课程文献中心 更多>>

关键词： 雅解沙把   金黄色葡萄球菌性乳腺炎   急性乳腺炎   傣药   细胞因子  

摘要： 目的:探讨傣药“雅解沙把”对金黄色葡萄球菌诱导大鼠乳腺炎的影响及作用机制。方法:将SD大鼠随机分为空白对照组、金黄色葡萄球菌大鼠乳腺炎模型组、雅解沙把低、中、高剂量组(0.3 g/kg、0.6 g/kg、0.9 g/kg),共5组,每组3只。造模后空白对照组与模型组灌胃生理盐水,其余组按对应剂量灌胃“雅解沙把”,每天1次,观察各组大鼠血清中CRP、IL-1β、IL-6、IL-8含量变化和各组大鼠乳腺组织的病理学变化。结果:空白对照组无乳腺肿块形成,其余组均有肿块形成;组织病理切片观察发现,模型组乳腺损伤程度明显高于“雅解沙把”低、中、高剂量组;各组血清中CRP、IL-1β、IL-6、IL-8的含量明显高于空白对照组,经治疗后实验组与模型组相比较,血清中CRP、IL-1β、IL-6、IL-8的表达下降(高剂量组均P<0.05,中剂量组L-1β、IL-6表达降低,具有统计学意义P<0.05,低剂量组IL-6表达降低,具有统计学意义P<0.05)。结论:“雅解沙把”能减轻大鼠急性乳腺炎的炎症表现,其作用机制可能与抑制促炎细胞因子IL-1β、IL-6、IL-8表达及NF-κB信号通路经典途径相关。

关键词： 抗原   SPF鸡   工艺参数   应用  

摘要： 为获得大收获量、高效价的制造疫苗用鸡传染性支气管炎鸡胚病毒液(抗原),试验从SPF鸡胚接种日龄、种毒接种剂量、接种后鸡胚孵育温度及孵育时间四方面进行探索研究。鸡传染性支气管炎病毒H120株、H52株抗原生产采用12日龄SPF鸡胚,每胚尿囊腔接种104.0EID50左右的种毒,接种后鸡胚置35.5℃,相对湿度65%~70%环境下孵育,弃去接毒后24 h前的死胚,至33 h,终止接毒鸡胚孵育,收获冷却后的鸡胚病毒液,其效价(病毒含量EID50)指标和收获量比现行常规法生产均有提高,试验研究取得的鸡传染性支气管炎抗原生产工艺参数可应用于实际生产。

关键词： 免疫球蛋白类,静脉内   低丙种球蛋白血症   B细胞非霍奇金淋巴瘤   CD20单抗  

摘要： 目的观察静注人免疫球蛋白(pH4)(简称IVIg)联合治疗对B细胞非霍奇金淋巴瘤(NHL)患者总免疫球蛋白(Ig)水平的影响,评估IVIg改善B细胞NHL经CD20单抗治疗后低丙种球蛋白血症的临床有效性。方法回顾性分析2018年1月至2022年6月期间于苏州大学附属第一医院血液科住院就诊的98例B细胞NHL并使用CD20单抗治疗后低丙种球蛋白血症患者的临床资料。其中,IVIg组70例、常规治疗组28例。为排除输注血浆对总Ig水平的干扰,对未使用血浆IVIg组(53例)和常规治疗组(25例)的总Ig水平进行统计分析。通过观察IVIg对于患者总Ig水平提升效果和持续时间,分析IVIg治疗效果,以及通过比较其他血液生化指标,分析IVIg的控制感染效果。并观察IVIg在临床中应用的安全性。结果IVIg组IVIg治疗后1~3 d内总Ig水平高于IVIg治疗前[(20.67±4.17)g/L对(17.16±1.76)g/L,P<0.001]。22例患者IVIg治疗后1~7 d、8~14 d、15~30 d的总Ig水平较治疗前差异均具有统计学意义(均P<0.001)。常规治疗组住院后1~3 d内总Ig水平均值较入院时差异无统计学意义[(18.12±1.84)g/L对(18.43±1.79)g/L,P>0.05]。IVIg组在IVIg治疗后1~3 d内总Ig水平达到20 g/L的患者比例显著高于入院1~3 d内的常规治疗组(57.69%对0,P<0.001)。12例入组时中性粒细胞水平低于正常值的IVIg组患者治疗后1~3 d、4~7 d、8~14 d的中性粒细胞水平均较治疗前升高(均P<0.05)。IVIg组治疗后新发感染患者比例低于常规治疗组[22.64%(12/53)对36.00%(9/25),P>0.05]。IVIg组(70例)中8例患者出现1~2级的不良反应,其中5例出现恶心呕吐、2例出现皮疹、1例肌肉关节痛,未观察到3级以上的不良反应。结论IVIg提高B细胞NHL患者CD20单抗治疗后Ig和中性粒细胞水平,对控制新发感染可能有一定作用。IVIg治疗B细胞NHL使用CD20单抗后低丙种球蛋白血症疗效确切且安全性良好。

