Male reproductive impairment linked to occupational ionizing radiation exposure in radiology workers.

Chitosan-based biopolymers for radioprotection: Mechanisms and biomedical applications in radiotherapy - A review.

SIRT2 mitigates radiation-induced oral mucositis by promoting homologous recombination-mediated DNA double-strand break repair in epithelial stem cells.

The evolving geopolitical landscape has heightened the probability of nuclear incidents, including accidental release or deliberate detonation, which can cause acute, life-threatening radiation injury to large populations. High-dose ionizing radiation (IR) is highly likely to cause radiation injury to the intestines and lead to intestinal radiation sickness. This study systematically explored the protective effect of cobalt chloride (CoCl2) on intestinal radiation injury and its preliminary mechanism from multiple levels, including cells, intestinal tissues, intestinal organoids, and live mice. The results showed that CoCl2 pretreatment could significantly enhance the radiation tolerance of mice, not only greatly improving the survival rate and multiple indicators such as intestinal injury score, but also maintaining the integrity of the small intestinal epithelial villi structure. At the same time, it promotes the proliferation and differentiation of intestinal organoids, inhibits the apoptosis of intestinal epithelial cells, and enhances the expression of barrier protection genes, thereby enhancing the intestinal resistance to radiation injury. Mechanism studies have shown that CoCl2 can up-regulate the expression of hypoxia-inducible factor-2 α (HIF-2α) via hypoxia-mimetic action and activate downstream signaling pathways related to cell proliferation, anti-apoptosis, and angiogenesis. This study initially clarified the mechanism by which CoCl2 protects the intestinal tract from radiation injury, providing a scientific basis and strategic support for the development of new radiation protection targets. Its in-depth research and application transformation are expected to play an important role in the future field of nuclear radiation protection.

Despite their established clinical benefits, breast cancer screening examinations expose women to ionizing radiation (IR) and call for vigilance regarding protocols and practices. This study estimates the population attributable risk (PAR) of radiation-induced breast cancer in France in 2019 that is attributable to past exposure to IR through screening performed in women aged 40 to 74 years old. Breast cancer screening practices were reconstituted for the period 1980 to 2019. Records of recent years were built based on French National Health Data System. An estimation was made for earlier years based on the available literature and expert knowledge. Women diagnosed with a history of breast cancer before mammography were excluded. Absorbed glandular doses to the breast were modeled based on existing literature and reports on French practices. Excess breast cancer cases were estimated using 2 radiation-risk models (Biologic Effects of Ionizing Radiation VII and the International Commission on Radiological Protection). Of roughly 55 000 new breast cancer cases diagnosed in 2019 in women at least 40 years old, we estimate that approximately 27 might be attributable to past exposures to IR associated with breast cancer screening between the ages of 50 and 74 years. This leads to a PAR of 0.048%. In addition, about 16 cases might be attributable to screening between ages 40 and 49 years, with a PAR of approximately 0.030%. The contribution of breast cancer screening to the breast cancer burden in France is limited. Efforts to limit the dose delivered to the breast must continue.

Ionizing radiation promotes lung injury by inducing ferroptosis-driven senescence in epithelial cells via NCOA4-mediated ferritinophagy.

The National Academy of Sciences Biological Effects of Atomic Radiation (BEAR) Genetics Panel recommended no second-generation genetic damage study of the offspring of the atomic bombings in Japan.

Ionizing radiation (IR) exerts complex, dose-dependent biphasic effects on the central nervous system (CNS). This review systematically elucidates the mechanisms underlying the impact of high- and low-dose radiation on neurocognitive function. High-dose radiation (HDR) triggers severe DNA damage, oxidative stress, and neuroinflammatory cascades, leading to neuronal dysfunction, suppression of neurogenesis, and failure of neural circuit reorganization, ultimately resulting in persistent cognitive decline. In contrast, low-dose radiation (LDR) exhibits a unique dual nature: within certain thresholds, it can activate endogenous protective pathways-including DNA repair and antioxidant defenses-thereby promoting neural plasticity and network homeostasis and demonstrating adaptive responses and neuroprotective potential. The research paradigm is shifting from the traditional linear no-threshold (LNT) model towards a dynamic homeostasis model. Future research should prioritize the development of neuroprotective strategies during radiotherapy for high-dose exposure, optimize irradiation modalities, and develop novel radioprotective agents to improve patient outcomes. For LDR, it is crucial to delineate its biological effects and explore its potential for intervening in neurodegenerative diseases. This review aims to provide an integrated theoretical framework for understanding the dose-dependent biphasic regulation of radiation on neurocognition and to outline future directions for developing related protective and therapeutic strategies.

