Radiation Medicine and Protection最新文献

Objective

Methods

Results

Conclusions

Objective

Methods

Results

Conclusion

Objective

Methods

Results

Conclusion

Objective

To investigate the effect and mechanism of Nup50 on radiation-induced DNA damage repair to radiation and explore the potential role of Nup50 as radioprotective target.

Methods

The Nup50 gene was knocked down in HUVEC cells using lentiviruses. Colony formation, CCK-8, and flow cytometry were performed to determine the viability, proliferation and apoptosis of HUVEC cells treated with γ-rays，respectively. The extent of DNA damage was evaluated by using comet assay and immunofluorescence staining against γ-H2AX. In addition, we explored the role of Nup50 in DNA damage response (DDR) pathways through western blotting assay. Finally, nuclear and chromatin fractionation were performed to determine the potential molecular mechanism underlying the radiation protection function of Nup50 knockdown.

Results

Nup50 knockdown increased the cellular resistance to ionizing radiation. The CCK-8 data showed that cell viability was significantly increased in the Nup50 knockdown group after radiation (t ​= ​4.23, P ​< ​0.01). The Nup50 knockdown group also showed more survived colonies (t ​= ​10.06, P ​< ​0.001), less apoptosis rate (t ​= ​3.78, P ​< ​0.05) and less unrepaired DNA damage. Furthermore, Nup50 knockdown increased radiation-activated phosphorylation levels of DNA-PKcs in HUVEC cells. Finally, the nuclear and chromatin fractionation data showed that inhibiting Nup50 increased the recruitment of DNA-PKcs to chromatin after DNA damage.

Conclusions

Our findings revealed that Nup50 knockdown promoted radioresistance in normal HUVEC cells by regulating DNA-PKcs pathway, suggesting Nup50 as a potential target for radiation protection.

Skin Exposure of skin to ionizing radiation can induce acute or chronic biological effects, resulting in radiation-induced skin injury (RSI). Premature cellular senescence, caused by oxidative stress and/or DNA damage from chemical or physical agents, leads to the decrease of cellular proliferation and physiological function. Persistent DNA damage and accumulation of senescent cells are associated with the progression of radiation-induced injury. Atopic dermatitis and RSI have similar inflammatory symptoms. The treatment of tacrolimus (TAC) in atopic dermatitis may be associated with premature cellular senescence. TAC can prevent the onset of cellular senescence by inactivating the p38 mitogen-activated protein kinase (p38 ​MAPK). The activation of p38 ​MAPK can induce the senescence-associated secretory phenotype (SASP) by enhancing the transcriptional activity of nuclear factor kappa-B (NF-κB), which ultimately leads to premature cellular senescence. FK506 binding protein 51 (FKBP51) exhibits resistance to ionizing radiation, but the mechanism of TAC regulation of ionizing radiation-induced premature senescence still needs further study. This review discusses the mechanism of cellular senescence in RSI and the role of TAC in both dermatitis and RSI.

Objective

To evaluate the health-care level (HCL), one of the most extensively used indicators to assess the level of medical exposure, and its influencing factors in China.

Methods

Based on the data from the China Statistical Yearbook of the National Bureau of Statistics and other public documents, HCL was calculated in terms of the number of physicians per head of population throughout the country. Multiple linear regression was used to analyze the association of HCL with main socioeconomic factors, including population size, area, number of administrative divisions and gross domestic product (GDP).

Results

Since 2015, there has been at least one physician for every 1,000 people in China on average. However, by 2019, there has yet been one physician for more than 1,000 people in each of two provinces. By 2020, there was at least one physician for every 1,000 people across all 31 provincial-level administrative districts (provinces). The population size and GDP were the influencing factors on HCL, with correlation coefficients of 0.416 and −0.583, respectively. Furthermore, a moderate correlation was found between HCL and the frequency of medical exposure (FME) to ionizing radiation (r ​= ​−0.620, P ​= ​0.028).

Conclusion

There has been at least one physician for every 1,000 people since 2015, but there are great differences between various provinces. HCL as an indicator to evaluate level of medical exposure is warranted further research in China.

This paper presents a comprehensive overview of the historical trajectory and development in biophoton studies over the past 100 years, with a particular focus on the recent progress regarding the pivotal role of biophoton in mediating radiation-induced bystander effects (RIBE). The exploration of biophoton mystery starts from the initial observation of mitogenetic radiation and continues to develop to the contemporary science of biophotonics. The properties and underlying mechanisms of biophoton emission are described with illustrative examples from diverse biological systems such as plants, animals and humans. The conclusive evidence of cell-to-cell communication facilitated by biophoton signaling is presented, followed by an elaborate interpretation of potential mechanisms through which biophoton mediates RIBE. The engagement of mitochondria and exosomes in this process is extensively clarified, by highlighting their significant roles in biophoton-mediated RIBE. The advances in biophoton research in respect of bystander response to ionizing radiation may offer profound insights into radiobiology and provide for possible future applications as well in radiation medicine and protection.

Bioinformatics has become increasingly integral to radiation biology, also known as radiobiology, providing substantial support through data storage, conversion, visualization, and sharing. This review aims to deepen understanding of bioinformatics application in radiobiology by introducing key databases and analytical tools in radiobiology, including general bioinformatics databases, radiobiology-specific databases, data processing tools, and statistical analysis tools for differentially expressed genes (DEGs) and LC/MS analysis. This review also discusses bioinformatics applications in radiobiological fields, such as radioresistance and immune cell enrichment. Despite these advances, challenges such as data interoperability remain. Methods and projects to address these issues, such as GeCo and GMQL, are also examined.

Objective

To assess if there is a relationship between residential radon exposure and two lung cancer histological types, small-cell carcinoma (diagnosed in people with a smoking history) and adenocarcinoma (the most commonly diagnosed histologic type in people who have never smoked) among males and females in Canada.

Methods

With survey data of long-term radon measurements in residential homes, long-term averaged tobacco consumption rates in the units of cigarettes per day per person and long-term averaged age-standardized lung cancer incidence rates at provincial level, simple linear fitting (ANOVA linear regression) was applied in this study to determine the effect on lung cancer induction by smoking and exposure to indoor radon, and to assess if there is a relationship between residential radon exposure and lung cancer histological types.

Results

Lung cancer incidence rates correlate very well with the tobacco consumption rates (P ​< ​0.05). However, females appear to be more likely than males to develop lung cancer at a given amount of cigarette consumption. For both small-cell carcinoma and adenocarcinoma, a statistically significant correlation between incidence rate and mean radon concentration was observed for females, the correlation was much stronger for adenocarcinoma (P ​= ​0.0057) than small-cell carcinoma (P ​= ​0.0483). However, there was no such correlation for males.

Conclusion

It is possible that female non-smokers are more susceptible to radon-induced lung cancer, and the joint effect of radon exposure and tobacco smoking may be worse in female smokers compared to males, such that higher incidence rate of adenocarcinoma among females compared to males were observed in recent decades, even though females never smoked more than males.