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关键词： Staphylococcus aureus   Colonization   Maternal infant health   Skin infection   Vaccine  

摘要： BACKGROUND:Staphylococcus aureus is the leading cause of infectious-related deaths. Vaccine development has been hampered by the recall of nonprotective immune responses from prior exposure, suggesting an effective vaccine may need to be given early in life. The goal of this pilot study was to correlate the maternal serologic response against S. aureus to an infant's risk for skin and soft tissue infection (SSTI) and colonization in the first year of life. METHODS:Pregnant women were enrolled and maternal-infant dyads followed for 12 months. Maternal 3rd trimester and cord blood were obtained to determine the anti-S. aureus IgG and anti-α-toxin (Hla) neutralizing antibody (NAb) titers. Serial surveys and skin swabs were obtained from mothers at enrollment and from infants longitudinally to ascertain S. aureus colonization status and the incidence of SSTI. RESULTS:63 pregnant women were enrolled, 54% with history of SSTI or asymptomatic S. aureus colonization at enrollment. Within 48-hours of delivery, 23% of infants had S. aureus colonization and 43% at 1-month. Maternal S. aureus colonization resulted in 7.4 increased odds of infant colonization at delivery. Higher cord blood anti-Hla Nab titer was associated with significantly lower risk for infant SSTI in the first year of life. CONCLUSIONS:S. aureus colonization occurs early in life, with over 40% of infants colonized by 1-month. These results are the first to demonstrate an association between higher transplacental anti-Hla NAb and protection against infant SSTI in the first year of life. Overall, these findings support Hla as a promising vaccine target.

关键词： 系统性红斑狼疮   体液免疫检验   抗核抗体  

摘要： 探析抗核抗体(ANA抗体)与体液免疫检验在系统性红斑狼疮(SLE)诊断中的应用效果。方法 选取淮海市中医院40例SLE患者(观察组)与40例健康体检者(对照组)(2023年7月-2025年5月),所有患者均进行ANA抗体与体液免疫检验,分析诊断结果。结果 ANA抗体阳性检出率方面,观察组是92.50%,对照组是7.50%,观察组显著提高(P<0.05)。观察组补体C3是(0.46±0.21)g/L,补体C4是(0.12±0.03)g/L,IgA是(1.20±0.69)g/L,IgG是(20.69±5.17)g/L,IgM是(2.95±0.43)g/L,对照组补体C3是(1.18±0.59)g/L,补体C4是(0.35±0.12)g/L,IgA是(1.18±0.65)g/L,IgG是(11.32±1.59)g/L,IgM是(1.24±0.32)g/L,观察组补体C3和补体C4更低,而IgG、IgM更高(P<0.05)。SLE活动组与SLE非活动组ANA抗体阳性检出率对比无明显差异(P>0.05)。SLE活动组补体C3、补体C4、IgA、IgG、IgM分别是(0.35±0.12)g/L、(0.09±0.03)g/L、(1.21±0.56)g/L、(22.63±3.34)g/L、(2.97±0.48)g/L;SLE非活动组分别是(0.56±0.14)g/L、(0.16±0.08)g/L、(1.19±0.58)g/L、(18.89±3.18)g/L、(2.39±0.41)g/L,SLE非活动组补体C3及补体C4更高,而IgG和IgM显著降低(P<0.05)结论 ANA抗体与体液免疫检验结合在SLE诊断中,能够清楚地反映患者补体情况和免疫情况,为疾病诊断和治疗提供参考,以便患者及早接受针对性治疗。

关键词： 支原体肺炎   血清补体C3   CRP   免疫球蛋白   诊断价值  

摘要： 探究血清补体C3、CRP及免疫球蛋白检验在支原体肺炎诊断中的临床意义。方法 该次研究时间为2023.01至2023.12,分析对象为支气体肺炎患者(疾病组)60例和健康体检者(健康组)60例。对其血清补体C3、CRP及免疫球蛋白(IgG、IgM、IgA)水平,进行对比分析,并绘制ROC,分析联合检验价值。结果 血清补体C3、CRP、IgG、IgM:疾病组>健康组,IgA:疾病组<健康组(P<0.05);血清补体C3、CRP、IgG、IgM:轻症<重症,IgA:轻症>重症(P<0.05);ROC示,AUC:联合检测>单独检测(P<0.05)。结论 血清补体C3、CRP、免疫球蛋白检验联合检测临床意义重大,可作为支原体肺炎辅助诊断重要指标,值得优选。