关键词： 社区获得性肺炎   老年   白细胞介素-12P70   4-羟基壬烯醛   钙结合蛋白S100A12  

摘要： 目的:探讨老年社区获得性肺炎(CAP)患者血清白细胞介素-12P70(IL-12P70)、4-羟基壬烯醛(4-HNE)、钙结合蛋白(S100A12)水平与病情严重程度及预后的相关性。方法:选取河北省胸科医院2022年4月至2024年6月收治的老年CAP患者158例作为研究组,另选取健康体检者158名作为对照组,对比研究组不同病情严重程度患者和对照组血清IL-12P70、4-HNE、S100A12水平、肺部感染评分(CPIS)、急性生理与慢性健康评价系统Ⅱ(APACHEⅡ)评分、肺功能指标[第1秒用力呼气容积(FEV1)、用力肺活量(FVC)],分析血清IL-12P70、4-HNE、S100A12与病情严重程度评分的相关性。研究组均随访28d,根据预后分为预后良好亚组与预后不良亚组,对比两亚组临床资料、血清IL-12P70、4-HNE、S100A12水平,分析血清IL-12P70、4-HNE、S100A12与预后的相关性及预测效能。结果:研究组血清IL-12P70、4-HNE、S100A12水平高于对照组(P<0.05);重症患者CPIS、APACHEⅡ评分、血清IL-12P70、4-HNE、S100A12水平高于非重症患者,FEV1、FVC低于非重症患者(P<0.05);Pearson相关性分析,血清IL-12P70、4-HNE、S100A12与CPIS、APACHEⅡ评分呈正相关,与FEV1、FVC呈负相关(P<0.05);随访28d,研究组预后不良33例,预后良好125例,分别纳入预后不良亚组与预后良好亚组。预后不良亚组年龄、重症比例、糖尿病比例、CPIS、APACHEⅡ评分、血清IL-12P70、4-HNE、S100A12水平高于预后良好亚组,FEV1、FVC低于预后良好亚组(P<0.05);Logistic回归分析,在校正年龄、糖尿病等其他因素前后,血清IL-12P70、4-HNE、S100A12均是老年CAP患者预后的独立影响因素(P<0.05);ROC曲线分析,血清IL-12P70、4-HNE、S100A12预测老年CAP预后的AUC为0.796、0.730、0.783,最佳截断值为5.24pg/mL、21.23mg/L、23.70ng/mL,敏感度为66.67%、63.64%、81.82%,特异度为82.40%、74.40%、68.80%;联合预测老年CAP预后的AUC为0.911,敏感度为84.85%,特异度为80.80%,较单独预测效能显著提高(Z=2.377、2.850、2.685,P=0.018、0.004、0.007);另选取同期老年CAP患者68例作为外部验证数据集样本,其中重症46例,非重症22例,随访28d,预后不良13例,预后良好55例。血清IL-12P70、4-HNE、S100A12联合预测外部验证数据集样本中68例患者预后情况为预后不良11例,预后良好57例,准确率为97.06%,提示预测效能较好。结论:血清IL-12P70、4-HNE、S100A12与老年CAP患者病情严重程度呈正相关,是预后的独立影响因素,联合检测能较为准确地预测预后情况。

