The National Institute of Radiological Sciences (放射線医学総合研究所) (NIRS) is a radiation research institute in Japan. The NIRS was established in 1957 as the Japan's only one institute of radiology. The NIRS maintains various ion accelerators in order to study the effects of radiation of the human body and medical uses of radiation.The National Institute of Radiological Sciences hospital established in 1961 is a research hospital with a basic focus on radiation therapy. In 1993 the HIMAC (Heavy Ion Medical Accelerator in Chiba) of NIRS was launched, and in 1997 the Research Center for Charged Particle Therapy was opened as one of the leading medical centers using carbon ions are in operation. On April 1, 2016, the Japan Atomic Energy Agency (JAEA) transferred some of its laboratories to the NIRS, and the NIRS body was renamed to the National Institutes for Quantum and Radiological Science and Technology (QST) which includes existing laboratories of the NIRS; the NIRS is currently a radiological research division of the QST.
A validation of the ITER real-time reconstruction algorithms for the plasma current, centroid position, boundary and for the poloidal beta has been performed using the data collected during the first operation of the JT-60SA tokamak. The accuracy of the reconstruction is evaluated against plasma equilibria computed with the CREATE-NL nonlinear code. As it will be shown, although the setup of the magnetic sensors during JT-60SA first operation included a reduced number of sensors compared to what envisaged in the ITER setup and for JT-60SA next campaigns, the ITER requirement on the estimation of the plasma current are met. This is not the case for the plasma centroid position and shape due to the small number of available flux loops and the absence of Mirnov coils which measure the normal component of the magnetic field. The obtained results for the real-time estimation of the plasma position and shape are anyway promising, taking into account that the lacking measurements will be available in the future, both for JT-60SA and at ITER. Finally, a fast method for the poloidal beta estimation is compared with the JT-60SA poloidal beta real-time estimation algorithm.
Enhanced bulk-etch-rate of PADC (polyallyl diglycol carbonate) detectors exposed to gamma rays has been found to be described well as an exponential function of the product of the radiation chemical yield of hydroxyl group (GOH) and the adsorbed dose (D) at different dose-rates between 0.41 and 8.14 Gy/s. The examined absorbed doses were ranging from 30 to 100 kGy, comparable with the local dose in proton tracks. By matching the bulk-etch-rates and the GOH values obtained under identical conditions on dose-rate, the following equation was derived for the relative bulk-etch-rate, Virra/Vb = exp(y.GOH.D), where, Virra and Vb denote the bulk-etch-rates after and before gamma irradiations, respectively, and y is an experimentally obtained constant in a unit of kg/mol, with a value of y = 5.98. In this relation, significant dose-rate dependence is explained as the dose-rate dependence of the GOH value. This means that the radiation damage that increases the bulk-etch-rate is the hydroxyl group itself, and y appears as a constant specific to PADC which relates the damage to bulk-etch-rate. Here, y is termed the "etching coefficient ".
Carbon-ion radiotherapy (CIRT) offers high-dose concentration and enhanced biological effects. Since 2016, a nationwide prospective registry study of CIRT for locally advanced non-small cell lung cancer (LA-NSCLC) has been conducted in Japan. This study aimed to evaluate clinical outcomes of CIRT in patients with LA-NSCLC who were ineligible for surgery or chemoradiotherapy (CCRT). Patients with inoperable LA-NSCLC treated with CIRT in Japan from May 2016 to June 2020 were included. Most patients received 64–72 Gy in 16 fractions per the Japanese Society for Radiation Oncology (JASTRO) unified policy. Elective nodal irradiation was allowed for nodal disease. No systemic therapy was administered before or after CIRT. Overall and progression-free survival were estimated by the Kaplan–Meier method; local failure was evaluated using the cumulative incidence function (CIF) with Gray’s test. Two-sided P < 0.05 was considered significant. Median follow-up was 28 months for all patients and 36 months for survivors. Of the 55 patients, clinical stages (UICC 8th) were: IIB (26), IIIA (17), and IIIB (12). A clinical diagnosis without histological confirmation was established in four patients (7.3
Congenital intestinal atresia (IA) is a birth defect characterised by the absence or closure of part of the intestine. Although genetic factors are implicated, mechanistic understanding has been hindered by the lack of suitable animal models. Here, we describe a medaka (Oryzias latipes) mutant, generated by N-ethyl-N-nitrosourea (ENU) mutagenesis, that develops IA during embryogenesis. Positional cloning identified a nonsense mutation in mypt1, encoding myosin phosphatase target subunit 1. Mutant embryos exhibited ectopic accumulation of F-actin and phosphorylated myosin regulatory light chain (Mrlc) in the intestinal epithelium, consistent with disrupted actomyosin regulation. These cytoskeletal abnormalities were accompanied by epithelial disorganisation, without notable alterations in cell proliferation, motility or apoptosis. Inhibition ofmyh11a, encoding smooth muscle (SM) myosin heavy chain, ameliorated the IA phenotype, whereas blebbistatin treatment completely rescued the defect, suggesting a non-contractile role prior to SM maturation. Together, these findings demonstrate that mypt1 loss disrupts intestinal morphogenesis through actomyosin dysregulation. Given the recent clinical identification of IA associated with MYPT1 variants, this medaka model offers a valuable platform to investigate the developmental and molecular basis of MYPT1-associated IA in humans.
For medical applications of photosensitization, it is crucial to identify the reactive species generated. Previous studies have shown that during photosensitization, the nitrone spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) converts singlet oxygen (1O2) to hydroxyl radical (•OH), producing the electron spin resonance (ESR) signal of DMPO-OH adduct. This signal is strongly enhanced by biological reductants such as reduced β-nicotinamide adenine dinucleotide phosphate, reduced glutathione, or phenolic compounds. In this study, we investigated the mechanism of DMPO-OH formation and the role of reductants during uroporphyrin-mediated photosensitization in an aqueous solution. Kinetic analyses revealed that the initial rate of DMPO-OH formation remained constant despite varying reductant concentrations. 1O2 was found to react with DMPO independently of reductants, as indicated by oxygen consumption. Similarly, the formation of •OH, monitored via 2,3-dihydroxybenzoic acid derived from salicylic acid, increased in the presence of DMPO regardless of the presence of reductants. Both DMPO-OH formation and oxygen consumption decreased under alkaline conditions. When the spin traps, 5-(diethoxyphosphoryl)-5-methyl-1-pyrroline-N-oxide (DEPMPO), 5-ethoxycarbonyl-5-methyl-1-pyrroline-N-oxide (EMPO), 5-tert-butoxycarbonyl-5-methyl-1-pyrroline-N-oxide (BMPO), and 3,3,5,5-tetramethyl-1-pyrroline-N-oxide (M4PO) were used, •OH adduct formation followed the order M4PO > DMPO > > DEPMPO, EMPO, BMPO; the opposite trend to that observed for pseudo-•OH adducts formation via nucleophilic substitution with water. These findings suggest that 1O2 electrophilically reacts with nitrone spin traps, and that •OH is likely released from the resulting hydroperoxide intermediate. Reductants may not contribute to the •OH generation but instead stabilize the DMPO-OH formed. This •OH adduct formation can be suppressed by using spin traps with electron-withdrawing substituents.
