内燃机车乘务员和轮轴工外周血淋巴细胞微核观察

本文作者对５１名内燃机车乘务员和车辆维修车间的３０名轮轴工外周血淋巴细胞微核进行了分析。结果表明,机车乘务员和轮轴工微核阳性检出率、微核细胞率和微核率均明显高于对照组（Ｐ＜０．０１）,而且随着作业工龄的延长,微核细胞率和微核率有接近显著（０．０５＜Ｐ＜０．０１）或显著（Ｐ＜０．０５）意义的增高。对两类作业工作人员微核增高的原因进行了讨论     

小剂量受照人员远期外周血淋巴细胞染色体畸变分析

本文对２６例小剂量（０．１０－０．３３Ｇｙ）受照人员受照２６－３１年后外周血淋巴细胞染色畸变和微核进行了分析。结果表明，受照组染色体畸变率和微核率都明显高于对照组，但染色体畸变率和微核率与受照剂量的相关关系已不存在；外照组染色体畸变率高略高于内照组，但在内照组中检出双着丝粒体和稳定性畸变，外照组中未检出。提示；不能排除在内照组人员体内仍有裂变产物内污染的存在。     

TLD质量核查调强放射治疗非均匀野剂量方法

目的核查放射治疗计划系统(TPS)计算病人治疗剂量的非均匀野剂量校正。方法将插有TLD的聚苯乙烯固体模体,聚苯乙烯/肺固体模体,聚苯乙烯/骨固体模体分别经CT扫描,影像分别传入TPS并计算高能X射线下监督单位数,使传递给中心束轴TLD剂量为2 Gy。在高能X射线下完成TLD照射,照射后的TLD经测量、剂量计算,D(TLD)与D(TPS)剂量比值在0.95~1.05范围为可接受范围。结果核查结果表明,光子线束均匀模体轴上(P)剂量和非均匀骨模体轴上(BP)剂量核查结果较好。非均匀肺模体轴上(LP)和离轴(LL)剂量核查结果误差很大。结论光子线束非均匀性剂量校正在放射治疗中是非常重要,尤其是肺组织。校正不当,对于肺组织剂量误差也可达到11.1%,离轴情况下更多达18.4%。对于骨组织剂量误差较小。     

五省市部分放射工作人员体检白细胞计数分析

目的比较不同放射工作人员的白细胞水平与一般人群的差异,并探索可能的影响因素。方法采用五个省(市)2011年、2012年和2013年的放射工作人员健康体检数据,与一般人群白细胞计数正常值进行比较,采用单因素分析和多元线性回归分析的方法,研究不同因素对放射工作人员白细胞计数的影响。结果本研究确认符合要求的研究对象共7314人,其中男性5595人(76.50%),女性1719人(23.50%),平均年龄为(37.71±10.14)岁,白细胞计数均值为(6.29±1.60)×109/L,一般人群白细胞计数为(6.50±1.53)×109/L,放射工作人员白细胞计数较一般人群低3.23%,差异有统计学意义(P<0.001)。女性的白细胞计数低于男性,且在年龄小于50岁的人群中,白细胞计数有随年龄增加而减少的趋势,差异均有统计学意义(P<0.05)。不同省市体检机构的放射工作人员白细胞计数也不同,且差异有统计学意义(P<0.05)。多元线性回归分析结果显示,在调整年龄、性别和地区因素后,不同职业照射类别人员的白细胞计数之间的差异无统计学意义(P>0.05)。结论放射工作人员白细胞计数在正常医学参考值范围内,但低于一般人群,可能与性别、年龄和不同地区体检机构之间的差异有关,尚不能认为与职业照射类别有关,需要进一步研究。     

The organochlorine p,p′-dichlorodiphenyltrichloroethane induces colorectal cancer growth through Wnt/β-catenin signaling

