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Thyroid cancer incidence increases worldwide annually, primarily due to factors such as ionizing radiation (IR), iodine intake, and genetics. Papillary carcinoma of the thyroid (PTC) accounts for about 80% of thyroid cancer cases. RET/PTC1 (coiled-coil domain containing 6 [CCDC6]-rearranged during transfection) rearrangement is a distinctive feature in over 70% of thyroid cancers who exposed to low doses of IR in Chernobyl and Hiroshima‒Nagasaki atomic bombings. This study aims to elucidate mechanism between RET/PTC1 rearrangement and IR in PTC. N-thy-ori-3-1 cells were subjected to varying doses of IR (2/1/0.5/0.2/0.1/0.05 Gy) of IR at different days, and result showed low-dose IR-induced RET/PTC1 rearrangement in a dose-dependent manner. RET/PTC1 has been observed to promote PTC both in vivo and in vitro. To delineate the role of different DNA repair pathways, SCR7, RI-1, and Olaparib were employed to inhibit non-homologous end joining (NHEJ), homologous recombination (HR), and microhomology-mediated end joining (MMEJ), respectively. Notably, inhibiting NHEJ enhanced HR repair efficiency and reduced IR-induced RET/PTC1 rearrangement. Conversely, inhibiting HR increased NHEJ repair efficiency and subsequent RET/PTC1 rearrangement. The MMEJ did not show a markable role in this progress. Additionally, inhibiting DNA-dependent protein kinase catalytic subunit (DNA-PKcs) decreased the efficiency of NHEJ and thus reduced IR-induced RET/PTC1 rearrangement. To conclude, the data suggest that NHEJ, rather than HR or MMEJ, is the critical cause of IR-induced RET/PTC1 rearrangement. Targeting DNA-PKcs to inhibit the NHEJ has emerged as a promising therapeutic strategy for addressing IR-induced RET/PTC1 rearrangement in PTC.

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Prenatal exposure to environmental factors may play an important role in the aetiopathogenesis of autism spectrum disorder (ASD). We aim to investigate the potential effects of low-dose x-rays from dental diagnostic x-rays on neurodevelopment and molecular mechanisms associated with ASD in developing zebrafish embryos. Zebrafish embryos were divided into four groups and exposed using a dental x-ray unit: control, 0.08, 0.15 and 0.30 seconds, which are exemplary exposure settings for periapical imaging. These exposure times were measured as 7.17, 23.17 and 63.83 mSv using optical stimulated luminescence dosimeters. At the end of 72 hours post-fertilization, locomotor activity, oxidant-antioxidant status, and acetylcholine esterase (AChE) activity were analyzed. Expression of genes related to apoptosis (bax, bcl2a, p53), neurogenesis (α1-tubulin, syn2a, neurog1, elavl3) and ASD (eif4eb, adsl2a, shank3) was determined by RT-PCR. Even at reduced doses, developmental toxicity was observed in three groups as evidenced by pericardial edema, yolk sac edema and scoliosis. Deleterious effects of dental x-rays on neurogenesis through impaired locomotor activity, oxidative stress, apoptosis and alterations in genes associated with neurogenesis and ASD progression were more pronounced in the 0.30s exposure group. Based on these results we suggest that the associations between ASD and low-dose ionizing radiation need a closer look.

