简介:摘要目的研究谷胱甘肽过氧化物酶1(glutathione peroxidase 1,GPX1)基因多态性与噪声性听力损失(noise-induced hearing loss,NIHL)易感性间的关系。方法于2019年5月,采用1∶1巢式病例-对照研究方法在噪声暴露队列研究的基础上,选择双耳高频(3 000、4 000、6 000 Hz)≥40 dB者为听力损失组,纯音听力测试任一耳语频(500、1 000、2 000 Hz)的任一频段听阈场≤25 dB,且纯音听力测试高频平均听阈<35 dB者为对照组,听力损失组和对照组各392人。对调查对象进行一般体格检查和基本信息调查,进行纯音听力测试和作业现场噪声测量。采用中高通量单核苷酸多态性分型检测技术(SNPscanTM法)检测GPX1基因的2个单核苷酸位点的多态性。检验对照组人群的哈迪-温伯格平衡(Hardy-Weinberg equilibrium,HWE)。应用logistic回归方法分析基因单核苷酸多态性(single nucleotide polymorphism,SNP)与NIHL易感性之间的关系。结果两组包括375名男性和17名女性,其中病例组平均年龄(40.9±8.2)岁,平均工龄(19.4±9.1)年,双耳高频平均听阈位移范围(51.3±8.9)dB;对照组平均年龄(40.3±8.2)岁,平均工龄(18.8±8.9)年,双耳高频平均听阈位移(12.5±10.2)dB,GPX1单核苷酸位点在对照组中的频率分布均符合Hardy-Weinberg平衡。调整研究样本吸烟因素后,发现rs1987628位点在共显性、显性遗传模型下与NIHL发生风险有关(P<0.05);与GG基因型携带者相比,听力损失组GA基因型携带者的NIHL的危险度显著升高,OR值为1.803(95%CI 1.215~2.676,P=0.003);GA+AA基因型携带者的NIHL的危险度显著升高,OR值为1.762(95%CI 1.197~2.593,P=0.004)。rs3448单核苷酸位点的基因型与NIHL危险度无相关性(P>0.05)。结论GPX1基因多态性可能是NIHL的遗传易感性因素。
简介:摘要 目的 通过检测P53和GPX1在骨巨细胞瘤(GCTB)组织中的表达,探讨它们的表达与临床病理特征的关系,及两者的相关性。方法 收集52例存档GCTB蜡块标本,用免疫组织化学S-P法检测P53和GPX1在GCTB组织中的表达。结果 (1)P53阳性表达率为38%,GPX1阳性表达率为52%;(2)P53及GPX1在GCTB中的表达与患者性别、年龄、肿瘤直径、肿瘤发生部位均无关,而与肿瘤病理分级及复发有关;(3)P53与GCTB的表达存在正相关性(P
简介:AbstractBackground:Glioma is the most common malignant brain tumor in adults. The standard treatment scheme of glioma is surgical resection combined alternative radio- and chemotherapy. However, the outcome of glioma patients was unsatisfied. Here, we aimed to explore the molecular and biological function characteristics of GPX7 in glioma.Methods:The multidimensional data of glioma samples were downloaded from Chinese Glioma Genome Atlas (CGGA). RT-qPCR method was used to identify the expression status of GPX7. Kaplan-Meier curves and Cox regression analysis were used to explore the prognostic value of GPX7. Gene Set Enrichment Analysis (GSEA) was applied to investigate the GPX7-related functions in glioma.Results:The results indicated that the expression of GPX7 in glioma was higher compared to that in normal brain tissue. Univariate and multivariate Cox regression analyses confirmed that the expression value of GPX7 was an independent prognostic factor in glioma. The GSEA analysis showed that GPX7 was significantly enriched in the cell cycle pathway, ECM pathway, focal adhesion pathway, and toll-like receptor pathway.Conclusions:The GPX7 was recommended as an independent risk factor for patients diagnosed with glioma for the first time and GPX7 could be potentially used as the therapy target in future. Furthermore, we attempted to explore a potential biomarker for improving the diagnosis and prognosis of patients with glioma.
简介:你知道不莱梅吗?噢——它是一个美丽快乐的地方。不莱梅在哪儿呢?噢——有梦想的地方就有不莱梅。没错儿,不莱梅这个地方,早就存在于“很久很久以前”的童话里了……
简介:摘要目的研究维生素D类似物paricalcitol激活维生素D受体/谷胱甘肽过氧化物酶4(VDR/GPX4)通路在呼吸机相关性肺损伤(VILI)中的作用。方法将24只雄性C57BL/6J小鼠随机分为对照组、大潮气量(HVT)致VILI模型组(HVT组)、paricalcitol对照组(P组)和paricalcitol预处理组(P+HVT组),每组6只。给予小鼠气管插管,按40 mL/kg的潮气量通气制备VILI模型;对照组仅气管插管,不予通气。P+HVT组小鼠于制模前1周腹腔注射paricalcitol 0.2 μg/kg,每日1次;P组仅在实验前1周腹腔注射paricalcitol 0.2 μg/kg,每日1次。通气4 h后处死小鼠取肺组织,通过肺湿/干质量(W/D)比值、苏木素-伊红(HE)染色和Masson染色评价肺损伤情况;采用蛋白质免疫印迹试验(Western blotting)和免疫组化法检测VDR、GPX4的表达;采用微量法检测丙二醛(MDA)和还原型谷胱甘肽(GSH)的含量。结果HVT通气4 h后小鼠出现明显肺损伤,表现为:与对照组相比,肺损伤评分和肺W/D比值明显升高〔肺损伤评分(分):0.430±0.035比0.097±0.025,肺W/D比值:4.860±0.337比3.653±0.332,均P<0.05〕,胶原纤维沉积明显增加,且肺组织MDA含量明显升高(nmol/g:212.420±8.757比97.073±5.308,P<0.05),GSH含量及VDR、GPX4的蛋白表达和免疫组化评分(IRS)明显降低〔GSH(μg/g):44.229±1.690比70.840±0.781;VDR蛋白(VDR/GAPDH):0.518±0.029比0.762±0.081,GPX4蛋白(GPX4/GAPDH):0.452±0.032比0.649±0.034;IRS评分(分):VDR为4.168±0.408比10.167±0.408,GPX4为4.333±1.033比10.333±0.516;均P<0.05〕。给予paricalcitol激活VDR后,与HVT组相比,P+HVT组小鼠肺损伤明显改善,表现为肺损伤评分和肺W/D比值明显降低〔肺损伤评分(分):0.220±0.036比0.430±0.035,肺W/D比值:4.015±0.074比4.860±0.337,均P<0.05〕,胶原纤维沉积减少,且肺组织MDA含量明显下降(nmol/g:123.840±8.082比212.420±8.757,P<0.05),GSH含量及VDR、GPX4的蛋白表达和IRS评分明显上调〔GSH(μg/g):63.094±0.992比44.229±1.690;VDR蛋白(VDR/GAPDH):0.713±0.056比0.518±0.029,GPX4蛋白(GPX4/GAPDH):0.605±0.008比0.452±0.032;IRS评分(分):VDR为9.000±0.632比4.168±0.408,GPX4为8.833±0.408比4.333±1.033;均P<0.05〕。结论维生素D类似物paricalcitol可通过激活VDR/GPX4通路改善肺组织氧化还原失衡,从而减轻VILI。