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  1. Article: The Use of Membranes (ST-100, oXiris, and M60) for Continuous Renal Replacement Therapy in a Child with Sepsis.

    Ying, Jiayun / Cai, Xiaodi / Lu, Guoping / Chen, Weiming

    Case reports in critical care

    2023  Volume 2023, Page(s) 2000781

    Abstract: Sepsis is a critical condition affecting patients worldwide. Systemic inflammatory response syndrome in sepsis contributes to organ dysfunction and mortality. The oXiris is a recently developed continuous renal replacement therapy (CRRT) hemofilter ... ...

    Abstract Sepsis is a critical condition affecting patients worldwide. Systemic inflammatory response syndrome in sepsis contributes to organ dysfunction and mortality. The oXiris is a recently developed continuous renal replacement therapy (CRRT) hemofilter indicated for the adsorption of cytokines from the bloodstream. In our study, in a septic child, CRRT with three filters, including the oXiris hemofilter, resulted in a downregulation of inflammatory biomarkers and a reduction of vasopressors. Herein, we described the first report of such usage in septic children.
    Language English
    Publishing date 2023-06-06
    Publishing country United States
    Document type Case Reports
    ZDB-ID 2927720-6
    ISSN 2090-6439 ; 2090-6420
    ISSN (online) 2090-6439
    ISSN 2090-6420
    DOI 10.1155/2023/2000781
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: [O-linked N-acetylglucosamine modification induced by lipopolysaccharide is involved in inflammatory signaling pathway in endothelial cells].

    Chen, Hehe / Shi, Yanhua / Ying, Jiayun / Dong, Zhuoya / Wang, Yan / Zheng, Yao / Ruan, Peisen

    Zhonghua wei zhong bing ji jiu yi xue

    2023  Volume 35, Issue 2, Page(s) 164–169

    Abstract: Objective: To explore whether the lipopolysaccharide (LPS)-induced modification of O-linked N-acetylglucosamine (O-GlcNAc) is involved in the inflammatory signaling pathway of endothelial cells.: Methods: Human umbilical vein endothelial cells (HUVEC) ...

    Abstract Objective: To explore whether the lipopolysaccharide (LPS)-induced modification of O-linked N-acetylglucosamine (O-GlcNAc) is involved in the inflammatory signaling pathway of endothelial cells.
    Methods: Human umbilical vein endothelial cells (HUVEC) were cultured in vitro, and cells in logarithmic growth phase were used for experiments. Cells were divided into blank control group, LPS group (2 000 mg/L LPS), O-GlcNAc transferase (OGT) overexpression (OGT-OE)+LPS group (plasmid transfection OGT+2 000 mg/L LPS), protein kinase C (PKC) inhibitor+LPS group (10 μmol/L Go 6983+2 000 mg/L LPS), RhoA inhibitor+LPS group (40 μmol/L Rhoin hydrochloride+2 000 mg/L LPS), phosphatidylinositol-3-kinase (PI3K) inhibitor+LPS group (1 μmol/L SL-2052+2 000 mg/L LPS), serine/threonine kinase (Akt) inhibitor+LPS group (10 μmol/L PP2+2 000 mg/L LPS) and small interfering RNA (siRNA) treated Akt (si-AKT)+LPS group (si-Akt+2 000 mg/L LPS). After 24 hours of LPS treatment, real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was used to detect the transcription levels of inflammatory cytokines [interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)]. The protein expression or phosphorylation of OGT, O-GlcNAc, Akt, extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (p38MAPK), nuclear factor-κB p65 (NF-κB p65), and signal transducer and activator of transcription 3 (STAT3) were determined by Western blotting.
    Results: Compared with the blank control group, the expression of OGT and the modification of O-GlcNAc in the LPS group were decreased, while the expressions of phosphorylated ERK, p38MAPK, and STAT3 were increased, and the transcript levels of inflammatory cytokines were also significantly increased [IL-6 mRNA (2
    Conclusions: The decreased level of O-GlcNAc modification in endothelial cells stimulated with LPS promotes partial activation of inflammatory signaling pathways, mainly involving ERK, p38MAPK, and STAT3, and affects the expression of inflammatory factors. AKT may be involved in the effect of LPS on the inhibition of O-GlcNAc modification.
    MeSH term(s) Humans ; Lipopolysaccharides/pharmacology ; Lipopolysaccharides/metabolism ; NF-kappa B/metabolism ; Acetylglucosamine/pharmacology ; Tumor Necrosis Factor-alpha/metabolism ; Intercellular Adhesion Molecule-1 ; Interleukin-6 ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Vascular Cell Adhesion Molecule-1 ; Signal Transduction ; Cytokines ; Human Umbilical Vein Endothelial Cells ; RNA, Small Interfering ; RNA, Messenger
    Chemical Substances Lipopolysaccharides ; NF-kappa B ; Acetylglucosamine (V956696549) ; Tumor Necrosis Factor-alpha ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Interleukin-6 ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Vascular Cell Adhesion Molecule-1 ; Cytokines ; RNA, Small Interfering ; RNA, Messenger
    Language Chinese
    Publishing date 2023-03-14
    Publishing country China
    Document type English Abstract ; Journal Article
    ISSN 2095-4352
    ISSN 2095-4352
    DOI 10.3760/cma.j.cn121430-20220314-00242
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Inhibition of the intracellular domain of Notch1 results in vascular endothelial cell dysfunction in sepsis.