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Objective To explore the differentially expressed mRNAs and related biological processes and pathways in fractional low-dose ionizing radiation (LDIR)-induced senescence of normal human bronchial epithelial (HBE) cells by high-throughput mRNA sequencing and bioinformatics techniques. Methods Senescence-associated β-galactosidase staining and senescence-associated secretion phenotype gene mRNA and protein expression levels were measured at 24 and 48 h after irradiating HBE cells 7 times at doses of 0, 50, 100, and 200 mGy, respectively. The differentially expressed genes were screened by high-throughput sequencing for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Results The senescence-positive area of fractional low-dose irradiated HBE cells increased in a dose-dependent manner (P < 0.05). The mRNA levels and protein expression of transforming growth factor-β1(TGF-β1) and matrix metalloproteinase-9(MMP-9) genes were increased in the 100 mGy × 7 and 200 mGy × 7 groups at 24 and 48 h after the end of irradiation compared with the control group. High-throughput sequencing showed that there were 882, 475, and 1205 differentially expressed mRNAs in each dose group compared with the control group. GO analysis showed that the differentially expressed mRNAs in each dose group were mainly enriched in biological processes such as cell cycle regulation, regulation of nitrogen compound metabolic process, regulation of cell division and response to stimulus. KEGG analysis showed that the differentially expressed mRNAs were mainly enriched in the pathways of cell cycle, cell senescence, and ferroptosis. Conclusion Fractional LDIR induced senescence in HBE cells, and differentially expressed mRNA-associated biological processes and pathways in senescent cells are related to cell cycle and cell senescence.

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Objective To investigate the mechanism of fractionated low-dose ionizing radiation (LDIR) in the induction of EA.hy926 cell senescence. Methods EA.hy926 cells were irradiated with X-ray at 0, 50, 100, and 200 mGy × 4, respectively, and cultured for 24, 48, and 72 h. Several indicators were measured, including the levels of cellular senescence-associated β-galactosidase (SA-β-gal) staining, mRNA levels of senescence-associated cell cycle protein-dependent kinase inhibitor genes CDKN1A and CDKN2A, reactive oxygen species (ROS), total antioxidant capacity (T-AOC), and phosphorylated H2A histone family member X (γ-H2AX). Results After 4 fractionated LDIR, compared with the control group, the treatment groups showed increased nucleus area, blurred cell edge, and increased SA-β-gal positive area (P < 0.05) at 24, 48 and 72 h. After 4 fractionated LDIR, the mRNA level of CDKN1A increased in the 100 and 200 mGy × 4 groups at 24 and 48 h (P < 0.05), and CDKN2A mRNA level increased in the 100 and 200 mGy × 4 groups at 48 and 72 h (P < 0.05). The fluorescence intensity of ROS increased in treatment groups at 24, 48, and 72 h after 4 fractionated LDIR (P < 0.05). After 4 fractionated LDIR, the T-AOC level increased in the 100 and 200 mGy × 4 groups at 24 h (P < 0.05), and T-AOC level increased in all treatment groups at 48 and 72 h (P < 0.05). After 4 fractionated LDIR, γ-H2AX fluorescence intensity increased in all treatment groups at 24 h (P < 0.05), and the fluorescence intensity increased in the 100 and 200 mGy × 4 groups at 48 and 72 h (P < 0.05). Conclusion Fractionated LDIR can induce cellular senescence in EA.hy926 cells by impacting the cellular oxidation-antioxidation and oxidative damage levels, and the effects were relatively evident at 100 and 200 mGy.

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Traumatic brain injury (TBI) and stroke share a common pathophysiology that worsens over time due to secondary tissue injury caused by sustained inflammatory response. However, studies on pharmacological interventions targeting the complex secondary injury cascade have failed to show efficacy. Here, we demonstrated that low-dose ionizing radiation (LDIR) reduced lesion size and reversed motor deficits after TBI and photothrombotic stroke. Magnetic resonance imaging demonstrated significant reduction of infarct volume in LDIR-treated mice after stroke. Systems-level transcriptomic analysis showed that genes upregulated in LDIR-treated stoke mice were enriched in pathways associated with inflammatory and immune response involving microglia. LDIR induced upregulation of anti-inflammatory- and phagocytosis-related genes, and downregulation of key pro-inflammatory cytokine production. These findings were validated by live-cell assays, in which microglia exhibited higher chemotactic and phagocytic capacities after LDIR. We observed substantial microglial clustering at the injury site, glial scar clearance and reversal of motor deficits after stroke. Cortical microglia/macrophages depletion completely abolished the beneficial effect of LDIR on motor function recovery in stroke mice. LDIR promoted axonal projections (brain rewiring) in motor cortex and recovery of brain activity detected by electroencephalography recordings months after stroke. LDIR treatment delayed by 8 h post-injury still maintained full therapeutic effects on motor recovery, indicating that LDIR is a promising therapeutic strategy for TBI and stroke.