Dichlorodiphenyltrichloroethane (DDT), an organochlorine pollutant, is associated with several types of cancer. However, the relationship between DDT and colorectal cancer is uncertain. In this study, the impact of p,p′-DDT on colorectal cancer growth was evaluated using both in vitro and in vivo models. Our results indicated that the proliferation of human colorectal adenocarcinoma DLD1 cells was significantly promoted after exposed to low concentrations of p,p′-DDT ranging from 10⁻¹² to 10⁻⁷ M for 96 h. Exposure to p,p′-DDT from 10⁻¹⁰ to 10⁻⁸ M led to upregulation of phospho-GSK3β (Ser9), β-catenin, c-Myc and cyclin D1 in DLD1 cells. RNA interference of β-catenin inhibited the proliferation of DLD1 cells stimulated by p,p′-DDT. Inhibiting of estrogen receptors (ERs) had no significant effect on the action of p,p′-DDT. Treatment with p,p′-DDT induced production of intracellular reactive oxygen species (ROS) and inhibited superoxide dismutase (SOD) activity in DLD1 cells. Treatment with N-acetyl-L-cysteine (NAC), a ROS inhibitor, suppressed the induction of Wnt/β-catenin signaling and DLD1 cell proliferation by p,p′-DDT. Moreover, in a mouse xenograft model, 5 nmol/kg p,p′-DDT resulted in increased tumor size, oxidative stress and Wnt/β-catenin signaling. These results indicated that low concentrations of p,p′-DDT promoted colorectal cancer growth through Wnt/β-catenin signaling, which was mediated by oxidative stress. The finding suggests an association between low concentrations of p,p′-DDT exposure and colorectal cancer progression.     

河南省义马煤业集团14415名接尘职工健康状况

目的分析煤矿企业接尘职工健康状况，探讨尘肺病和其他疾病的防治对策。方法回顾调查2003、2004和2005年义马煤业集团接尘14415名职工职业健康检查、尘肺病诊断资料。结果职业健康检查异常率30．36％，观察期、尘肺（Ⅰ-Ⅲ期，均为新诊断）、肺结核和胸膜炎检出率分别为9．52％、2．33％、1．03％和0．24％。胸片、血压、心电图、尿常规、肝功能、血常规和肺功能异常率分别为13．12％、10．87％、8．80％、2．50％、1．70％、1．21％和0．99％。结论不仅做好尘肺病防治工作，还要做好心血管和肺结核等疾病的防治工作。     

《职业性放射性甲状腺疾病诊断》标准解读

为准确掌握和理解国家职业卫生标准《职业性放射性甲状腺疾病诊断》(GBZ 101-2020),本文就该标准发布的重要意义、修订的相关背景、修订的基本原则、主要技术内容修订依据和标准的应用等内容进行说明。指导职业病诊断医师在职业性放射性甲状腺疾病诊断中能够把握好诊断的原则,作出正确的诊断,避免标准应用中产生困惑,从而更好地保障放射工作人员的职业健康权益。     

Valproic acid induced liver injury: An insight into molecular toxicological mechanism

Valproic acid (VPA) is an anti-seizure drug that causes idiosyncratic liver injury. 2-propyl-4-pentenoic acid (Δ⁴VPA), a metabolite of VPA, has been implicated in VPA-induced hepatotoxicity. This review summarizes the pathogenesis involved in VPA-induced liver injury. The VPA induce liver injury mainly by i) liberation of Δ⁴VPA metabolites; ii) decrease in glutathione stores and antioxidants, resulting in oxidative stress; iii) inhibition of fatty acid β-oxidation, inducing mitochondrial DNA depletion and hypermethylation; a decrease in proton leak; oxidative phosphorylation impairment and ATP synthesis decrease; iv) induction of fatty liver via inhibition of carnitine palmitoyltransferase I, enhancing nuclear receptor peroxisome proliferator-activated receptor-gamma and acyl-CoA thioesterase 1, and inducing long-chain fatty acid uptake and triglyceride synthesis. VPA administration aggravates liver injury in individuals with metabolic syndromes. Therapeutic drug monitoring, routine serum levels of transaminases, ammonia, and lipid parameters during VPA therapy may thus be beneficial in improving the safety profile or preventing the progression of DILI.