关键词： KHSRP   乙酰化   兔多克隆抗体   肿瘤  

摘要： 目的:制备人源KHSRP位点特异性乙酰化修饰的兔多克隆抗体,探讨其在肿瘤样本检测中的潜在价值和临床意义。方法:设计并合成KHSRP蛋白Lys205(K205)乙酰化的氨基酸修饰肽段,在肽段羧基末端偶联网络匙孔血蓝蛋白(KLH),形成抗原-载体偶联物。5次抗原免疫新西兰大白兔后采血分离血清,间接ELISA测定血清抗体效价,亲和层析法纯化特异性多克隆抗体,Western blot及免疫组化(IHC)检测抗体特异性。结果:终兔血清抗体的ELISA效价>5.12×10^(5),能够用于Western blot和IHC特异性检测K205乙酰化的KHSRP蛋白。结论:KHSRP在肿瘤中的作用可能与其表面乙酰化修饰密切相关,本研究成功制备了抗人源KHSRP乙酰化兔多克隆抗体,为评估肿瘤细胞KHSRP乙酰化水平与肿瘤发生发展的生物关联奠定基础。

关键词： B7H6   B7 Homolog 6   BST2   Bone marrow stromal cell antigen 2   CAR   Chimeric Antigen Receptor   CCA   Cholangiocarcinoma   CD161   C-type lectin-like membrane receptor   CD40   Cluster of Differentiation 40   CD1d   Cluster of differentiation 1 d   CDK   Cyclin-Dependent Kinase   CDKN1A   Cyclin Dependent kinase inhibitor 1A   COL1A1   Collagen type I alpha 1 chain   CRLF1   Cytokine receptor-like factor 1   CSF1   Colony Stimulating Factor 1   DNMT   DNA Methyltransferase   DysiNKT   Dysfunctional iNKT cell   DNA   Deoxyribonucleic Acid   EMT   Epithelial-Mesenchymal transition   FBS   Fetal Bovine Serum   FGFR   Fibroblast growth factor receptor   FYN   Src family tyrosine kinase   GFP   Green Fluorescence Protein   GMPR   Guanosine Monophosphate Reductase   GR   Growth Rate Inhibition   GvHD   Graft-Vs-Host Disease   HDAC   Histone Deacetylases   IFI6   Interferon alpha inducible protein 6   IFI30   Interferon-gamma inducible protein 30   IFNγ   Interferon Gamma   IL   Interleukin   INKT   Invariant Natural Killer T cell   IPSC   Induced Pluripotent Stem Cell   Jak3   Janus Kinase 3   LCK   Lymphocyte specific protein Tyrosine kinase   M2   Macrophage 2   MDSC   Myeloid-Derived Suppressor Cell   MICA   MHC class I polypeptide-related sequence A   MICB   MHC class I polypeptide-related sequence B   MHC   Major Histocompatibility Complex   MRNA   messenger Ribonucleic Acid   MTORC1   Mammalian Target of Rapamycin Complex 1   NF-κB   Nuclear factor kappa-light-chain-enhancer of activated B cells   NK   Natural Killer cell   NKG7   Natural Killer Cell Granule Protein 7   NKp30   Natural Cytotoxicity Triggering Receptor 3   PBMC   Peripheral blood mononuclear cells   PI3K   Phosphoinositide 3-kinase   PKC   Protein Kinase C   PCOLCE   Procollagen C-endopeptidase Enhancer   Rag2   Recombination Activating Gene 2 Protein   SPP1   Secreted Phosphoprotein 1   STAT5   Signal transducer and activator of transcription 5   STAT3   Signal transducer and activator of transcription 3   TCR   T Cell Receptor   T   reg   Regulatory T cells   TAM   Tumor-Associated Macrophage   Th2   T Helper 2   TIM3   T cell immunoglobulin and mucin domain-containing protein 3   TKI   Tyrosine Kinase inhibitor   TLR4   Toll-like receptor 4   TME   Tumor Microenvironment  