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Although ionizing radiation (IR) is widely used for therapeutic and research purposes, studies on low-dose ionizing radiation (LDIR) are limited compared with those on other IR approaches, such as high-dose gamma irradiation and ultraviolet irradiation. High-dose IR affects DNA damage response and nucleotide-protein crosslinking, among other processes; however, the molecular consequences of LDIR have been poorly investigated. Here, we developed a method to profile RNA species crosslinked to an RNA-binding protein, namely, human antigen R (HuR), using LDIR and high-throughput RNA sequencing. The RNA fragments isolated via LDIR-crosslinking and immunoprecipitation sequencing were crosslinked to HuR and protected from RNase-mediated digestion. Upon crosslinking HuR to target mRNAs such as PAX6, ZFP91, NR2F6, and CAND2, the transcripts degraded rapidly in human cell lines. Additionally, PAX6 and NR2F6 downregulation mediated the beneficial effects of LDIR on cell viability. Thus, our approach provides a method for investigating post-transcriptional gene regulation using LDIR.

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Diabetic liver injury (DLI) can result in several diseases of the liver, including steatohepatitis, liver fibrosis, cirrhosis, and liver cancer. Low­dose ionizing radiation (LDIR) has hormetic effects in normal/disease conditions. However, whether LDIR has a beneficial effect on DLI has not been assessed previously. MicroRNA (miR)­155 and its target gene suppressor of cytokine signaling 1 (SOCS1) play critical roles in modulating hepatic proliferation, apoptosis, and immunity. However, whether a miR­155­SOCS1 axis is involved in high glucose (HG) induced hepatic damage remains to be determined. In the present study, mouse hepatocyte AML12 cells were treated with 30 mM glucose (HG), 75 mGy X­ray (LDIR), or HG plus LDIR. The expression levels of miR­155 and SOCS1 were determined by reverse transcription­quantitative PCR and western blotting. Additionally, apoptosis was measured using flow cytometry. The release of inflammatory factors, including TNF­α, IL­1ß, IL­6, IL­10, and IFN­Î³, after HG and/or LDIR treatment was detected by ELISA. The results showed that HG may induce hepatic apoptosis by upregulating the levels of miR­155 and downregulating the levels of SOCS1. HG also stimulated the secretion of TNF­α, IL­1ß, IL­6, and IL­10. However, LDIR blocked the HG­induced activation of a miR­155­SOCS1 axis and suppressed the release of inflammatory factors. These results indicated that a miR­155­SOCS1 axis plays a role in HG­induced liver injury, and LDIR may exert a hepatoprotective effect by regulating the miR­155­SOCS1 axis.

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Understanding the structural and antibiotic resistance changes of microbial communities in space environments is critical for identifying potential pathogens that may pose health risks to astronauts and for preventing and controlling microbial contamination. The research to date on microbes under simulated space factors has primarily been carried out on single bacterial species under the individual effects of microgravity or low-dose radiation. However, microgravity (MG) and low-dose ionizing radiation (LDIR) coexist in the actual spacecraft environment, and microorganisms coexist as communities in the spacecraft environment. Thus, the microbial response to the real changes present during space habitation has not been adequately explored. To address this knowledge gap, we compared the dynamics of community composition and antibiotic resistance of synthetic bacterial communities under simulated microgravit, low-dose ionizing radiation, and the conditions combined, as it occurs in spacecraft. To ensure representative bacteria were selected, we co-cultured of 12 bacterial strains isolated from spacecraft cleanrooms. We found that the weakened competition between communities increased the possibility of species coexistence, community diversity, and homogeneity. The number of Bacilli increased significantly, while different species under the combined conditions showed various changes in abundance compared to those under the individual conditions. The resistance of the synthetic community to penicillins increased significantly under low doses of ionizing radiation but did not change significantly under simulated microgravity or the combined conditions. The results of functional predictions revealed that antibiotic biosynthesis and resistance increased dramatically in the community under space environmental stress, which confirmed the results of the drug sensitivity assays. Our results show that combined space environmental factors exert different effects on the microbial community structure and antibiotic resistance, which provides new insights into our understanding of the mechanisms of evolution of microorganisms in spacecraft, and is relevant to effective microbial pollution prevention and control strategies.

