Radiation Injury
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Life ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 99
Weihong Li ◽  
Shixiang Zhou ◽  
Meng Jia ◽  
Xiaoxin Li ◽  
Lin Li ◽  

Accurate dose assessment within 1 day or even 12 h after exposure through current methods of dose estimation remains a challenge, in response to a large number of casualties caused by nuclear or radiation accidents. P53 signaling pathway plays an important role in DNA damage repair and cell apoptosis induced by ionizing radiation. The changes of radiation-induced P53 related genes in the early stage of ionizing radiation should compensate for the deficiency of lymphocyte decline and γ-H2AX analysis as novel biomarkers of radiation damage. Bioinformatic analysis was performed on previous data to find candidate genes from human peripheral blood irradiated in vitro. The expression levels of candidate genes were detected by RT-PCR. The expressions of screened DDB2, AEN, TRIAP1, and TRAF4 were stable in healthy population, but significantly up-regulated by radiation, with time specificity and dose dependence in 2–24 h after irradiation. They are early indicators for medical treatment in acute radiation injury. Their effective combination could achieve a more accurate dose assessment for large-scale wounded patients within 24 h post exposure. The effective combination of p53-related genes DDB2, AEN, TRIAP1, and TRAF4 is a novel biodosimetry for a large number of people exposed to acute nuclear accidents.

2022 ◽  
Kiran Maan ◽  
Ruchi Baghel ◽  
Radhika Bakhshi ◽  
Seema Dhariwal ◽  
Ritu Tyagi ◽  

A comprehensive overview of combining data from LC-MS and NMR using multiblock-OPLSDA analysis, correlation networking and pathway enrichment. This provided novel avenues for understanding biological perturbations post radiation injury.

2022 ◽  
Laura E. Ewing ◽  
Prabath G. Biju ◽  
Rupak Pathak ◽  
Stepan Melnyk ◽  
Martin Hauer-Jensen ◽  

ScienceAsia ◽  
2022 ◽  
Vol 48 (1) ◽  
pp. 89
Jin Xie ◽  
Ke Zhu ◽  
Qingya Wang ◽  
Pei Zhao ◽  
Lihua Pan ◽  

2021 ◽  
Vol 11 (2) ◽  
pp. 29-34
Alok Kumar Soni ◽  
Ankita Soni ◽  
Neeraj Upmanyu ◽  
Gurusamy Mathu Kannan

2021 ◽  
Vol 66 (6) ◽  
pp. 34-38
T. Bichkova ◽  
I. Andrianova ◽  
O. Nikitenko ◽  
N. Stavrakova ◽  
I. Parfenova ◽  

Purpose: Assessing the role of various factors in the formation of radioresistance is an important branch of radiobiology. The quality of drinking water, as it turned out, can significantly affect radioresistance. Against the background of studying the antiradiation properties of various types of water, differing in mineral and isotopic composition, the problem of the influence of tap water on the course of radiation injury remained underestimated. This circumstance determined the purpose of the work: to evaluate the modifying effect of tap water on the course of acute radiation sickness after X-ray irradiation of mice at an average lethal dose. Material and methods: Female ICR (CD-1) mice were irradiated with an average lethal dose once – 6.5 Gy of X-ray irradiation. After irradiation, half of the mice received tap water as drinking water, and the other half received artificially mineralized drinking water. Results: Keeping animals on tap water significantly reduced the survival rate of mice both with a single dose (log-rank test p=0.02, χ2=5.38) compared with animals receiving artificially mineralized distilled water. In addition, in the group of mice that received tap water, an increase in the rate of death of mice and a lower preservation of the group mass of animals during the development of acute radiation injury was noted. Conclusion: Tap water, used as drinking water, increases the damaging effect of radiation when X-rays are irradiated in mice.

2021 ◽  
W. June Brickey ◽  
Michael A. Thompson ◽  
Zhecheng Sheng ◽  
Zhiguo Li ◽  
Kouros Owzar ◽  

Radiation can be applied for therapeutic benefit against cancer or may result in devastating harm due to accidental or intentional release of nuclear energy. In all cases, radiation exposure causes molecular and cellular damage, resulting in the production of inflammatory factors and danger signals. Several classes of innate immune receptors sense the released damage associated molecules and activate cellular response pathways, including the induction of inflammasome signaling that impacts IL-1β/IL-18 maturation and cell death. A previous report indicated inflammasomes aggravate acute radiation syndrome. In contrast, here we find that inflammasome components do not exacerbate gamma-radiation-induced injury by examining heterozygous and gene-deletion littermate controls in addition to wild-type mice. Absence of some inflammasome genes, such as caspase-1/11 and Nlrp3, enhance susceptibility of treated mice to acute radiation injury, indicating importance of the inflammasome pathway in radioprotection. Surprisingly, we discover that the survival outcome may be sex-dependent as more inflammasome-deficient male mice are susceptible to radiation-induced injury. We discuss parameters that may influence the role of inflammasomes as radioprotective or radioexacerbating factors in recovery from radiation injury including the use of littermate controls, the sex of the animals, differences in microbiota within the colonies and other experimental conditions. Under the conditions tested, inflammasome components do not exacerbate radiation injury, but rather provide protective benefit.

2021 ◽  
Vol 3 (Supplement_6) ◽  
pp. vi9-vi10
Motomasa Furuse ◽  
Shinji Kawabata ◽  
Masahiko Wanibuchi ◽  
Hiroyuki Shiba ◽  
Koji Takeuchi ◽  

Abstract Background: Re-irradiation had a higher rate of radiation injury because recurrent MG had already irradiated in the first-line treatment. Recently, combination therapy of re-irradiation and bevacizumab showed a lower incidence of radiation injury than re-irradiation alone. Boron neutron capture therapy (BNCT), a tumor-selective particle radiation therapy, also increased radiation injury for recurrent MG, despite the greater focus on tumor cells. In this study, we evaluated the efficacy of BNCT plus bevacizumab with early induction after BNCT. Methods: Patients with recurrent MG were prospectively enrolled in this study. BNCT was performed using Kyoto University Research Reactor as a neutron source. Bevacizumab of 10 mg/kg was initiated 1–4 weeks after BNCT and was continued every 2–3 weeks until disease progression. Newly-diagnosed (de novo) glioblastoma was categorized as primary GBM (pGBM). Other MG were categorized as non-pGBM. Results: Kyoto University Research Reactor stopped irradiation for clinical use in February 2019. Twenty-five patients (14 pGBM and 11 non-pGBM) were treated with this combination therapy between June 2013 and February 2019. The median Overall survival (OS) after BNCT was 21.4 months for pGBM and 73.6 months for non-pGBM, respectively (p = 0.0428). The median progression-free survival (PFS) after BNCT was 8.3 months for pGBM and 15.6 months for non-pGBM, respectively (p = 0.0207). The objective response rate was 72 %. Alopecia occurred in all patients. Adverse events ≥ grade 3 were grade 3 proteinuria in four patients, grade 5 myocardial infarction in one patient, and grade 5 meningitis in one patient. Conclusion: BNCT plus bevacizumab showed a long OS and a long PFS, compared to our previous studies of BNCT alone for recurrent MG. Bevacizumab could provide beneficial effects not only for tumor itself, but also radiation injury. Further research with a larger sample using accelerator-based BNCT and bevacizumab is required to elucidate the efficacy and safety of this combination therapy.

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