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关键词： 子宫内膜异位症   环氧合酶-2   癌胚抗原  

摘要： 目的分析子宫内膜异位症(EMS)患者癌胚抗原(CEA)、环氧合酶-2(COX-2)表达水平及临床意义。方法选取2022年6月至2024年6月青岛市市南区妇幼保健计划生育服务中心收治的87例EMS患者为EMS组,同期选取50例非EMS妇科良性疾病患者为对照1组、50例健康体检女性为对照2组。对比各组CEA、COX-2水平,以修订的美国生殖医学协会(r-AFS)EMS分期为依据,比较不同临床分期EMS患者的CEA、COX-2水平,分析EMS患者CEA、COX-2与r-AFS评分的相关性。结果三组CEA、COX-2水平比较,有统计学差异(P<0.05);对照1组CEA、COX-2水平较对照2组更高(P<0.05);EMS组CEA、COX-2水平较对照1组、对照2组更高(P<0.05)。不同临床分期的EMS患者CEA、COX-2水平比较,有统计学差异(P<0.05);Ⅱ期患者CEA、COX-2水平较Ⅰ期患者更高(P<0.05);Ⅲ期患者CEA、COX-2水平较Ⅰ、Ⅱ期患者更高(P<0.05);Ⅳ期患者CEA、COX-2水平较Ⅰ、Ⅱ、Ⅲ期患者更高(P<0.05)。CEA、COX-2与r-AFS评分呈正相关(r=0.544、0.538,P<0.05)。结论EMS患者CEA、COX-2呈高表达,且与r-AFS评分呈正相关。

关键词： 中性粒细胞   淋巴细胞   载脂蛋白B   载脂蛋白A1   高脂血症   急性胰腺炎  

摘要： 目的探讨分析发病48小时内中性粒细胞/淋巴细胞比率(NLR)、载脂蛋白B/载脂蛋白A1(Apo B/A1)评估高脂血症性急性胰腺炎(HLAP)严重程度的意义。方法选取2021年1月至2024年1月我院收治的HLAP患者63例,纳入疾病组,根据修订亚特兰大分级系统将患者分为轻度51例、中重度/重度12例,同期选取62例62例血常规及血脂正常的非腹痛的相对健康者,纳入相对健康组,对所有入选对象进行NLR、Apo B/A1检测,分析其评估HLAP严重程度的作用。结果疾病组NLR、Apo B/A1较相对健康组明显更高(P<0.05)。轻度组NLR、Apo B/A1低于中重度/重度组(P<0.05)。联合评估较单项评估的灵敏度、特异度及准确性明显更高(P<0.05)。Spearman分析可见,NLR、Apo B/A1与HLAP严重程度呈显著正相关(P<0.05)。结论NLR、Apo B/A1对HLAP有较好的诊断评估价值,能有效评估HLAP的病情程度,为临床治疗提供依据。

关键词： 神经痛,带状疱疹后   龙胆泻肝汤   针刺疗法   免疫,细胞   针刺镇痛   白细胞介素35  

摘要： 目的观察加味龙胆泻肝汤联合疏肝调神针刺法治疗肝经郁热型带状疱疹后神经痛的疗效及对细胞免疫、血清白细胞介素35(IL-35)、CX3C趋化因子受体1(CX3CR1)的影响。方法将102例肝经郁热型带状疱疹后神经痛患者按照随机数字表法分为2组,对照组51例予常规西医治疗,治疗组51例在对照组治疗基础上予加味龙胆泻肝汤联合疏肝调神针刺法治疗。比较2组临床疗效,并比较2组治疗前后中医证候、贝克焦虑量表(BAI)、带状疱疹简明疼痛量表(ZBPI)、皮肤病生活质量指数(DLQI)量表评分,检测2组患者治疗前后低氧诱导因子-1α(HIF-1α)、人神经损伤诱导蛋白1(NINJ1)、IL-35、CX3CR1、微小核糖核酸-21(miR-21)水平及辅助性T淋巴细胞17(Th17)/调节性T淋巴细胞(Treg)比值。结果2组临床疗效比较差异有统计学意义(P<0.05),治疗组临床疗效优于对照组。治疗后,2组各项中医证候评分、BAI、ZBPI、DLQI评分均较本组治疗前降低(P<0.05),且治疗组均低于对照组(P<0.05)。治疗后,2组CX3CR1、Th17/Treg、HIF-1α、NINJ1、miR-21水平均较本组治疗前降低(P<0.05),且治疗组均低于对照组(P<0.05);治疗后,2组IL-35水平均较本组治疗前升高(P<0.05),且治疗组高于对照组(P<0.05)。结论加味龙胆泻肝汤联合疏肝调神针刺法治疗肝经郁热型带状疱疹后神经痛,可调节患者细胞免疫,减轻炎症损伤,促进神经损伤修复,提高镇痛效应,缓解病情,提升生活质量及临床疗效。