    Liu, Tingyan / Zhang, Caiyan / Ying, Jiayun / Wang, Yaodong / Yan, Gangfeng / Zhou, Yufeng / Lu, Guoping

    Frontiers in immunology

    2023  Volume 14, Page(s) 1134556

    Abstract: Background: Notch signaling is critical for regulating the function of vascular endothelial cells (ECs). However, the effect of the intracellular domain of Notch1 (NICD) on EC injury in sepsis remains unclear.: Methods: We established a cell model of ...

    Abstract Background: Notch signaling is critical for regulating the function of vascular endothelial cells (ECs). However, the effect of the intracellular domain of Notch1 (NICD) on EC injury in sepsis remains unclear.
    Methods: We established a cell model of vascular endothelial dysfunction and induced sepsis in a mouse model
    Results: We found that LPS, interleukin 6, and serum collected from septic children could inhibit the expression of NICD and its downstream regulator Hes1, which impaired endothelial barrier function and led to EC apoptosis through the AKT pathway. Mechanistically, LPS decreased the stability of NICD by inhibiting the expression of a deubiquitylating enzyme, ubiquitin-specific proteases 8 (USP8). Melatonin, however, upregulated USP8 expression, thus maintaining the stability of NICD and Notch signaling, which ultimately reduced EC injury in our sepsis model and elevated the survival rate of septic mice.
    Conclusions: We found a previously uncharacterized role of Notch1 in mediating vascular permeability during sepsis, and we showed that inhibition of NICD resulted in vascular EC dysfunction in sepsis, which was reversed by melatonin. Thus, the Notch1 signaling pathway is a potential target for the treatment of sepsis.
    MeSH term(s) Animals ; Mice ; Endothelial Cells/metabolism ; Lipopolysaccharides ; Melatonin/pharmacology ; Sepsis/metabolism ; Signal Transduction
    Chemical Substances Lipopolysaccharides ; Melatonin (JL5DK93RCL) ; Notch1 protein, mouse
    Language English
    Publishing date 2023-05-02
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1134556
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Sulodexide improves vascular permeability via glycocalyx remodelling in endothelial cells during sepsis.