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The growing use of ionizing radiation (IR)-based diagnostic and treatment methods has been linked to increasing chronic diseases among patients and healthcare professionals. However, multiple factors such as IR dose, dose-rate, and duration of exposure influence the IR-induced chronic effects. The predicted links between low-dose ionizing radiation (LDIR) and health risks are controversial due to the non-availability of direct human studies. The studies pertaining to LDIR effects have importance in public health as exposure to background LDIR is routine. It has been anticipated that data from epidemiological and clinical reports and results of preclinical studies can resolve this controversy and help to clarify the notion of LDIR-associated health risks. Accumulating scientific literature shows reduced cancer risk, cancer-related deaths, curtailed neuro-impairments, improved neural functions, and reduced diabetes-related complications after LDIR exposure. In addition, it was found to alter evolutionarily conserved stress response pathways. However, the picture of molecular signaling pathways in LDIR responses is unclear. Besides, there is limited/no information on biomarkers of epidemiological LDIR exposure. Therefore, the present review discusses epidemiological, clinical, and preclinical studies on LDIR-induced positive effects in three chronic diseases (cancer, dementia, and diabetes) and their associated molecular mechanisms. The knowledge of LDIR response mechanisms may help to devise LDIR-based therapeutic modalities to stop disease progression. Modulation of these pathways may be helpful in developing radiation resistance among humans. However, more clinical evidence with additional biochemical, cellular, and molecular data and exploring the side effects of LDIR are the major areas of future research.

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Development of the hippocampus is critical for its normal maturation. However, there is no systematic study on the effects of low-dose (≤2 Gy) neonatal X-ray exposure on different cells at different developmental stages of the mouse hippocampus. The present study demonstrated that irradiation with 2 Gy at postnatal day (PD) 3 in mice induced anxiety and impairment of spatial learning and memory in adult mice. Neuroinflammatory cells were observed in the dentate gyrus (DG) and CA3 areas of the hippocampus at PD3 + 1. X-ray irradiation impaired neuronal complexity and neurogenesis. However, the number of astrocytes and microglia in the hippocampus was increased the first day after irradiation, and then decreased 21 days later. The protein expression levels of NF-κB, C/EBP homologous protein (CHOP), and γH2 A histone family member X (γH2 AX) increased from 7 to 21 days after irradiation, or till 90 days after irradiation for IL-1ß, whereas those of hippocampal sirtuin1 (SIRT1) decreased after 21 days of irradiation at PD3. These results suggest that neonatal X-ray irradiation-induced neuroinflammation impaired neuroplasticity and neurogenesis in the hippocampus, leading to the anxiety and spatial memory disorder during adulthood. The mechanisms involved in the induction of developmental neurotoxicity following low-dose irradiation may involve the inflammation-mediated signaling pathway IL-1ß/ SIRT1/CHOP.

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Due to the continuous development of nuclear power technology and the wide application of ionizing radiation in China, an increasing number of occupational groups and the general public have been exposed to the low-dose ionizing radiation environment. Consequently, research has focused on related health effects (carcinogenic and non-carcinogenic effects). There is no consensus on the health effects of long-term low-dose ionizing radiation exposure on populations. This article reviews the health effects of low-dose ionizing radiation identified worldwide to provide a scientific basis for investigating the mechanisms of such effects and developing population protection strategies.