关键词： Biomarker   Inflammation   Interleukin   Prognosis   Renal cell carcinoma   Tumorigenesis  

摘要： Background:Renal cell carcinoma(RCC)is a prevalent malignancy characterized by a rising incidence and significant ***(ILs)are crucial in regulating immune cell trafficking and exhibit anti-tumor ***,limited research has explored the expression levels and prognostic significance of interleukins in ***:In this comprehensive study,we performed a detailed analysis of interleukins in RCC patients using multiple bioinformatics tools,including Oncomine,UALCAN,GEPIA,Kaplan-Meier plotter,cBioPortal,GeneMANIA,TRRUST,STRING,and Linked ***:Our analysis demonstrated a significant upregulation in the transcriptional levels of IL4,IL7,IL15,IL16,IL23A,IL26,and IL32 were significantly upregulated in RCC tissues,indicating their potential involvement in the pathogenesis of this *** contrast,IL1A,IL11,and IL27 were downregulated,indicating their potential function as tumor *** correlations were identified between the expression levels of IL11,IL23A,IL27,IL32,and the pathological stage of RCC *** expression levels of IL1A,IL4,IL11,IL15,IL16,IL23A,IL26,IL27,and IL32 were significantly correlated with improved *** differentially expressed interleukins primarily function in cytokine-cytokine receptor interactions and immune response-regulating signaling *** A10(HOXA10),v-myb myeloblastosis viral oncogene homolog(avian)(MYB),v-rel reticuloendotheliosis viral oncogene homolog A(avian)(RELA),and nuclear factor of kappa light polypeptide gene enhancer in B-cells 1(NFKB1)are key transcription factors for ILs,while LCK proto-oncogene(LCK),LYN proto-oncogene(LYN),spleen associated tyrosine kinase(SYK),Janus kinase 3(JAK3),and FER tyrosine kinase(FER)are IL *** expression significantly correlated with the infiltration of six distinct immune cell ***1A potentially exerts an anti-tumor effect in RCC prognosis by inducing neutrophil extracellular traps(NETs).Additionally,NFK

关键词： 口蹄疫病毒   非复制型mRNA   非编码区   蛋白表达  

摘要： 口蹄疫(foot-and-mouth disease, FMD)是目前全球范围内最重要的动物传染病之一,所有偶蹄动物均易感。疫苗免疫是口蹄疫防控的首要选择。mRNA疫苗可以在体外快速设计合成和大规模生产,且能够诱导高效的保护性免疫应答,具有开发速度快、易制备、生物安全风险低等优点。其中,非编码区的设计是增强mRNA疫苗表达和效力的关键。为了获得高效的FMD mRNA疫苗,本研究体外合成了3种具有不同非编码区的口蹄疫P12A3C DNA与对应的mRNA,通过比较其在不同时间点和细胞系中的表达量差异,发现mRNA P12A3C-UTR3表达量优异且普适性最好。本研究为口蹄疫mRNA疫苗的研制奠定了基础,也为高效mRNA的序列设计提供了理论依据。

关键词： 胱抑素C   C反应蛋白质   糖类抗原125   急性冠脉综合征   相关  

摘要： 目的分析血清胱抑素C(CysC)、超敏C反应蛋白(hs-CRP)、糖类抗原125(CA125)与非ST段抬高型急性冠状动脉综合征患者病情严重程度的相关性。方法将郑州人民医院2023年1月至2024年3月就诊的92例非ST段抬高型急性冠状动脉综合征患者归为A组,同期院内健康体检者81名归为B组,将A组分为非ST段抬高型心肌梗死组(22例)与不稳定性心绞痛组(70例),对比各组研究对象血清CysC、hs-CRP、CA125水平及全球急性冠状动脉事件注册(GRACE)评分,并根据GRACE评分将A组患者分为低危组(21例)、中危组(48例)、高危组(23例),对比3组患者血清CysC、hs-CRP、CA125水平,并分析血清CysC、hs-CRP、CA125水平与GRACE评分的相关性。结果非ST段抬高型心肌梗死组、不稳定性心绞痛组患者的血清CysC、hs-CRP、CA125水平及GRACE评分相较于B组呈升高趋势(F=92.509、283.679、2346.068、440.602,P均<0.001)。低危组、中危组、高危组非ST段抬高型急性冠状动脉综合征患者血清CysC、hs-CRP、CA125水平呈升高趋势(F=11.397、24.129、51.789,P<0.001)。血清CysC、hs-CRP、CA125水平与患者GRACE评分表现为正相关(r=0.486、0.476、0.482,P<0.05)。结论非ST段抬高型急性冠状动脉综合征患者体内血清CysC、hs-CRP、CA125的浓度处于较高水平,且这些标志物的浓度会随着患者病情的加剧而逐渐上升,以上血清学指标水平变化与非ST段抬高型急性冠状动脉综合征严重程度呈正相关,可反映患者的病情严重程度、炎症反应情况。

