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Objective To investigate the effect of sufentanil (suf) on hepatic injury in burn sepsis rats by regulating Janus kinase 2 (JAK2)/signal transduction and transcriptional activator 3 (STAT3) signaling pathway. Methods SD rats were randomly divided into the control group, the model group, the suf low-dose group (0.75 µg/kg), the suf high-dose group (3 µg/kg), the imipenem group (90 mg/kg) and the suf high-dose + kumamycin group (3 µg/kg suf+4 mg/kg kumamycin). Serum liver function indexes including alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected. The pathological changes of liver tissue were observed by HE staining. The contents of tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1) and interleukin (IL)-6 were detected by enzyme-linked immunosorbent assay (ELISA). Terminal deoxynucleotide transferase mediated dUTP nick end labeling (TUNEL) staining was used to detect hepatocyte apoptosis. Western blot assay was used to detect the expression of p-JAK2 and p-STAT3 proteins in liver tissue. Results Compared with the control group, the model group showed elevated serum levels of ALT and AST, swelling of liver cells and infiltration of numerous inflammatory cells in liver tissue. The levels of TNF-α, MCP-1 and IL-6 in liver tissue, apoptosis rate of liver cells, and expression levels of p-JAK2 and p-STAT3 proteins were increased (P＜0.05). Compared with the model group, serum levels of ALT and AST were reduced in the suf low-dose group and the suf high-dose group, and pathological damages of liver tissue were improved. The contents of TNF- α, MCP-1 and IL-6 in liver tissue, the apoptosis rate of liver cells, and the expression levels of p-JAK2 and p-STAT3 proteins were reduced (P＜0.05). Moreover, changes in above indicators were significantly higher in the suf high dose group of suf than those in the suf low dose group (P＜0.05), and there was no significant difference compared with the imipenem group. Kumamycin inhibited the improvement effect of high-dose suf on liver injury in rats with burn sepsis (P＞0.05). Conclusion Sufentanil may improve liver injury in burn-induced sepsis rats by inhibiting the JAK2/STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To study the evaluation value of prognosis of neutrophil CD64 index combined with serum apolipoprotein M (APOM) and high mobility group protein B1 (HMGB1) in patients with sepsis caused by bacterial bloodstream infection. Methods: 251 patients with sepsis caused by bacterial bloodstream infection were divided into survival group and death group according to whether they experienced mortality after 28 days of admission. The influencing factors of 28 d mortality were analyzed by Logistic regression model, the value of CD64 index, serum APOM, HMGB1 and conventional infection indicators in predicting 28 d mortality in patients with sepsis caused by bacterial bloodstream infection were analyzed by receiver operating characteristic (ROC) curve. Results: Compared with survival group, the neutrophil CD64 index and HMGB1 in death group were significantly increased, and the serum APOM was significantly decreased (P<0.05). High APACHEII score, high procalcitonin, high neutrophil CD64 index, high C-reactive protein, high HMGB1, and low APOM were risk factors for 28 d mortality in patients with sepsis caused by bacterial bloodstream infection (P<0.05). ROC curve showed that, the area under the curve (AUC) of procalcitonin, C-reactive protein, neutrophil CD64 index, APOM and HMGB1 in predicting the 28 d mortality risk of sepsis patients caused by bacterial bloodstream infection was 0.917, which was greater than that predicted by single index. Conclusion: The increase of neutrophil CD64 index, HMGB1 and the decrease of APOM are related to the risk of 28 d mortality in patients with sepsis caused by bacterial bloodstream infection, and combined with procalcitonin and C-reactive protein has a high predictive value. [ABSTRACT FROM AUTHOR]

脓毒症是一种由宿主对感染反应失调引起的全身炎症反应综合征, 具有高发病率、高病死率的特点。脓 毒症的发病机制复杂, 至今仍尚未明确。孟德尔随机化 (MR) 分析使用与暴露因素相关的遗传变异作为工具变量, 将基因组数据纳入流行病学研究设计中, 能够更为准确地推断暴露因素与健康结局之间的因果关系。近年来, 随着 全基因组关联研究大样本数据的发布, MR分析在脓毒症相关危险因素与发病风险及预后的关系方面取得一定进 展。MR分析作为一种强有力的流行病学研究方法, 在脓毒症领域可明确相关危险因素对脓毒症发病风险或预后 是否起到诱导作用, 有助于识别高危人群、及时制定干预措施并进一步探索针对脓毒症的潜在防治策略, 以避免或 延缓疾病发生发展及改善患者预后。 [ABSTRACT FROM AUTHOR]

BACKGROUND: Sepsis complicated by myocardial injury is characterized by a high mortality. Metformin can prevent sepsis-induced myocardial dysfunction byexerting anti-inflammatory effects, improving oxidative stress, and reducing apoptosis. However, it is unclear whether metformin-induced autophagy plays an important role in the protective effect against sepsis-induced myocardial injury. OBJECTIVE: To explore the effect of metformin pretreatment on myocardial injury in septic mice. METHODS: A total of 40 male Kunming mice were randomly divided into sham operation group, model group, metformin group, and metformin+ 3-methyladenine group, with 10 mice in each group. The latter two groups were intraperitoneally injected with metformin for 14 days at a fixed time every day, and the metformin+3-methyladenine group was intraperitoneally injected with 3-methyladenine 1 hour before modeling. Twenty-four hours after the last injection of metformin, cecal ligation and perforation were used to construct a model of myocardial injury in septic mice. The sham operation group was not ligated and perforated. All mice were sacrificed 24 hours after surgery, and blood and myocardial specimens were collected. The levels of inflammatory factors and myocardial injury markers in serum were detected by ELISA. The mRNA expression of autophagy markers LC3B and p62 in myocardial tissue was detected by RT-qPCR. The protein expression of LC3B, Beclin-1, p62, p-AMPK, and AMPK in myocardial tissue was detected by western blot. The pathological changes in myocardial tissue were detected by hematoxylin-eosin staining. RESULTS AND CONCLUSION: Autophagy was inhibited in septic mice with myocardial injury. Compared with the sham operation group, the levels of serum tumor necrosis factor-α, interleukin-1β, interleukin-6, creatine kinase isoenzyme, and troponin T were increased in the model group (P < 0.05), but there was no significant difference in p62, LC3II/LC3I, and p-AMPK/AMPK between the two groups (P > 0.05). Compared with the model group, the levels of tumor necrosis factor-α, interleukin-6, creatine kinase isoenzyme, troponin T, and p62 were decreased in the metformin group (P < 0.05), while LC3II/LC3I, p-AMPK/ AMPK and Beclin-1 level were increased (P < 0.05). Compared with the metformin group, the levels of tumor necrosis factor-α, interleukin-6, creatine kinase isoenzyme, troponin T, and p62 were increased in the metformin+3-methyladenine group (P < 0.05), while LC3II/LC3I and Beclin-1 level were decreased (P < 0.05). Myocardial hematoxylin-eosin staining indicated that myocardial fibers arranged normally in the sham operation group, but disorderedly in the model group, with interstitial edema and a large number of infiltrated inflammatory cells. A small amount of vacuolar changes were observed in the metformin group. The arrangement of myocardial fibers in the metformin+3-methyladenine group was slightly disordered, with more vacuolar changes. To conclude, metformin pretreatment may reduce myocardial injury in septic mice by activating the AMPK signaling pathway and inducing autophagy. [ABSTRACT FROM AUTHOR]

Objective To investigate the mechanism of fisetin inhibiting the activation of microglia NOD-like receptor family protein 3 (NLRP3) inflammasome in microglia and alleviating cognitive impairment after sepsis. Methods C57BL/6 mice were used to establish the sepsis model by cecal ligation and puncture. Mice were divided into four groups: the sham group, the sepsis group, the sepsis+caspase-1 knockout group (sepsis+Cas-1-/- group) and the sepsis+fisetin group. Evans blue was used to detect the permeability of blood-brain barrier (BBB). Morris water maze was used to evaluate the cognitive function of mice. Western blot assay and immunofluorescence double staining were used to detect the expression of NLRP3 inflammasome-related proteins including caspase-1, N-terminal fragment of the GSDMD (GSDMD-N), interleukin (IL)-1β, IL-18 and mitophagy-related proteins (Pink1, Parkin and LC3-Ⅱ) in brain tissue and microglia. Results Compared with the sham group, expression levels of caspase-1, GSDMD-N, IL-1β and IL-18 were significantly increased in the sepsis group (P＜0.05). Compared with the sepsis group, expression levels of caspase-1, GSDMD-N, IL-1β and IL-18 were significantly decreased in the sepsis+Cas-1-/- group (P＜0.05). The expression levels of Pink1, Parkin and LC3- Ⅱ were significantly higher in the sepsis+fisetin group than those of the sepsis group (P＜0.05), and expression levels of caspase-1, GSDMD-N, IL-1β and IL-18 were significantly lower (P＜0.05). After fisetin intervention, the permeability of BBB was decreased and the cognitive impairment (decreased escape latency and increased frequencies of crossing the platform) was alleviated in the sepsis+fisetin group compared with those of the sepsis group (P＜0.05). Conclusion Fisetin may alleviate central inflammation and cognitive impairment after sepsis by inhibiting the activation of microglial NLRP3 inflammasome through activating mitophagy. [ABSTRACT FROM AUTHOR]

Sepsis patients have low survival rates, high mortality rates, and poor prognosis, making early identification of pathogens particularly crucial. Metagenomic next-generation sequencing (mNGS) enables unbiased detection of all microorganisms in clinical samples, providing greater sensitivity, accuracy, and efficiency in early detection of sepsis pathogenic microorganism compared to traditional culture techniques. With the continuous development of next-generation sequencing technology, the clinical application value of mNGS in sepsis diagnosis will further improve. This article reviews the advantages, clinical applications, progress, challenges, and prospects of mNGS in the early diagnosis of sepsis. [ABSTRACT FROM AUTHOR]