关键词： 脓毒症休克   预后分析   TNF-α   oXiris滤器  

摘要： 分析脓毒性休克患者采用oXiris滤器治疗对IL-6、CRP、PCT、TNF-α的影响。方法 纳入2023年1月1日-2024年3月1日12例江阴市人民医院重症医学科脓毒症休克患者,将oXiris滤器作为连续线肾脏替代治疗的工具,针对基本资料实施回顾性分析、验证分析登,比较IL-6、CRP、PCT、TNF-α,监测血流动力学状态,分析血乳酸和血小板计数,而后观察氧合指数、预后情况、安全性等。结果 IL-6、CRP、PCT、TNF-α综合分析后,治疗后降幅明显,和治疗前的差异较大,P<0.05。12例患者有66.67%的就救治存活率,有50.00%的并发症发生率,平均ICU住院时间为(12.7±7.5)d。治疗后MAP表现出较为明显的增幅,HR则表现出明显的降幅,P<0.05;治疗后PLT、SaO2等均升高,P<0.05;治疗前后Lac并未表现出明显区别,P>0.05;SOFA评分、NE比较中,治疗后均比较低,P<0.05;结论 oXiris滤器可降低IL-6、CRP、PCT、TNF-α水平,还能减少NE用量,调节氧合状态,提高MAP、HR稳定性,维持较高救治存活率,实现较好预后,适用于脓毒症休克患者。

摘要： Colorectal cancer (CRC) is increasingly common in younger individuals and strongly linked to chronic inflammation. Gut microbiota and pathways like NF-κB/STAT3 play key roles, which highlights the therapeutic potential of natural compounds that target intestinal immunity and microbial balance. To investigate the therapeutic effects of pectic polysaccharides (PPs) from in inflammation-associated CRC the modulation of of gut microbiota and NF-κB/IL-6/STAT3 signaling pathways. C57BL/6 mice were subjected to azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced CRC and treated with PP (100 mg/kg/day), the STAT3 inhibitor W2014-S (10 mg/kg), or fecal microbiota transplantation (FMT) from PP-treated donors. Histopathology, immunohistochemistry (IHC), Western blot, immunofluorescence (IF), 16S rRNA sequencing, and SCFA analysis were performed to assess inflammation, signaling pathways, gut microbiota composition, and metabolic changes. PP intervention significantly mitigated AOM/DSS-induced weight loss, intestinal lesions, and disease activity index (DAI) scores while suppressing NF-κB and STAT3 activation. PP restored gut microbiota diversity, reduced pro-inflammatory genera, and regulated SCFA levels, particularly hexanoic those of and isohexanoic acids. FMT from PP-treated donors similarly attenuated colitis and inhibited NF-κB/STAT3 pathways. PP alleviates CRC and is associated with modulation of gut microbiota, SCFA metabolism, and NF-κB/IL-6/STAT3 signaling, offering a potential therapeutic strategy for inflammation-driven CRC.

关键词： Lupus nephritis   Podocyte injury   IFN-(3   HERC5   IRF3  

摘要： Podocytes may mediate local production of Type I interferon (IFN-I), which play a crucial role in the pathogenesis of lupus nephritis (LN). ISGylation is widely involved in the innate immune activation and IFN-I production. Here, we discovered that in patients with LN and pristane-induced model mouse the staining of HERC5, a E3 protein ligase in ISGylation, was markedly elevated in renal glomerulus and associated with podocyte injury. Knockdown of HERC5 in Human podocyte cells significantly decreased the transcription level of Ifn-b1 and subsequently pro-inflammatory factors Tnf-alpha, Il-6, and Cxcl10, while increasing anti-inflammatory factor Il-10 levels, and reduced podocyte injury induced by LN plasma or IFN-(3. Conversely, overexpression of HERC5 reversed the above results, that increased IFN-(3 generation and excessive activation, and induced podocyte injury. Mechanistically, HERC5 interacts with and facilitates the ISGylation of IRF3, preventing its ubiquitination and subsequent degradation. This interaction stabilizes IRF3, enhancing its activity and leading to sustained IFN-(3 production and inflammation. In conclusion, our study identifies HERC5 as a key regulator in LN, promoting IRF3 activation and driving sustained IFN-(3 production and overactivation. This process induces an inflammatory phenotype in podocytes, contributing to their self-injury.

关键词： HDAC6 inhibitor   MHC class II complex   Esophageal cancer treatment  

摘要： Objective: This study aimed to investigate the therapeutic potential of the novel HDAC6 inhibitor 9r in esophageal cancer (EC). Specifically, it focused on evaluating 9r's ability to inhibit tumor growth, migration, and apoptosis while enhancing antitumor immunity through the modulation of MHC class II signaling pathways. Methods: The study employed in vitro experiments using TE-1 and MEC25 esophageal cancer cells to assess antitumor effects of compound 9r. RNA sequencing and bioinformatics analysis were utilized to explore the molecular mechanisms underlying its action, particularly its impact on MHC class II pathways. In vivo experiments were conducted using a murine MEC25 cell xenograft model to evaluate tumor growth inhibition and immune activation. Techniques such as flow cytometry, RT-qPCR, Western blotting, and immunohistochemistry were used for functional validation. Results: Compound 9r significantly suppressed TE-1 cell proliferation, migration, and induced apoptosis in vitro. RNA-seq analysis revealed that 9r upregulated MHC class II-related genes (e.g., HLA-DRA, CD74), which were further enhanced by IFN-gamma co-stimulation. In vivo studies demonstrated that 9r inhibited tumor growth in MEC25 xenografts while increasing CD4+ and CD8+ T cell infiltration in both tumor tissue and spleen. Immunohistochemistry confirmed reduced Ki-67 expression and increased acetylation of alpha-tubulin, indicating HDAC6 inhibition. The compound exhibited minimal toxicity in treated mice. Conclusion: The HDAC6 inhibitor 9r effectively suppresses esophageal cancer progression through dual mechanisms: direct tumor inhibition and enhancement of antitumor immune responses via MHC class II pathway activation. These findings establish 9r as a promising candidate for esophageal cancer treatment and provide a foundation for further clinical development.