Perovskite solar cells (PSCs) offer unique advantages for space-based energy harvesting, combining cost-effective manufacturing with flexible, high power-to-weight devices that can reduce payload mass in deployable structures. Despite this promise, few reports have demonstrated the viability of this technology in realistic, space-based scenarios, where they are subjected to large temperature variations and hard radiation. Here, we present a comprehensive analysis of PSC performance in low Earth orbit (LEO). The champion rigid cell exhibited relatively stable in-orbit performance at ∼80% of initial efficiency over a 44-day measurement interval that concluded nearly 100 days after launch, corresponding to ∼1600 orbital eclipse cycles and temperature ranges from -25 to 35°C. Mission data was systematically compared with laboratory measurements of rigid and ultrathin flexible PSCs across temperatures from -80 to +80°C and upon exposure to high-energy proton radiation. Flexible devices retained over 92% efficiency after a proton dose equivalent to 50 years in orbit. Despite this radiation tolerance, mitigating pre-flight environmental degradation remains a challenge for ultrathin substrates. Combined, this study bridges the gap between short suborbital demonstrations and long-term orbital performance, highlighting the potential of PSCs as a low-cost, resilient alternative for light harvesting, even in harsh space environments.

A bstract We derive a factorization formula for boosted double resonant top-antitop pair production in e + e − annihilation with a semileptonic top quark decay in the phase space region where the b -jet invariant mass is small. The decaying top quark state is defined through invariant mass measurements on the final states in the top and antitop hemispheres, and the b -jet is defined from clustering all hadrons in the top hemisphere. The factorization does not rely on the narrow width limit and accounts for the QCD off-shell and interference effects. The approach employs Soft-Collinear-Effective Theory and boosted Heavy-Quark-Effective-Theory and relies on a combination of factorization theorems known from e + e − dijet production and inclusive semileptonic heavy meson endpoint decays. The result provides a first principles treatment of the dominant hadronization effects, which can be determined from e + e − event shapes. In the factorization a new distribution function arises, called the ultra-collinear-soft (ucs) function, which encodes the Fermi motion of the decaying top quark within the state defined from the invariant mass measurement. The ucs function is a differential generalization of the inclusive bHQET jet function and shares properties of the shape function in semileptonic heavy meson decays. In frames where the top quark is very slow, it describes the coherent soft radiation arising from top production, propagation and decay, and encodes all effects that are non-factorizable from the perspective of the NW limit. Its form and renormalization depend on two light-cone momenta related to the top-jet and b -jet directions and their relative angle. Due to the large top quark width, the ucs function can be computed perturbatively, and we determine the QCD corrections at 𝒪( α s ). The anomalous dimension is known to three loops.

Bone marrow mesenchymal stem/stromal cells (BM-MSCs) are important components of bone marrow, possessing multipotent differentiation potential and the ability to support hematopoiesis. Exposure to ionizing radiation (IR) induces cellular damage in BM-MSCs, such as DNA lesions and mitochondrial dysfunction. Despite their relative radioresistance, most surviving BM-MSCs enter senescence post-irradiation. This senescent state disrupts the bone marrow niche, impairs stem cell proliferation and differentiation, and contributes to acute radiation syndrome (ARS) and myelosuppression. To clarify the impact of IR on BM-MSCs, this review systematically summarizes the general mechanisms of radiation-induced cellular senescence, examines the effects of different radiation types (e.g., gamma rays, X-rays, and heavy-ion radiation) and doses on BM-MSCs senescence, and outlines senotherapeutic strategies targeting BM-MSCs senescence. The analysis indicates that the senescence of BM-MSCs caused by IR is type- and dose-dependent. The review identifies key factors in IR-induced BM-MSCs senescence to guide targeted interventions, highlighting the need for future studies to elucidate the underlying mechanisms of IR-induced BM-MSCs senescence.

