目的探究血清晚期糖基化终产物受体(RAGE)、高迁移率族蛋白B1(high mobility group protein B1,HMGB1)水平与重症肺炎(SP)急性呼吸窘迫综合征(ARDS)发病及γ-干扰素(IFN-γ)/白细胞介素4(IL-4)变化的关系。方法前瞻性选取2020年3月至202...目的探究血清晚期糖基化终产物受体(RAGE)、高迁移率族蛋白B1(high mobility group protein B1,HMGB1)水平与重症肺炎(SP)急性呼吸窘迫综合征(ARDS)发病及γ-干扰素(IFN-γ)/白细胞介素4(IL-4)变化的关系。方法前瞻性选取2020年3月至2022年2月我院收治的100例SP患儿为研究对象,根据患儿是否发生继发性ARDS将患儿分为ARDS组(n=56)和对照组(n=44),收集患儿一般资料,采集外周血以酶联免疫吸附法进行RAGE、HMGB1、IFN-γ和IL-4表达水平检测,采用多因素logistic回归分析SP患儿继发ARDS的影响因素,采用Pearson相关性分析其与IFN-γ/IL-4的相关性,并采用受试者工作曲线(ROC)分析RAGE、HMGB1表达对SP患儿继发ARDS的预测价值。结果两组SP患儿性别、年龄、体温以及发病季节之间无显著差异,ARDS组致病菌种类多于对照组,PaO_(2)/FiO_(2)和APS评分、血清RAGE、HMGB1、IFN-γ和IL-4表达水平以及IFN-γ/IL-4比值均高于对照组(P<0.05)。经多因素logistic回归分析可知,致病菌种类、PaO_(2)/FiO_(2)、RAGE、HMGB1表达、IFN-γ、IL-4和IFN-γ/IL-4均为SP患儿继发ARDS的影响因素。经Pearson相关检验,SP患儿血清RAGE、HMGB1表达水平与IFN-γ、IL-4和IFN-γ/IL-4均呈正相关(P<0.05)。经ROC曲线分析可得,血清RAGE、HMGB1水平预测SP患儿发生ARDS的AUC分别为0.707和0.750,灵敏度分别为73.2%、64.3%,特异度分别为68.2%、77.3%,两者联合预测的AUC为0.848,灵敏度和特异度分别为80.4%和81.8%。结论SP继发ARDS患儿血清中RAGE、HMGB1表达水平较高,与IFN-γ/IL-4呈正相关,监测患儿血清RAGE、HMGB1表达对SP患儿继发ARDS的风险有一定的预测价值。展开更多
目的:观察电针对便秘型肠易激综合征(IBS-C)模型大鼠抑郁样行为及血清IL-4的影响,探讨电针改善便秘型肠易激综合征抑郁样行为的机制。方法:采用冰水灌胃法制备IBS-C模型大鼠,造模成功后随机分为模型对照组、电针干预组、手针干预组、温...目的:观察电针对便秘型肠易激综合征(IBS-C)模型大鼠抑郁样行为及血清IL-4的影响,探讨电针改善便秘型肠易激综合征抑郁样行为的机制。方法:采用冰水灌胃法制备IBS-C模型大鼠,造模成功后随机分为模型对照组、电针干预组、手针干预组、温针干预组,另设空白对照组,每组5只。电针干预组、手针干预组、温针干预组分别给予“足三里”、“天枢”、“三阴交”组合电针、手针、温针等干预措施,持续7天,干预结束后评估各组大鼠的一般情况和体重变化,利用强迫游泳实验(FST)和糖水偏好实验(SPT)检测各组大鼠抑郁行为学表现,利用酶联免疫吸附试验(ELISA)检测各组大鼠血清中IL-4含量。结果:与空白对照组相比,模型组大鼠AWR评分显著升高(P P P P < 0.05),以电针组为著。结论:电针治疗可以显著改善IBS-C大鼠抑郁行为学表现,对于IBS-C康复治疗具有重要的临床意义,其作用机制可能与调节IBS-C模型大鼠炎症因子IL-4的水平有关。展开更多
Background:S100A8 is a member of the S100 protein family and plays a pivotal role in regulating inflammation and tumor progression.This study aimed to comprehensively assess the expression patterns and functional role...Background:S100A8 is a member of the S100 protein family and plays a pivotal role in regulating inflammation and tumor progression.This study aimed to comprehensively assess the expression patterns and functional roles of S100A8 in glioma progression.Methods:Glioma tissues were collected from 98 patients who underwent surgical treatment at Fudan University Shanghai Cancer Center.S100A8 expression in glioma tissues was analyzed using immunohistochemistry(IHC)to establish its correlation with clinicopathological features in patients.The expression and prognostic effect of S100A8 in glioma were analyzed using TCGA and CGGA public databases.Then,we investigated the role of S100A8 in glioma through a series of in vivo and in vitro experiments including Transwell,wound healing,CCK8,and intracranial tumor models.Subsequently,bioinformatics analysis,single-cell sequencing and coimmunopre-cipitation(Co-IP)were used to explore the underlying mechanism.Results:S100A8 was upregulated in gliomas compared to paracancerous tissues,and this phenotype was sig-nificantly correlated with poor prognosis.Subgroup analysis showed that S100A8 expression was higher in the high-grade glioma(HGG)group than that in the low-grade glioma(LGG)group.S100A8 overexpression in glioma cell lines promoted cell proliferation,migration and invasion,while silencing S100A8 reversed these effects.In vivo experiments showed that S100A8 knockdown can significantly reduce the tumor burden of glioma cells.Notably,S100A8 was observed to stimulate microglial M2 polarization by interacting with TLR4,which subse-quently induced NF-𝜅B signaling and IL-10 secretion within the tumor microenvironment.Conclusions:S100A8 promotes tumor progression by inducing phenotypic polarization of microglia through the TLR4/IL-10 signaling pathway in glioma.It might represent a therapeutic target for further basic research or clinical management of glioma.展开更多