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@#<b>Objective</b> To investigate the effects of lowdose ionizing radiation (LDIR) on oxidative stress and damage repair in human bronchial epithelial (HBE) cells. <b>Methods</b> HBE cells were divided into 0, 50, 100, and 200 mGy groups, and cultured for 24 and 48 h after X-ray irradiation, respectively. The cell viability, levels of glutathione (GSH), malondialdehyde (MDA), and 8-hydroxy-2’-deoxyguanosine (8-OHdG), and transcriptional levels of DNA damage repair genes <i>PPP2R2D</i> and <i>TP53</i> were measured. <b>Results</b> At 24 h after irradiation, there was no significant difference in the cell viability between the dose groups and the control group (<i>P</i> > 0.05); all dose groups had significantly increased MDA level, dose-dependently decreased GSH level, dose-dependently increased 8-OHdG level, and significantly increased mRNA level of <i>PPP2R2D</i> gene (all <i>P</i> < 0.05); the mRNA expression level of <i>TP53</i> gene was significantly increased in the 50 mGy group (<i>P</i> < 0.05). At 48 h after irradiation, there were the highest cell viability, significantly decreased MDA and 8-OHdG levels, and significantly increased mRNA expression levels of <i>PPP2R2D</i> and <i>TP53</i> genes in the 50 mGy group compared with the control group (all <i>P</i> < 0.05); the GSH level in the 100 mGy group was significantly increased (<i>P</i> < 0.05). <b>Conclusion</b> LDIR, especially radiation at 50 mGy, can affect the oxidative-antioxidant level in HBE cells and the transcript-level differential expression of DNA damage repair genes.

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As the environmental nuclear radiation pollution caused by nuclear-contaminated water discharge and other factors intensifies, more plant-microorganism-soil systems will be under long-term low-dose ionizing radiation (LLR). However, the regulatory mechanisms of the plant-microorganism-soil system under LLR are still unclear. In this study, we study a system that has been stably exposed to low-dose ionizing radiation for 10 years and investigate the response of the plant-microorganism-soil system to LLR based on the decay of the absorbed dose rate with distance. The results show that LLR affects the carbon and nitrogen migration process between plant-microorganism-soil through the "symbiotic microbial effect." The increase in the intensity of ionizing radiation led to a significant increase in the relative abundance of symbiotic fungi, such as Ectomycorrhizal fungi and Rhizobiales, which is accompanied by a significant increase in soil lignin peroxidase (LiP) activity, the C/N ratio, and C%. Meanwhile, enhanced radiation intensity causes adaptive changes in the plant functional traits. This study demonstrates that the "symbiotic microbial effect" of plant-microorganism-soil systems is an important process in terrestrial ecosystems in response to LLR.