目的 分析外周血中性粒细胞/淋巴细胞 (NLR) 联合乳酸清除率 (LCR) 与脓毒症并发肝损伤的关系, 并评估 NLR, LCR 单独及联合检测对脓毒症并发肝损伤的预测效能. 方法 302例脓毒症患者中, 并发急性肝损 伤 89例 (肝损组), 未并发肝损伤 213例 (非肝损组), 比较两组 NLR, 6h LCR. 肝损组中, 胆汁淤积型 38例, 混合型 40例, 肝细胞损伤型11例, 轻度肝损伤42例, 中度肝损伤33例, 重度肝损伤14例, 比较不同类型, 不同程度肝损伤 患者NLR, 6 h LCR. 采用多因素Logistic回归分析NLR, LCR与脓毒症并发肝损伤的相关性. 采用ROC评价NLR, LCR 对 脓 毒 症 并 发 肝 损 伤 的 预 测 效 能. 结 果 肝 损 组 外 周 血 NLR, 6 h LCR 分 别 为 19. 25 ± 5. 70, -57. 5% (-127. 6%, -17. 7%), 非肝损组分别为14. 03 ± 5. 06, 24. 1% (-12. 9%, 47. 6%), 两组比较, P均<0. 05. 不同程度肝损 伤患者6 h LCR比较, P均<0. 05. 多因素Logistic回归分析结果显示, NLR, 6 h LCR, APACHEⅡ评分, SOFA评分, 总 胆红素, 凝血酶原时间是脓毒症并发肝损伤的独立危险因素. NLR预测脓毒症并发肝损伤发生的ROC下面积 (AUC) 为0. 786 (95% CI: 0. 717~ 0. 854), 6 h LCR的AUC为0. 816 (95% CI: 0. 763~ 0. 868), 而NLR联合6 h LCR预测脓毒症 并发肝损伤的AUC为0. 857 (95% CI: 0. 807~ 0. 908), 当取最佳截断值0. 398时, 灵敏度为69. 7%, 特异度为90. 6%, 优 于单一指标对脓毒症相关肝损伤的预测效能. 结论 外周血NLR及6 h LCR是脓毒症并发肝损伤的危险因素; NLR 及6 h LCR单独及联合检测对脓毒症并发肝损伤均有一定预测效能, 联合检测预测效能更高. [ABSTRACT FROM AUTHOR]

Objective: To study the clinical value of serum heparin binding protein (HBP), neopterin (neopterin) and ubiquitin specific protease 13 (USP13) in predicting the clinical outcome of patients with sepsis. Methods: 157 patients with sepsis who were admitted to our hospital from June 2021 to June 2023 were selected, and patients were divided into non-shock group (n = 93) and shock group (n = 64) according to whether septic shock occurred, the levels of serum HBP, neopterin and USP13 were compared between two groups. The 28 d mortality of 157 patients with sepsis were counted, the data of death group and survival group and the levels of serum HBP, neopterin and USP13 were compared, the influencing factors of 28 d death in patients with sepsis upon admission were analyzed by multivariate Logistic regression model, the predictive value of serum HBP, neopterin and USP13 of 28 d death in patients with sepsis upon admission were analyzed by receiver operating characteristic (ROC) curve. Results: Compared with non-shock group, the serum HBP and neopterin in shock group were significantly increased (P < 0.05) and the serum USP13 was significantly decreased (P < 0.05) . 157 patients with sepsis admitted for 28 d and 47 deaths, with an incidence of 29.94%. Compared with survival group, the acute physiology and chronic health status score II (APACHE-II), the proportion of complicated with diabetes mellitus, sequential organ failure assessment score (SOFA), HBP and neopterin in death group were significantly increased (P < 0.05) and serum USP13 was significantly decreased (P < 0.05) Multivariate Logistic regression analysis showed that, elevated APACHE II score, elevated SOFA score, complicated with diabetes mellitus, elevated HBP, elevated neopterin and decreased USP13 were risk factors for 28 d death in patients with sepsis upon admission (P < 0.05) ROC curve showed that, the area under the curve (AUC) (95%CI) of serum HBP, neopterin, USP13, HBP+neopterin, neopterin+USP13, HBP+USP13, HBP+neopterin+USP13 for predicting 28 d death in patients with sepsis upon admission were 0.722 (0.627~0.818), 0.768 (0.691~0.844), 0.647 (0.547~0.747), 0.849 (0.779~0.919), 0.845 (0.780~0.910), 0.832 (0.755~0.910), 0.923 (0.876~0.969), the combined prediction efficiency of HBP+neopterin+USP13 was significantly better than that of single or two tests (P<0.05). Conclusion: High levels of serum HBP, neopterin, and low levels of serum USP13 are associate with 28 d death and septic shock in patients with sepsis, Detection of serum HBP, neopterin combine with USP13 can effectively predict 28 d death in patients with sepsis upon admission. [ABSTRACT FROM AUTHOR]

Objective To observe the inhibitory effect of caudal vein injection of senescence marker protein 30（SMP30） on myocardial injury in septic mice and to explore its mechanism. Methods Sixty male C57BL/6 mice were randomly divided into the Con+empty vector group, LPS+empty vector group, and LPS+SMP30 group, with 20 mice in each. Mice in the Con+empty vector group and LPS+empty vector group were injected with adeno-null associated virus vector via the tail vein, and mice in the LPS+SMP30 group were injected with SMP30 adeno-associated virus vector via the tail vein. After 2 weeks of adeno-associated virus vector injection, mice in the LPS+empty vector group and LPS+SMP30 group were intraperitoneally injected with lipopolysaccharide（LPS） to establish the sepsis models, while mice in the Con+empty vector group were given intraperitoneal injection of the same volume of normal saline. Left ventricular ejection fraction（LVEF） and left ventricular fraction shortening（LVFS） were measured by echocardiography at 24 h after LPS injection.Serum and heart tissues were collected after the mice were killed, and serum levels of creatine kinase-MK（CK-MB), lactic dehydrogenase（LDH） and cTnI, and myocardial levels of malondialdehyde（MDA), superoxide dismutase（SOD） and glutathione peroxidase（GSH-Px） were detected by ELISA. TUNEL staining was used to detect cardiomyocyte apoptosis.Macrophage infiltration was detected by immunofluorescence staining. The myocardial reactive oxide species（ROS） production was detected by dihydroethidium fluorescent probe. Interleukin（IL）-1β, tumor necrosis factor（TNF）-α and IL-6mRNA levels were detected by qRT-PCR. The protein expression levels of myocardial tissues SMP30, silent information regulator 1（SIRT1), Ac-NF-κB p65, and Ac-FOXO1 were detected by Western blotting. Results Compared with the Con+empty vector group, the values of LVEF and LVFS decreased, the levels of serum CK-MB, LDH and cTnI increased, the apoptosis rate increased, the myocardial macrophage infiltration was more obvious, the mRNA levels of IL-1β, IL-6, TNF-α increased, the productions of ROS and MDA increased, the activities of SOD and GSH-Px decreased, the expression of SIRT1 down-regulated, and the expression levels of Ac-NF-κB p65 and Ac-FOXO1 increased in the LPS+empty vector group（all P＜0. 01). Compared with LPS+empty vector group, the values of LVEF and LVFS increased, the levels of serum CK-MB, LDH and cTnI decreased, the apoptosis rate decreased, the myocardial macrophage infiltration decreased, the mRNA levels of IL-1β, IL-6, TNF-α decreased, the productions of ROS and MDA decreased, the activities of SOD and GSH-Px increased, the expression of SIRT1 increased, and the expression levels of Ac-NF-κB p65 and AcFOXO1 decreased in the LPS+SMP30 group（all P＜0. 01). Conclusion The caudal vein injection of SMP30 can up-regulate SMP30 expression in mice with sepsis, inhibit myocardial inflammatory response and oxidative stress level, thereby alleviating myocardial injury, and its mechanism may be related to activating the SIRT1 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To establish a nomogram model for tsutsugamushi disease complicated with sepsis based on Lasso regression, so as to provide a reference for the diagnosis and treatment of tsutsugamushi disease complicated with sepsis. Methods We selected patients with scrub typhus patients admitted to Kunming Third People’s Hospital from June 2012 to December 2023 as the research subjects (n = 235), with scrub typhus patients patients with sepsis as the experimental group (n = 138) and scrub typhus patients patients without sepsis as the control group (n = 97), Lasso regression was used to screen the influencing factors of scrub typhus combined with sepsis, and a nomogram model was constructed through logistic regression. The effectiveness of the model was evaluated using receiver operating characteristic (ROC) curves and calibration curves, and clinical utility analysis was performed using decision curve analysis (DCA). Results The results of multivariate analysis through logistic regression showed: that age (OR = 1.039, 95%CI: 1.017～1.061), PLT (OR = 0.995, 95%CI: 0.990～1.000), UA (OR = 1.004, 95%CI: 1.001 ～1.008) and IgA (OR = 0.680, 95%CI: 0.472 ～0.979) were independent influencing factors of scrub typhus combined with sepsis. The area under the ROC curve (AUC) was 0.721 (95%CI: 0.656～0.786, P < 0.001), the sensitivity of the model was 69.1%, and the specificity was 63.1%. The calibration curve indicates that the model had good consistency, and the DCA indicated that the model had a high net benefit value. Conclusion Patients with scrub typhus are associated with increased age and UA levels and decreased PLT and IgA levels, and have a higher risk of secondary sepsis. [ABSTRACT FROM AUTHOR]