Gastrointestinal (GI) carcinomas are among the leading cause of cancer-related deaths worldwide, and chemoradioresistance severely limits the long-term effectiveness of their treatment. Aldo-keto reductase family 1 member C3 (AKR1C3) is a therapeutic target in cancer treatment, particularly for addressing therapy resistance. The objective of present study was to explore the potential of natural, structurally similar coumarins to target AKR1C3 and improve sensitivity of cancer cells to chemotherapy and ionizing radiation (IR). Upon identification of potential targets, interactome mapping and gene set enrichment analyses were carried out, and the expression of AKR1C3 was assessed in GI samples. Coumarins were subjected to molecular docking and dynamics simulations to provide insight into their binding propensity with AKR1C3. For experimental validation, umbelliprenin (UMB) was extracted from Ferula persica by preparative thin layer chromatography, and then, KYSE-30 cells were treated with UMB, alone and in combination with paclitaxel (PTX) for 48h. Additionally, cells were pretreated with UMB, exposed to IR (3-6Gy), and recovered for 72h. At the end of combinatorial treatments, cells were evaluated for viability and apoptosis. Predictions indicated AKR1C3 as a potential target of esculetin, scopoletin, umbelliferone and UMB. Enrichment analyses confirmed the involvement of AKR1C3 in several biological processes and pathways, and expression analyses indicated upregulation of AKR1C3 in pancreatic, liver and esophageal carcinomas. Molecular docking and dynamics simulations revealed favorable and stable interactions of coumarins with the NADPH binding site of AKR1C3. Experimental studies revealed significant (p < 0.0001) enhancement in the cytotoxicity and apoptosis-inducing effects of 5 nM PTX upon combinatorial use with 100 µM UMB. Moreover, 48h pretreatment with UMB significantly (p < 0.01) enhanced IR-induced cytotoxicity and apoptosis. The present findings highlight the potential of natural coumarins, particularly UMB, to inhibit the reductase activity of AKR1C3, thereby enhancing the efficacy of chemotherapy and radiotherapy. This positions UMB as a promising candidate for overcoming chemoradioresistance in GI carcinomas and paves the way for the development of innovative therapeutic strategies.

The 1956 recommendation by the US National Academy of Sciences (NAS) Biological Effects of Atomic Radiation (BEAR) I Genetics Panel to transition from a threshold to a linear dose response model for hereditary effects had a profound impact on environmental/occupational risk assessment, affecting policies/practices of US regulatory agencies, having much influence on regulations worldwide to the present. The recommendation gained influence due to the authority of the NAS, the prestige of the Panel, and the claim of a striking degree of uniformity among six independent estimates of radiation-induced hereditary risk. This claim was orchestrated by panelist James Crow who removed conflicting findings from the nine panelists who submitted estimates, acting with the approval of the entire Panel. These misrepresentations were ensured by the US NAS President who refused to share the Panel's technical reports and related documents with the scientific community. Ironically, the mouse mutation rate data used by the panelists who calculated risk estimates for either mouse or Drosophila were incorrect due to falsification by panelist William Russell without their knowledge. This action led to greatly exaggerated mutation risks and enhanced their overall false impression of agreement/scientific convergence. The actions of Crow were such that the already grossly inflated and falsified risk estimates of the panelists were made to appear in reasonably good agreement. These massive and compounded errors and deceptions have significantly affected regulatory practices for cancer risk assessment in the US and globally to the present. The present paper provides for the first time in the scientific literature an assessment of the unpublished technical reports of each of the nine participating geneticists of the BEAR I Genetics Panel and provides the basis for the above critical conclusions.