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Objective: To investigate the effect of low-dose X-ray ionizing radiation on thyroid function of radiation workers. Methods: From January to December 2021, a total of 1039 medical workers in some tertiary hospitals in Wuhan were selected as the survey subjects, of which 518 radiation workers were selected as the exposure group, and 521 non-radiation workers were selected as the control group. The general conditions of the two groups were collected, and 5 indicators of thyroid function were measured, including total thyroxine (TT(4)) , total triiodothyronine (TT(3)) , free triiodothyronine (FT(3)) , thyroid stimulating hormone (TSH) , and free thyroxine (FT(4)) . The annual cumulative dose of ionizing radiation exposure in the exposure group was collected. Pearson χ(2) test and independent sample t test were used to compare the general conditions, 5 indicators of thyroid function and abnormal rate between the two groups. Linear regression model was used to analyze the correlation between the annual cumulative dose and 5 indicators of thyroid function in the exposure group. Binary logistic regression was used to analyze the influencing factors of thyroid dysfunction in the exposure group. Results: The TT(4) levels of the workers in the control group and the exposure group were (7.95±1.07) µg/dl and (8.26±1.41) µg/dl, respectively, and the FT(4) levels were (16.33±2.19) pmol/L and (17.15±2.42) pmol/L, respectively, the rate of thyroid dysfunction was 4.80% (25/521) and 8.49% (44/518) , and the above differences were statistically significant (P<0.05) . Linear regression analysis showed that the annual cumulative dose of the exposure group was significantly correlated with TT(4), TT(3), FT(4), and TSH (P<0.05) . For every 1 mSv increase in the annual cumulative dose, TT(4) increased by 1.661 µg/dl, FT(4) increased by 1.422 pmol/L, TT(3) decreased by 0.113 ng/ml, and TSH decreased by 0.731 µIU/ml. Binary logistic regression analysis showed that the older the radiation workers, the higher the risk of thyroid dysfunction (OR=1.080, 95% CI: 1.016-1.148, P=0.013) ; the greater the annual cumulative dose, the higher the risk of thyroid dysfunction (OR=6.400, 95%CI: 1.796-22.811, P=0.004) . Conclusion: The annual cumulative dose of low-dose X-ray ionizing radiation is positively correlated with thyroid function TT(4) and FT(4) of radiation workers, and negatively correlated with TT(3) and TSH; the greater the age and annual cumulative dose, the higher the risk of thyroid dysfunction.

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Mass rearing of insects of high biological quality is a crucial attribute for the successful implementation of sterile insect release programs. Various ontogenetic stages of Spodoptera litura (Fabr.) were treated with a range of low doses of ionizing radiation (0.25-1.25 Gy) to assess whether these gamma doses could elicit a stimulating effect on the growth and viability of developing moths. Doses in the range of 0.75 Gy to 1.0 Gy administered to eggs positively influenced pupal weight, adult emergence, and growth index, with a faster developmental period. The enhanced longevity of adults derived from eggs treated with 0.75 Gy and 1.0 Gy, and for larvae and pupae treated with 1.0 Gy, indicated a hormetic effect on these life stages. Furthermore, the use of these hormetic doses upregulated the relative mRNA expression of genes associated with longevity (foxo, sirtuin 2 like/sirt1, atg8) and viability/antioxidative function (cat and sod), suggesting a positive hormetic effect at the transcriptional level. These results indicated the potential use of low dose irradiation (0.75-1 Gy) on preimaginal stages as hormetic doses to improve the quality of the reared moths. This might increase the efficiency of the inherited sterility technique for the management of these lepidopteran pests.

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BACKGROUND: The thyroid-gut axis has a great influence on the maintenance of human health; however, we know very little about the effects of low-dose ionizing radiation (LDR) on thyroid hormone levels and gut microbiota composition. AIM: To investigate the potential effects of low-dose X-ray radiation to male C57BL/6J mice. METHODS: Peripheral blood was collected for enzyme-linked immunosorbent assay (ELISA), and stool samples were taken for 16S ribosomal RNA (rRNA) gene sequencing after irradiation. RESULTS: We found that LDR caused changes in thyroid stimulating hormone (TSH) levels in the irradiated mice, suggesting a dose-dependent response in thyroid function to ionizing radiation. No changes in the diversity and richness of the gut microbiota were observed in the LDR-exposed group in comparison to the controls. The abundance of Moraxellaceae and Enterobacteriaceae decreased in the LDR-exposed groups compared with the controls, and the Lachnospiraceae abundance increased in a dose-dependent manner in the radiated groups. And the abundances of uncultured_bacterium_g_Acinetobacter, uncultured_bacterium_ o_Mollicutes_RF39, uncultured_bacterium_g_Citrobacter, and uncultured_ bacterium_g_Lactococcus decreased in the radiated groups at the genus level, which showed a correlation with radiation exposure and diagnostic efficacy. Analysis of functional metabolic pathways revealed that biological metabolism was predicted to have an effect on functional activities, such as nucleotide metabolism, carbohydrate metabolism, and glycan biosynthesis and metabolism. Furthermore, Kyoto Encyclopedia of Genes and Genomes pathway annotation also suggested that changes in the gut microbiota were related to processing functions, including translation, replication and repair. CONCLUSION: LDR can change thyroid function and the gut microbiota, and changes in the abundances of bacteria are correlated with the radiation dose.