Objective To explore the effects of dapnetin's regulation of STING/TBK1/IRF3 signaling pathway on immune inflammatory response in sepsis rats. Methods In this study, 80 male Sprague Dawley (SD) rats were selected and randomly divided into four groups, 20 rats in the sham-operation group, the remaining 60 mice with sepsis were constructed according to cecal ligation puncture (CLP) method and were intraperitoneally injected with different doses of dapnetin. They were divided into no-dapnetin model group (0 mg/kg), low-dose group (2.5 mg/kg), and high-dose group (5 mg/kg), with 20 mice in each group. The model group and sham-operation group were intraperitoneally injected with 0.1% DMSO. The survival rate of rats in each group after 72 h of CLP modeling was observed. Lung, kidney, liver and spleen tissues were collected for histopathological analysis. Serum inflammatory factors (TNF-α, IL-6, and IL-1β) were detected by ELISA, T lymphocyte subsets in peripheral blood were detected by flow cytometry, and STING/TBK1/IRF3 signaling pathway protein expression was detected by Western blotting. Results Compared with sham-operation group, the survival rate of rats in model group was reduced (P<0.05), each organ tissue injury was significant, serum inflammatory factors (TNF-α, IL-6, and IL-1β) levels were increased (P<0.05), CD4+ ratio and CD4+/CD8+ ratio in peripheral blood were decreased (P<0.05), while CD8+ ratio and Th1/Th2 ratio were increased (P<0.05), the protein expressions of STING, p-TBK1/TBK1 and p-IRF3/IRF3 were downregulated (P<0.05) . Compared with the model group, dapnetin in high-dose group improved the survival rate of rats (P<0.05), the injury of all organs and tissues was reduced, and the level of serum inflammatory factors was decreased (P<0.05), CD4+ ratio and CD4+/CD8+ ratio in peripheral blood were increased (P<0.05), while CD8+ ratio and Th1/Th2 ratio were decreased (P<0.05), the protein expressions of STING, p-TBK1/TBK1 and p-IRF3/IRF3 were increased (P<0.05) . Conclusion Dapnetin can improve the immune inflammatory response of sepsis rats by regulating STING/TBK1/IRF3 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To investigate the relationship between serum a proliferation-inducing ligand (APRIL), leucine-rich a-2 glycoprotein 1 (LRG1), multiligand proteoglycan-1 (Syndecan-1) and renal function and short-term prognosis in patients with sepsis combined with acute kidney injury (AKI). Methods: 247 patients with sepsis admitted to Jinan Fifth People's Hospital from January 2021 to January 2023 were selected, and patients were divided into non-AKI group (122 cases) and AKI group (125 cases) according to whether AKI was combined, patients with sepsis combine with AKI were divided into death group and survival group according to the 30 days clinical outcome. Serum APRIL, LRGI and Syndecan-1 were detected by enzyme-linked immunosorbent assay, and renal function indexes [urinary albumin/creatinine ratio (UACR), estimated glomerular filtration rate (eGFR)] were calculated. The correlation between serum APRIL, LRGI, Syndecan-1 and UACR and eGFR in patients with sepsis combine with AKI were analyzed by Spearman correlation analysis. The influencing factors of short-term prognosis in patients with sepsis combine with AKI were analyzed by multivariate Logistic regression, the predictive value of serum APRIL, LRG1 and Syndecan-1 levels for short-term prognosis in patients with sepsis combine with AKI were analyzed by receiver operating characteristic (ROC) curve. Results: The levels of serum APRIL, LRG1, Syndecan-1 and UACR in AKI group were higher than those in non-AKI group, and eGFR was lower than that in non-AKI group (P<0.05). Spearman correlation analysis showed that, serum APRIL, LRG1 and Syndecan-1 were positively correlated with UACR and negatively correlated with eGFR in patients with sepsis combine with AKI (P<0.05). The 30 day mortality rate of 125 patients with sepsis combine with AKI was 40.80%. The levels of serum APRIL, LRG1, Syndecan-1 and UACR in death group were higher than those in survival group, and eGFR was lower than that in survival group (P<0.05). Multivariate Logistic regression analysis showed that, the increase of acute physiology and chronic health evaluation II (APACHE II) score, sequential organ failure assessment (SOFA) score, UACR, APRIL, LRG1 and Syndecan-1 were independent risk factors for short-term prognosis in patients with sepsis combine with AKI, and the increase of eGFR was an independent protective factor (P<0.05). The area under the curve of combined prediction of serum APRIL, LRG1 and Syndecan-1 levels was 0.908, which was greater than that of serum APRIL, LRG1 and Syndecan-1 levels alone. Conclusion: The increase of serum APRIL, LRG1 and Syndecan-1 levels are closely relate to the decrease of renal function in patients with sepsis combine with AKI, and are independent risk factors for poor short-term prognosis in patients with sepsis combined with AKI. The combination of serum APRIL, LRG1 and Syndecan-1 levels has a high value in predicting the short-term prognosis in patients with sepsis combine with AKI. [ABSTRACT FROM AUTHOR]

Objective: To compare the changes in serum renin angiotensin aldosterone (RAAS) system indicators and serum high mobility group protein 1 (HMGB1), soluble myeloid cell trigger receptor-1 (sTREM-1), and Toll like receptor-4 (TLR4) levels in patients with sepsis complicated by acute kidney injury (AKI) after intermittent hemodialysis (IHD) and continuous blood purification (CBP) treatment. Methods: 107 patients with sepsis combine with AKI admitted to our hospital from January 2019 to June 2023 were selected. Patients were divided into intermittent group (n=53, receiving IHD treatment) and continuous group (n=54, receiving CBP treatment) according to the random number table method. The RAAS system indexes, serum sTREM-1, HMGB1, TLR4, renal function and immune function indexes were compared between two groups. Results: After treatment, the renin activity (PRA), aldosterone (ALD), angiotensin I (AngI), sTREM-1, HMGB1, TLR4, urea nitrogen (BUN) and serum creatinine (Scr) in two groups decreased, and those in continuous group were lower than those in intermittent group (P<0.05). After treatment, CD8 decreased in both groups, and continuous group was lower than than in intermittent group. CD3, CD4, CD4/CD8" increased, and continuous group were higher than those in intermittent group (P<0.05). Conclusion: Compared with IHD treatment, CBP treatment of sepsis combine with AKI, which can further improve renal function, improve immune function, regulate RAAS system indexes and serum sTREM-1, HMGB1, TLR4 levels. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of prunella vulgaris extract on inflammation, macrophage phenotype, and phagocytic ability in septic mice, and analyze whether Toll like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway involved in its mechanism. Methods C57BL/6 mice were divided into the control group, the model group and the prunella vulgaris extract low (25 mg/kg), medium (50 mg/kg) and high (100 mg/kg) dose groups. Except for the control group, all other groups of mice were injected intraperitoneally with lipopolysaccharide (LPS) to prepare sepsis model. Each group was given corresponding medication by gavage. After 24 hours of administration, serum tumor necrosis factor-α (TNF-α), interleukin (IL) -1β, high mobility group protein B1 (HMGB1), IL-10 levels, the proportion of M1 type (CD11b+ F4/80+ ) and M2 type (CD206+ F4/80+ ) macrophages in peritoneal macrophages, the phagocytotic capacity of macrophages, the expression of inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) and arginase 1 (Arg1) mRNA in peritoneal macrophages and expression levels of TLR4, NF- κB p65 and their phosphorylated proteins in macrophages were detected. Results Compared with the control group, serum TNF-α, IL-1β, HMGB1, proportion of M1 type macrophages in abdominal cavity, mean fluorescence intensity and phagocytotic capacity of macrophages, iNOS mRNA, TLR4, phosphorylated NF-κB p65 (pNF-κB p65)/NF-κB p65 protein expression were increased in the model group (P＜0.05). IL-10, proportion of M2 type macrophages and Arg1 mRNA expression were decreased (P＜0.05). Compared with the model group, serum TNF-α, IL-1β, HMGB1, proportion of M1 type macrophages in abdominal cavity, iNOS mRNA, TLR4, p-NF-κB p65/NF-κB p65 protein expression were decreased successively in the prunella vulgaris extract low, medium and high dose groups (P＜0.05). IL-10, proportion of M2 macrophages, mean fluorescence intensity and phagocytotic capacity of macrophages and Arg1 mRNA expression were increased successively (P＜0.05). Conclusion By inhibiting TLR4/NF- κB pathway, prunella vulgaris extract may inhibit the polarization of peritoneal macrophages into M1 type and promote their polarization to M2 type, enhance macrophage phagocytic ability and alleviate LPS induced inflammatory response in septic mice. [ABSTRACT FROM AUTHOR]

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Copyright of China Tropical Medicine is the property of China Tropical Medicine Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the effect of Traditional Chinese Medicine nursing interventions on sleep quality and gastrointestinal function in patients with sepsis. Methods Totally 84 patients with sepsis accompanied with gastrointestinal function disorder were randomly divided into the control group and observation group, with 42 cases in each group. The conventional nursing mode was adopted in the control group, while the Traditional Chinese medicine nursing interventions including dietary nursing by syndrome differentiation, acupoint massage, Chinese herbal medicine foot bath and hot compress were carried out in the observation group. Acute Physiological and Chronic Health Score (APACHE II) score, Pittsburgh Sleep Quality Index (PSQI) score, improvement in gastrointestinal function, general comfort questionnaire scale (GCQ) score and satisfaction were compared between the two groups. Results Scores of PSQI and APACHE II in the observation group were lower than those in the control group(P＜0. 01). The recovery rate of the observation group was 80. 95%(34/42), which was higher than 64. 29%(27/42)of the control group(P＜0. 05). The GCQ score and patient satisfaction rate in the observation group were higher than those in the control group (P＜0. 05). Conclusion Acupoint massage combined with Traditional Chinese medicine interventions nursing are effective to improve the sleep quality and gastrointestinal function of patients with sepsis. (目的 观察中医特色护理改善脓毒症患者睡眠质量及胃肠功能的效果。方法 选取重症医学科脓毒症胃肠功能障碍患者84例, 随机分为对照组和观察组, 各42例。对照组采用常规护理模式, 观察组采用辨证施膳、穴位按摩、中药足浴、中药热敷等中医特色护理干预。比较两组患者的急性生理与慢性健康评分(APACHE Ⅱ)评分、匹兹堡睡眠质量指数(PSQI)评分, 胃肠功能改善情况、舒适状况量表(GCQ)评分和满意度。结果 观察组患者PSQI和APACHE Ⅱ评分均低于对照组, 差异有统计学意义(P＜0. 01)。干预后, 观察组胃肠功能改善率80. 95%(34/42), 高于对照组的64. 29%(27/42), 差异有统计学意义(P＜0. 05)。观察组患者GCQ量表总分和满意度高于对照组, 差异有统计学意义(P＜0. 05)。结论 穴位按摩联合中医特色护理模式能有效改善脓毒症患者睡眠质量和胃肠功能, 提高患者舒适度。)