文摘目的探究血清晚期糖基化终产物受体(RAGE)、高迁移率族蛋白B1(high mobility group protein B1,HMGB1)水平与重症肺炎(SP)急性呼吸窘迫综合征(ARDS)发病及γ-干扰素(IFN-γ)/白细胞介素4(IL-4)变化的关系。方法前瞻性选取2020年3月至2022年2月我院收治的100例SP患儿为研究对象,根据患儿是否发生继发性ARDS将患儿分为ARDS组(n=56)和对照组(n=44),收集患儿一般资料,采集外周血以酶联免疫吸附法进行RAGE、HMGB1、IFN-γ和IL-4表达水平检测,采用多因素logistic回归分析SP患儿继发ARDS的影响因素,采用Pearson相关性分析其与IFN-γ/IL-4的相关性,并采用受试者工作曲线(ROC)分析RAGE、HMGB1表达对SP患儿继发ARDS的预测价值。结果两组SP患儿性别、年龄、体温以及发病季节之间无显著差异,ARDS组致病菌种类多于对照组,PaO_(2)/FiO_(2)和APS评分、血清RAGE、HMGB1、IFN-γ和IL-4表达水平以及IFN-γ/IL-4比值均高于对照组(P<0.05)。经多因素logistic回归分析可知,致病菌种类、PaO_(2)/FiO_(2)、RAGE、HMGB1表达、IFN-γ、IL-4和IFN-γ/IL-4均为SP患儿继发ARDS的影响因素。经Pearson相关检验,SP患儿血清RAGE、HMGB1表达水平与IFN-γ、IL-4和IFN-γ/IL-4均呈正相关(P<0.05)。经ROC曲线分析可得,血清RAGE、HMGB1水平预测SP患儿发生ARDS的AUC分别为0.707和0.750,灵敏度分别为73.2%、64.3%,特异度分别为68.2%、77.3%,两者联合预测的AUC为0.848,灵敏度和特异度分别为80.4%和81.8%。结论SP继发ARDS患儿血清中RAGE、HMGB1表达水平较高,与IFN-γ/IL-4呈正相关,监测患儿血清RAGE、HMGB1表达对SP患儿继发ARDS的风险有一定的预测价值。
文摘目的:观察电针对便秘型肠易激综合征(IBS-C)模型大鼠抑郁样行为及血清IL-4的影响,探讨电针改善便秘型肠易激综合征抑郁样行为的机制。方法:采用冰水灌胃法制备IBS-C模型大鼠,造模成功后随机分为模型对照组、电针干预组、手针干预组、温针干预组,另设空白对照组,每组5只。电针干预组、手针干预组、温针干预组分别给予“足三里”、“天枢”、“三阴交”组合电针、手针、温针等干预措施,持续7天,干预结束后评估各组大鼠的一般情况和体重变化,利用强迫游泳实验(FST)和糖水偏好实验(SPT)检测各组大鼠抑郁行为学表现,利用酶联免疫吸附试验(ELISA)检测各组大鼠血清中IL-4含量。结果:与空白对照组相比,模型组大鼠AWR评分显著升高(P P P P < 0.05),以电针组为著。结论:电针治疗可以显著改善IBS-C大鼠抑郁行为学表现,对于IBS-C康复治疗具有重要的临床意义,其作用机制可能与调节IBS-C模型大鼠炎症因子IL-4的水平有关。
基金supported by the National Natural Science Foundation of China(grant numbers:82103429 and 82173177).
文摘Background:S100A8 is a member of the S100 protein family and plays a pivotal role in regulating inflammation and tumor progression.This study aimed to comprehensively assess the expression patterns and functional roles of S100A8 in glioma progression.Methods:Glioma tissues were collected from 98 patients who underwent surgical treatment at Fudan University Shanghai Cancer Center.S100A8 expression in glioma tissues was analyzed using immunohistochemistry(IHC)to establish its correlation with clinicopathological features in patients.The expression and prognostic effect of S100A8 in glioma were analyzed using TCGA and CGGA public databases.Then,we investigated the role of S100A8 in glioma through a series of in vivo and in vitro experiments including Transwell,wound healing,CCK8,and intracranial tumor models.Subsequently,bioinformatics analysis,single-cell sequencing and coimmunopre-cipitation(Co-IP)were used to explore the underlying mechanism.Results:S100A8 was upregulated in gliomas compared to paracancerous tissues,and this phenotype was sig-nificantly correlated with poor prognosis.Subgroup analysis showed that S100A8 expression was higher in the high-grade glioma(HGG)group than that in the low-grade glioma(LGG)group.S100A8 overexpression in glioma cell lines promoted cell proliferation,migration and invasion,while silencing S100A8 reversed these effects.In vivo experiments showed that S100A8 knockdown can significantly reduce the tumor burden of glioma cells.Notably,S100A8 was observed to stimulate microglial M2 polarization by interacting with TLR4,which subse-quently induced NF-𝜅B signaling and IL-10 secretion within the tumor microenvironment.Conclusions:S100A8 promotes tumor progression by inducing phenotypic polarization of microglia through the TLR4/IL-10 signaling pathway in glioma.It might represent a therapeutic target for further basic research or clinical management of glioma.
