帕瑞昔布对宫颈癌腹腔镜手术患者炎性因子及镇痛效果的影响

目的 分析帕瑞昔布对宫颈癌腹腔镜手术患者炎性因子及镇痛效果的影响.方法 选择宫颈癌患者90例,参照抽签法将患者随机分为对照组与试验组,每组各45例.所有患者均行腹腔镜宫颈癌切除术治疗,对照组患者于麻醉诱导前输注生理盐水,试验组患者于麻醉诱导前输注帕瑞昔布,对比两组患者术后炎性因子[肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-8(IL-8)]水平、视觉模拟评分法(VAS)得分、24 h舒芬太尼用量及不良反应发生情况.结果 术后,试验组患者的炎性因子水平明显低于对照组患者(P<0.01);术后12 h、术后24 h,试验组患者的VAS评分均低于对照组患者,两组患者的VAS评分在组间(F=6.814,P=0.000)、不同时间点间(F=6.785,P=0.002)、组间+不同时间点间(F=5.672,P=0.014)相互比较,差异均有统计学意义;术后24 h,试验组患者的舒芬太尼用量低于对照组患者(P<0.05);试验组患者的不良反应总发生率明显低于对照组患者(P<0.01).结论 帕瑞昔布能够有效调节宫颈癌腹腔镜手术患者炎性因子的分泌,进而发挥镇痛作用.     

细胞因子在分化型甲状腺癌诊疗中的应用进展

甲状腺癌是内分泌系统常见的恶性肿瘤之一,其发病率呈逐年上升趋势.甲状腺癌以分化型甲状腺癌(differentiated thyroid carcinoma,DTC)为主,尽管多数DTC患者经规范化治疗后预后良好,但由于部分肿瘤的病理类型侵袭性较高或肿瘤组织分化程度较低,病情进展迅速导致患者总生存时间显著缩短.近年来,有...     

黄芪多糖对NOD鼠胰岛细胞因子基因表达的影响

目的　探讨黄芪多糖 (APS)以NOD小鼠 1型糖尿病免疫干预的分子机制。方法　应用RT CPR技术分别检测APS处理组和对照组NOD小鼠所有胰腺组织内 15条细胞因子mRNA的表达水平。结果　与对照组相比 ,APS组IL 1β、IL 2、IL 6、IL 12、TNF α、INF γ、Fas、iNOS的mRNA表达水平明显下调 ,IL 4、IL 5、IL 10、TGF β、Bcl 2、SOD的mRNA表达水平明显上调。结论　APS能纠正NOD小鼠Th1/Th2型细胞 /细胞因子的免疫失衡状态 ,预防或延缓 1型糖尿病的发生     

温肾健脾方对大鼠慢性创面愈合的影响

目的:探讨温肾健脾中药对慢性创面愈合的影响及可能作用机制.方法:采用大鼠背部开放性创面模型,用肌注氢化可的松的方法造成慢性难愈性创面,以辛葡康为阳性对照药,应用免疫组化、流式细胞术等方法,观察创面愈合时间、新生上皮宽度、肉芽组织形态学变化、肉芽组织细胞周期、表皮生长因子(epidermal growth factor, EGF)、转化生长因子β1 (transforming growth factor-β1, TGF-β1)及纤维连接蛋白(fibronectin, FN)等指标.结果:温肾健脾方治疗组与辛葡康对照组平均创面愈合时间分别为(17.0±1.9)和(18.8±1.9) d,较模型组及空白组明显缩短(P<0.05);治疗14 d后,治疗组及对照组新生上皮宽度分别为(3.73±0.19)和(3.21±0.15)mm,较模型组及空白组明显增宽(P<0.05);治疗组新生毛细血管丰富,成纤维细胞数量多,而对照组、模型组及空白组新生毛细血管及成纤维细胞数量均较治疗组明显减少(P <0.05);治疗组S期细胞比例较对照组、模型组及空白组明显提高(P<0.05);治疗组及对照组与模型组及空白组比较,EGF、TGF-β1、FN蛋白表达均增强(P<0.05).结论:温肾健脾方有促进大鼠慢性难愈创面修复的作用,其机制与调节细胞周期,上调EGF、TGF-β1细胞因子蛋白表达水平,促进间质FN的表达有关.     

Cell division control 42 elevates during infliximab therapy,and its increment relates to treatment response in ulcerative colitis patients

BackgroundCell division control 42 (CDC42) regulates multiple processes of inflammation and/or immunity in autoimmune diseases and also relates to the treatment efficacy of biologic regimens clinically. This study aimed to explore the longitudinal change in CDC42 during infliximab (IFX) treatment and its correlation with IFX response in ulcerative colitis (UC) patients.MethodsActive UC patients (N = 48) who received IFX were recruited, and their CDC42 expressions in peripheral blood mononuclear cells (PBMCs) were detected before treatment (W0) and at 12 weeks after treatment (W12) using RT‐qPCR. Also, CDC42 in PBMCs from UC patients with remission (N = 20) and health controls (HCs) (N = 20) were detected.ResultsCDC42 was reduced in active UC patients compared with UC patients with remission (p = 0.014) and HCs (p < 0.001). Besides, CDC42 was negatively correlated with CRP (p = 0.025), TNF‐α (p = 0.024), IL‐1β (p = 0.045), IL‐17A (p = 0.039), and Mayo score (p = 0.015) in active UC patients, but did not relate to ESR, disease duration, or IL‐6 (all p > 0.05), while CDC42 was only negatively related to CRP in UC patients with remission (p = 0.046). Interestingly, CDC42 was increased at W12 after IFX treatment in active UC patients (p < 0.001). Specifically, CDC42 was elevated during treatment in active UC patients with IFX response (p < 0.001), but did not obviously change in those without IFX response (p = 0.061). Furthermore, CDC42 at W12 was higher in active UC patients with IFX response compared with those without IFX response (p = 0.049).ConclusionCell division control 42 serves as a potential biomarker for monitoring disease progression and IFX response in UC patients.     