BACKGROUND: Sepsis-induced systemic inflammation leads to rapid bone mass loss; however, there is a lack of effective treatments. Ulinastatin is an antiinflammatory drug, but its protective effect and mechanism on bone under sepsis-induced systemic inflammation are still unclear. OBJECTIVE: To explore whether ulinastatin can relieve acute bone loss caused by lipopolysaccharide. METHODS: (1) Animal experiment. Thirty male C57BL/6 mice were randomly divided into three groups (n=10 per group): control group, model group and experimental group. The control group was injected intraperitoneally with normal saline, the model group was injected intraperitoneally with lipopolysaccharide, and the experimental group was injected intraperitoneally with lipopolysaccharide and ulinastatin. In the experimental group, ulinastatin was injected continuously for 3 days. After intraperitoneal injection of ulinastatin for 14 days, femoral tissues were taken for CT scanning and pathological observation. (2) Cell experiment. C57BL/6 mouse primary osteoblasts were isolated and divided into three groups: the control group was routinely cultured, lipopolysaccharide was added to the model group, and lipopolysaccharide with ulinastatin was added to the experimental group. Cell proliferation and osteogenic differentiation were detected. C57BL/6 mouse bone marrow mononuclear cells were isolated and divided into three groups: the control group was routinely cultured, lipopolysaccharide was added to the model group, and lipopolysaccharide and ulinastatin were added to the experimental group. Osteoclast differentiation was detected. RESULTS AND CONCLUSION: (1) Animal experiment. CT scanning and hematoxylin-eosin staining showed that bone mass in lipopolysaccharide-treated mice was reduced but increased after treatment with ulinastatin. Tartrate resistant acid phosphatase staining showed that the number of osteoclasts in bone tissue increased in the model group, but significantly decreased in the experimental group compared with the model group. (2) Cell experiment. Cell counting kit-8 assay showed that lipopolysaccharide treatment inhibited the proliferation of osteoblasts, and ulinastatin elevated the proliferation of osteoblasts after lipopolysaccharide treatment. Alkaline phosphatase staining, alizarin red staining and osteogenesis-related gene (alkaline phosphatase, Runx2, osteocalcin, osteoblastin, nuclear factor κB receptor-activating factor ligand, osteoprotegerin) detection showed that lipopolysaccharide treatment inhibited osteogenic differentiation of osteoblasts and elevated the nuclear factor κB receptor-activating factor ligand/osteoprotegerin ratio; ulinastatin did not have any significant effect on the reduction of osteoblast function induced by lipopolysaccharide but decreased the nuclear factor κB receptor-activating factor ligand/osteoprotegerin ratio. Tartrate resistant acid phosphatase staining and osteoclast-related gene (tartrate resistant acid phosphatase and matrix metalloproteinase 9) detection showed that lipopolysaccharide treatment could promote osteoclast differentiation of bone marrow monocytes, while ulinastatin could inhibit lipopolysaccharide-induced osteoclast differentiation of bone marrow monocytes. (3) Overall, ulinastatin can significantly inhibit lipopolysaccharide-induced bone loss, mainly through promoting osteoblast proliferation and directly or indirectly inhibiting osteoclast differentiation to alleviate bone loss and achieve osteoprotective effects. [ABSTRACT FROM AUTHOR]

Objective To investigate the predictive value of soluble growth-stimulated expressed gene 2 protein （sST2） in predicting sepsis-associated acute kidney injury （SA-AKI）. Methods From January 2020 to December 2023， a total of 395 sepsis patients with sepsis from the Emergency Department， Affiliated Hospital of Nantong University were enrolled in this retrospective observational study. These patients were further categorized into two groups: AKI group （114 cases） and non-AKI group （281 cases）. Clinical data and laboratory indicators were collected within 24 hours after admission. ROC curve analysis was used to evaluate the diagnostic ability of sST2 for SA-AKI. Logistic regression analysis was performed to assess independent risk factors for the development of SA-AKI. Concurrently， two predictive models for SA-AKI were constructed， and the predictive ability of sST2 for SA-AKI was assessed using the Area Under the Curve （AUC）， the Net Reclassification Index （NRI） and the Integrated Discrimination Improvement （IDI）. Results T The levels of sST2 were significantly higher in the AKI group compared to the non-AKI group （P < 0.001）. The AUC predicted by sST2 （0.839， 95% CI: 0.799 ~ 0.874） in sepsis patients with AKI was significantly superior to other laboratory indicators （P < 0.000 1）. An sST2 concen-tration greater than 85 ng/mL independently increased the risk for SA-AKI （OR: 14.315， 95% CI: 5.867 ~ 34.926， P < 0.001）. Incorporating sST2 into the prediction model substantially improved the AUC values （0.954 vs. 0.909， P < 0.000 1）， NRI（ 21.48%， 95% CI: 11.48% ~ 31.49%， P < 0.000 1） and IDI（ 8.62%， 95% CI: 5.75% ~ 11.49%， P < 0.000 1）. Conclusion sST2 has the potential to serve as a promising biomarker for prognosticating AKI in septic patients. [ABSTRACT FROM AUTHOR]

革兰阴性菌感染性脓毒症是由于宿主对革兰阴性菌感染反应失调而导致的一种危及生命的器官功能障 碍综合征，患者病情凶险，病死率较高。革兰阴性菌的细胞壁中含有脂多糖（LPS），可与宿主细胞膜上的CD14受体 结合而激活免疫细胞，并通过Toll样受体4（TLR4）识别LPS，从而调控NF-κB和MAPK信号通路，导致细胞因子产生 并进一步激活凝血和补体级联反应，从而引发全身炎症反应和器官衰竭。近年来，oXiris-连续性肾脏替代治疗 （oXiris-CRRT）在革兰阴性菌感染性脓毒症的治疗中展现了多方面的优势，相较于其他传统治疗方法效果更为显 著。oXiris-CRRT通过针对性清除血液中的内毒素和炎症介质，可有效减轻革兰阴性菌感染性脓毒症患者的过度炎 症反应，纠正凝血功能障碍和血流动力学异常，从而提升器官功能，减轻患者病情并降低短期死亡风险。 [ABSTRACT FROM AUTHOR]

脓毒症是由感染引起的生理、病理和生化异常的一个综合征，其中肾损伤是脓毒症最常见的并发症，脓毒 症相关肾损伤与短期病死率和不良长期疾病相关。目前，脓毒症相关肾损伤病理生理机制尚不明确。脓毒症患者 常合并高水平尿酸，随着尿酸水平的升高，脓毒症相关肾损伤的发生率将大幅增加。研究显示，高水平尿酸是脓毒 症患者发生肾损伤的独立危险因素，但两者的具体作用机制尚不清楚。高水平尿酸可通过促炎、促氧化应激等途径 导致肾脏糖萼脱落、上皮细胞向间充质细胞转化、肾脏细胞焦亡、铁死亡等的发生，从而导致急性肾损伤甚至慢性肾 病的发生，进而增加脓毒症患者病死率。 [ABSTRACT FROM AUTHOR]

Objective: To study the clinical value of serum fibroblast growth factor-21 (FGF-21) and fibroblast growth factor-23 (FGF-23) detection in patients with sepsis combined with acute kidney injury (AKI). Methods: 202 patients with sepsis admitted to Baiyun Hospital Affiliated to Guizhou Medical University and the Affiliated Hospital of Guizhou Medical University from May 2020 to August 2023 were selected, and patients were divided into non-AKI group (n=109) and AKI group (n=93) according to whether they were combine with AKI, 70 healthy volunteers who underwent physical examinations in our hospital were selected as health group during the same period. Patients were divided into death group and survival group according to the 28-day clinical outcome of patients with sepsis combine with AKI. Serum FGF-21 and FGF-23 levels were detected. The influencing factors of 28-day death in patients with sepsis combine with AKI were analyzed by multivariate Logistic regression model, the predictive value of serum FGF-21 and FGF-23 for 28-day death in patients with sepsis combined with AKI were analyzed by receiver operating characteristic (ROC) curve. Results: Compared with healthy group, the levels of serum FGF-21 and FGF-23 in non-AKI group and the AKI group were significantly increased (P<0.05). Compared with non-AKI group, the serum levels of FGF-21 and FGF-23 in AKI group were significantly increased (P<0.05). Among 93 patients with sepsis combined with AKI, 26 died within 28 days, with a mortality rate of 27.96%. Compared with survival group, the serum FGF-21 and serum FGF-23 in death group were significantly increased (P<0.05). Multivariate Logistic regression analysis showed that AKI stage Ⅱ～Ⅲ, increased APACHE II score, increased SOFA score, increased serum FGF-21 and increased serum FGF-23 were risk factors for 28-day death in patients with sepsis combine with AKI (P<0.05). ROC curve results showed that, the AUC, sensitivity and specificity of FGF-21 combine with FGF-23 in predicting 28-day death in patients with sepsis combine with AKI were 0.798, 0.769 and 0.791 respectively, which were significantly better than those of single detection. Conclusion: Serum FGF-21 and FGF-23 are highly express in patients with sepsis combined with AKI, which are relate to 28 deaths in patients with sepsis combined with AKI. The combined detection of serum FGF-21 and FGF-23 has a high predictive value for 28-day death in patients with sepsis combined with AKI. [ABSTRACT FROM AUTHOR]