Radiation-based medical techniques and devices provide significant benefits to patients through the diagnosis, treatment, and management of illness and disease. Documenting trends and frequency of use offer important insights into radiation protection and help address gaps in the documentation of medical exposures. Here, we present the retrospective Canadian data collected for the recent United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) global survey on medical exposure. The global survey included three modality categories: diagnostic and interventional radiology, nuclear medicine, and radiotherapy and reports the total number of devices, physicians, examinations, and procedures. Due to the inability to collect high-quality dose data from Canadian sources, the average doses for specific examinations and treatments were estimated using internationally pooled data. The total annual per capita dose from medical exposures was determined to be 1.56 mSv, excluding radiotherapy, resulting in approximately 47% of all radiation doses received by Canadians, compared to natural, industrial, and consumer product sources. This assessment of Canadian medical radiation exposures contributes to global improvement of patient protection, helps establish trends, and identifies where Canadian data collection is lacking, particularly dose data.

According to the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) publications, contributions of terrestrial gamma doses are mainly from the presence of 40K, and of 238U and 232Th together with their progeny in various rocks and soils. A survey of soil distributions of radionuclides 40K, 238U, and 232Th was performed at the Nevada National Security Site (NNSS) using in situ gamma-ray spectrometry with a high-purity germanium (HPGe) detector. The average activity concentrations of 40K, 238U, and 232Th in natural soils at the NNSS are 867 Bq kg-1 (range from 150 ± 8 to 1297 ± 56 Bq kg-1), 50 Bq kg-1 (range from 29 ± 3 to 74 ± 8 Bq kg-1), and 56 Bq kg-1 (range from 11 ± 2 to 96 ± 10 Bq kg-1), respectively. The concentration at each location is significantly associated with its geological lithology. The terrestrial gamma dose rates around the NNSS were estimated from 26 to 144 nSv h-1 with mean value of 93 nSv h-1. Our results provide useful information about the natural background radiation and radiological effects of naturally occurring radionuclides at the NNSS.

Reactive oxygen species (ROS) potentially affected survival rate after ionizing radiation in scallops.

Yinhuo Tang alleviates ionizing radiation injury via modulating PI3K-Akt signaling and metabolomics in mice.

Radiation Dose and Lymphedema Risk After Immediate Lymphatic Reconstruction and Axillary Lymph Node Dissection: Radiation Dose and Lymphedema Risk after ALND and IL.

NCOA4-Mediated Ferroptosis Drives cGAS-STING-Dependent Inflammation in Radiation Dermatitis: Protective Modulation by Cu-ATSM.

Senescent cells accumulate with age and after exposure to various stresses, contributing to chronic diseases and cancer, effects largely driven by the senescence-associated secretory phenotype (SASP). Recent evidence indicates that a subset of senescent cells exhibits immunogenic properties. However, the extent to which immunogenicity depends on the cell type and the senescence inducer remains unclear. In this study, we evaluated the immunogenic properties of various human cell types induced to senesce following exposure to ionizing radiation (IR) or oncogenic RAS. Specifically, we used human dermal fibroblasts (HDF) and induced pluripotent stem cell (iPSC)-derived myoblasts (i-MB), endothelial cells (i-EC), lung progenitor cells (i-LPC), along with immune cells from autologous donors. Our results showed that cell types exhibit a distinct SASP and express a variety of inhibitory immune ligands. Notably, senescent HDF displayed a unique immunopeptidome but failed to elicit specific immune responses from CD8+ T cells or NK cells. Similarly, senescent i-EC and i-LPC exhibited limited immunogenicity. In contrast, RAS-induced senescent myoblasts demonstrated immunogenicity, characterized by T cell activation, NK cell-mediated cytotoxicity, and immune cell recruitment in an orthotopic humanized mouse model. These findings highlight the influence of cell type and senescence inducer on immunogenicity and suggest that targeted strategies will be necessary to address the deleterious consequences of the accumulation of distinct senescent cell types.