    Ying, Jiayun / Zhang, Caiyan / Wang, Yaodong / Liu, Tingyan / Yu, Zhenhao / Wang, Kexin / Chen, Weiming / Zhou, Yufeng / Lu, Guoping

    Frontiers in immunology

    2023  Volume 14, Page(s) 1172892

    Abstract: Background: Degradation of the endothelial glycocalyx is critical for sepsis-associated lung injury and pulmonary vascular permeability. We investigated whether sulodexide, a precursor for the synthesis of glycosaminoglycans, plays a biological role in ... ...

    Abstract Background: Degradation of the endothelial glycocalyx is critical for sepsis-associated lung injury and pulmonary vascular permeability. We investigated whether sulodexide, a precursor for the synthesis of glycosaminoglycans, plays a biological role in glycocalyx remodeling and improves endothelial barrier dysfunction in sepsis.
    Methods: The number of children with septic shock that were admitted to the PICU at Children's Hospital of Fudan University who enrolled in the study was 28. On days one and three after enrollment, venous blood samples were collected, and heparan sulfate, and syndecan-1 (SDC1) were assayed in the plasma. We established a cell model of glycocalyx shedding by heparinase III and induced sepsis in a mouse model via lipopolysaccharide (LPS) injection and cecal ligation and puncture (CLP). Sulodexide was administrated to prevent endothelial glycocalyx damage. Endothelial barrier function and expression of endothelial-related proteins were determined using permeability, western blot and immunofluorescent staining. The survival rate, histopathology evaluation of lungs and wet-to-dry lung weight ratio were also evaluated.
    Results: We found that circulating SDC1 levels were persistently upregulated in the non-alive group on days 1 and 3 and were positively correlated with IL-6 levels. Receiver operating characteristic curve analysis showed that SDC1 could distinguish patients with mortality. We showed that SDC1-shedding caused endothelial permeability in the presence of heparinase III and sepsis conditions. Mechanistically, sulodexide (30 LSU/mL) administration markedly inhibited SDC1 shedding and prevented endothelial permeability with zonula occludens-1 (ZO-1) upregulation via NF-κB/ZO-1 pathway. In mice with LPS and CLP-induced sepsis, sulodexide (40 mg/kg) administration decreased the plasma levels of SDC1 and increased survival rate. Additionally, sulodexide alleviated lung injury and restored endothelial glycocalyx damage.
    Conlusions: In conclusion, our data suggest that SDC1 predicts prognosis in children with septic shock and sulodexide may have therapeutic potential for the treatment of sepsis-associated endothelial dysfunction.
    MeSH term(s) Animals ; Mice ; Endothelial Cells ; Shock, Septic ; Capillary Permeability ; Glycocalyx ; Lipopolysaccharides ; Lung Injury ; Sepsis/drug therapy ; Glycosaminoglycans/pharmacology ; Body Weight
    Chemical Substances glucuronyl glucosamine glycan sulfate (75HGV0062C) ; Lipopolysaccharides ; Glycosaminoglycans
    Language English
    Publishing date 2023-08-08
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1172892
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Establishment of a Rat Model of Capillary Leakage Syndrome Induced by Cardiopulmonary Resuscitation After Cardiac Arrest.

    Zhang, Xiao-Lei / Cheng, Ye / Xing, Chun-Lin / Ying, Jia-Yun / Yang, Xue / Cai, Xiao-di / Lu, Guo-Ping

    Current medical science

    2023  Volume 43, Issue 4, Page(s) 708–715

    Abstract: Objective: Cardiopulmonary resuscitation (CPR) after cardiac arrest (CA) is one of the main causes of capillary leakage syndrome (CLS). This study aimed to establish a stable CLS model following the CA and cardiopulmonary resuscitation (CA-CPR) model in ...