Sepsis is a life-threatening organ dysfunction caused by the imbalance of host immune response to infection, which immune regulation mechanism is complex and has not been clarified. Programmed death receptor-1 （PD-1）/programmed death receptor ligand-1 （PD-L1） is a negative co-inhibitory molecule that has attracted much attention in recent years. Studies have shown that PD-1/PD-L1 signaling pathway plays an important immunosuppressive role in sepsis. There are differences in immune regulation mechanisms in heart, liver, spleen, lung and kidney, which has not been clarified. Immune regulation of PD-1/PD-L1 in different organs of sepsis is reviewied in this article, which could to provide a new direction for the study of sepsis. [ABSTRACT FROM AUTHOR]

Sepsis represents a major challenge for global health. Early identification and standardized treatment are crucial for improving the survival rate of septic patients, who often receive their first systemic evaluation in the emergency departments. Therefore, emergency department plays an important role in the management of sepsis. However, great barriers still exist in the early detection and administration of sepsis, due to lack of specific physical manifestations and diagnostic markers, poor compliance with sepsis bundles, etc. This article elaborates the research progress of early identification and nursing care of emergency sepsis patients, and the key role of emergency nurses in sepsis management, in order to promote the standardized management of emergency sepsis patients, reduce the morbidity and mortality of sepsis, and improve the treatment outcome and prognosis of patients. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of γ -aminobutyric acid (GABA) signaling pathway on endoplasmic reticulum (ER) stress and mitochondrial autophagy in septic rats with acute lung injury (ALI). Methods SD rats were randomly grouped into the control (CON) group, the model group, the GABA signaling pathway activator Baclofen group (the Baclofen group), the GABA signaling pathway inhibitor dicentrine group (the BIC group), with 6 rats in each group. The Baclofen group received intraperitoneal injection of 5 mg/kg Baclofen, and the BIC group received intraperitoneal injection of 1 mg/kg BIC, once a day, for two consecutive weeks. The CON group and the model group were injected with an equal amount of physiological saline via intraperitoneal injection. Enzyme linked immunosorbent assay was applied to detect serum levels of superoxide dismutase (SOD) and malondialdehyde (MDA) and levels of cytochrome C (Cyt.C) and Nicotinamide adenine dinucleotide phosphate (NADPH) in bronchoalveolar lavage fluid (BALF). Transmission electron microscopy (TEM) was applied to observe the ultrastructure of lung tissue cells. HE staining was applied to observe the pathological morphology of lung tissue. TUNEL staining was applied to observe the apoptosis of lung tissue. Western blot assay was applied to detect expression levels of GABAAR, GRP78 and CHOP proteins in lung tissue. Results Compared with the model group, the lung swelling, congestion and inflammatory cell infiltration were improved in the Baclofen group, and the lung injury score, MDA content, apoptosis index, Cyt.C and NADPH levels, GRP78, and CHOP protein levels were reduced (P＜0.05). The number of autophagic vacuoles in phagocytic mitochondria, SOD content and GABAAR protein level were increased (P＜ 0.05), however, the trend of above indicators in the BIC group was opposite to that in the Baclofen group. Conclusion Upregulation of GABA signaling pathway may have an improvement effect on ALI in sepsis rats. [ABSTRACT FROM AUTHOR]

Objective: To investigate the changes of serum brain natriuretic peptide (BNP), procalcitonin (PCT) and recombinant single Ig IL1 related receptor (SIGIRR) in patients with emergency abdominal infection-related sepsis and their relationship with prognosis. Methods: 318 patients with emergency abdominal infection who were received by our hospital from January 2020 to October 2023 were divided into simple infection group (n=233) and sepsis group (n=85) according to whether sepsis occurred. The baseline data and serum BNP, PCT and SIGIRR levels were compared between groups. Pearson correlation analysis was used to explore the correlation between serum indicators and clinical data. The patients in sepsis group were classified into survival group (n=56) and death group (n=29) by means of survival status within 28 days, and the baseline data, serum BNP, PCT and SIGIRR were compared. Binary logistics equation was used to analyze the related influencing factors of prognosis of patients with sepsis. ROC curve was adopted to analyze the diagnostic value of serum BNP, PCT and SIGIRR levels on prognosis of sepsis group. Results: There were significant differences in pathogen types, WBC, CRP, ALB, APACHE II score and SOFA score between simple infection group and sepsis group (P<0.05). The levels of serum BNP, PCT and SIGIRR in simple infection group were significantly lower than those in sepsis group (P<0.05). Pearson correlation analysis showed that the levels of BNP, PCT and SIGIRR in sepsis group were positively correlated with WBC, CRP, APACHE II score and SOFA score (P<0.05), and were negatively correlated with ALB (P<0.05). Among patients with sepsis, the levels of serum BNP, PCT and SIGIRR were significantly higher in death group than those in survival group(P<0.05). Binary logistics regression analysis showed that serum BNP, PCT and SIGIRR levels were associated with poor prognosis in patients with sepsis(P<0.05). ROC curve revealed that the AUCs of serum BNP, PCT, SIGIRR alone and in combination in predicting the poor prognosis in patients with sepsis were 0.876, 0.826, 0.779 and 0.976, the sensitivities were 86.21%, 82.76%, 75.86% and 96.55%, and the specificities were 75%, 75%, 71.43% and 69.64% respectively, and the combined diagnostic value was higher. Conclusion: BNP, PCT and SIGIRR have a certain correlation with patients with abdominal infection-related sepsis, and can be used as reference indicators for clinical diagnosis, treatment and prognosis evaluation. [ABSTRACT FROM AUTHOR]

Objective: To investigate the mechanism of nucleotides binding oligomeric domain like receptor protein 3 (NLRP3) inflammasome on the intestinal inflammatory response and intestinal mucosal injury in septic rats through the JAK/STAT3 signaling pathway. Methods: Thirty healthy and clean grade male Wistar rats were chosed and randomly divided into three groups: sham surgery group, model group, and NLRP3 inhibitor group, with 10 rats in each group. The model group and inhibitor group were subjected to cecal ligation and perforation for modeling. The inhibitor group was intraperitoneally injected with NLRP3 inhibitor MCC950 (10 mg/kg) 30 minutes before modeling, and the model group was injected with equal amount of physiological saline. The 24-hour survival status of rats in each group were observed, ileal pathological score was performed with HE staining, serum tumor necrosis factor-α(TNF-α) and interleukin-1β (IL-1β) were detected using ELISA method, NF-κB p65, NLRP3, apoptosis related spot protein (ASC), aspartate specific cysteine protease-1(Caspase-1), p-JAK, and p-STAT3 proteins levels in small intestine tissues were detected by Western blot method. Results: ① Compared with the sham surgery group, the mortality rate and pathological score of the model group rats significantly increased, serum TNF-α and IL-1β levels were higher, tissue NF-κB p65, NLRP3, ASC, Caspase-1, p-JAK, and p-STAT3 proteins relative expressions were significantly higher, too (P<0.05). ② Compared with the model group, the mortality rate and pathological score of the inhibitor group rats significantly reduced, serum TNF-α and IL-1β was significantly lower, levels of NF-κB p65, NLRP3, ASC, Caspase-1, p-JAK, and p-STAT3 proteins were significantly less, too(P<0.05). There were still significantly statistical differences between the inhibitor group and the sham surgery group in the above indicators (P<0.05). Conclusion: NLRP3 inflammasome may enhance the intestinal inflammatory response and injury intestinal mucosal in septic rats by activating JAK/STAT3 signaling pathway, targeting intervention of NLRP3 could reverse intestinal injury. [ABSTRACT FROM AUTHOR]

Macrophages are crucial immune cells in the body, with functions including phagocytosis, antigen presentation, immune defense, and inflammation regulation. Macrophages polarize into distinct subtypes within diverse microenvironments to further exert their immunoregulatory functions. Sepsis is a life ⁃threatening organ dysfunction caused by a dysregulated host response to infection, and it is the primary cause of mortality in critically ill patients. Macrophage polarization plays a significant role at different stages of the inflammatory response in sepsis, thereby influencing the clinical outcomes of septic patients. This review provides an overview of the characteristics of macrophage polarization and its role in sepsis immunity and organ dysfunction, aiming to offer new insights for improving the prognosis and treatment of septic patients. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Contemporary Pediatrics is the property of Xiangya Medical Periodical Press and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Traditional Chinese Drug Research & Clinical Pharmacology is the property of Traditional Chinese Drug Research & Clinical Pharmacology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Sichuan University (Medical Science Edition) is the property of Editorial Board of Journal of Sichuan University (Medical Sciences) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Severe acute pancreatitis (SAP) is the most serious type of acute pancreatitis (AP) and a common critical disease in clinic. With the continuous improvement of medical level, the mortality rate in the early stage of SAP has decreased significantly, and the peak of death is mainly concentrated in the later stage of the disease and the main cause of death in the later stage is secondary sepsis after infection of pancreatic or peripancreatic necrosis. If the risk of secondary sepsis in SAP can be predicted early it can guide the medical staff to carry out appropriate early monitoring and intervention to improve the clinical outcome of patients, The article reviewed the application progress of blood markers to predict secondary sepsis in SAP. [ABSTRACT FROM AUTHOR]