摘要： In this study, we explored the potential of histone deacetylase (HDAC) inhibitors, with a focus on Vorinostat, to restore the functionality of invariant natural killer T (iNKT) cells—a unique subset of T cells with potent anti-tumor activity that are often impaired within the tumor microenvironment. Using aggressive cholangiocarcinoma (CCA) cell lines lacking CD1d molecules, we observed a marked decline in iNKT cell reactivity within 48 h of exposure to CCA cells. Through a systematic approach that included the utilization of the L1000FWD search engine, Vorinostat emerged as a promising candidate for mitigating iNKT cell dysfunction. Vorinostat induced significant molecular alterations in iNKT-nonresponsive CCA cells, enhancing CD1d expression, the production of inflammatory cytokines and the activation of T cell receptor (TCR) signaling pathways. These changes effectively reactivated iNKT cells and restored their anti-tumor functionality. In the mouse xenograft model, combined treatment with Vorinostat significantly inhibited tumor growth. These findings suggest that Vorinostat may offer a novel therapeutic strategy for patients with cholangiocarcinoma who are resistant to conventional chemotherapy.

关键词： 反复呼吸道感染   小儿热速清颗粒   C反应蛋白   白细胞分化抗原   免疫球蛋白  

摘要： 目的探讨小儿热速清颗粒治疗儿童反复呼吸道感染的临床疗效。方法选取2022年8月至2024年8月医院收治的82例反复呼吸道感染患儿为研究对象,按照随机数字表法分为对照组和观察组,各41例。对照组给予头孢克肟颗粒治疗,观察组在对照组基础上联合小儿热速清颗粒治疗,比较两组临床疗效、症状缓解时间、炎性指标[肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、C反应蛋白(CRP)]、白细胞分化抗原、免疫球蛋白[免疫球蛋白M(IgM)、免疫球蛋白A(IgA)、免疫球蛋白G(IgG)]及不良反应。结果观察组治疗总有效率高于对照组(P<0.05);观察组各项临床症状缓解时间均短于对照组(P<0.05);观察组治疗后CRP、IL-6、CD8^(+)、TNF-α水平均低于对照组,CD3^(+)、CD4^(+)水平均高于对照组(P<0.05);观察组治疗后IgA、IgG、IgM水平均高于对照组(P<0.05);两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论小儿热速清颗粒治疗儿童反复呼吸道感染可有效缓解患儿临床症状,提高免疫球蛋白水平,抑制机体炎症反应,改善T细胞亚群,且不会明显增加不良反应。

摘要： Background Aptamers are RNA-or DNA-based oligomers with high protein-specific binding properties that have demonstrated effectiveness in targeting various proteins and treating diseases such as cancer. However, their application in regulating chronic respiratory diseases, such as chronic rhinosinusitis, is not well established. Methods In this study, we used the anti-IL-4R alpha aptamer (anti-IL-4R alpha apt) to investigate its impact on IL-4 signalling and related T-helper 2 (Th2)-type inflammation in nasal polyp tissue. To achieve this, we treated nasal polyp tissue extracted from chronic rhinosinusitis with nasal polyps (CRSwNP) patients who had undergone polypectomy with the anti-IL-4R alpha apt. Furthermore, to evaluate the effects of the anti-IL-4R alpha apt on NP formation, we established an eosinophilic mouse model of CRSwNP to mimic the Th2 inflammatory pathogenesis observed in CRSwNP. Results Interestingly, we observed that treatment with anti-IL-4R alpha apt resulted in a significant reduction in IL-4-STAT6 signalling and Th2-mediated inflammation, as demonstrated by an similar to 2-fold decrease in the levels of IL-4R alpha, phosphorylated STAT6 (p-STAT6) and GATA3 in treated nasal polyp (NP) tissues compared to the untreated uncinate process (p<0.001). Notably, we observed that the administration of the anti-IL-4R alpha apt effectively reduced NP formation and Th2-mediated inflammation, as shown by an similar to 3-fold reduction in the percentages of IL-4R alpha, p-STAT6 and GATA3 positive cells in the nasal tissues of this mouse model (p<0.001). Conclusion Given that the anti-IL-4R alpha apt demonstrated comparable efficacy to dupilumab-an anti-IL-4R alpha therapy proven effective for CRSwNP-this research highlights the potential therapeutic efficacy of aptamers in managing chronic inflammatory conditions such as those seen in CRSwNP.