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While previous studies have focused on the health effects of occupational exposure of radiations on medical radiation workers, few have analyzed the dose-response relationship between low radiation doses and changes in blood parameters. Even fewer studies have been conducted on industrial worker populations. Using a prospective cohort study design, this study collected health examination reports and personal dose monitoring data from 705 industrial irradiation workers who underwent regular physical examinations at Dongguan Sixth People's Hospital. The dose-response effects of low-dose ionizing radiation on blood parameters were assessed using a generalized linear model and restricted cubic spline model. Red blood cell counts decreased then increased, before decreasing again with increasing ionizing radiation. This was in contrast to the curve of the total platelet count after irradiation. Additionally, a radiation dose of 2.904 mSv was the turning point for the nonlinear curve of hemoglobin count changes. In conclusion, long-term, low-dose ionizing radiation affects blood cell levels in industrial irradiation workers. There is a nonlinear dose-response relationship between red blood cell, platelet, and hemoglobin counts and the cumulative radiation dose. These findings should alert radiation workers to seek preventive medical treatment before the occurrence of any serious hematopoietic disease.

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We report the case of a patient in Massachusetts with early-stage Alzheimer's disease who was treated with low doses of ionizing radiation to the brain. He requested this treatment after reading about a patient with severe Alzheimer's in Michigan who improved remarkably after receiving 4 CT scans. After his first treatment in April 2016, mental clarity improved. His impaired conversation, reading, and sense of humor were restored, especially his virtuosic clarinet jazz-playing. However, executive function remained deficient. He requested a treatment every 2 weeks, but his neurologist denied this, fearing opposition to this treatment, a diagnostic procedure that used ionizing radiation. Limited recovery was observed after each CT scan, lasting from several weeks to months, depending on the endpoints/behavior and the periodicity. Despite the positive responses, the physician was reluctant to continue beyond 6 due to concerns about adverse effects and disapproval for prescribing them. The patient began hyperbaric oxygen therapy as an alternative. But after 43 treatments, no conclusive benefit was observed. The patient died in September 2020 at age 77. This experience suggests CT scans may have value in treating Alzheimer's patients and restoring, at least temporarily, important aspects of normal life activities. Such observations need testing and validation.

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Epidemiological studies of children's cancer risks associated with background gamma radiation exposure have used geographic exposure models to estimate exposure at their locations of residence. We measured personal exposure to background gamma radiation, and we investigated the extent to which it was associated with children's whereabouts. We collected data on whereabouts and exposure to background gamma radiation over a 5-day period among children aged 4-15 years in Switzerland. We used D-Shuttle dosimeters to measure children's exposure, and we asked parents to write their children's activities in diaries. We used Poisson mixed-effects and linear regression models to investigate the association of hourly and overall doses, respectively, with children's reported whereabouts. During the observed time, 149 participating children spent 66% indoors at home; 19% indoors away from home; and 15% outdoors. The mean personal exposure was 85.7 nSv/h (range 52.3 nSv/h-145 nSv/h). Exposure was 1.077 (95% CI 1.067, 1.087) times higher indoors than outdoors and varied by building material and (predicted) outdoor dose rates. Our study provides detailed information about children's patterns of exposure to background gamma radiation in Switzerland. Dwelling building materials and outdoor dose rates are important determinants of children's exposure. Future epidemiological studies may benefit from including information about building materials.

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