Objective: To explore the effect of Annexin A1 (ANXA1) peptidomimetic Ac2-26 on acute kidney injury (AKI) and neutrophil apoptosis in septic rats. Methods: Experimental groups included control group, Ac2-26 group, AKI group, AKI+Ac2-26 group, with 15 rats in each group. After cecal ligation and perforation were used to establish a sepsis-induced AKI model, Ac2-26 was intravenously infused for treatment, once a day for 14 days; after the end, ELISA was used to detect levels of serum creatinine (Scr), urea nitrogen( BUN), IL-1β, IL-6 and TNF-α; HE staining and periodic acid Schiff( PAS) staining were used to observe the pathological changes of rat kidney tissues in each group; immunohistochemical staining was used to detect expression of ANXA1 in kidney tissue of each group of rats; neutrophils were isolated from rat peripheral blood, Giemsa staining and trypan blue staining were used to detect cell purity and viability; Annexin V-FITC/PI double staining method and TUNEL staining were used to determine apoptosis level of neutrophils in each group. Results: Compared with control group, levels of Scr and BUN in serum of rats in AKI group were increased (P<0.05), levels of IL-1β, IL-6 and TNF-α also increased (P<0.05), renal tubules and glomeruli in kidney tissue were both significantly damaged, accompanied by a large number of inflammatory cell infiltration, and pathological score increased (P<0.05), while proportion of ANXA1 positive staining area was decreased (P<0.05); neutrophils identified by Giemsa staining and trypan blue staining had complete morphology and high activity; compared with control group, apoptosis rate of neutrophils in AKI group was decreased( P<0.05), and the positive rate of TUNEL was decreased( P<0.05). Compared with AKI group, levels of Scr and BUN in serum of rats in AKI+Ac2-26 group were decreased (P<0.05), levels of IL-1β, IL-6 and TNF-α also decreased (P<0.05), pathological manifestations of renal tubules and glomeruli in renal tissue were significantly reduced, and pathological score was reduced (P<0.05), while the proportion of ANXA1 positive staining area was increased (P<0.05), at the same time, apoptosis rate of rat neutrophils was increased (P<0.05), positive rate of TUNEL was also increased (P<0.05). Conclusion: ANXA1 peptidomimetic Ac2-26 can increase expression of ANXA1 in kidney tissue of AKI in septic rats, promote neutrophil apoptosis, and have a protective effect on kidney tissue damage in rats caused by sepsis. [ABSTRACT FROM AUTHOR]

Objective To analyze the risk factors for acute kidney injury (AKI) in patients with sepsis and construct a Nomogram predictive model. Methods A total of 180 patients with sepsis from March 2020 to September 2022 were selected as the research subjects and divided into an AKI group (n=75) and a non-AKI group (n=105) based on the presence of AKI. The predictive value of continuous variables was analyzed by ROC experiments, and logistic regression was used to analyze the risk factors for AKI in patients with sepsis. The clinical efficacy of the Nomogram model was validated using internal data. Results There were no statistically significant differences in general data between the two groups (P＞0.05). Compared with the non-AKI group, the AKI group had a higher proportion of males, more cases of pulmonary infection, lower mean arterial pressure (MAP), higher levels of lactate, white blood cell count, and multiple organ dysfunction syndrome (MODS) score (P<0.05). The AUC values for MAP, lactate, procalcitonin, white blood cell count, and MODS score were 0.823, 0.921, 0.663, 0.948, and 0.946, respectively. Male gender, pulmonary infection, MAP (≤89 mmHg), lactate (>2.13 mmol/L), white blood cell count(＞15×109·L-1), and MODS score (>6 points) were all risk factors for AKI in patients with sepsis (P<0.05). The C-index for predicting the risk of AKI in patients with sepsis using the Nomogram model was 0.763 (95%CI: 0.651-0.832). Conclusion Male gender, pulmonary infection, low MAP, high lactate, elevated white blood cell count, and increased MODS score are risk factors for AKI in patients with sepsis. The nomogram model constructed based on these variables can effectively predict the occurrence of AKI in patients with sepsis. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the changes of human leukocyte elastase ( HLE) and monocyte-surface lipopolysaccharide receptor (mCD14) levels in patients with sepsis receiving adjuvant treatment of ulinastatin, and the value of early detection of serum HLE and mCD14 levels in treatment responsiveness. METHODS: A total of 196 patients with sepsis admitted into this hospital from 2020 to 2022 were selected and given ulinastatin based on classical conventional therapeutic regimen, which were divided into good-response group (38 cases) and poor-response group (158 cases) according to different therapeutic effect. The serum HLE and mCD14 levels of two groups were detected before and after treatment. Clinical data were collected by the electronic medical record system, and both groups were matched 1 ∶ 1 according to the nearest matching method. Influencing factors of treatment responsiveness of ulinastatin in adjuvant treatment of sepsis were analyzed and the predictive model was established, the value of early detection of serum HLE and mCD14 levels in treatment responsiveness was analyzed by receiver operating characteristic (ROC) curve. RESULTS: The serum HLE level was lower and the mCD14 level was higher in both groups after treatment than those before treatment, with statistically significant differences (P<0. 05). The severity in the poor-response group after propensity score matching, procalcitonin (PCT), C-reactive protein (CRP) and HLE levels in the poor-response group before and after treatment were higher than those in the good-response group, while the mCD14 level in the poorresponse group before and after treatment was lower than that in the good-response group, with statistically significant differences (P<0. 05). The severity, PCT, CRP and HLE levels before treatment were the risk factors of treatment responsiveness of ulinastatin for the adjuvant treatment of sepsis patients, and the mCD14 level before treatment was a protective factor for the treatment responsiveness (P<0. 05); a joint prediction model was established, P = 1 / [1 + 1 / exp (0. 826 × severity + 0. 941 × PCT before treatment + 0. 694 × CRP before treatment + 1. 112 × HLE before treatment - 0. 963 × mCD14 before treatment - 3. 968)], with good calibration ability; the drug-time area under the curve ( AUC) for the prediction of treatment responsiveness by the HLE and mCD14 levels before treatment was respectively 0. 777 and 0. 779, while the AUC for the prediction of treatment responsiveness by the combined prediction model was 0. 947, which was higher than the AUC for HLE and mCD14 assessed individually, with statistically significant differences ( P < 0. 05 ). CONCLUSIONS: The application of ulinastatin in the adjuvant treatment of sepsis can decrease the serum HLE level and elevate mCD14 level, the decrease in blood HLE levels and the increase in mCD14 levels are closely related to treatment response, and the combined detection of these markers can further enhance their predictive value. [ABSTRACT FROM AUTHOR]

To investigate the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) gene transfected bone marrow mesenchymal stem cells (BMSCs) on vascular endothelial injury, coagulation function and inflammatory factors in septic mice. 60 SD mice were divided into Sham group, model (Model) group, BMSCs group and GM-CSF-BMSCs group, with 15 mice in each group, sepsis model of mice was prepared by cecal ligation and puncture. The expression of GM-CSF gene was detected by real-time fluorescence quantitative polymerase chain reaction (qRT-PCR). The tail bleeding time of 24h mice was recorded. The levels of plasma prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT) and fibrinogen (Fib) were detected. The levels of serum interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-1 and IL-10 were detected by ELISA. The morphology of vascular tissue was observed by hematoxylin-eosin (HE) staining. Apoptosis of vascular endothelial cells was detected by TUNEL method. The expression of vascular tissue factor (TF), tissue factor pathway inhibitor (TFPI), antithrombin (ATIII), vascular cell adhesion molecule 1 (VCAM1) and protease-activated receptor 1 (PAR1) were detected by Western blot. Compared with BMSCs in CK group, the expression of GM-CSF mRNA in BMSCs in Transfection group was significantly increased (P<0.05). Compared with Sham group, the vascular morphology of the mice in Model group was significantly damaged, the tail bleeding time, Fib content, serum IL-10 level and ATIII protein expression in vascular endothelial tissue of the mice in Model group were significantly decreased, PT, APTT, TT time, serum IL-6, TNF-α, IL-1 levels, apoptosis rate, TF, TFPI, VCAM1, PAR1 protein expression in vascular endothelial tissue were significantly increased (P<0.05). Compared with Model group, the damage of vascular morphology and structure in BMSCs group and GM-CSF-BMSCs group was significantly reduced, the tail bleeding time, Fib content, serum IL-10 level and ATIII protein expression in vascular endothelial tissue were significantly increased, PT, APTT time, serum IL-6, TNF-α, IL-1 level, apoptosis rate, TF, TFPI, VCAM1 and PAR1 protein expression in vascular endothelial tissue were significantly decreased (P<0.05). The detection indexes in GM-CSF-BMSCs group were better than those in BMSCs group (P<0.05). GM-CSF transfected BMSCs can reduce the inflammatory response and vascular endothelial cell injury in septic mice, and improve coagulation function. [ABSTRACT FROM AUTHOR]

Objective: To observe the effects of yiqi tongfu decoction combined with ulinastatin on patients with sepsis gastrointestinal dysfunction. Methods: 98 patients with sepsis gastrointestinal dysfunction were divided into control group (treated with ulinastatin) and treatment group (treated with yiqi tongfu decoction on the basis of control group) according to the random number table method, 49 cases in each group. The gastrointestinal hormones [motilin (MOT), gastrin (GAS)], intestinal flora [Bifidobacterium, Lactobacillus, Enterobacter, Enterococcus, Bacteroides] and intestinal barrier markers [diamine oxidase (DAO) and D lactic acid] were compared between two groups. Results: After treatment, compared with control group, DAO, D lactic acid, GAS level, Enterobacter, Enterococcus, and Bacteroides colonies in treatment group decreased, while the MOT level, Bifidobacterium, and Lactobacillus colonies increased (P<0.05). Conclusion: Yiqi tongfu decoction combined with ulinastatin may improve the levels of intestinal flora, gastrointestinal hormones and intestinal barrier markers in patients with septic gastrointestinal dysfunction. [ABSTRACT FROM AUTHOR]