摘要： People living with HIV and who initiated antiretroviral therapy (PLH) at the chronic stage of the infection are generally exposed to persistent inflammation. We here assessed the impact of the interferon (IFN)/JAK-STAT pathway on myeloid cells from PLH and the potential of a JAK1/2 inhibitor, Baricitinib, to prevent IFN-driven myeloid cell activation. Peripheral blood mononuclear cells (PBMCs) from 16 chronically infected and virologically suppressed PLH were compared to 15 healthy uninfected individuals (UI) before and after exposure to type 1 IFN, type 2 IFN, and Baricitinib. First, we report an increased activation profile on monocytes and type 2 conventional dendritic cells (cDC2s) from PLH compared to UI, associated with a higher expression of PD-L1 and CD11b ex-vivo, and elevated transcription of pd-l1, cxcl-10 and ifnar1. Then, we unveil the role of type 1 and 2 IFN as inducers of PD-L1 expression at the transcriptional and protein level and highlight an increased response to IFN in PLH myeloid cells, associated with the delay before antiretroviral therapy initiation and the level of CD4 T cell depletion. Last, we describe the preventive effects of Baricitinib on IFN-driven PD-L1 expression. Our study shows that PLH harbor signs of myeloid cell activation, associated with increased type 1 and 2 IFN-signaling, which could be reversed by JAK1/2 inhibitors in vitro.

关键词： 肿瘤浸润淋巴细胞   非小细胞肺癌   免疫治疗   预后   生物标志物  

摘要： 非小细胞肺癌(non-small cell lung cancer,NSCLC)是肺癌中最常见的类型,占肺癌的80%以上。尽管近年来NSCLC的诊断和治疗已经有所突破,但是患者的预后仍然较差,5年生存率仅15%。目前,免疫检查点抑制剂(immune checkpoint inhibitors,ICIs)已被批准用于治疗肺癌。虽然其具有高效、持久、低毒等优点,但仅少部分NSCLC患者从免疫治疗中持久获益。随着肿瘤浸润淋巴细胞(tumor-infiltrating lymphocytes,TILs)在NSCLC中的预后作用逐渐受到关注,寻找更有效的预后指标成为了NSCLC研究的重点。本综述系统分析TILs在NSCLC免疫治疗疗效预测中的作用机制、临床证据及评估方法,旨在为未来研究和临床应用提供参考。

关键词： Antiviral innate immunity   RLR   Stress granule   IFN   TRBP  

摘要： Stress granules (SGs) are dense aggregates of RNA and proteins that form in response to various cellular stresses. Virus-induced SGs, known as antiviral SGs (avSGs), play a crucial role in regulating retinoic acid-inducible gene I-like receptors (RLRs)-mediated antiviral innate immunity. However, the regulation of avSG formation remains not fully understood. In this study, we demonstrate that TAR-RNA binding protein (TRBP), an RNA silencing regulator, negatively regulates type I interferon (IFN) expression by inhibiting avSG formation in response to RNA virus infection. Overexpression of TRBP inhibits both IFN-beta promoter activity and avSG formation following viral infection or the viral RNA mimic, polyinosinic-polycytidylic acid transfection. TRBP knockout cells exhibit enhanced phosphorylation and activation of IFN regulatory factor-3 (IRF-3) and increased IFN-beta mRNA expression compared to wild-type cells. Additionally, depletion of G3BP1 and G3BP2, which are essential for SG formation, abolishes the inhibitory effect of TRBP on IRF-3 phosphorylation. Mechanistically, TRBP physically interacts with double-stranded RNA (dsRNA)-dependent protein kinase R (PKR), a key kinase involved in avSG formation, via its dsRNA-binding domains, and inhibits PKR activation. In summary, our findings reveal a novel function for TRBP as a negative regulator of RLR-mediated signaling through PKR-dependent inhibition of avSG formation.