目的 分析总结综合性医院门诊放疗过程中新型冠状病毒肺炎(简称新冠肺炎)流程防护的有效管理措施.方法 根据疫情防控要求,结合中国人民解放军总医院第一医学中心放疗门诊诊疗过程中可能存在的问题,回顾性梳理在新冠肺炎疫情下放疗门诊诊疗过程中采取的流程调整、环境分区、患者防控及消杀等防控措施,并对防控成效进行效果评价.结果 在门诊放疗过程中采取针对性的防护措施,通过加强入口管理、严格陪护管理以及预约治疗等举措,总结出一套行之有效的新冠肺炎疫情期间门诊放疗防控模式.2020年1月至12月本单位共收治患者1959例,实现科室医护技患"零感染",防控成效良好.结论 新冠肺炎疫情期间,综合性医院放疗门诊放疗流程防控必须采取行之有效严谨管理措施,做好治疗流程、环境和人员的防控,最大限度地降低医护技患的感染风险,确保医护技患的安全,保证门诊放疗工作安全有序的开展.

目的:探讨细胞中重要的DNA感受器干扰素基因刺激因子(STING)在小鼠单核巨噬细胞(RAW264.7)细胞活化中的作用.方法:收集60Coγ射线照射后小鼠肺泡上皮细胞(MLE-12)的培养上清,对RAW264.7细胞进行刺激,使用蛋白免疫印迹(Western Blot)检测刺激后RAW264.7细胞中STING蛋白的表达,使用酶联免疫吸附测定(ELISA)法检测处理后RAW264.7细胞经典激活的巨噬细胞(M1)型和非经典激活的巨噬细胞(M2)型相关细胞因子的表达水平.结果:Western Blot检测结果显示,刺激后RAW264.7细胞中STING蛋白的表达水平显著上调;ELISA检测结果表明,刺激后RAW264.7细胞上清中的肿瘤坏死因子α(TNF-α)和白细胞介素-1(IL-1)显著增加;脱氧核糖核酸酶I(DNase I)处理能够抑制RAW264.7细胞中STING通路的激活.ELISA检测结果表明,DNase I能够抑制RAW264.7细胞向M1型极化.结论:辐射诱导的MLE-12细胞死亡能够释放DNA,从而激活RAW264.7细胞中的环磷酸鸟苷-腺苷酸合成酶(cGAS)-STING信号通路,进而促进其向M1型极化.

Objective:To explore the regulatory effect of glutathione S-transferase P1(GSTP1) on the radiosensitivity of mouse Lewis lung cancer (LLC) cells.Methods:GSTP1-shRNA lentivirus and negative control lentivirus were used to respectively infect the LLC cells, and stable transgenic strains were selected. Real-time PCR and Western blot were conducted to quantitatively measure the expression levels of GSTP1 mRNA and protein in the LLC cells to verify the knockdown effect. The cell counting kit-8(CCK-8) assay was used to detect cell viability after irradiation. The colony formation assay was utilized to assess the cell proliferation ability after irradiation. Flow cytometry was performed to assess the level of cell apoptosis after irradiation. The tumor-bearing mice were established and irradiated to detect the changes in the tumor volume after irradiation. TUNEL staining was employed to detect the level of tumor apoptosis after irradiation. Immunofluorescence was used to detect the number of CD 4+ CD 8+ T cells in the tumor after irradiation. Results:Real-time PCR and Western blot showed that after shRNA lentivirus interference, the expression levels of GSTP1 mRNA and protein were significantly down-regulated. Down-regulation of GSTP1 reduced cell viability and proliferation, and increased the rate of cell apoptosis after irradiation. The tumor volume of the tumor-bearing mice after irradiation in the GSTP1 knockdown group was significantly smaller than that in the NC group, whereas the tumor apoptosis rate was significantly higher and the number of infiltrating CD 4+ CD 8+ T cells in the tumor was remarkably higher compared with those in the control group. Conclusion:Knockdown of GSTP1 can significantly increase the radiosensitivity of LLC cells and enhance the infiltration of lymphocytes in tumor tissues.

Protein phosphatase 2A (PP2A) is a serine/threonine phosphatase that serves as a key regulator of cellular physiology in the context of apoptosis, mitosis, and DNA damage responses. Canonically, PP2A functions as a tumor suppressor gene. However, recent evidence suggests that inhibiting PP2A activity in tumor cells may represent a viable approach to enhancing tumor sensitivity to chemoradiotherapy as such inhibition can cause cells to enter a disordered mitotic state that renders them more susceptible to cell death. Indeed, there is evidence that inhibiting PP2A can slow tumor growth following radiotherapy in a range of cancer types including ovarian cancer, liver cancer, malignant glioma, pancreatic cancer, and nasopharyngeal carcinoma. In the present review, we discuss current understanding of the role of PP2A in tumor radiotherapy and the potential mechanisms whereby it may influence this process.

Radiotherapy is an important strategy for NSCLC. However, although a variety of comprehensive radiotherapy‐based treatments have dominated the treatment of NSCLC, it cannot be avoided to overcome the growing radioresistance during radiotherapy. The purpose of this study was to elucidate the radiosensitizing effects of NSCLC via knockdown GTSE1 expression and its mechanism. Experiments were performed by using multiple NSCLC cells such as A549, H460 and H1299. Firstly, we found GTSE1 conferred to radioresistance via clonogenic assay and apoptosis assay. Then, we detected the level of DNA damage through comet assay and γH2AX foci, which we could clearly observe knockdown GTSE1 enhance DNA damage after IR. Furthermore, through using laser assay and detecting DNA damage repair early protein expression, we found radiation could induce GTSE1 recruited to DSB site and initiate DNA damage response. Our finding demonstrated that knockdown GTSE1 enhances radiosensitivity in NSCLC through DNA damage repair pathway. This novel observation may have therapeutic implications to improve therapeutic efficacy of radiation.

Radiotherapy is one of the most important treatments for chest tumours. Although there are plenty of strategies to prevent damage to normal lung tissues, it cannot be avoided with the emergence of radiation-induced lung injury. The purpose of this study was to investigate the potential radioprotective effects of glucosamine, which exerted anti-inflammatory activity in joint inflammation. In this study, we found glucosamine relieved inflammatory response and structural damages in lung tissues after radiation via HE staining. Then, we detected the level of epithelial-mesenchymal transition marker in vitro and in vivo, which we could clearly observe that glucosamine treatment inhibited epithelial-mesenchymal transition. Besides, we found glucosamine could inhibit apoptosis and promote proliferation of normal lung epithelial cells in vitro caused by radiation. In conclusion, our data showed that glucosamine alleviated radiation-induced lung injury via inhibiting epithelial-mesenchymal transition, which indicated glucosamine could be a novel potential radioprotector for radiation-induced lung injury.