目的 探讨泻热祛毒汤辅助治疗脓毒症胃肠功能障碍的临床疗效及药理机制。方法 选取脓毒症胃肠 功能障碍患者 72 例, 随机分为观察组和对照组各 36 例。对照组采用西医治疗, 观察组采用西医治疗联合泻热祛毒 汤治疗, 疗程 7 d。治疗前、治疗 7 d 比较两组胃肠功能障碍评分、急性生理和慢性健康状况评分系统 (APACHE Ⅱ) 评分和马歇尔 (Marshall) 评分。治疗后 28 d, 统计两组患者生存情况, 计算累计生存率。治疗前、治疗 7 d 检测两组 血清肠黏膜屏障功能指标 (D-乳酸、二氨氧化酶)、炎症因子 (PCT、CRP、IL-6) 水平。结果 治疗 7 d, 观察组胃肠功 能障碍评分、APACHEⅡ 评分、Marshall 评分以及血清 D-乳酸、二氨氧化酶、PCT、CRP、IL-6 水平低于对照组 (P 均< 0. 05)。治疗 28 d, 观察组累计生存率 (86. 1% vs 75. 0%, P<0. 05)。结论 泻热祛毒汤对脓毒症胃肠功能障碍患者 有良好疗效, 其药理机制与促进肠道黏膜屏障功能恢复及抑制炎症反应相关。 [ABSTRACT FROM AUTHOR]

This article summarized the experience of integrated Chinese and western medicine nursing of a patient with septic gastrointestinal injury-intestinal obstruction (toxic megacolon). According to the theory of pathogenesis integration of Chinese and western medicine, the appropriate nursing technology of Chinese medicine was implemented in three stages. The first stage was clearing heat and detoxification, smoothing the liver and awakening the blood, including ear bloodletting; In the second stage, measures was taken to promote lung qi, including Traditional Chinese Medicine retention enema and auricular acupoint pressure; In the third stage, the skin needle therapy and Traditional Chinese Medicine hot package therapy were carried out. After 40 days of treatment, the patient's body temperature returned to the normal level, the symptoms of abdominal pain, abdominal distension and diarrhea disappeared, and the pressure ulcer treatment was continued in our hospital. (本文总结1例基于“中西医病机融通理论”治疗脓毒症胃肠损伤-肠痹(中毒性巨结肠)患者的护理体会。通过护理评估和中医辨证, 在常规护理的基础上, 依据“中西医病机融通理论”, 分3个阶段实施耳部放血、中药保留灌肠、耳穴贴压、中药热奄包、皮内针疗法等中医适宜护理技术, 缓解患者不适症状, 改善胃肠功能。)

Objective We systematically analyze the changes in the count and function of platelet at the early sepsis based on clinical study and single cell sequencing. Methods Clinical data of sepsis patients at the early stage were collected and had been compared between different prognostic groups in the prospective case⁃control study. The independent risk factors of death were analyzed by logistic regression, and the predictive efficacy of clinical indicators was evaluated by receiver operating characteristic （ROC） curve. The healthy volunteers and sepsis patients were recruited. Clinical researchers collected peripheral venous blood samples for sorting cell samples to carry out single⁃cell RNA sequencing （sc⁃RNA seq）. Through bioinformatics techniques, we analyzed the changes in platelet count， the significantly differential⁃expressed genes and its enriched functional signaling pathways in the early stages of sepsis. Results （1） A total of 224 patients were enrolled, with a 90 day survival rate of 70.5%. Compared with the survival group, the count of platelet and MAP in the death group at the early stage of sepsis were significantly lower, but the plasma lactate content and SOFA score were significantly higher.（2） Based on single cell sequencing technology, cells are annotated as six groups. The proportion of innate immune cells （neutrophils， monocytes， and dendritic cells） was significantly increased in the early stage of sepsis compared to the healthy volunteers （2.15∶1）， while platelets significantly decreased （0.31∶1）.（3） Through bioinformatics technology, CD41/ CD42a/CD61 was identified as platelet specific molecules, with significantly increased expression levels in sepsis. Three molecules can distinguish platelets together.（4）771 genes were significantly upregulated and 1101 genes were significantly downregulated in platelets of patients with sepsis, including core molecules involved in physiological functions such as cell adhesion, chemotaxis, and immune response. Functional analysis suggests that differentially expressed genes are enriched in coagulation, immune functions and cell death, participating in oxidative phosphorylation, leukocyte chemotaxis， iron death, and NOD like receptor signaling pathways. Conclusion Reduced platelet count is associated with poor prognosis in the early stage of sepsis. The specific high expression molecules CD41/ CD42a/CD61 that are significantly upregulated in platelets can serve as biomarkers for platelets. Platelets not only mediate cell adhesion and coagulation cascade， but also participate in functional changes such as immune cell chemotaxis, inflammatory response, and the pathological death of inflammatory cells. [ABSTRACT FROM AUTHOR]

Objective To analyze the clinical characteristics and risk factors of septic patients with bacterial infections.Methods A total of 2 158 patients with positive bacterial cultures from October 1, 2019, to September 30, 2020, were collected, including 229 cases in the septic group and 1 929 cases in the non-septic group. General information, laboratory test results, medical history of underlying diseases, and clinical manifestations were collected and compared between the two groups. Relevant risk factors were screened using T-test or approximate T-test for continuous variables, Pearson chi-square test, Fisher′s exact test for categorical variables, and non-conditional logistic regression model. Results Compared with the non-septic group, there were statistically significant differences in gender, age, smoking, alcohol consumption, congestive heart failure, chronic kidney disease (CKD), chronic hepatitis B, liver cirrhosis, and malignant tumors (all P＜0.05) . Male gender (OR=2.17, P＜0.01), age (OR=1.01, P＜0.05), and chronic hepatitis B (OR=1.86, P＜0.05) were identified as independent risk factors for sepsis. Conclusion Sepsis was significantly associated with male gender, older age, smoking, and alcohol consumption. Patients with congestive heart failure, CKD, chronic hepatitis B, liver cirrhosis, and malignant tumors were more likely to develop sepsis. Male gender, older age, and chronic hepatitis B were independent risk factors for sepsis. [ABSTRACT FROM AUTHOR]

Sepsis associated encephalopathy (SAE) is a common complication in patients with sepsis. It is characterized by brain dysfunction, and a considerable proportion of patients have long-term cognitive impairment. The central nervous system is one of earliest regions affected by peripheral inflammation caused by sepsis. As resident immune cells of central nervous system, microglia can coordinate inflammatory responses in brain and play an important role in the innate and adaptive immune responses of brain. Therefore, it plays a crucial role in the occurrence and development of SAE. In this paper, the functional phenotypes of microglia and their role in SAE are reviewed to explore the potential value of microglia in the prevention and treatment of SAE. [ABSTRACT FROM AUTHOR]

Objective To investigate the clinical features and risk factors of sepsis-induced cardiomyopathy in children with sepsis, aiming to provide reference for enhancing the diagnosis and treatment levels of clinicians. Methods Clinical data of children with sepsis were retrospectively analyzed. All patients were divided into the sepsis-induced cardiomyopathy group and non-sepsisinduced cardiomyopathy group according to whether sepsis-induced cardiomyopathy occurred.Clinical characteristics and outcomes were compared between two groups. The risk factors of sepsis-induced cardiomyopathy were analyzed. Results Three hundred and ninty-eight children with sepsis were included in this study, and the incidence of sepsis-induced cardiomyopathy was 15.58% (62/398) . The age of children in the sepsis-induced cardiomyopathy group was 49 (18, 108) months, older than 19 (6, 52) months in the nonsepsis-induced cardiomyopathy group. The incidence of septic shock in the sepsis-induced cardiomyopathy group was 83.87% (52/62), which was higher than 42.56% (143/336) in the non-sepsis-induced cardiomyopathy group. The mortality rate in the sepsis-induced cardiomyopathy group was 29.03% (18/62), significantly higher than 14.58% (49/336) in the non-sepsis-induced cardiomyopathy group. All differences were statistically significant (all P < 0.05) .Multivariate Logistic regression analysis showed that the influence of age on sepsis-induced cardiomyopathy was statistically significant (OR=1.010, 95%CI 1.003-1.017, P = 0.006) . The higher the lactic acid level, the higher the risk of sepsis-induced cardiomyopathy, with statistical significance (OR=1.163, 95%CI 1.034-1.308, P = 0.012) . The higher the cTnI level, the higher the risk of sepsis-induced cardiomyopathy, with statistical significance (OR=9.929, 95%CI 4.651-21.197, P < 0.001) . Conclusions Compared with children with non-sepsis-induced cardiomyopathy, children with sepsis-induced cardiomyopathy are more prone to septic shock and have higher mortality. Age, lactic acid and cTnI levels are the independent influencing factors for sepsis-induced cardiomyopathy in children. [ABSTRACT FROM AUTHOR]