关键词： 结直肠癌   细胞焦亡   炎癌转化   生长因子   细胞因子  

摘要： 结直肠癌作为全球范围内发病率和死亡率均居高不下的恶性肿瘤之一，对人类健康构成了严重威胁。而且结直肠癌的早期诊断率相对较低，许多患者在确诊时已处于中晚期，治疗效果和预后均不理想。然而目前大多数结直肠癌的研究都还停留在外科层面，对于内部细胞和分子的作用机制研究较少。随着对肿瘤生物学的深入研究，炎症与肿瘤之间的密切联系逐渐被揭示，细胞焦亡作为新型程序性细胞死亡方式，在肿瘤免疫及微环境调控中备受关注。本研究系统梳理结直肠癌炎癌转化及细胞焦亡的研究进展，分析两者相互作用机制及细胞焦亡在疾病发展中的作用。研究发现，慢性炎症通过细胞因子、生长因子等调控未分化细胞向癌症干细胞转化，构建促癌微环境；细胞焦亡由炎症体激活引发，经caspase家族及gasdermin家族蛋白介导，既可促进肿瘤细胞死亡，又通过释放IL-1β、IL-18等细胞因子影响肿瘤微环境，其作用具有双重性。针对炎癌转化和细胞焦亡的靶向策略展现出治疗潜力。本研究为理解结直肠癌发病机制提供了细胞分子层面的理论依据，为开发精准靶向治疗方案奠定基础，有助于推动结直肠癌治疗技术从外科为主向多机制联合干预发展，改善患者预后。

关键词： Liver fibrosis   MASLD   Myofibroblast   NAFLD   Translational research  

摘要： Aims Non-alcoholic fatty liver disease (NAFLD), also known as metabolic dysfunction associated steatotic liver disease (MASLD), represents a spectrum of chronic liver diseases that eventually lead to cirrhosis and hepatocellular carcinoma. Liver fibrosis is both a pathological feature and a contributing factor in NAFLD. In the present study we investigated whether targeting pre-B cell leukemia transcription factor 1 (PBX1) and interleukin 7 receptor (IL7R) might ameliorate liver fibrosis in the context of NAFLD. Methods and materials NAFLD was induced in C57/B6j mice by feeding with a choline-deficient amino acid defined high-fat diet (CDAA-HFD). Key findings Both PBX1 expression and IL7R expression were up-regulated in hepatic stellate cells (HSCs) isolated from the mice fed the CDAA-HFD compared to those isolated from the control mice. Myofibroblast-specific PBX1 depletion, by injecting the mice with AAV6 carrying short-hairpin RNA (shRNA) against PBX1, significantly attenuated liver fibrosis induced by CDAA-HFD feeding. Similarly, myofibroblast-specific IL7R depletion significantly mitigated liver fibrosis. Of note, liver injury and steatosis were not influenced by either PBX1 or IL7R depletion. Importantly, IL7R blockade with a neutralizing antibody likewise diminished NAFLD-associated liver fibrosis. Finally, a positive correlation between PBX1 expression, IL7R expression, and myofibroblast activation was identified in liver specimens from NAFLD patients. Significance Our data demonstrate the feasibility of targeting the PBX1-IL7R axis for the intervention of NAFLD-associated liver fibrosis.

关键词： 系统护理   急性淋巴细胞白血病   生命质量   睡眠质量   心理状态  

摘要： 观察急性淋巴白血病(ALL)行系统护理的影响。方法 采集ALL病例(72例;均本院就诊;2023.02-2025.02期间收治),1:1原则随机分组,CG组、XT组(组内病例例数比36:36),前者常规护理,后者系统护理;对干预效果进行对比。结果 ①生命质量:t1,组内评分上升,组间PWB(t值4.734),SWB(t值3.615),EWB(t值5.071),FWB(t值4.580),CG组XT组(P<0.05)。③心理状态:t1,组内评分下降,组间HAMA(t值3.923),HAMD(t值3.182),CG组>XT组(P<0.05)。④认可度;XT组>CG组(x2=5.063,P<0.05)。结论 ALL行系统护理干预作用显著,可提高生命质量、睡眠质量,利于心理状态调节,认可度高,具备推广价值。