusses the association between blood pressure (BP) variability at different time periods within first 24 hours after admission and the functional outcome in acute ischemic stroke (AIS). We observed BP variability within first 24 hours after admission and evaluated the association between BP variability at different time periods (4 am-8 am, 10 am-2 pm, 4 pm-8 pm, 10 pm-2 am) and the functional outcome in AIS. National Institute of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS) were applied to evaluate short- (7 days) and long-term functional outcome. The 24 hours after admission and early morning (4 am-8 am) systolic blood pressure (SBP) variability were associated with poor outcome at day 7 (adjusted OR = 1.567, 95% CI = 1.076-2.282; adjusted OR = 1.507, 95% CI = 1.028-2.209, respectively). Compared with the impact of the 24-hour BP variability on long-term functional outcome, the early morning SBP was proved to be a strongly independent predictor for functional outcome at 3 months (adjusted OR = 1.505, 95% CI = 1.053-2.152), 6 months (adjusted OR = 1.560, 95% CI = 1.048-2.226), and 12 months (adjusted OR = 1.689, 95% CI = 1.104-2.584). The BP variability in other time period groups was shown to have no influence on functional outcome. In addition, attempts to explain early morning BP variability with baseline characteristic factors at admission found that baseline SBP is the most influential (2.71%) factor. About 95.87% of the SBP variability in early morning was unexplained. In our study, early morning SBP variability is the strongest independent predictor for functional outcome in (AIS) patients, and baseline SBP after admission should be monitored as a control indicator of early morning SBP variability in the treatment of AIS patients. [ABSTRACT FROM AUTHOR]

[Display omitted] • Electrostimulated reduction–oxidation process for azo dye removal was proposed. • Intermittent electrostimulation enhanced biocathode reductive decolorization. • Oxygen-assisted bioanode achieved intermediates mineralization and electron recovery. • Differences in voltage supply strategies regulated electrode microbiome evolution. • The possible degradation mechanism for electrostimulated azo dye removal was revealed. The electro-stimulated microbial process offers promise in overcoming the intrinsic drawbacks of the conventional reduction–oxidation process for azo dyes removal. However, the lack of available electron donors, continuous external power supply, and weak anodic oxidation are the major challenges for this process to achieve efficient azo dye biodegradation. Herein, an intermittent electric field stimulated reduction–oxidation coupled process was developed to enhance Alizarin Yellow R (AYR) biodegradation. Introducing a weak intermittent electrostimulation considerably boosted the anaerobic cathodic reduction and micro-oxygen-assisted anodic oxidation process, as evidenced by the higher AYR decolorization, p -phenylenediamine, and 5-aminosalicylic acid bio-mineralization efficiency than that in the bio-processes with continuous and without electrostimulation, respectively. The endogenous organics generated during AYR degradation could serve as an effective electron source for anodic microorganisms to drive the biocathode decolorization. Compared to continuous electrostimulation, intermittent electrostimulation exhibited better electron transfer capability and created a more favorable oxidation–reduction potential (ORP) for reductive decolorization of AYR and bio-mineralization of its intermediate products. Microbial community analysis revealed that more functional consortia capable of electroactivity (e.g. Geobacter and Pseudomonas) and AYR metabolism (e.g. Bosea , Sphingopyxis , and Achromobacter) were enriched by intermittent electrostimulation than continuous electrostimulation. The molecular ecological network analysis indicated that synthetic metabolisms between electroactive and AYR metabolizing bacteria might play major roles in electro-microbial-mediated AYR removal. This study reveals the potential and mechanism of intermittent electric field stimulated reduction–oxidation coupled process for enhanced azo dye biodegradation, which opens an appealing avenue for enhanced azo dye removal from wastewater. [ABSTRACT FROM AUTHOR]