    Abstract Objective: Cardiopulmonary resuscitation (CPR) after cardiac arrest (CA) is one of the main causes of capillary leakage syndrome (CLS). This study aimed to establish a stable CLS model following the CA and cardiopulmonary resuscitation (CA-CPR) model in Sprague-Dawley (SD) rats.
    Methods: We conducted a prospective, randomized, animal model study. All adult male SD rats were randomly divided into a normal group (group N), a sham operation group (group S), and a cardiopulmonary resuscitation group (group T). The SD rats of the three groups were all inserted with 24-G needles through their left femoral arteries and right femoral veins. In group S and group T, the endotracheal tube was intubated. In group T, CA induced by asphyxia (AACA) was caused by vecuronium bromide with the endotracheal tube obstructed for 8 min, and the rats were resuscitated with manual chest compression and mechanical ventilation. Preresuscitation and postresuscitation measurements, including basic vital signs (BVS), blood gas analysis (BG), routine complete blood count (CBC), wet-to-dry ratio of tissues (W/D), and the HE staining results after 6 h were evaluated.
    Results: In group T, the success rate of the CA-CPR model was 60% (18/30), and CLS occurred in 26.6% (8/30) of the rats. There were no significant differences in the baseline characteristics, including BVS, BG, and CBC, among the three groups (P>0.05). Compared with pre-asphyxia, there were significant differences in BVS, CBC, and BG, including temperature, oxygen saturation (SpO
    Conclusion: The CA-CPR model in SD rats induced by asphyxia could reproduce CLS with good stability and reproducibility.
    MeSH term(s) Animals ; Male ; Rats ; Asphyxia/complications ; Cardiopulmonary Resuscitation/adverse effects ; Cardiopulmonary Resuscitation/methods ; Heart Arrest/therapy ; Prospective Studies ; Rats, Sprague-Dawley ; Reproducibility of Results
    Language English
    Publishing date 2023-07-05
    Publishing country China
    Document type Journal Article
    ZDB-ID 2931065-9
    ISSN 2523-899X ; 2096-5230
    ISSN (online) 2523-899X
    ISSN 2096-5230
    DOI 10.1007/s11596-023-2695-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Malat1 regulates PMN-MDSC expansion and immunosuppression through p-STAT3 ubiquitination in sepsis.

    Wang, Yaodong / Zhang, Caiyan / Liu, Tingyan / Yu, Zhenhao / Wang, Kexin / Ying, Jiayun / Wang, Yao / Zhu, Ting / Li, Jingjing / Hu, Xiuchuan Lucas / Zhou, Yufeng / Lu, Guoping

    International journal of biological sciences

    2024  Volume 20, Issue 4, Page(s) 1529–1546

    Abstract: Myeloid-derived suppressor cells (MDSCs) expand during sepsis and contribute to the development of persistent inflammation-immunosuppression-catabolism syndrome. However, the underlying mechanism remains unclear. Exploring the mechanisms of MDSCs ... ...

    Abstract Myeloid-derived suppressor cells (MDSCs) expand during sepsis and contribute to the development of persistent inflammation-immunosuppression-catabolism syndrome. However, the underlying mechanism remains unclear. Exploring the mechanisms of MDSCs generation may provide therapeutic targets for improving immune status in sepsis. Here, a sepsis mouse model is established by cecal ligation and perforation. Bone marrow cells at different sepsis time points are harvested to detect the proportion of MDSCs and search for differentially expressed genes by RNA-sequence. In lethal models of sepsis, polymorphonuclear-MDSCs (PMN-MDSCs) decrease in early but increase and become activated in late sepsis, which is contrary to the expression of metastasis-associated lung adenocarcinoma transcript 1 (Malat1).
    MeSH term(s) Animals ; Mice ; Disease Models, Animal ; Immunosuppression Therapy ; Myeloid-Derived Suppressor Cells/metabolism ; Sepsis/metabolism
    Chemical Substances Malat1 long non-coding RNA, mouse ; Stat3 protein, mouse
    Language English
    Publishing date 2024-02-11
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2179208-2
    ISSN 1449-2288 ; 1449-2288
    ISSN (online) 1449-2288
    ISSN 1449-2288
    DOI 10.7150/ijbs.92267
    Database MEDical Literature Analysis and Retrieval System OnLINE

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