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目的 探讨血乳酸/白蛋白 (LAR) 与老年脓毒症合并急性胃肠功能损伤患者病情及预后的关系。 方法 选择老年脓毒症合并急性胃肠功能损伤患者 247例，入组时存在胃肠功能障碍 143例 (AGI分级Ⅰ级 68例、 Ⅱ级75例) 、胃肠功能衰竭104例 (AGI分级Ⅲ级51例、Ⅳ级53例) ，随访12个月判断预后。比较不同胃肠功能损伤 程度及预后情况患者的一般资料［性别、年龄、BMI、查尔森共病指数 (CCI) 、急性生理学与慢性健康状况量表系统Ⅱ (APACHEⅡ) 评分、序贯器官衰竭评估 (SOFA) 评分、平均动脉压 (MAP) ］及实验室相关指标［降钙素原 (PCT) 、乳酸 (LAC) 、白蛋白 (ALB) 、LAR］，绘制有统计学差异的相关指标预测患者急性胃肠功能损伤严重程度及预后的受试者 工作特征 (ROC) 曲线，计算曲线下面积 (AUC) ，分析其预测价值。根据 LAR的最佳临界值，将患者分为 LAR低、高 水平者，比较其胃肠功能衰竭发生率和生存率。结果 247例患者随访12个月生存105例、死亡142例，其中AGI分 级为Ⅰ、Ⅱ、Ⅲ、Ⅳ级的老年脓毒症患者生存率分别为61. 8% (42/68) 、44. 0% (33/75) 、31. 4% (16/51) 、26. 4% (14/53) ， 随着AGI分级的增加老年脓毒症患者生存率逐渐降低 (P<0. 05) 。胃肠功能障碍的老年脓毒症患者LAR、LAC、SOFA 评分均低于胃肠功能衰竭者 (P均<0. 05) ，二者性别构成比及年龄、BMI、CCI、APACHEⅡ评分、MAP、PCT、ALB比较 P均>0. 05；ROC曲线分析结果显示，LAR预测老年脓毒症患者急性胃肠功能损伤程度的AUC及95% CI为80. 365 8 (74. 767 1～85. 934 4) ，最佳临界值为1. 315、敏感度为77. 88%、特异度为74. 13%，均高于LAC、SOFA评分；LAR低 水平者121例、LAR高水平者126例，LAR低水平者胃肠功能衰竭发生率低于LAR高水平者 (P<0. 05) 。生存的老年 脓毒症患者APACHEⅡ评分、SOFA评分、LAR、LAC均低于死亡者且ALB高于死亡者 (P均<0. 05) ，二者性别构成比 及年龄、BMI、CCI、MAP、PCT比较P均>0. 05；ROC曲线分析结果显示，LAR预测老年脓毒症患者预后的AUC及95% CI为 84. 070 0 (74. 796 6～86. 017 3) ，最佳临界值为 1. 030、敏感度为 83. 10%、特异度为 65. 38%，AUC 及敏感度均 高于 APACHEⅡ评分、SOFA 评分、LAC、ALB；LAR 低水平者生存率高于 LAR 高水平者 (P<0. 05) 。结论　老年 脓毒症合并急性胃肠功能损伤患者LAR水平升高与胃肠道功能损伤程度加重及预后不良有关。 [ABSTRACT FROM AUTHOR]

Obejective: To investigate the relationship between serum procalcitonin (PCT), apolipoprotein M (APOM), soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) and prognosis in patients with sepsis due to bacterial bloodstream infection (BSI). Methods: 185 patients with sepsis due to bacterial BSI (sepsis group) were selected in Beijing Chaoyang Hospital Affiliated to Capital Medical University from January 2021 to October 2023, patients were divided into death group (61 cases) and survival group (124 cases) according to the prognosis within 28 days, and 87 healthy volunteers (control group) were selected from our hospital during the same period. Serum PCT level was detected by electrochemiluminescence, and serum APOM and sTREM-1 levels were detected by enzyme-linked immunosorbent assay. The factors affecting the prognosis of patients with sepsis due to bacterial BSI were analyzed by univariate and multivariate Logistic regression models. The predictive value of serum PCT, APOM and sTREM-1 on the prognosis of patients with sepsis due to bacterial BSI were analyzed by receiver operating characteristic (ROC) curve. Results: Compared with control group, the levels of serum PCT and sTREM-1 in sepsis group were increased, and the level of APOM was decreased (P<0.05). The 28-day mortality rate of 185 patients with sepsis due to bacterial BSI was 32.97% (61/185). Compared with survival group, the levels of serum PCT and sTREM-1 in death group increased, and the level of APOM decreased (P<0.05). The results of the multifactor analysis show that gram-negative bacterial infection, septic shock, increased neutrophil/lymphocyte ratio (NLR), increased sequential organ failure assessment (SOFA) score, increased acute physiology and chronic health evaluation II (APACHE II) score, increased serum PCT and sTREM-1 were independent risk factors for death in patients with sepsis due to bacterial BSI, and increased serum APOM was an independent protective factor (P<0.05). The area under the curve of combined detection of serum PCT, APOM and sTREM-1 in predicting the death of patients with sepsis due to bacterial BSI was 0.908, which was greater than 0.785, 0.779 and 0.783 predicted by serum PCT, APOM and sTREM-1 alone. Conclusion: The increase of serum PCT and sTREM-1 levels and the decrease of APOM level in patients with sepsis due to bacterial BSI are relate to the occurrence of poor prognosis, the combine detection of serum PCT, APOM and sTREM-1 has a high predictive value for the death of patients with sepsis due to bacterial BSI. [ABSTRACT FROM AUTHOR]

Objective To explore the effect of adiponectin (APN) on acute kidney injury in mice with sepsis and its related mechanism. Methods Twenty-four male C57BL/6 mice were randomly divided into the control group (CON group), model group (LPS group) and experimental group (LPS+APN group) . We prepared the sepsis models by intraper‑ itoneal injection of 10 mg/kg lipopolysaccharide (LPS) . Mice in the CON group were injected with equal volume of 0. 9% sodium chloride injection intraperitoneally, and mice in the experimental group were injected with 0. 1 mg/kg APN via the tail vein at 8 h before modeling for intervention. Mice were sacrificed at 24 h after modeling, and venous blood was taken to detect renal injury indicators such as creatinine and urea nitrogen. HE staining was used to observe and evaluate the pathological changes of mouse renal tissues. The content of reactive oxygen species was detected by dihydroethidium (DHE) . The mRNA expression levels of NLRP3, IL-1β and TNF-α in the renal tissues were detected by real-time quanti‑ tative PCR, and the expression levels of NLRP3, Caspase-1 and IL-1β were detected by Western blotting. Results Compared with the model group, after APN pretreatment, renal function and histopathological injury were alleviated, the content of reactive oxygen species in renal tissues significantly decreased, the mRNA expression levels of NLRP3, IL-1β and TNF-α significantly decreased, and the expression levels of NLRP3, Caspase-1 and IL-1β significantly decreased (all P<0. 05) . Conclusion APN has a protective effect on acute renal injury mice with sepsis, and its mechanism may be re‑ lated to the inhibition of NLRP3 inflammatome and pyroptosis-related pathway. [ABSTRACT FROM AUTHOR]

Objective: To screen key differentially expressed genes （DEGs） in dead mice with sepsis by spleen high-throughput sequencing combined with bioinformatics. Methods: ①A mouse sepsis model was set up by intraperitoneal injection of lipopolysaccharide （LPS）, a 7-day survival curve of mice was drawn, and the modeling doses of survival group and death group were screened out. ②Expressions of TNF-α, IL-1β, IL-6 and IL-10 in peripheral blood of mice in control group, survival group and death group were verified by ELISA. ③High-throughput sequencing was conducted on spleens of survival group and death group, and the key genes were screened by bioinformatics analysis of DEGs. ④Expressions of key genes and proteins were detected by RT-PCR and Western blot. Results: ①LPS dosage in survival group was 15 mg/kg （with a mortality of 30%）, and LPS dosage in death group was 30 mg/kg（ with a mortality of 80%）. ②Expression levels of IL-6, TNF-α and IL-1β in sepsis mice were significantly higher than those of control group, while expression level of IL-10 was decreased （P<0.05）. Comparison of sepsis model groups showed that levels of pro-inflammatory factors in death group were higher than those in survival group, while level of IL-10 was lower than that in survival group （P<0.05）. ③A total of 2 999 DEGs in survival group and death group were screened out by bioinformatics, among which 1 185 genes were up-regulated and 1 814 genes were down-regulated. Top 5 DEGs enrichment pathways were screened out: "hematopoietic cell lineage" "primary immunodeficiency" "African trypanosomiasis" "leishmaniasis" and "B-cell receptor signaling pathway". Ifit1, Ifit3 and Mx1 were three key genes that were screened out. ④Compared with survival group, expressions of genes and proteins of Ifit1, Ifit3 and Mx1 were down-regulated in spleen tissues of the death group （P<0.05）. Conclusion: By high-throughput sequencing and bioinformatics, Ifit1, Ifit3 and Mx1 are screened out as key genes related to the death outcome of sepsis, which probably influence the outcome of sepsis through the immune mechanism related to virus infection. [ABSTRACT FROM AUTHOR]

Objective To evaluate the application of combined measurement of chromogranin A (CgA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and modified quick Sequential Organ Failure Assessment (qSOFA) score in the prognostic assessment of pediatric sepsis. Methods Clinical data of 188 pediatric sepsis patients admitted to our hospital from March 2020 to April 2023 were selected. The patients were divided into sepsis group (n = 113) and severe sepsis group (n = 75) based on the severity of their condition. CgA, TNF-α, and IL-6 levels were compared between the two groups. The relationship between CgA, TNF-α, IL-6 levels, modified qSOFA score, and the prognosis of children was analyzed to explore their predictive value for the prognosis of children. Results CgA, TNF-α, IL-6, and modified qSOFA scores in the severe sepsis group were higher than those in the sepsis group (P < 0.05) . Patients in the deceased group had higher CgA, TNF a, IL-6, and modified qSOFA scores compared to the survival group (P < 0.05) . Using the prognosis of children as the independent variable (survival = 0, death = 1), multiple logistic regression analysis of CgA, TNF-α, IL-6, and modified qSOFA scores showed that these indicators would impact the prognosis of children (P < 0.05) . The AUC values of receiver operating characteristic (ROC) curves for predicting adverse prognosis in patients using CgA, TNF, IL-6, and modified qSOFA scores were 0.926, 0.875, 0.863, 0.862, respectively. The AUC value of combined application was 0. 994, higher than individual predictions (P < 0.05) . Conclusion Combined measurement of CgA, TNF-α, IL-6, and modified qSOFA scores significantly increases in pediatric patients with severe sepsis and deceased patients. Their combined application has a high predictive value for adverse prognosis in children, assisting in the clinical treatment of pediatric sepsis. [ABSTRACT FROM AUTHOR]