Th17 cell‐derived miR‐155‐5p modulates interleukin‐17 and suppressor of cytokines signaling 1 expression during the progression of systemic sclerosis

Background miR‐155‐5p is associated with autoimmune diseases. T helper 17 (Th17) cells, interleukin (IL)‐17, and suppressor of cytokines signaling 1 (SOCS1) have important roles in the pathogenesis of systemic sclerosis (SSc). The purpose of this study was to explore the role of miR‐155‐5p in the regulation of IL‐17 and SOCS1 expression in Th17 cells and the subsequent effect on SSc disease progression.MethodsTh17 cells were isolated from peripheral blood mononuclear cells of SSc patients and healthy controls (HCs). RT‐qPCR and western blotting were used to examine the expression patterns of miR‐155‐5p, IL‐17, and SOCS1. Luciferase reporter assays were performed to confirm SOCS1 as a target of miR‐155‐5p. RNA pull‐down assays were performed to detect the interaction of IL‐17 and SOCS1 with miR‐155‐5p. In situ hybridization was performed to analyze the co‐expression pattern of miR‐155‐5p and IL17A in Th17 cells.ResultsThe levels of Th17 cell‐derived miR‐155‐5p were significantly up‐regulated in SSc patients compared with HCs, and its levels were negatively correlated with SOCS1 levels. Meanwhile, miR‐155‐5p positively regulated IL‐17 expression levels in Th17 cells isolated from SSc patients as the disease progressed. Using pmirGLO vectors, SOCS1 was confirmed as a target of miR‐155‐5p. The binding status of IL‐17 and SOCS1 to miR‐155‐5p was related to SSc progression. An increase in the co‐localization of miR‐155‐5p and IL‐17 was associated with greater SSc progression.ConclusionsIL‐17 and SOCS1 expression modulated by Th17 cell‐derived miR‐155‐5p are critical for SSc progression, which may provide novel insights into the pathogenesis of SSc.     

左氧氟沙星联合阿奇霉素治疗呼吸道合胞病毒感染30例

目的 观察左氧氟沙星联合阿奇霉素对呼吸道合胞病毒感染（RSV）和哮喘患者淋巴液、血液中T细胞亚群及干扰素γ、白细胞介素-4（IL-4）的变化.方法 选择60例呼吸道合胞病毒和哮喘感染的患儿,随机分为联合组和对照组,各30例.联合组采用左氧氟沙星联合阿奇霉素治疗,对照组单纯使用左氧氟沙星,治疗周期为30 d.治疗前后均采用流式细胞仪检测外周血T细胞亚群,酶联免疫吸附法（ELISA）检测IL-4、干扰素γ水平.结果 两组血液中CD3＋,CD4＋,IL-4,转化型生长因子（TGF）β1水平均较治疗前明显降低（P＜0.05）,而干扰素γ水平明显升高（P＜0.05）.组间比较对照组CD3＋,CD4＋,IL-4,转化型生长因子（TGF）β1水平均较联合组高,干扰素γ低于联合组（P＜0.05）.联合组中发生哮喘的患儿有5例（16.67％）,少于对照组的10例（33.33％）,差异具有统计学意义（P＜0.05）.结论 左氧氟沙星联合阿奇霉素治疗RSV感染引起的毛细支气管炎,可通过作用于患者免疫细胞提高治疗效果.     

MALT1 in asthma children: A potential biomarker for monitoring exacerbation risk and Th1/Th2 imbalance‐mediated inflammation

BackgroundMucosa‐associated lymphoid tissue lymphoma translocation protein 1 (MALT1) participates in the immune‐related allergic response and inflammation flare, while its clinical role in asthma children is still unknown. Herein, this study aimed to investigate MALT1 expression, and its correlation with exacerbation risk, T helper (Th)1, Th2 cells (and their secreted cytokines), as well as inflammatory cytokines in asthma children.MethodsSixty children with asthma exacerbation and 60 children with remission asthma were enrolled in this study; then their blood MALT1, Th1, Th2 cells, tumor necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6), interferon‐gamma (IFN‐γ), and interleukin‐4 (IL‐4) were detected. Besides, blood MALT1 in another 20 health controls was also determined.ResultsMucosa‐associated lymphoid tissue lymphoma translocation protein 1 was highest in children with asthma exacerbation, followed by children with remission asthma, and lowest in health controls (p < 0.001). MALT1 could distinguish children with asthma exacerbation from children with remission asthma (area under the curve (AUC): 0.757, 95% CI: 0.670–0.843). In children with asthma exacerbation, MALT1 was negatively linked with IFN‐γ (p = 0.002) and Th1 cells (p = 0.050), but positively related to Th2 cells (p = 0.027) and exhibited a positive correlation trend (without statistical significance) with IL‐4 (p = 0.066); meanwhile, MALT1 was positively correlated with exacerbation severity (p = 0.010) and TNF‐α (p = 0.003), but not linked with IL‐6 (p = 0.096). In children with remission asthma, MALT1 only was negatively associated with Th1 cells (p = 0.023), but positively linked with TNF‐α (p = 0.023).ConclusionMucosa‐associated lymphoid tissue lymphoma translocation protein 1 serves as a potential biomarker for monitoring exacerbation risk and Th1/Th2 imbalance‐mediated inflammation of asthma children.